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Cardionerds: A Cardiology Podcast

作者: CardioNerds
最近更新: 5天前
Welcome to CardioNerds, where we bring you in-depth discussions with leading experts, case reports, ...

Recent Episodes

437. Atrial Fibrillation: The Diagnosis and Management of Atrial Flutter with Dr. Joshua Cooper

437. Atrial Fibrillation: The Diagnosis and Management of Atrial Flutter with Dr. Joshua Cooper

In this episode, the CardioNerds (Dr. Naima Maqsood, Dr. Akiva Rosenzveig, and Dr. Colin Blumenthal) are joined by renowned educator in electrophysiology, Dr. Joshua Cooper, to discuss everything atrial flutter; from anatomy and pathophysiology to diagnosis and management. Dr. Cooper’s expert teaching comes through as Dr. Cooper vividly describes atrial anatomy to provide the foundational understanding to be able to understand why management of atrial flutter is unique from atrial fibrillation despite their every intertwined relationship. A foundational episode for learners to understand atrial flutter as well as numerous concepts in electrophysiology. Audio editing for this episode was performed by CardioNerds intern Dr. Bhavya Shah.  CardioNerds Atrial Fibrillation PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls "The biggest mistake is failure to diagnose”. Atrial flutter, especially with 2:1 conduction, is commonly missed in both inpatient and outpatient settings so look carefully at that 12-lead EKG so you can mitigate the stroke and tachycardia induced cardiomyopathy risk  Decremental conduction of the AV node makes it more challenging to rate control atrial flutter than atrial fibrillation  Catheter Ablation is the first line treatment for atrial flutter and is highly successful, but cardioversion can be utilized as well prior to pursuing ablation in some cases.  Class I AADs like propafenone and flecainide may stability the atrial flutter circuit by slowing conduction and thus may worsen the arrhythmia. Therefore, the preferred anti-arrhythmic medication in atrial flutter are class III agents.  Atrial flutter can be triggered by firing from the left side of the heart, so in patients with both atrial fibrillation and flutter, ablating atrial fibrillation makes atrial flutter less likely to recur.  BONUS PEARL: Dr. Cooper’s youtube video on atrial flutter is a MUST SEE!  Notes Notes: Notes drafted by Dr. Akiva Rosenzveig  What are the distinguishing features of atrial fibrillation and flutter?  Atrial flutter is an organized rhythm characterized by a wavefront that continuously travels around the same circuit leading to reproducible P-waves on surface EKG as well as a very mathematical and predictable relationship between atrial and ventricular activity  Atrial fibrillation is an ever changing, chaotic rhythm that consists of small local circuits that interplay off each other. Consequently, no two beats are the same and the relationship between the atrial activity and ventricular activity is unpredictable leading to an irregularly irregular rhythm  What are common atrial flutter circuits?  Cavo-tricuspid isthmus (CTI)-dependent atrial flutter is the most common type of flutter. It is characterized by a circuit that circumnavigates the tricuspid valve.  Typical atrial flutter is characterized by the circuit running in a counterclockwise pattern up the septum, from medial to lateral across the right atrial roof, down the lateral wall, and back towards the septum across the floor of the right atrium between the IVC and the inferior margin of the tricuspid valve i.e. the cavo-tricuspid isthmus. Surface EKG will show a gradual downslope in leads II, III, and AvF and a rapid rise at end of each flutter wave.   Atypical CTI-dependent flutter follows the same route but in the opposite direction (clockwise). Therefore, we will see positive flutter waves in the inferior leads   Mitral annular flutter is more commonly seen in atrial fibrillation patients who’ve been treated with ablation leading to scarring in the left atrium.  Roof-dependent flutter is characterized by a circuit that travels around left atrium circumnavigating a lesion (often from prior ablation), traveling through the left atrial roof, down the posterior wall, and around the pulmonary veins  Surgical/scar/incisional flutter is seen in people with a history of prior cardiac surgery and have iatrogenic scars in right atrium due to cannulation sites or incisions  How does atrial flutter pharmacologic management differ from other atrial arrhythmias?  The atrioventricular (AV) node is unique in that the faster it is stimulated, the longer the refractory period and the slower it conducts. This characteristic is called decremental conduction. In atrial fibrillation, the atrial rate is so fast that the AV node becomes overwhelmed and only lets some of those signals through to the ventricles creating an irregular tachycardia but at lower rates. In atrial flutter, the atrial rate is slower, therefore the AV node has more capability to conduct allowing for higher ventricular rates. Therefore, to achieve rate control one will need a higher dose of AV blocking medications. Atrial tachycardia may require even higher doses due to the increased ability of the AV node to conduct, as the atrial rates are slower than in atrial flutter.  Sodium channel blockers (Class I) such as flecainide and propafenone slow wavefront propagation, making it easier for the AV node to handle the atrial rates. This will end up leading to increased ventricular rates which can be dangerously fast. That is why AV nodal blockers should be used in conjunction with flecainide and propafenone.  What is the role of cardioversion in atrial flutter management?  Due to high success rate with atrial flutter ablation, ablation is the first line treatment. However, sometimes cardioversion may be utilized in patients depending on how symptomatic they are and how long it will take to get an ablation. Cardioversion may also be utilized preferentially when the atrial flutter was triggered by infection or cardiac surgery to see if it will come back.   If cardioversion is pursued, the patient will need to be anticoagulated due to the stroke risk after the procedure due to post-conversion stunning.  How effective is atrial flutter ablation?  The landmark Natale et al study in 2000 demonstrated 80% success rate after radiofrequency ablation as compared to 36% in patients on anti-arrhythmic therapy. The LADIP study in 2006 further corroborated these findings. Contemporary data shows above 90% success rate of atrial flutter ablation.  In patients who have had both atrial fibrillation and atrial flutter, most electrophysiologists would ablate both. However, in patients with atrial fibrillation, the atrial flutter usually is initiated by trigger spots firing in the left atrium. Once the atrial fibrillation is ablated, the flutter will become less likely. Therefore, there are those who say there’s no need to ablate the flutter circuit as well. Alternatively, if a patient has severe comorbidities and/or is high risk for ablation, one may consider performing the atrial flutter ablation only since atrial flutter is harder to manage medically compared with atrial fibrillation.   How do you manage atrial flutter in the acute inpatient setting?  In the inpatient setting, electrical cardioversion is often limited by blood pressure and the hypotensive effects of the sedatives required. If one is awake and too hypotensive, chemical cardioversion can be pursued. The most effective anti-arrhythmic for this is ibutilide. Amiodarone is not effective for acute cardioversion. Since ibutilide prolongs refractoriness in atrial and ventricular tissue, there’s a risk of long QT induced torsades de pointes. Pretreating with magneisum reduces the risk to 1-2%.  References Jolly WA, Ritchie WT. Auricular flutter and fibrillation. 1911. Ann Noninvasive Electrocardiol. 2003;8(1):92-96. doi:10.1046/j.1542-474x.2003.08114.x  McMichael J. History of atrial fibrillation 1628-1819 Harvey - de Senac - Laënnec. Br Heart J. 1982;48(3):193-197. doi:10.1136/hrt.48.3.193  Lee KW, Yang Y, Scheinman MM; University of Califoirnia-San Francisco, San Francisco, CA, USA. Atrial flutter: a review of its history, mechanisms, clinical features, and current therapy. Curr Probl Cardiol. 2005;30(3):121-167. doi:10.1016/j.cpcardiol.200  2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2024;149(1):e167. doi:10.1161/  Cosío F. G. (2017). Atrial Flutter, Typical and Atypical: A Review. Arrhythmia & electrophysiology review, 6(2), 55–62. https://doi.org/10.15420/aer.2017.5.2  https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-11/Atrial-flutter-common-and-main-atypical-forms Natale A, Newby KH, Pisanó E, et al. Prospective randomized comparison of antiarrhythmic therapy versus first-line radiofrequency ablation in patients with atrial flutter. J Am Coll Cardiol. 2000;35(7):1898-1904. doi:10.1016/s0735-1097(00)00635-5  Da Costa A, Thévenin J, Roche F, et al. Results from the Loire-Ardèche-Drôme-Isère-Puy-de-Dôme (LADIP) trial on atrial flutter, a multicentric prospective randomized study comparing amiodarone and radiofrequency ablation after the first episode of symptomatic atrial flutter. Circulation. 2006;114(16):1676-1681. doi:10.1161/CIRCULATIONAHA.106.638395  https://www.acc.org/Membership/Sections-and-Councils/Fellows-in-Training-Section/Section-Updates/2015/12/15/16/58/Atrial-Fibrillation#:~:text=The%20first%20'modern%20day'%20account,in%20open%20chest%20animal%20models.&text=In%201775%2C%20William%20Withering%20first,(purple%20foxglove)%20in%20AFib.

5天前
30:07
436. Heart Failure: Pre-Heart Transplant Evaluation and Management with Dr. Kelly Schlendorf

436. Heart Failure: Pre-Heart Transplant Evaluation and Management with Dr. Kelly Schlendorf

In this episode, the CardioNerds (Dr. Rachel Goodman, Dr. Shazli Khan, and Dr. Jenna Skowronski) discuss a case of AMI-shock with a focus on listing for heart transplant with faculty expert Dr. Kelly Schlendorf. We dive into the world of pre-transplant management, discuss the current allocation system, and additional factors that impact transplant timing, such as sensitization. We conclude by discussing efforts to increase the donor pool.  Audio editing for this episode was performed by CardioNerds Intern, Julia Marques Fernandes. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Heart Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls The current iteration of heart allocation listing is based on priority, with status 1 being the highest priority.  The are multiple donor and recipient characteristics to consider when listing a patient for heart transplantation and accepting a heart offer.  Desensitization is an option for patients who need heart transplantation but are highly sensitized.  Protocols vary by center.  Acceptance of DCD hearts is one of many efforts to expand the donor pool   Notes Notes: Notes drafted by Dr. Rachel Goodman  Once a patient is determined to be a candidate for heart transplantation, how is priority determined?  The current iteration of heart listing statuses was implemented in 2018.  Priority is determined by acuity, with higher statuses indicating higher acuity and given higher priority.  Status 1 is the highest priority status, and Status 7 is inactive patients. (1,2)  What criteria should be considered in organ selection when listing a patient for heart transplant?  Once it is determined that a patient will be listed for heart transplantation, there are certain criteria that should be assessed.  These factors may impact pre-transplant care and/or donor matching (3).  (1) PVR  (2) Height/weight   (3) Milage listing criteria  (4) Blood typing/cPRA/HLA typing  What is desensitization and why would it be considered?  Desensitization is an attempt to reduce or remove anti-HLA antibodies in the recipient.  It is done to increase the donor pool.  In general, desensitization is reserved for patients who are highly sensitized.  Desensitization protocols vary by transplant center, and some may opt against it.  When considering desensitization, it is important to note two key things: first, there is no promise that it will work, and second desensitization involves the use of immunosuppressive agents, thereby putting patients at increased risk of infection and cytopenia. (4)  Can you explain DCD and DBD transplant?  DBD: donor that have met the requirements for legal definition of brain death.   DCD: donors that have not met the legal definition of brain death but have been determined to have circulatory death.  Because the brain death criteria have not been met, organ recovery can only take place once death is confirmed based on cessation of circulatory and respiratory function. Life support is only withdrawn following declaration of circulatory death—once the heart has stopped beating and spontaneous respirations have stopped. (5,6)  References 1: Maitra NS, Dugger SJ, Balachandran IC, Civitello AB, Khazanie P, Rogers JG. Impact of the 2018 UNOS Heart Transplant Policy Changes on Patient Outcomes. JACC Heart Fail. 2023;11(5):491-503. doi:10.1016/j.jchf.2023.01.009  2:  Shore S, Golbus JR, Aaronson KD, Nallamothu BK. Changes in the United States Adult Heart Allocation Policy: Challenges and Opportunities. Circ Cardiovasc Qual Outcomes. 2020;13(10):e005795. doi:10.1161/CIRCOUTCOMES.119.005795  3:  Copeland H, Knezevic I, Baran DA, et al. Donor heart selection: Evidence-based guidelines for providers. J Heart Lung Transplant. 2023;42(1):7-29. doi:10.1016/j.healun.2022.08.030  4: Kittleson MM. Management of the sensitized heart transplant candidate. Curr Opin Organ Transplant. 2023;28(5):362-369. doi:10.1097/MOT.0000000000001096  5:  Kharawala A, Nagraj S, Seo J, et al. Donation After Circulatory Death Heart Transplant: Current State and Future Directions. Circ Heart Fail. 2024;17(7):e011678. doi:10.1161/CIRCHEARTFAILURE.124.011678  6: Siddiqi HK, Trahanas J, Xu M, et al. Outcomes of Heart Transplant Donation After Circulatory Death. J Am Coll Cardiol. 2023;82(15):1512-1520. doi:10.1016/j.jacc.2023.08.006

3周前
32:11
435. Atrial Fibrillation: Chronic Management of Atrial Fibrillation with Dr. Edmond Cronin

435. Atrial Fibrillation: Chronic Management of Atrial Fibrillation with Dr. Edmond Cronin

CardioNerds (Dr. Kelly Arps, Dr. Naima Maqsood, and Dr. Elizabeth Davis) discuss chronic AF management with Dr. Edmond Cronin. This episode seeks to explore the chronic management of atrial fibrillation (AF) as described by the 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. The discussion covers the different AF classifications, symptomatology, and management including medications and invasive therapies. Importantly, the episode explores current gaps in knowledge and where there is indecision regarding proper treatment course, as in those with heart failure and AF. Our expert, Dr. Cronin, helps elucidate these gaps and apply guideline knowledge to patient scenarios. Audio editing for this episode was performed by CardioNerds intern Dr. Bhavya Shah. CardioNerds Atrial Fibrillation PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Review the guidelines- Catheter ablation is a Class I recommendation for select patient groups  Appropriately recognize AF stages- preAF conditions, symptomatology, classification system (paroxysmal, persistent, long-standing persistent, permanent)  Be familiar with the EAST-AFNET4 trial, as it changed the approach of rate vs rhythm control  Understand treatment approaches- lifestyle modifications, management of comorbidities, rate vs rhythm control medications, cardioversion, ablation, pulmonary vein isolation, surgical MAZE  Sympathize with patients- understand their treatment goals  Notes Notes: Notes drafted by Dr. Davis.    What are the stages of atrial fibrillation?   The stages of AF were redefined in the 2023 guidelines to better recognize AF as a progressive disease that requires different strategies at the different therapies  Stage 1 At Risk for AF: presence of modifiable (obesity, lack of fitness, HTN, sleep apnea, alcohol, diabetes) and nonmodifiable (genetics, male sex, age) risk factors associated with AF  Stage 2 Pre-AF: presence of structural (atrial enlargement) or electrical (frequent atrial ectopy, short bursts of atrial tachycardia, atrial flutter) findings further pre-disposing a patient to AF  Stage 3 AF: patient may transition between these stages  Paroxysmal AF (3A): intermittent and terminates within ≤ 7 days of onset  Persistent AF (3B): continuous and sustained for > 7 days and requires intervention  Long-standing persistent AF (3C): continuous for > 12 months   Successful AF ablation (3D): freedom from AF after percutaneous or surgical intervention  Stage 4 Permanent AF: no further attempts at rhythm control after discussion between patient and clinician   The term chronic AF is considered obsolete and such terminology should be abandoned   What are common symptoms of AF?   Symptoms vary with ventricular rate, functional status, duration, and patient perception  May present as an embolic complication or heart failure exacerbation  Most commonly patients report palpitations, chest pain, dyspnea, fatigue, or lightheadedness. Vague exertional intolerance is common  Some patients also have polyuria due to increased production of atrial natriuretic peptide  Less commonly can present as tachycardia-associated cardiomyopathy or syncope  Cardioversion into sinus rhythm may be diagnostic to help determine if a given set of symptoms are from atrial fibrillation to help guide the expected utility of more aggressive rhythm control strategies.   What are the current guidelines regarding rhythm control and available options?  COR-LOE 1B: In patients with reduced LV function and persistent (or high burden) AF, a trial of rhythm control should be recommended to evaluate whether AF is contributing to the reduced LV function   COR-LOE 2a-B: In patients with reduced LV function and persistent (or high burden) AF, a trial of rhythm control should be recommended to evaluate whether AF is contributing to the reduced LV function. In patients with a recent diagnosis of AF (<1 year), rhythm control can be useful to reduce hospitalizations, stroke, and mortality. In patients with AF and HF, rhythm control can be useful for improving symptoms and improving outcomes, such as mortality and hospitalizations for HF and ischemia. In patients with AF, rhythm-control strategies can be useful to reduce the likelihood of AF progression.  COR-LOE 2b-C: In patients with AF where symptoms associated with AF are uncertain, a trial of rhythm control (eg, cardioversion or pharmacological therapy) may be useful to determine what if any symptoms are attributable to AF.  COR-LOE 2b-B: In patients with AF, rhythm-control strategies may be useful to reduce the likelihood of development of dementia or worsening cardiac structural abnormalities.  While both rate and rhythm control can improve AF symptoms, several studies (such as AF-CHF) show improved quality of life with rhythm control  EAST-AFNET 4 was significant in that it showed rhythm control was associated with a 25% reduction in the combined endpoint of mortality rate, stroke, and hospitalizations due to HF or ACS  Acute rhythm control can be achieved with electrical or pharmacological cardioversion. Electrical is more effective and faster than pharmacological and is preferred for patients with hemodynamic instability attributable to AF. However, both approaches involved considerations for anticoagulation and thromboembolic risk. Pharmacologic options for cardioversion include ibutilide, amiodarone, flecainide, propafenone, procainamide, dofetilide, and sotalol.   COR-LOE 1-A: In patients with symptomatic AF in whom antiarrhythmic drugs have been ineffective, contraindicated, not tolerated or not preferred, and continued rhythm control is desired, catheter ablation is useful to improve symptoms.  AF ablation is also a suitable first-line option in some patients with paroxysmal AF to reduce recurrence and burden. Patient selection is important. Younger patients, those with minimal atrial enlargement, less myocardial fibrosis, and less persistent forms are more likely to have successful ablations, meaning less likely to have recurrence of AF after ablation.   HFrEF patients derive greater benefit than others from AF ablation in terms of improved functional status, LV function, and cardiovascular outcomes  Surgical ablation can be considered in those undergoing cardiac surgery for some other etiology such as valve surgery or CABG and is associated with increased survival, but some risk of pacemaker placement and renal dysfunction  How would you monitor for AF recurrence in post-ablation or cardioversion? Is there a role for monitoring in every patient?  Cardiac monitoring may be advised to AF patients for various reasons, such as for detecting recurrences, screening, or response to therapy  Long-term surveillance to detect recurrent AF can be beneficial and can be accomplished by various modalities, including wearable devices, smart watches, random monitoring (Holter, event, mobile telemetry), and implantable loop recorders. This is especially helpful in those who had AF-induced cardiomyopathy, especially if their LVEF recovered after rate/rhythm control. This is a population in whom recurrence of AF would want to be promptly noted and addressed.   Loop recorders can also be helpful in detecting subclinical AF or in patients with stroke or TIA of undetermined cause (COR-LOE 2a-B)  What AF burden warrants intervention?  It is important to recognize that AF is a chronic condition and tends to recur, so treatment often is focused on reducing risk of recurrence   Patient-clinician shared decision making is important when deciding when/how to intervene, as there is no cut-off for “significant” burden (COR-LOE 1-B)  What are some options for antiarrhythmic drugs and their characteristics?  Antiarrhythmic drugs are reasonable for long-term maintenance of sinus rhythm for patients with AF who are not candidates for, or decline, catheter ablation, or who prefer antiarrhythmic therapy  Amiodarone can be used in patients with or without HFrEF, as opposed to many other anti-arrhythmics that are (relatively) contraindicated in HFrEF or should be used with caution in such patients, such as flecainide, propafenone, dronedarone, and sotalol. However, due to its adverse effects and multiple drug interactions, is should be used only in patients in which other antiarrhythmic drugs are contraindications, ineffective, or not preferred. Dofetilide can also be used in patients with HFrEF.   In patients on amiodarone, labs should be checked regularly for thyroid, liver and kidney functions. There is also a role for pulmonary function testing and chest x-rays to monitor for pulmonary fibrosis, but frequency is not clearly established. It should be noted that amiodarone-induced lung toxicity occurs between 6 months and 2 years of use.   Flecainide is well tolerated, but is contraindicated in patients with significant coronary artery disease and possibly structural heart disease in general. It can also lead to the development of atrial flutter.   Dofetilide and sotalol require regular renal function monitoring and QTC monitoring  When should AV node ablation (AVNA) be considered?  In patients with AF and uncontrolled rapid ventricular response refractory to rate-control medications (who are not candidates for or in whom rhythm control has been unsuccessful), AVNA can be useful to improve symptoms and QOL (COR-LOE 2a-B)  AVNA is effective for rate control and does not require continuation of medications; however,

3周前
47:54
434. Heart Failure: Advanced Therapies Evaluation with Dr. Michelle Kittleson

434. Heart Failure: Advanced Therapies Evaluation with Dr. Michelle Kittleson

CardioNerds kicks off its advanced therapies series with Chair of the CardioNerds Heart Failure Council, Dr. Jenna Skowronski, co-chair of the series, Dr. Shazli Khan, and Episode FIT lead, Dr. Jason Feinman. In this first episode, they discuss the process of advanced therapies evaluation with Dr. Michelle Kittleson, Professor of Medicine and Director of Education in Heart Failure and Transplantation at Cedars-Sinai. In this case-based discussion, they cover the signs and symptoms of end-stage heart failure, the initial management strategies, and the diagnostic workup required when considering advanced therapies. Importantly, they discuss the special considerations for pursuing left-ventricular assist device (LVAD) versus heart transplantation as well as the multidisciplinary, team-based approach needed when advanced therapies are indicated.  Notes were drafted by Dr. Shazli Khan.  Audio editing for this episode was performed by CardioNerds Intern, Julia Marques Fernandes. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Heart Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Guideline-directed medical therapy (GDMT) is indicated in all heart failure patients and improves survival, but progressive symptoms and intolerance to GDMT can be warning signs of disease progression. The I-NEED-HELP mnemonic is an excellent reference when considering referral for advanced therapies (Figure).   Management of acute decompensation includes diuretics and possible inotropic support. The inotropic agent used should be whichever best suits your specific patient. Milrinone may result in more hypotension, whereas dobutamine may result in more tachycardia. Tachycardic and normotensive patients may do better with milrinone, while hypotensive patients with normal heart rates may do better with dobutamine. Notably, DoReMi found no difference between milrinone and dobutamine for patients with cardiogenic shock.  The initial diagnostic evaluation includes an echocardiogram, right heart catheterization (RHC), and often cardiopulmonary exercise testing (CPET) to objectively assess the status of the heart. Comprehensive labs, imaging and cancer screening are also needed to assess all other organs.   When making the decision to pursue advanced therapies, always ask:   Is the heart sick enough?   Is the rest of the body well enough?   These two questions provide a framework to guide if patients are optimal candidates for transplant versus LVAD.   The advanced therapies evaluation is a team sport! Patients will meet not only with advanced heart failure cardiologists, but also cardiac surgeons, psychiatrists, social workers, nutritionists and pharmacists. All team members are of critical value in the process.   Notes 1.) What are the key features of advanced cardiomyopathy, and when should providers consider referral for advanced therapies?   Advanced cardiomyopathy may present as recurrent hospitalizations for decompensated heart failure, intolerance to GDMT with symptomatic orthostasis and hypotension, and progressive symptoms of heart failure despite medical therapy.   The I-NEED-HELP mnemonic is a helpful tool to identify patients at risk of heart failure and is defined as follows: Need for Inotropic support, New York Heart Association (NYHA) Class IV symptoms, End-Organ Dysfunction, Ejection fraction <20%, Defibrillator shocks for ventricular arrhythmias, Recurrent HF hospitalizations, Escalating diuretic dose, Low blood pressure and Progressive intolerance of GDMT. See the Figure designed by Dr. Gurleen Kaur.  When patients demonstrate any of the above warning signs, they should be referred to advanced heart failure specialists for consideration of advanced therapies.   2.) What diagnostic testing is pursued when working up patients for advanced therapies? How does this workup differ whether you are in the inpatient or outpatient setting?  Work-up generally answers two key questions: is the heart sick enough and is the rest of the body well enough?  Workup includes an echocardiogram that may show specific features concerning for end-stage heart failure (EF <20%, dilated and remodeled left ventricle, reduced right ventricular function, etc.).   A RHC provides information on the filling pressures of the heart for management in the acute setting, but also helps give an objective measure of the cardiac output to assess how sick the heart is. Importantly the RHC also provides key information on the presence of pulmonary hypertension.  Obtaining a comprehensive metabolic panel provides valuable information on end-organ dysfunction, as kidney or liver abnormalities are suggestive of worsening disease.  Outpatients presenting for referral may also undergo CPET as an objective confirmation of decreased functional capacity. Typically, a peak VO2 max of <14 mL/kg/min is indicative of advanced disease.  CT imaging, as well as other cancer screening tools, may be employed to ensure there is no systemic disease that would prohibit advanced therapies.   3.) Who makes up the multidisciplinary advanced therapies team?   The ACC/AHA/HFSA 2022 guidelines for heart failure support using a multidisciplinary team approach in managing HF. This collaborative care model has been shown to reduce hospital admissions and healthcare expenses while enhancing patient adherence to self-care practices and recommended medical treatments.  The multidisciplinary team consists of cardiologists, cardiac surgeons, advanced practice providers, psychiatrists, pharmacists, social workers, nutritionists, and other specialists.  4.) What are the medical factors to consider when deciding between transplant versus LVAD, and what social determinants of health play a role?   The medical evaluation and workup done during the advanced therapies evaluation help answer two crucial questions: Is the heart sick enough? Is the rest of the body well enough? All patients should be assessed for extracardiac disease that may impact survival after advanced therapies.   While selection between transplant versus LVAD varies by program and institution, general principles considered include the allocation system and regional wait times, patient’s age, and extracardiac comorbidities.   Generally, patients being considered for heart transplantation should be devoid of conditions that have a five-year survival of <70% or a ten-year survival of <50%.  This is also because patients undergoing organ transplantation require immunosuppressive medications, which may further exacerbate their other systemic conditions.   Social support and internal motivation also play a role, as it is important for patients to attend multiple follow-up appointments and maintain strict adherence to their immunosuppressive medications.   Graphic - Stage D (Advanced) Heart Failure  Designed by Dr. Gurleen Kaur  References Morris AA, Khazanie P, Drazner MH, et al; American Heart Association Heart Failure and Transplantation Committee of the Council on Clinical Cardiology; Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Cardiovascular Radiology and Intervention; Council on Hypertension. Guidance for timely and appropriate referral of patients with advanced heart failure: a scientific statement from the American Heart Association. Circulation. 2021;144(15):e238-e250. doi:10.1161/CIR.0000000000001016  https://www.ahajournals.org/doi/10.1161/CIR.0000000000001016 Truby LK, Rogers JG. Advanced heart failure: epidemiology, diagnosis, and therapeutic approaches. JACC Heart Fail. 2020;8(7):523-536. doi:10.1016/j.jchf.2020.01.014 https://www.sciencedirect.com/science/article/pii/S2213177920302080?via%3Dihub  Heidenreich PA, Bozkurt B, Aguilar D, Allen LA, Byun JJ, Colvin MM, Deswal A, et al; ACC/AHA Joint Committee Members. 2022 AHA/ACC/HFSA guideline for the management of heart failure: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2022;145(18):e895-e1032. doi:10.1161/CIR.0000000000001063 https://www.ahajournals.org/doi/10.1161/CIR.0000000000001063  Guglin M, Zucker MJ, Borlaug BA, Breen E, Cleveland J, Johnson MR, Panjrath GS, et al; ACC Heart Failure and Transplant Member Section and Leadership Council. Evaluation for heart transplantation and LVAD implantation: JACC Council perspectives. J Am Coll Cardiol. 2020;75(12):1471-1487. doi:10.1016/j.jacc.2020.01.034 https://www.sciencedirect.com/science/article/pii/S0735109720304150?via%3Dihub

2个月前
14:01
433. The Evolution and Future of Cardio-Obstetrics with Dr. Afshan Hameed, Dr. Doreen DeFaria Yeh, Dr. Garima Sharma, and Dr. Rina Mauricio

433. The Evolution and Future of Cardio-Obstetrics with Dr. Afshan Hameed, Dr. Doreen DeFaria Yeh, Dr. Garima Sharma, and Dr. Rina Mauricio

In this second episode of a collaborative series with the AHA Women in Cardiology (WIC) Committee, CardioNerds (Dr. Gurleen Kaur and Dr. Anna Radhakrishnan) are joined by four leading experts in Cardio-Obstetrics to explore this rapidly evolving field. Dr. Rina Mauricio (Director of Women's Cardiovascular Health and Cardio-Obstetrics at UT Southwestern Medical Center), Dr. Afshan Hameed (Director of Maternal Fetal Medicine and Cardio-Obstetrics at UC Irvine), Dr. Doreen DeFaria Yeh (Co-director of the MGH Cardiovascular Disease and Pregnancy Program), and Dr. Garima Sharma (Director of Women's Cardiovascular Health and Cardio-Obstetrics at Inova) define Cardio-Ob as encompassing not only care of women during pregnancy, but also the complex decision-making that extends through the preconception and postpartum periods. From counseling patients with pre-existing or congenital heart disease before pregnancy to managing cardiovascular health during pregnancy and after delivery, they trace how the field has developed in response to the urgent need to address maternal mortality. Listeners will gain valuable insight into the multidisciplinary teamwork, patient-centered decision-making, and advocacy that drive this field - along with the importance of expanding Cardio-Ob education for clinicians and trainees, and innovations and system-level changes shaping its future. Audio editing by CardioNerds academy intern, Grace Qiu. This episode was planned in collaboration with the AHA CLCD Women in Cardiology Committee with mentorship from Dr. Monika Sanghavi.  The PA-ACC & CardioNerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

2个月前
31:35
432. Journal Club: The TRANSFORM-AF Trial with Dr. Sanjeev Saksena and Dr. Varun Sundaram

432. Journal Club: The TRANSFORM-AF Trial with Dr. Sanjeev Saksena and Dr. Varun Sundaram

Dr. Jeanne De Lavallaz and Dr. Ramy Doss discuss the results of the  TRANSFORM-AF Trial with expert faculty Dr. Sanjeev Saksena and Dr. Varun Sundaram.   The TRANSFORM-AF trial enrolled 2,510 patients with atrial fibrillation (AF), type 2 diabetes, and obesity across 170 Veterans Affairs hospitals to evaluate the impact of diabetes-dose GLP-1 receptor agonists on AF-related outcomes. Participants were assigned to receive either a GLP-1 receptor agonist, a DPP-IV inhibitor, or a sulfonylurea. The primary composite outcome included AF-related hospitalizations, cardioversions, ablation procedures, and all-cause mortality. Over a median follow-up of 3.2 years, GLP-1 use was associated with a 13% reduction in major AF-related events compared to other therapies. The study population was predominantly male, with a high prevalence of severe obesity (BMI >40 kg/m²) in whom the benefit appeared most pronounced. Notably, the observed benefit occurred despite only modest additional weight loss, suggesting potential non-weight-mediated effects of GLP-1 therapy  This episode was planned in collaboration with  Heart Rhythm TV with mentorship from Dr. Daniel Alyesh and Dr. Mehak Dhande.  CardioNerds Journal Club PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

2个月前
21:38
431. Atrial Fibrillation: Acute Management of Atrial Fibrillation with Dr. Jonathan Chrispin

431. Atrial Fibrillation: Acute Management of Atrial Fibrillation with Dr. Jonathan Chrispin

Dr. Naima Maqsood, Dr. Kelly Arps, and Dr. Jake Roberts discuss the acute management of atrial fibrillation with guest expert Dr. Jonathan Chrispin. Episode audio was edited by CardioNerds Intern Dr. Bhavya Shah. This episode reviews acute management strategies for atrial fibrillation. Atrial fibrillation is the most common chronic arrhythmia worldwide and is associated with increasingly prevalent comorbidities, including advanced age, obesity, and hypertension. Atrial fibrillation is a frequent indication for hospitalization and a complicating factor during hospital stays for other conditions. Here, we discuss considerations for the acute management of atrial fibrillation, including indications for rate versus rhythm control strategies, treatment targets for these approaches, considerations including pharmacologic versus electrical cardioversion, and management in the post-operative setting. CardioNerds Atrial Fibrillation PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls A key component to the management of acute atrial fibrillation involves addressing the underlying cause of the acute presentation. For example, if a patient presents with rapid atrial fibrillation and signs of infection, treatment of the underlying infection will help improve the elevated heart rate. Selecting a rate control versus rhythm control strategy in the acute setting involves considerations of comorbid conditions such as heart failure and competing risk factors such as critical illness that may favor one strategy over another. Recent data strongly supports the use of rhythm control in heart failure patients. Patients should be initiated on anticoagulation prior to pursuing a rhythm control strategy. There are several strategies for rate control medications with therapies including beta-blockers, non-dihydropyridine calcium channel blockers, and digoxin. The selection of which agent to use depends on additional comorbidities and the overall clinical assessment. For example, a patient with severely decompensated low-output heart failure may not tolerate a beta-blocker or calcium channel blocker in the acute phase due to hypotension risks but may benefit from the use of digoxin to provide rate control and some inotropic support. Thromboembolic prevention remains a cornerstone of atrial fibrillation management, and considerations must always be made in terms of the duration of atrial fibrillation, thromboembolic risk, and risks of anticoagulation. While postoperative atrial fibrillation is more common after cardiac surgeries, there is no major difference in management between patients who undergo cardiac versus non-cardiac procedures. Considerations involve whether the patient has a prior history of atrial fibrillation, surgery-specific bleeding risks related to anticoagulation, and monitoring in the post-operative period to assess for recurrence. Notes 1. Our first patient is a 65-year-old man with obesity, hypertension, obstructive sleep apnea, and pre-diabetes presenting for evaluation of worsening shortness of breath and palpitations. The patient has no known history of heart disease. Telemetry shows atrial fibrillation with ventricular rates elevated to 130-140 bpm. What would be the initial approach to addressing the acute management of atrial fibrillation in this patient? What are some of the primary considerations in the initial history and chart review? An important first step involves taking a careful history to understand the timing of symptom onset and potential underlying causes contributing to a patient’s acute presentation with rapid atrial fibrillation. Understanding the episode trigger determines management by targeting reversible causes of the acute presentation and elucidating whether the episode is triggered by a cardiac or non-cardiac condition. For example, if a patient presents with a few days of infectious symptoms, treating the infection is likely to lead to improvements in heart rate. Determining the tempo of symptoms has further importance for assessing the risk of thromboembolism and anticoagulation consideration. 2. How would the initial evaluation be different for patients who have a new diagnosis of atrial fibrillation compared to those who have a known prior history of this arrhythmia? The acuity of symptom onset plays an essential role in these considerations. For example, a patient may describe symptoms that have been ongoing for several months, which indicate a diagnosis beyond the acute phase of their presentation and would involve different considerations than for a patient who first noticed symptoms within the past few hours. One way to view RVR rates in a patient with longstanding or permanent atrial fibrillation is to consider this vital sign as that patient’s version of sinus tachycardia in response to another physiologic process. In that setting, you would not try an approach to directly lower their heart rate but would instead attempt to determine and address the underlying cause of their presentation. An additional consideration for patients without known prior atrial fibrillation is that they have likely never been on any rate-controlling agents and may have variable initial responses to these interventions. 3. In cases for which acute rate control of atrial fibrillation is indicated, what is the recommended heart rate target and how quickly should we aim to reach that target? The initial first step in management should focus on addressing the underlying cause of the patient’s elevated heart rate while in atrial fibrillation. Once those factors are addressed and elevated heart rates persist, a rate-controlling agent can be considered. Often, a primary reason for rate control is for symptom relief since patients can be very symptomatic from an elevated heart rate alone.  A reasonable goal for the intermediate setting is to achieve a heart rate of less than 100-110 bpm. One study compared lenient (resting heart rate <110 bpm) versus strict (resting heart rate <80 bpm and heart rate during moderate exercise <110 bpm) rate control in patients with atrial fibrillation and found no difference in outcomes related to mortality, hospitalization for heart failure, stroke, embolism, bleeding, or life-threatening arrhythmic events but that lenient control was easier to achieve.1 For this reason, aggressive rate control in the acute setting may not have a significant impact apart from symptom relief. There are not often clear indications to rapidly lower a patient’s heart rate, for example, from 140 to 90 bpm. Conversely, lowering a patient’s heart rate too rapidly can be detrimental by causing bradycardia or hypotension with excessive use of nodal blocking agents. 4. What are some of the considerations for the selection of rate-controlling agents? Beta-blockers and non-dihydropyridine calcium channel blockers remain the mainstay of therapies used for rate control. The choice between these agents often depends on the comorbidities present. For example, if a patient has a known reduced LVEF, you may often avoid calcium channel blockers and opt for careful titration of beta-blockers. Often, the use of beta-blockers also allows for the management of additional comorbidities, including heart failure and coronary disease. Digoxin is another agent to consider when a patient presents with acutely decompensated heart failure with a low LVEF and may not tolerate a beta-blocker or calcium channel blocker due to the risk of hypotension or worsening cardiogenic shock. Digoxin provides rate control while adding some positive inotropy. In terms of chronic management, digoxin use can be more challenging with close follow-up required to monitor levels. In some cases, amiodarone can be used as an acute rate-control agent, but there is a risk of conversion to sinus rhythm and thromboembolism if not on anticoagulation. 5. In what clinical scenarios might it be more optimal to consider an upfront rhythm control strategy? Recent data support the benefit of an upfront rhythm control approach in heart failure patients, with complications including cardiovascular death, stroke, or hospitalization for worsening of heart failure or for acute coronary syndrome, reduced in heart failure patients managed with any early rhythm control strategy.2,3 In certain patients with known atrial fibrillation and heart failure, cardioversion can be considered as a strategy to help improve their heart failure symptoms. In these patients, initiating an anti-arrhythmic drug (AAD) prior to cardioversion can improve the likelihood of remaining in sinus rhythm after cardioversion. 6. Our second patient is a 58-year-old woman with a history of heart failure with reduced EF presenting to the ED with progressive lower extremity swelling and shortness of breath. She has a prior diagnosis of paroxysmal atrial fibrillation, and her most recent echo demonstrated an LVEF of 35%. She is found to have bilateral lower extremity pitting edema to her knees and elevated jugular venous pressure while requiring 2L of oxygen by nasal cannula. She is in rapid atrial fibrillation on presentation. Interrogation of her primary prevention ICD shows that she has been in atrial fibrillation for the past 3 weeks. In this scenario involving a patient with an acute heart failure exacerbation, are there considerations for a more upfront rhythm control strategy and perhaps electrical cardioversion? In this scenario, there is an indication for utilizing an early rhythm control strategy. Even if an initial trial of diuresis and beta-blockers is used initially,

2个月前
18:40
430. Women Leaders in Advanced Heart Failure and Transplant Cardiology with Dr. Mariell Jessup and Dr. Nosheen Reza

430. Women Leaders in Advanced Heart Failure and Transplant Cardiology with Dr. Mariell Jessup and Dr. Nosheen Reza

In this powerful kickoff to a collaborative series with the AHA Women in Cardiology (WIC) Committee, CardioNerds (Dr. Apoorva Gangavelli, Dr. Gurleen Kaur, and Dr. Jenna Skowronski) explore the evolving landscape of women in advanced heart failure and transplant cardiology, featuring insights from two inspiring leaders in the field. Dr. Mariell Jessup, Chief Science and Medical Officer of the American Heart Association, reflects on her decades-long journey in heart failure cardiology, from navigating early career barriers to becoming a trailblazer in clinical leadership and research. Dr. Nosheen Reza, an advanced heart failure and transplant cardiologist at the University of Pennsylvania, shares how Dr. Jessup’s pioneering work has inspired her own career and shaped her approach to mentorship, advocacy, and academic development. Together, they discuss the systemic challenges women continue to face, the importance of sponsorship, and the evolving culture within cardiology. Listeners will gain a multigenerational perspective on how far the field has come and what is still needed to ensure equity, excellence, and innovation in advanced heart failure care. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Narratives in Cardiology Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! References DeFilippis EM, Moayedi Y, Reza N. Representation of Women Physicians in Heart Failure Clinical Practice. Card Fail Rev. 2021;7:e05. Published 2021 Mar 31. doi:10.15420/cfr.2020.31

3个月前
46:18
429. Walking Both Paths: A Physician and Patient in Adult Congenital Heart Disease with Dr. Leigh Reardon

429. Walking Both Paths: A Physician and Patient in Adult Congenital Heart Disease with Dr. Leigh Reardon

CardioNerds (Dr. Abby Frederickson, Dr. Claire Cambron, and Dr. Rawan Amir) are joined by Dr. Leigh Reardon for a powerful conversation on navigating adult congenital heart disease as both a patient and provider. Dr. Reardon shares his personal journey with congenital heart disease and how it shaped his path to becoming an expert in the field himself. The discussion highlights patient-centered perspectives, barriers to care within the healthcare system, and the importance of advocacy and empathy. This episode was planned by the CardioNerds ACHD Council. CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

3个月前
44:45
428. Atrial Fibrillation: The Impact of Modifiable Risk Factors and Lifestyle Management on Atrial Fibrillation with Dr. Prash Sanders

428. Atrial Fibrillation: The Impact of Modifiable Risk Factors and Lifestyle Management on Atrial Fibrillation with Dr. Prash Sanders

Dr. Kelly Arps, Dr. Naima Maqsood, and Dr. Sahi Allam discuss modifiable risk factors and lifestyle management of atrial fibrillation with Dr. Prash Sanders. Atrial fibrillation is becoming more prevalent across the world as people are living longer with cardiovascular disease. While much of our current focus lies on the pharmacological and procedural management of atrial fibrillation, several studies have shown that targeted reduction of risk factors, such as obesity, sleep apnea, hypertension, and alcohol use, can also significantly reduce atrial fibrillation burden and symptoms. Today, we discuss the data behind lifestyle management and why it is considered the “4th pillar” of atrial fibrillation treatment. We also explore ways to incorporate prevention strategies into our general cardiology and electrophysiology clinics to better serve the growing atrial fibrillation population. Audio editing for this episode was performed by CardioNerds Intern, Julia Marques Fernandes.  CardioNerds Atrial Fibrillation PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls More people have atrial fibrillation because it is being detected earlier using wearable technology, and patients are living longer with subclinical or clinical cardiovascular disease  There are 3 components of atrial fibrillation: an electrical “trigger” + a susceptible substrate (due to age, sex, genetics) + “perpetuators” that cause the trigger to continue stimulating the substrate (lifestyle risk factors such as obesity, smoking, diabetes, etc.)  Obesity is the highest attributable risk factor for atrial fibrillation. Treating obesity often helps to treat other risk factors, such as hypertension and sleep apnea.  Counseling is patient-dependent. Most patients are unable to make major behavioral changes cold-turkey and will need to make small, incremental changes.  Dr. Sanders’ tip: He tells his own patients that “atrial fibrillation is the body’s response to stress.” The key to treating atrial fibrillation is to control your underlying stressors - procedures and medications are simply band-aids that do not fix the root of the problem.  Notes Notes drafted by Dr. Allam. 1. How common is atrial fibrillation?  Atrial fibrillation is the most common sustained arrhythmia. Currently, an estimated 50-60 million individuals worldwide are estimated to have atrial fibrillation, or roughly 1 in 4 individuals over the age of 45.1  The rising global prevalence of atrial fibrillation can be attributed to the aging of the population, increased rates of obesity, and greater accumulation of cardiovascular risk factors and survival with clinical cardiovascular disease.2 Atrial fibrillation is also being detected earlier through digital and wearable devices.2  Annually, we spend approximately $5,312 per adult on the management of atrial fibrillation in the United States.3  2. What is the underlying pathophysiology of atrial fibrillation? How do risk factors like sleep apnea or obesity “trigger” atrial fibrillation?  For atrial fibrillation to occur, there is an electrical “trigger”, a susceptible substrate (due to age, sex, genetics), and “perpetuators” that allow the trigger to continue stimulating the substrate.2  90% of electrical “triggers” come from the pulmonary veins  “Perpetuators” influence how the autonomic nervous system interacts with the triggers and substrate to perpetuate atrial fibrillation. Sleep apnea, obesity, and other risk factors are the “perpetuators”  Over time, as atrial fibrillation recurs, the substrate remodels to result in persistent atrial fibrillation.  3. What are some of the risk factors for atrial fibrillation and what are the possible benefits of controlling them?  Reference 4 provides an excellent review of the individual risk factors   Tobacco use  Nicotine patches/gums and counseling are associated with successful nicotine cessation in RCTs.   In the long term, nicotine itself can cause atrial fibrosis. However, it is safe to use patches and gums in the short term to abet cessation.  Obesity  The highest attributable risk factor for atrial fibrillation. Treating obesity often helps to treat other risk factors, such as hypertension and sleep apnea  In addition to regular exercise, reducing caloric intake can help combat obesity. Eating more fiber-laden food such as vegetables instead of carbohydrates, limiting portions, sugary drinks, and alcohol, and increasing fasting periods can all help decrease weight.  GLP-1 agonists can significantly reduce obesity and improve both symptoms and mortality for patients with comorbid conditions, such as HFpEF.  Obstructive sleep apnea  This is an evolving area of research with upcoming randomized trial data  Sleep apnea is probably not a static condition. Our likelihood of having sleep apnea changes with how rested we are, how much we’ve exercised, or whether we’ve consumed alcohol, etc. The testing and treatment of the future will reflect the changeable nature of sleep apnea.  Current data:  In the atrial fibrillation ablation population, treatment of sleep apnea was associated with an improvement in time to arrhythmia recurrence.   Another observational study from Norway, which included various patients who used dental sleep appliances, found no significant difference in atrial fibrillation between those who were treated for sleep apnea and those who were not. It was severely underpowered to detect a difference.  Caffeine  There is no evidence to support cessation of caffeine in patients with atrial fibrillation  For patients with bothersome palpitations, caffeine cessation can be tried if it improves their symptoms  Alcohol use  Per data from the UK Biobank, a single drink of alcohol daily does not increase your risk for developing atrial fibrillation. However, multiple drinks per day will increase your risk.  A proof-of-concept study showed that patients who abstained from alcohol for at least 6 months had complete resolution of atrial fibrillation. However, the dropout rate was very high as most patients could not completely abstain from alcohol  Dr. Sanders recommends alcohol consumption of ≤ 3 drinks/week, which is the cutoff used in lifestyle management studies.   Heart Failure  For patients with heart failure, the 4 pillars of heart failure management are also crucial to treating atrial fibrillation. SGLT2 inhibitors in particular are likely to confer benefits. 40-50% of patients in the SGLT2 inhibitor clinical trials had co-morbid atrial fibrillation.  About half of patients undergoing atrial fibrillation ablation appear to have HFpEF based on their hemodynamics.  4. Can atrial fibrillation be treated with only lifestyle modifications?  Potentially. This is an evolving area of research without much published data. Empirically, Dr. Sanders has noticed that in patients referred for atrial fibrillation ablation, aggressive lifestyle modifications result in 40% of them no longer requiring ablation. After a 10-year follow-up, 20% still do not require ablation.  However, ablation is still an effective modality to achieve rhythm control. It is also becoming a safer procedure owing to novel techniques, such as pulse field ablation.   In the future, we foresee most patients utilizing a combination of lifestyle modification and rhythm control strategies (ablation and/or medications) to control their atrial fibrillation.  5. What are the benefits of exercise in patients with atrial fibrillation? How much exercise do you recommend to your patients? Also, on the other end of the spectrum, does participation in endurance sports paradoxically promote atrial fibrillation?  The ACTIVE-AF study tested whether an intensive aerobic exercise regimen, up to 210 minutes per day, is safe and effective in controlling atrial fibrillation. Intensive exercise was associated with a significant reduction in atrial fibrillation burden and symptoms as well as an increase in quality of life and maintenance of sinus rhythm.5   Endurance athletes do have an approximately 5-fold higher risk of atrial fibrillation compared to sedentary people.6 However, this occurs at very high levels of exercise, exceeding 4 hours per day. Low to moderate levels of exercise have been shown to reduce rates of atrial fibrillation.4,5  6. How should we counsel patients about lifestyle management? Are there any good resources to use?  Dr. Sanders’ tip: Counseling is patient-dependent. For the majority of patients, the key to behavioral change is to make incremental adjustments over time, accompanied by encouragement. Some patients respond well to continuous feedback from digital devices. We can also supplement pharmacological therapies, such as medications to assist with weight loss or tobacco/alcohol cessation, to behavioral counseling.  Risk factor modification should be the central pillar of atrial fibrillation management and reviewed early on with patients in their atrial fibrillation course. It may be beneficial to have clinic sessions specifically dedicated to lifestyle counseling, which can be run by a multidisciplinary team of electrophysiologists, general cardiologists, and nurse educators.  7. How should we explain what atrial fibrillation is to our patients?  Dr. Sanders’ tip: He tells his own patients that “atrial fibrillation is the body’s response to stress. It occurs because the heart is not coping well with increased stress. Procedures and medications for atrial fibrillation are simply band-aids that do not fix the root of the problem, but controlling the risk factors contributing to increased stress will.

3个月前
35:55
427. Management of Asymptomatic Severe Aortic Stenosis with Dr. Parth Desai and Dr. Tony Bavry

427. Management of Asymptomatic Severe Aortic Stenosis with Dr. Parth Desai and Dr. Tony Bavry

CardioNerds (Drs. Amit Goyal, Elizabeth Davis, and Keerthi Gondi) discuss the approach to asymptomatic severe aortic stenosis with expert faculty Drs. Parth Desai and Tony Bavry.   They review the natural history of aortic stenosis, current guidelines for treating severe aortic stenosis, multiparametric risk stratification, trial data on aortic valve replacement for patients with asymptomatic severe aortic stenosis, and a practical approach for our patients today.   This episode was supported by an educational grant from Edwards Lifesciences. All CardioNerds education is planned, produced, and reviewed solely by CardioNerds. Managing asymptomatic severe aortic stenosis | AKH CME Enjoy this Circulation Paths to Discovery article to learn more about the CardioNerds mission and journey.  US Cardiology Review is now the official journal of CardioNerds! Submit your manuscripts here.  CardioNerds Aortic Stenosis SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

4个月前
36:07
426. Case Report: A Ruptured Saccular Aortic Aneurysm into the Right Ventricle – University of Tennessee, Nashville ​

426. Case Report: A Ruptured Saccular Aortic Aneurysm into the Right Ventricle – University of Tennessee, Nashville ​

CardioNerds join Dr. Neel Patel, Dr. Victoria Odeleye, and Dr. Jay Ramsay from the University of Tennessee, Nashville, for a deep dive into cardiovascular medicine in the vibrant city of Nashville. They discuss the following case: A 57-year-old male with a history of prior cardiac surgery, hypertension, and polysubstance use presented with syncope and chest pain. Initial workup revealed a large saccular ascending aortic aneurysm. While under conservative management, he experienced acute hemodynamic collapse, leading to the discovery of an unprecedented aorto-right ventricular fistula. This episode examines the clinical presentation, diagnostic journey, and management challenges of this rare and complex aortic pathology, highlighting the role of multimodal imaging and the interplay of multifactorial risk factors. Expert commentary is provided by Dr. Andrew Zurick III. Episode audio was edited by CardioNerds Intern student Dr. Pacey Wetstein.   US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Saccular Aneurysm Risk: Saccular aortic aneurysms, though less common than fusiform, carry a higher inherent rupture risk due to concentrated wall shear stress, often exacerbated by prior cardiac surgery, chronic hypertension, and polysubstance use.     Unprecedented Rupture: The direct rupture of an aortic aneurysm into a cardiac chamber, specifically the right ventricle, is an exceedingly rare event, with no prior reported cases in the literature, highlighting the unpredictable nature of complex aortic pathology.     Hemodynamic Catastrophe: A large aorto-right ventricular fistula creates a massive left-to-right shunt, leading to acute right ventricular pressure and volume overload, culminating in rapid cardiogenic shock and refractory right ventricular failure.     Multimodal Imaging Imperative: Multimodal imaging (CT angiography for anatomy, TTE/TEE for real-time hemodynamics and fistula detection, CMR for tissue characterization) is indispensable for rapid diagnosis and comprehensive characterization of life-threatening cardiovascular emergencies.     High-Risk Intervention: Emergent surgical repair of a ruptured aortic aneurysm with an aorto-right ventricular fistula is a high-risk procedure associated with significant mortality, underscoring the need for prompt multidisciplinary care and realistic outcome expectations.     Notes - Notes (drafted by Dr Neel Patel):  What are the unique characteristics and rupture risk of saccular aortic aneurysms?  Saccular aortic aneurysms are less common than fusiform aneurysms.     They are generally considered more prone to rupture due to higher wall shear stress concentrated at the neck of the aneurysm, acting as a focal point of weakness.     Contributing Factors to Aneurysm Formation and Rupture in this Case:  Prior Cardiac Surgery: Aortic cannulation during the VSD/ASD repair decades ago likely created a localized structural weakness or predisposition.     Chronic, Poorly Controlled Hypertension: Imposed relentless systemic stress on the arterial walls, accelerating dilation and weakening.     Polysubstance Use: Particularly stimulants like cocaine and methamphetamines, which directly contribute to vascular damage by inducing severe, uncontrolled hypertension and direct arterial wall injury. This significantly increases the risk of aneurysm formation and rupture, especially with pre-existing conditions.     The direct rupture of an aortic aneurysm into a cardiac chamber, specifically the right ventricle, is an exceedingly rare event, with no prior reported cases in the literature, making this a "first of its kind" report.     What are the hemodynamic consequences and management challenges associated with aorto-right ventricular fistulas?  Hemodynamic Impact: A large aorto-right ventricular fistula results in a significant anatomic left-to-right shunt, where blood from the high-pressure aorta is shunted directly into the lower-pressure right ventricle.     This leads to acute right ventricular pressure and volume overload, causing rapid right ventricular dilation, increased right ventricular wall stress, and ultimately, acute right ventricular failure.     This directly explained the sudden onset of cardiogenic shock, as the right ventricle was unable to maintain forward flow, leading to systemic hypoperfusion and shock.     Management Challenges:  The patient required emergent, extremely high-risk salvage aortic aneurysm repair surgery.     Marked hemodynamic instability occurred immediately after anesthesia induction (systolic blood pressure dropped to 50 mmHg), necessitating immediate initiation of external cardiopulmonary bypass.     Intra-operatively, a large (2 cm diameter) hole in the ascending aorta communicating with the saccular aneurysm was found, along with a massive (4-5 cm) fistula into the right ventricular outflow tract (RVOT) area, just proximal to the pulmonic valve, with several smaller holes.     Surgical repair involved a 5x10 cm bovine pericardial patch for the right ventricular wall and replacement of a 5 cm segment of the ascending aorta with a 34 mm gelweave straight graft.     Post-operative Course: Severely complicated by severe coagulopathy and extensive bleeding (requiring multiple blood products and a Cabral fistula).     Continued severe right ventricular dysfunction necessitated the placement of a Right Ventricular Assist Device (RVAD).     Despite support, hemodynamic function continued to decline, with severely depressed Left Ventricular (LV) function observed.     The patient ultimately passed away due to refractory right heart failure and hemodynamic collapse, highlighting the extremely high mortality risk associated with such complex, emergent cardiac surgical interventions.     What is the role of multimodal imaging in diagnosing this complex and rare cardiovascular emergency?  CT Angiography: Crucial for initial identification and comprehensive characterization of the large saccular ascending aortic aneurysm, providing precise dimensions, revealing layered thrombus, and understanding anatomical relationships. Its high spatial resolution and wide field of view are excellent for aortic assessment.     Transthoracic and Transesophageal Echocardiography (TTE/TEE): Absolutely critical for real-time diagnosis of the fistula during acute deterioration. Bedside echocardiography, particularly TEE, allowed for visualization of the new continuous, turbulent flow from the aorta directly into the right ventricle, quantification of acute right ventricular dilation, and estimation of significantly increased RVSP. Its accessibility and real-time capabilities are unmatched for acute hemodynamic assessment and shunt detection.     Cardiac MRI (CMR): Provided additional tissue characterization of the aneurysm, confirming partial thrombosis and, importantly, showing no significant late gadolinium enhancement (LGE) in the myocardium, which was reassuring regarding the absence of significant myocardial scar related to the aneurysm itself. CMR offers superior soft tissue characterization compared to CT.     Complementary Nature: This case demonstrated the complementary nature of these modalities: CT provided the initial anatomical roadmap, echocardiography offered real-time hemodynamic assessment and immediate diagnosis of the acute rupture and shunt, and CMR contributed valuable tissue characterization. Imaging choices are guided by clinical questions, urgency, and specific information needed for critical management decisions.     What are the multi-factorial risk factors contributing to complex aortic disease, including the often-overlooked impact of polysubstance use?  Prior Cardiac Surgery: The patient's history of open-heart surgery decades prior, involving aortic cannulation for cardiopulmonary bypass, is a recognized risk factor for the subsequent development of iatrogenic aneurysms, creating a localized structural weakness or predisposition.     Chronic, Poorly Controlled Hypertension: Imposes relentless systemic stress on the arterial walls, accelerating dilation and weakening, significantly contributing to aneurysm progression.     Polysubstance Use:  The patient's long-standing history of polysubstance use, particularly stimulants like cocaine and methamphetamines, represents a significant contributing factor to his vascular pathology.     These substances are not merely comorbidities; they directly contribute to vascular damage.     Chronic stimulant use can induce severe, uncontrolled hypertension and direct arterial wall injury.     This significantly increases the risk of aneurysm formation and rupture, especially when combined with pre-existing conditions like essential hypertension and prior cardiac surgery.     Multi-hit Phenomenon: This case illustrates a multi-factorial pathology where various insults on vascular integrity over time converge to create a highly complex and catastrophic cardiovascular event. The presence of these factors emphasizes the critical importance of a thorough social history in cardiovascular risk assessment, moving beyond a superficial listing to understanding the profound pathophysiological impact on vascular health.     References - Lavall D, Schäfers HJ, Böhm M, Laufs U. Aneurysms of the ascending aorta. Dtsch Arztebl Int. 2012 Mar;109(13):227-33. doi: 10.3238/arztebl.2012.0227. Epub 2012 Mar 30. PMID: 22532815; PMCID: PMC3334714.  Shang EK, Nathan DP, Boonn WW, Lys-Dobradin IA,

4个月前
36:09
425. Case Report: The Hidden Culprit – Unraveling the Cause of Malignant Ventricular Arrhythmias in a Young Adult – Trinity Health Livonia Hospital

425. Case Report: The Hidden Culprit – Unraveling the Cause of Malignant Ventricular Arrhythmias in a Young Adult – Trinity Health Livonia Hospital

CardioNerds guest host Dr. Colin Blumenthal joins Dr. Juma Bin Firos and Dr. Aishwarya Verma from the Trinity Health Livonia Hospital to discuss a fascinating case involving malignant ventricular arrhythmias. Expert commentary is provided by Dr. Mohammad-Ali Jazayeri. Audio editing for this episode was performed by CardioNerds Intern,Julia Marques Fernandes.  This case explores the puzzling presentation of exercise-induced ventricular tachycardia in a young, otherwise healthy male who suffered recurrent out-of-hospital cardiac arrests. With no traditional risk factors and an unremarkable ischemic workup, the challenge lay in uncovering the underlying cause of his malignant arrhythmias. Electrophysiology studies and advanced imaging played a pivotal role in systematically narrowing the differentials, revealing an unexpected arrhythmogenic substrate. This episode delves into the diagnostic dilemma, the role of EP testing, and the critical decision-making surrounding ICD placement in a patient with a concealed but life-threatening condition.  US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls- Malignant Ventricular Arrhythmias This case highlights the challenges and importance of diagnosing and managing ventricular arrhythmias in young, seemingly healthy individuals. Here are five key takeaways from the episode:  Electrophysiology (EP) studies play a crucial role in identifying arrhythmogenic substrates in patients with exercise-induced ventricular tachycardia (VT) without obvious structural heart disease. In this case, substrate mapping revealed late abnormal ventricular afterdepolarizations in the basal inferior left ventricle, providing valuable insights into the underlying mechanism.  Cardiac MRI can be a powerful tool for detecting subtle myocardial abnormalities. The subepicardial late gadolinium enhancement (LGE) in the lateral and inferior LV walls suggested an underlying myocardial process, even when other imaging modalities appeared normal.  The VT morphology can provide clues about the underlying mechanism. In this case, the right bundle branch block pattern with a northwest axis and shifting exit sites pointed towards a scar-mediated mechanism rather than a channelopathy or idiopathic VT.  Implantable cardioverter-defibrillator (ICD) placement is crucial for secondary prevention of sudden cardiac death (SCD) in patients with malignant ventricular arrhythmias, even in young individuals. The patient's initial deferral of ICD implantation highlights the importance of shared decision-making and patient education in these complex cases.  "Scar-mediated VT introduces the risk of new arrhythmogenic substrates over time, reinforcing the need for ICD therapy even when catheter ablation is considered." This pearl emphasizes the dynamic nature of the arrhythmogenic substrate and the importance of long-term risk mitigation strategies.  Notes - Malignant Ventricular Arrhythmias Notes were drafted by Juma Bin Firos.  1. What underlying pathologies cause ventricular arrhythmias in young patients without overt structural heart disease? Myocardial fibrosis: Detected via late gadolinium enhancement (LGE) on cardiac MRI Present in 38% of nonischemic cardiomyopathy cases Increases sudden cardiac death (SCD) risk 5-fold Often localized to subepicardial regions, particularly in the inferolateral left ventricle (LV) May precede overt systolic dysfunction by years Subclinical cardiomyopathy: 67% of young VT patients show subtle cardiac dysfunction Suggests VT may be the first manifestation of cardiomyopathy Can include early-stage genetic cardiomyopathies (e.g., ARVC, LMNA mutations) Often associated with preserved ejection fraction (EF >50%) Arrhythmogenic substrate: EP studies localize re-entry circuits to specific regions: Basal inferior LV near the mitral annulus (as in this case) Right ventricular outflow tract (RVOT) in idiopathic VT Papillary muscles or fascicular regions Substrate can exist even with normal EF and no visible structural abnormalities on echocardiography Channelopathies: Long QT syndrome (LQTS): QTc >460ms in males, >470ms in females Brugada syndrome: Coved ST elevation in V1-V3 Catecholaminergic polymorphic VT (CPVT): Normal resting ECG, bidirectional VT with exercise Short QT syndrome: QTc <330ms Inflammatory conditions: Myocarditis: Can cause transient or persistent arrhythmogenic substrate Cardiac sarcoidosis: Patchy inflammation and fibrosis, often affecting the septum 2. How do electrophysiology studies differentiate scar-mediated VT from channelopathies? Substrate mapping: Identifies late abnormal potentials (LAPs) with 92% specificity for re-entry circuits Utilizes multi-electrode catheters (e.g., Penta Ray) for high-density mapping LAPs indicate slow conduction through fibrotic tissue, key for re-entry Absent in purely electrical disorders like channelopathies Inducibility: Programmed electrical stimulation (PES) protocols: Up to triple extra stimuli at multiple sites (RV apex, RVOT, LV) Burst pacing at cycle lengths down to 200-250ms Scar-mediated VT is often inducible with aggressive stimulation Polymorphic VT/VF induction suggests a structural substrate Channelopathies like Catecholaminergic polymorphic ventricular tachycardia CPVT) typically requires isoproterenol or exercise for induction VT morphology analysis: Right bundle branch block (RBBB) + northwest axis localizes to LV basal inferior wall Left bundle branch block (LBBB) + inferior axis suggests RVOT origin Fascicular VT: RBBB + left anterior or posterior fascicular block pattern Papillary muscle VT: RBBB or LBBB with variable axis Entrainment mapping: Performed during sustained monomorphic VT Post-pacing interval minus tachycardia cycle length (PPI-TCL) <30ms indicates critical isthmus Not applicable to polymorphic VT or channelopathies Electroanatomic voltage mapping: Low voltage areas (<1.5mV bipolar) indicate scar tissue Normal voltage throughout suggests functional (non-scar) VT mechanism 3. What are key management considerations for recurrent VT/VF in young patients? ICD for secondary prevention: Class I indication after cardiac arrest or sustained VT without a reversible cause Reduces mortality from 13% (8-year untreated) to <5%, especially with LGE present Device selection: Single-chamber ICD if no pacing indication Subcutaneous ICD (S-ICD) in young patients to avoid transvenous lead complications Consider cardiac resynchronization therapy defibrillator (CRT-D) if LBBB or wide QRS LifeVest limitations: Bridges ≤3 months; not a long-term solution Recurrent arrests double mortality vs. prompt ICD implantation Compliance issues: must be worn consistently to be effective Oral antiarrhythmic medications: Amiodarone: Effective for acute VT suppression Long-term use limited by side effects (thyroid, liver, pulmonary toxicity) Beta-blockers: First line for most VT/VF, especially exercise-induced Sotalol: Alternative for those with preserved LV function Mexiletine: Adjunct for frequent ICD shocks, especially with LQT3 Catheter ablation: Consider early in the course for recurrent ICD shocks Success rates 60-80% for scar-related VT May reduce ICD shocks and improve quality of life Limitations: deep intramural or epicardial substrates may require specialized approaches Lifestyle modifications: Exercise restrictions: Avoid high-intensity activities that trigger arrhythmias Stress management: Consider cognitive behavioral therapy or mindfulness training Avoidance of QT-prolonging medications in LQTS patients Genetic testing and family screening: Recommended for suspected inherited arrhythmia syndromes Can guide management and risk stratification for family members 4. Why does exercise exacerbate arrhythmia risk in these patients? Sympathetic surge: Increases myocardial oxygen demand Enhances automaticity and triggered activity Can unmask concealed conduction abnormalities Hemodynamic changes: Increased preload and afterload stress fibrotic regions Volume shifts may alter electrolyte concentrations locally Metabolic factors: Lactic acid accumulation can promote ectopic beats Catecholamine release exacerbates ion channel dysfunction in channelopathies Exercise-induced VT/VF correlates with 8× higher SCD risk vs. rest-onset arrhythmias: Warrants activity restrictions tailored to individual risk profile May indicate more malignant substrate or advanced disease process Treadmill testing: Should guide therapy in asymptomatic patients with exercise-related VT Protocols: Bruce protocol for general assessment Modified protocols (e.g., longer stages) for specific arrhythmia provocation Endpoints: Induction of sustained VT/VF Achieving target heart rate (85% of age-predicted maximum) Development of concerning symptoms (pre-syncope, chest pain) Cardiac rehabilitation: Supervised exercise programs can improve outcomes Gradual increase in intensity with continuous monitoring Helps define safe exercise thresholds for patients 5. How does LGE on cardiac MRI refine risk stratification? Late gadolinium enhancement (LGE) on cardiac MRI acts like a "scar map" of the heart, revealing areas of damaged or fibrotic tissue. These scars create electrical instability,

4个月前
54:43
424. Treatment of Transthyretin Amyloid Cardiomyopathy (ATTR-CM) with Dr. Justin Grodin

424. Treatment of Transthyretin Amyloid Cardiomyopathy (ATTR-CM) with Dr. Justin Grodin

CardioNerds (Drs. Rick Ferraro and Georgia Vasilakis Tsatiris) discuss ATTR cardiac amyloidosis with expert Dr. Justin Grodin. This episode is a must-listen for all who want to know how to diagnose and treat ATTR with current available therapies, as well as management of concomitant diseases through a multidisciplinary approach. We take a deep dive into the importance of genetic testing, not only for patients and families, but also for gene-specific therapies on the horizon. Dr. Grodin draws us a roadmap, guiding us through new experimental therapies that may reverse the amyloidosis disease process once and for all.  Audio editing by CardioNerds academy intern, Christiana Dangas. This episode was developed in collaboration with the American Society of Preventive Cardiology and supported by an educational grant from BridgeBio.  Enjoy this Circulation Paths to Discovery article to learn more about the CardioNerds mission and journey.  US Cardiology Review is now the official journal of CardioNerds! Submit your manuscripts here.  CardioNerds Cardiac Amyloid PageCardioNerds Episode Page Pearls: You must THINK about your patient having amyloid to recognize the pattern and make the diagnosis. Start with a routine ECG and TTE, and look for a disproportionately large heart muscle with relatively low voltages on the ECG.  Before you diagnose ATTR amyloidosis, AL amyloidosis must be ruled out (or ruled in) with serum light chains, serum/urine immunofixation, and/or tissue biopsy.  Genetic testing is standard of care for all patients and families with ATTR amyloidosis, and the future is promising for gene-specific treatments. Current FDA-approved treatments for TTR amyloidosis are TTR stabilizers and TTR silencers, but TTR fibril-depleting agents are on their way.  Early diagnosis of ATTR affords patients maximal benefit from current amyloidosis therapies.   TTR amyloidosis patients require a multidisciplinary approach for success, given the high number of concomitant diseases with cardiomyopathy.  Notes: Notes: Notes drafted by Dr. Georgia Vasilakis Tsatiris.  What makes you most suspicious of a diagnosis of cardiac amyloidosis from the typical heart failure patient?  You must have a strong index of suspicion, meaning you THINK that the patient could have cardiac amyloidosis, to consider it diagnostically. Some characteristics or “red flags” to not miss:   Disproportionately thick heart muscle with a relatively low voltages on EKG   Bilateral carpal tunnel syndrome – estimated that 1 in 10 people >65 years old will have amyloidosis   Previously tolerated antihypertensive medications  Atraumatic biceps tendon rupture   Bilateral carpal tunnel syndrome  Spinal stenosis   Concomitant with other diseases: HFpEF, low-flow low-gradient aortic stenosis  How would you work up a patient for cardiac amyloidosis?   Start with a routine ECG (looking for disproportionally low voltage) and routine TTE (looking for thick heart muscle)  CBC, serum chemistries, hepatic function panel, NT proBNP, and troponin levels  NOTE: It is critical to differentiate between amyloid light chain (AL amyloidosis) and transthyretin ATTR amyloidosis, as both make up 95-99% of amyloidosis cases.   Obtain serum free light chains, serum & urine electrophoresis, and serum & urine immunofixation to rule out AL amyloidosis. (See table below)  AL Amyloidosis ATTR Amyloidosis  → Positive serum free light chains and immunofixation (Abnormal M protein) → Tissue biopsy (endomyocardial, fat pad) to confirm diagnosis → Negative serum free light chains and immunofixation (ruled out AL amyloidosis) → Cardiac scintigraphy (Technetium pyrophosphate with SPECT imaging)  What treatment options do we have to offer now for ATTR CM, and how has this compared to prior years?   Before 2019, treatment options were limited outside of cardiac transplantation and prophylactic liver transplants for hereditary ATTR amyloidosis.  Treatments since 2019 have utilized the amyloidogenic cascade:  TTR protein is formed in the liver and circulates in the bloodstream.   Current treatments aim to either slow ATTR progression by stopping deposition or clearing amyloid deposits  Only FDA-approved treatments are for stopping deposition, while agents that clear amyloid deposits remain investigational. Two classes of agents that stop amyloid deposition are TTR stabilizers and TTR Silencers. (See table below)  TTR Stabilizers TTR Silencers Tafamidis (ATTR-ACT, 2018) Acoramidis (ATTRibute-CM, 2024)  Inotersen (Clinical Trial, 2018) Eplontersen (Clinical Trial, 2023) Patisiran (Clinical Trial, 2018)  Vutrisiran* (Clinical Trial, 2022)   Mechanism: prevents dissociation of, or stabilizes, the TTR tetramer to halt disease progression Mechanism: inhibit the liver’s production of TTR in the bloodstream via small interfering RNAs (siRNAs)/antisense oligonucleotides Route of administration: PO (pills) Route of Administration: IV infusions *Vutrisiran is a subQ injection q3months Outcomes: improve morbidity and mortality in both wildtype (wtATTR) and hereditary ATTR (hATTR) amyloidosis Outcomes: only approved for treatment of hATTR with polyneuropathy  Agents that clear amyloid deposits are still in clinical trials (ALXN2200, Coramitug PRX004).  Liver transplantation is the only method of clearing amyloid fibril deposits until the FDA approves a fibril-depleting agent, as perhaps one of the aforementioned agents.   How do you use genetic testing in your practice? How does the role of genetic testing impact treatment options for patients and their families?   Genetic testing = standard of care; everyone with ATTR-CM should get genetic sequencing!  Family screening is also important, as hATTR is an autosomal dominant disease. Patients and families can be referred to genetic counseling, become educated on the GINA Act, and choose to start cascade screening for family members.  Family members can be affected in different ways, as penetrance can occur at different ages   Due to current FDA labeling patients must have hereditary ATTR with polyneuropathy and a pathologic variant to qualify for TTR silencer treatment. Patients can have concomitant cardiomyopathy but must also have polyneuropathy and pathologic variant.   TTR stabilizers are approved for ATTR cardiomyopathy regardless of the presence of the pathogenic TTR variant.   Are there differences in treatment response between wtATTR or hATTR? What about differences in men and women?  Epidemiological studies suggest variant (hereditary) ATTR patients have more aggressive disease than wildtype ATTR patients.   Since current treatments do not cure the disease and work to slow progression, patients with advanced stages of disease do not show much benefit from current therapies.  Whether it is wild type or hereditary, diagnosing ATTR as early as possible will afford patients the greatest therapeutic impact of current treatments.   The current data does not suggest a therapeutic difference in response between men and women with ATTR cardiac amyloidosis  What is the role of CRISPR/Cas9 in the treatment of cardiac amyloidosis?   ATTR amyloidosis is an elegant disease model because it is one gene responsible for one protein and ultimately one disease process.  NTLA 2001 (currently in a phase-three clinical trial, link to phase one) is an agent administered in a single infusion to silence hepatic production of TTR indefinitely.  We are awaiting promising results from this trial at the time of this recording.  How can we best call on our friends in other subspecialities to take care of the concomitant diseases – peripheral neuropathy, symptomatic atrial fibrillation, aortic stenosis? Do any ATTR specific treatments show improvement in these manifestations?  TTR amyloidosis patients need a multidisciplinary care model for success.  Carpal tunnel syndrome is common in ATTR amyloidosis, so referrals to neurology and hand surgery are common  Patients with autonomic dysfunction secondary to autonomic neuropathy could benefit from neurology referral for blood pressure strategies and gastroenterology due to gut dysmotility and constipation.  Electrophysiology (EP) referral is common for atrial fibrillation and atrial flutter  ATTR is a disease of aging, so collaborating with geriatricians is important to help coordinate care and establish the patient’s individualized goals.    What is your management of subclinical ATTR and strategies for early detection?  Again, having a strong index of suspicion for cardiac amyloidosis is prudent.    The most common TTR variant that causes hATTR on earth is the V122I mutation (PV142I), which is very common in Western African ancestry. We suspect 1.5 million carriers of this variant in the USA alone, which puts individuals at 2-3x higher risk for heart failure than their age, sex, and race-matched non-carrier controls.  Expert consensus suggests monitoring individuals with this variant about 10 years before when the proband (i.e. if patient was diagnosed at 70, family members start screening at 60).   Initial work-up should include standard tests: ECG, echocardiogram, blood work.  Upcoming clinical trial will enroll patients in this critical 10-year window and randomize them into acoramadis vs placebo to see if treatment before symptom/disease onset can prevent amyloid disease.  References Arbelo E, Protonotarios A, Gimeno JR, et al. 2023 ESC Guidelines for the management of cardiomyopathies: Developed by the task force on the management of cardiomyopathies of the European Society of Cardiology (ESC). Eur Heart J. 2023;44(37):3503-3626. doi:10.1093/eurheartj/ehad194  Maron MS, Masri A, Nassif ME, et al.

4个月前
44:38
423. Case Report: The Malignant Murmur – More Than Meets the Echo in Nonbacterial Thrombotic Endocarditis – Baylor College of Medicine

423. Case Report: The Malignant Murmur – More Than Meets the Echo in Nonbacterial Thrombotic Endocarditis – Baylor College of Medicine

CardioNerds (Dr. Rick Ferraro and Dr. Dan Ambinder) join Dr. Sahar Samimi and Dr. Lorraine Mascarenhas from Baylor College of Medicine, Houston, Texas, at the Houston Rodeo for some tasty Texas BBQ and a tour of the lively rodeo grounds to discuss an interesting case full of clinical pearls involving a patient with nonbacterial thrombotic endocarditis (NBTE). Expert commentary is provided by Dr. Basant Arya. Episode audio was edited by CardioNerds Intern Dr. Bhavya Shah. (Photo by Xu Jianmei/Xinhua via Getty Images)Xinhua News Agency via Getty Images We discuss a case of a 38-year-old woman with advanced endometrial cancer who presents with acute abdominal pain, found to have splenic and renal infarcts, severe aortic regurgitation, and persistently negative blood cultures, ultimately diagnosed with nonbacterial thrombotic endocarditis (NBTE). We review the definition and pathophysiology of NBTE in the context of malignancy and hypercoagulability, discuss initial evaluation and echocardiographic findings, and highlight important management considerations. Emphasis is placed on the complexities of anticoagulation choice, the role of valvular surveillance, and the need for coordinated, multidisciplinary care.   US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls- Nonbacterial Thrombotic Endocarditis Eliminate the Usual Suspects. NBTE is a diagnosis of exclusion! Always rule out infective endocarditis (IE) first with serial blood cultures and serologic tests.  More than Meets the Echo. Distinguishing NBTE from culture-negative endocarditis can be tricky. Look beyond the echo—focus on clinical context (underlying malignancy, autoimmune issues) and lab findings to clinch the diagnosis.  TEE for the Win... Mostly. While TEE is more sensitive than TTE, NBTE vegetations can be sneaky and may embolize quickly. Don’t hesitate to use advanced imaging (i.e., cardiac MRI, CTA) or repeat imaging if you still suspect NBTE.  Choose your champion. In cancer-associated NBTE, guideline recommendations for anticoagulation choice are lacking. Consider DOACs and LMWH as agents of choice, but ultimately use shared decision-making to guide management.  No obvious trigger? Go hunting for hidden malignancies or autoimmune disorders. A thorough workup is essential to uncover the driving force behind NBTE.  Check out this state-of-the-art review for a comprehensive, one-stop summary of NBTE: European Heart Journal, 46(3), 236–245. Please note that the figures and tables referenced in the following notes are adapted from this review.  notes- Nonbacterial Thrombotic Endocarditis Notes were drafted by Dr. Sahar Samimi.  What is nonbacterial thrombotic endocarditis (NBTE)?   NBTE, previously known as marantic endocarditis, is a rare condition in which sterile vegetations form on heart valves.1  It occurs most commonly in association with malignancies and autoimmune conditions (i.e, antiphospholipid antibody syndrome or systemic lupus erythematosus).1 In addition, NBTE has been reported in association with COVID-19 infection, burns, sepsis, and indwelling catheters.2  Precise mechanisms remain unclear, but an interplay of endothelial injury, hypercoagulability, hypoxia, and immune complex deposition contributes to the formation of these sterile vegetations. 1  How do we diagnose NBTE?  Physicians should have a high level of suspicion for NBTE in at-risk patients (e.g., with active malignancy) who present with recent or recurrent embolic events (i.e., stroke, splenic, renal, or mesenteric infarct, and acute coronary syndrome).1  Once vegetations are observed, the diagnosis of NBTE is focused on ruling out IE, followed by looking for the underlying etiology, if not already evident.1 A focused clinical assessment, including a thorough history, physical exam, and relevant microbiological and serological tests, should aim to rule out IE using the modified Duke criteria.3  Persistently negative blood cultures after adequate sampling increase the likelihood of NBTE but do not exclude culture-negative endocarditis. Vegetations found in patients with risk factors raise the suspicion for NBTE, whereas signs of systemic infection—such as ongoing fever, recent antibiotic exposure, or potential zoonotic sources—may point instead toward CNE.1  New diagnostic techniques, including specialized serology and metagenomic sequencing, have significantly enhanced our ability to detect elusive pathogens in CNE.1  How should imaging be approached in suspected NBTE?  In cases of suspected endocarditis, guidelines from the American College of Cardiology, the American Heart Association, and the European Society of Cardiology recommend starting the assessment with a TTE to visualize potential valvular vegetations. 4,5  TTE is less sensitive than TEE, particularly for detecting smaller vegetations < 5 mm that are often associated with NBTE. Therefore, a subsequent TEE is recommended due to its superior ability to detect subtle valvular abnormalities. 4,5  Echocardiographic features of vegetations alone do not reliably distinguish NBTE from IE; hence, clinical context, along with laboratory and microbiological findings, is crucial for accurate diagnosis. 1  Uncertainty may remain following a TEE or in cases where TEE is not feasible. In such situations, advanced imaging techniques like cardiac MRI and CT scanning are emerging tools for more detailed cardiac tissue characterization. 1  What are the management strategies for NBTE?  NBTE’s complexity necessitates a multidisciplinary treatment strategy, with each patient’s prognosis shaped by individual clinical factors. 1  Primary therapy involves anticoagulation, alongside targeted management of malignancy or autoimmune disorder driving the hypercoagulable state. 1  While the criteria for surgical intervention are similar to those used in IE, surgery generally has a more limited role in NBTE. 1  What factors into choosing the anticoagulation agent?  Anticoagulation outcomes in NBTE can vary greatly: some patients have vegetations resolve, while others experience disease progression to new valves despite therapy.1  Because NBTE-specific evidence remains sparse, the underlying clinical context primarily guides the choice of anticoagulant:  Multiple case reports describe DOAC failure with recurrent embolization in patients with cancer and NBTE. 6-8  LMWH remains a mainstay for patients with cancer or when patients experience thrombotic complications on DOACs. 1  Warfarin is the preferred anticoagulant among patients with thrombotic antiphospholipid syndrome. 9  The duration of anticoagulation should take into consideration the status of the underlying disease, the presence of valvular lesions on follow-up imaging, and an individualized assessment of risks and benefits. 1  References - Nonbacterial Thrombotic Endocarditis Ahmed O, King NE, Qureshi MA, et al. Non-bacterial thrombotic endocarditis: a clinical and pathophysiological reappraisal. European Heart Journal. 2025;46(3):236-49.  Balata D, Mellergård J, Ekqvist D, et al. Non-bacterial thrombotic endocarditis: a presentation of COVID-19. European journal of case reports in internal medicine. 2020;7(8).   Li JS, Sexton DJ, Mick N, et al. Proposed modifications to the Duke criteria for the diagnosis of infective endocarditis. Clin Infect Dis 2000;30: 633–8.   Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol 2021;77:e25–197.   Vahanian A, Beyersdorf F, Praz F, et al.; ESC/EACTS Scientific Document Group. 2021 ESC/EACTS Guidelines for the management of valvular heart disease. Eur Heart J. 2022 Feb 12;43(7):561-632.   Mantovani F, Navazio A, Barbieri A, Boriani G. A first described case of cancer- associated non-bacterial thrombotic endocarditis in the era of direct oral anticoagulants. Thromb Res 2017;149:45–7.   Panicucci E, Bruno C, Ferrari V, Suissa L. Recurrence of ischemic stroke on direct oral anticoagulant therapy in a patient with marantic endocarditis related to lung cancer. J Cardiol Cases 2021;23:242–5.  Shoji MK, Kim JH, Bakshi S, et al. Nonbacterial thrombotic endocarditis due to primary gallbladder malignancy with recurrent stroke despite anticoagulation: case report and literature review. J Gen Intern Med 2019;34:1934–40.   Khairani CD, Bejjani A, Piazza G, et al. Direct oral anticoagulants vs vitamin K antagonists in patients with antiphospholipid syndromes: meta-analysis of randomized trials. J Am Coll Cardiol 2023;81:16–30.  Case Media TTE and TEE

5个月前
32:05
422. Diagnosis of Transthyretin Amyloid Cardiomyopathy (ATTR-CM) with Dr. Venkatesh Murthy

422. Diagnosis of Transthyretin Amyloid Cardiomyopathy (ATTR-CM) with Dr. Venkatesh Murthy

Drs. Rick Ferraro and Sneha Nandy discuss ‘Diagnosis of ATTR Cardiac Amyloidosis’ with Dr. Venkatesh Murthy.  In this episode, we explore the diagnosis of ATTR cardiac amyloidosis, a condition once considered rare but now increasingly recognized due to advances in imaging and the availability of effective therapies. Dr. Venkatesh Murthy, a leader in multimodality imaging, discusses key clinical and laboratory features that should raise suspicion for the disease. We also examine the role of nuclear imaging and genetic testing in confirming the diagnosis, as well as the importance of early detection. Tune in for expert insights on navigating this challenging diagnosis and look out for our next episode on treatment approaches for cardiac amyloidosis! Audio editing for this episode was performed by CardioNerds Intern, Julia Marques Fernandes. Enjoy this Circulation Paths to Discovery article to learn more about the CardioNerds mission and journey.  US Cardiology Review is now the official journal of CardioNerds! Submit your manuscripts here.  CardioNerds Cardiac Amyloid PageCardioNerds Episode Page Pearls: - Diagnosis of Transthyretin amyloid cardiomyopathy 1. Recognizing the Red Flags – ATTR cardiac amyloidosis often presents with subtle but telling signs, such as bilateral carpal tunnel syndrome, low-voltage ECG, and a history of lumbar spinal stenosis or biceps tendon rupture. If you see these features in a patient with heart failure symptoms, think amyloidosis!    2. “Vanilla Ice Cream with a Cherry on Top” – On strain echocardiography, apical sparing is a classic pattern for cardiac amyloidosis. While helpful, it’s not foolproof—multimodal imaging and clinical suspicion are key!   3. Nuclear Imaging is a Game-Changer – When suspicion for cardiac amyloidosis is high à a positive PYP scan with SPECT imaging (grade 2 or 3 myocardial uptake) in the absence of monoclonal protein (ruled out by SPEP, UPEP, and free light chains) is diagnostic for ATTR amyloidosis—no biopsy needed!   4. Wild-Type vs. Hereditary? Know the Clues – Older patients (70+) are more likely to have wild-type ATTR, while younger patients (40s-60s), especially those with neuropathy and a family history of heart failure, should raise suspicion for hereditary ATTR. Genetic testing is crucial for distinguishing between the two. Note that some ATTR variants may predispose to a false negative PYP scan!  5. Missing Amyloidosis = Missed Opportunity – With multiple disease-modifying therapies now available, early diagnosis is critical. If you suspect cardiac amyloidosis, don’t delay the workup—early treatment improves outcomes!   Notes - Diagnosis of Transthyretin amyloid cardiomyopathy What clinical features should raise suspicion for ATTR cardiac amyloidosis?   ATTR cardiac amyloidosis is underdiagnosed because symptoms overlap with other forms of heart failure.   Red flags include bilateral carpal tunnel syndrome (often years before cardiac symptoms), low-voltage ECG despite increased LV wall thickness, heart failure with preserved ejection fraction (HFpEF) with a restrictive pattern, and history of lumbar spinal stenosis, biceps tendon rupture, and/or peripheral neuropathy, including possible autonomic dysfunction (e.g., orthostatic hypotension).  Remember: If an older patient presents with heart failure and unexplained symptoms like neuropathy or musculoskeletal issues, think amyloidosis!   What is the differential diagnosis for a thick left ventricle (LVH) and how does ATTR amyloidosis fit into it?    Hypertension: Most common cause of LVH, typically with a history of uncontrolled high blood pressure.   Aortic stenosis: May present with concentric LVH.   Hypertrophic cardiomyopathy (HCM): Genetic disorder typically presenting with asymmetric LVH, especially in younger patients.   Infiltrative cardiomyopathy: Often due to amyloidosis, sarcoidosis, or hemochromatosis.  Storage disorder: Fabry’s, Danon, Pompe, etc.  What are the key imaging modalities used to diagnose ATTR cardiac amyloidosis?   Echocardiography: Thickened LV walls (>12 mm) with a restrictive filling pattern, Speckled appearance on 2D echo (not specific), apical sparing on strain imaging (“Vanilla ice cream with a cherry on top”).  Cardiac MRI (CMR): Late gadolinium enhancement (LGE) in a global subendocardial pattern, T1 mapping & extracellular volume (ECV) expansion are supportive findings.  Nuclear Scintigraphy (99mTc-PYP scan): Gold standard noninvasive test for ATTR. Grade 2 or 3 uptake (equal to or greater than bone uptake) is diagnostic if monoclonal protein is absent in the right clinical scenario.   What lab tests are used to diagnose ATTR cardiac amyloidosis?   Check troponin and NTproBNP (useful for staging)  Rule out AL amyloidosis with monoclonal protein studies like serum protein electrophoresis (SPEP) and urine protein electrophoresis (UPEP) with immunofixation and serum free light chain (FLC) assay (to detect clonal plasma cell disorders)   Why is ruling out AL amyloidosis critical before diagnosing ATTR?   They are treated very differently- AL amyloidosis is an oncologic emergency requiring chemotherapy, while ATTR is treated with medications.  If workup for AL amyloidosis, such as SPEP/UPEP or serum free light chains ratio, comes back positive, you do not need to pursue further testing for ATTR amyloidosis.   When should genetic testing be performed in suspected ATTR amyloidosis?   All patients diagnosed with ATTR amyloidosis should undergo genetic testing to distinguish wild-type from hereditary forms.   Wild-type ATTR:  More common in older men (≥70 years), no known mutation, sporadic occurrence, often presents with predominantly cardiac involvement   Familial ATTR: Autosomal dominant inheritance, more common in Black patients (V122I mutation), more likely to have neuropathy and earlier onset of heart failure (4th or 5th decade). Specific variants have typical geographic distribution and predilection to causing neuropathy and/or cardiomyopathy.  When is a biopsy necessary to confirm ATTR amyloidosis?    Biopsy is not needed if PYP scan is positive (Grade 2-3) and AL amyloidosis is ruled out.   If the diagnosis remains uncertain, a biopsy can be performed of either a fat pad or salivary gland biopsy (easier, lower sensitivity) or an endomyocardial biopsy (gold standard but invasive).  References - Diagnosis of Transthyretin amyloid cardiomyopathy Dorbala S, Ando Y, Bokhari S, et al. ASNC/AHA/ASE/EANM/HFSA/ISA/SCMR/SNMMI expert consensus recommendations for multimodality imaging in cardiac amyloidosis: Part 1 of 2-evidence base and standardized methods of imaging [published correction appears in J Nucl Cardiol. 2021 Aug;28(4):1761-1762. doi: 10.1007/s12350-021-02711-w.]. J Nucl Cardiol. 2019;26(6):2065-2123. doi:10.1007/s12350-019-01760-6  https://pubmed.ncbi.nlm.nih.gov/31468376 Writing Committee, Kittleson MM, Ruberg FL, et al. 2023 ACC Expert Consensus Decision Pathway on Comprehensive Multidisciplinary Care for the Patient With Cardiac Amyloidosis: A Report of the American College of Cardiology Solution Set Oversight Committee [published correction appears in J Am Coll Cardiol. 2023 Mar 21;81(11):1135. doi: 10.1016/j.jacc.2023.02.013.]. J Am Coll Cardiol. 2023;81(11):1076-1126. doi:10.1016/j.jacc.2022.11.022  https://pubmed.ncbi.nlm.nih.gov/36697326

5个月前
13:38
421. Case Report: Switched at Birth: A Case of Congenital Heart Disease Presenting in Adulthood – New York Presbyterian Queens

421. Case Report: Switched at Birth: A Case of Congenital Heart Disease Presenting in Adulthood – New York Presbyterian Queens

CardioNerds (Dr. Claire Cambron and Dr. Rawan Amir) join Dr. Ayan Purkayastha, Dr. David Song, and Dr. Justin Wang from NewYork-Presbyterian Queens for an afternoon of hot pot in downtown Flushing. They discuss a case of congenital heart disease presenting in adulthood. Expert commentary is provided by Dr. Su Yuan, and audio editing for this episode was performed by CardioNerds Intern, Julia Marques Fernandes. A 53-year-old woman with a past medical history of hypertension visiting from Guyana presented with 2 days of chest pain. EKG showed dominant R wave in V1 with precordial T wave inversions. Troponin levels were normal, however she was started on therapeutic heparin with plan for left heart catheterization. Her chest X-ray revealed dextrocardia and echocardiogram was suspicious for the systemic ventricle being the morphologic right ventricle with reduced systolic function and the pulmonic ventricle being the morphologic left ventricle. Patient underwent coronary CT angiography which confirmed diagnosis of congenitally corrected transposition of the great arteries (CCTGA) as well as minimal non-obstructive coronary artery disease. Her chest pain spontaneously improved and catheterization was deferred. Patient opted to follow with a congenital specialist back in her home country upon discharge.   US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls- A Case of Congenital Heart Disease Presenting in Adulthood Congenitally Corrected Transposition of the Great Arteries (CCTGA) is a rare and unique structural heart disease which presents as an isolated combination of atrioventricular and ventriculoarterial discordance resulting in physiologically corrected blood flow.   CCTGA occurs due to L looping of the embryologic heart tube. As a result, the morphologic right ventricle outflows into the systemic circulation, and the morphologic left ventricle outflows into the pulmonary circulation.   CCTGA is frequently associated with ventricular septal defects, pulmonic stenosis, tricuspid valve abnormalities and dextrocardia.   CCTGA is often asymptomatic in childhood and can present later in adulthood with symptoms of morphologic right ventricular failure, tricuspid regurgitation, or cardiac arrhythmias.   Systemic atrioventricular valve (SAVV) intervention can be a valuable option for treating right ventricular failure and degeneration of the morphologic tricuspid valve.  notes- A Case of Congenital Heart Disease Presenting in Adulthood Notes were drafted by Ayan Purkayastha.  What is the pathogenesis of Congenitally Corrected Transposition of the Great Arteries?   Occurs due to disorders in the development of the primary cardiac tube   Bulboventricular part of the primary heart forms a left-sided loop instead of right-sided loop, leading to the normally located atria being connected to morphologically incompatible ventricles   This is accompanied by abnormal torsion of the aortopulmonary septum (transposition of the great vessels)   As a result, there is ‘physiologic correction’ of blood flow. Non-oxygenated blood flows into the right atrium and through the mitral valve into the morphologic left ventricle, which pumps blood into the pulmonary artery. Oxygenated blood from the pulmonary veins flows into the left atrium and through the tricuspid valve to the morphologic right ventricle, which pumps blood to the aorta. Compared with standard anatomy, the flow of blood is appropriate, but it is going through the incorrect ventricle on both sides.  Frequent conditions associated with CCTGA include VSD, pulmonic stenosis and dextrocardia   What is the presentation of Congenitally Corrected Transposition of the Great Arteries?   In cases without concomitant deficits CCTA is asymptomatic early in life and often for several decades. Cyanosis and dyspnea are common presenting symptoms.   Systemic right ventricular dysfunction due to high systemic pressures over time  Arrythmias, commonly AV block, due to abnormal structure of the conduction system   Tricuspid valve regurgitation resulting from dilation of the right ventricle and tricuspid valve annulus  What is Dextrocardia and how is it associated with CCTGA?   Dextrocardia is a cardiac positional anomaly where the heart is located in the right hemithorax with base to apex axis directed to the right and caudad   Dextrocardia can occur in up to 20% cases of CCTGA   Can be associated with both situs solitus (normal anatomic arrangement of chest and abdominal organs) or situs inversus (chest and abdominal organs are mirrored from their normal positions)   How is CCTGA Diagnosed?    Transthoracic echocardiography is the primary diagnostic tool in CCTGA   Assessment of the systemic RV function is crucial but can be challenging. Techniques such as speckle tracking echocardiography and global longitudinal strain can help with assessment of systemic RV function   Cardiac MRI can also provide accurate measurements of ventricular volumes as well as quantification of valvular regurgitation   What is the long-term management of CCTGA in adults?   Many patients with CCTGA and no associated lesions have long life expectancies with minimal or non-specific symptoms     Symptoms of circulatory failure occur mainly in 5th and 6th decades of life   The 2018 AHA/ACC Guidelines for the Management of Adults with Congenital Heart Disease recommends the following routine follow-up and testing intervals for CCTGA  Physiologic stage A: Outpatient ACHD follow up every 12 months with ECG(12 months), TTE(12-24 months), Holter monitor(12-60 months), CMR/CCT and exercise test(36-60 months)   Physiologic stage B: outpatient ACHD follow up every 12 months with ECG and TTE(12 months), Holter monitor(12-60 months), CMR/CCT and exercise test(36-60 months)    Physiologic stage C: outpatient ACHD follow up every 6-12 months with ECG and TTE(12 months), pulse oximetry at each visit, Holter monitor(12-36 months), CMR/CCT and exercise test(12-24 months)   Physiologic stage D: outpatient ACHD follow up every 3-6 months, ECG and TTE every 12 months, pulse oximetry at each visit, Holter monitor, CMR/CCT and exercise test every 12 months   What is the role of Systemic Atrioventricular Valve Surgery (SAVV) for treatment of CCTGA as an adult?   In CCTGA the morphologic tricuspid valve acts as the SAVV and is subject to functional deterioration from high systemic pressures   Tricuspid valve regurgitation is a key prognostic overall survival determinant in CCTGA patients   Studies have shown that 94% of patients with CCTGA suffered from intrinsic tricuspid valve abnormalities   SAV surgery remains a valuable option with low early mortality and good long-term outcomes, especially with ejection fraction > 40%.   The 2018 AHA/ACC Guidelines for the Management of Adults with Congenital Heart Disease recommends tricuspid valve replacement for symptomatic adults with CCTGA and severe TR and preserved or mildly depressed systemic ventricular function (class IB recommendation).   References - A Case of Congenital Heart Disease Presenting in Adulthood 1.        Baruteau AE, Abrams DJ, Ho SY, Thambo JB, McLeod CJ, Shah MJ. Cardiac Conduction System in Congenitally Corrected Transposition of the Great Arteries and Its Clinical Relevance. J Am Heart Assoc. 2017;6(12). doi:10.1161/JAHA.117.007759  2.        Susheel Kumar TK. Congenitally corrected transposition of the great arteries. J Thorac Dis. 2020;12(3):1213-1218. doi:10.21037/jtd.2019.10.15  3.        Osakada K, Ohya M, Waki K, Nasu H, Kadota K. Congenitally Corrected Transposition of the Great Arteries at Age 88 Years. CJC Open. 2020;2(6):726-728. doi:10.1016/j.cjco.2020.08.003  4.        Munaf M, Farooqui S, Kazmi SK, Ul-Haque I. Congenitally Corrected Transposition of Great Arteries with Dextrocardia, Patent Ductus Arteriosus, Atrial Septal Defects and Ventricular Septal Defects in a 15-Year-Old Marfanoid Habitus Patient: A Case Study. Cureus. Published online July 1, 2020. doi:10.7759/cureus.8937  5.        Abdelrehim AA, Stephens EH, Miranda WR, et al. Systemic Atrioventricular Valve Surgery in Patients With Congenitally Corrected Transposition of the Great Vessels. J Am Coll Cardiol. 2023;82(23):2197-2208. doi:10.1016/j.jacc.2023.09.822  6.        Lippmann MR, Maron BA. The Right Ventricle: From Embryologic Development to RV Failure. Curr Heart Fail Rep. 2022;19(5):325-333. doi:10.1007/s11897-022-00572-z  7.        Brida M, Diller GP, Gatzoulis MA. Systemic Right Ventricle in Adults with Congenital Heart Disease. Circulation. 2018;137(5):508-518. doi:10.1161/CIRCULATIONAHA.117.031544  8.        Bevilacqua F, Pasqualin G, Ferrero P, et al. Overview of Long-Term Outcome in Adults with Systemic Right Ventricle and Transposition of the Great Arteries: A Review. Diagnostics. 2023;13(13). doi:10.3390/diagnostics13132205  9.        Maldjian PD, Saric M. Approach to dextrocardia in adults: Review. American Journal of Roentgenology. 2007;188(6 SUPPL.). doi:10.2214/AJR.06.1179  10.      Kandakure PR, Katta Y, Batra MJ, Timmanwar A, Lakka VK, Reddy B. Dextrocardia and corrected transposition of the great arteries with rheumatic tricuspid stenosis: a unique association. Indian J Thorac Cardiovasc Surg. 2019;35(2):230-232. doi:10.1007/s12055-018-0778-0  11.      Stout KK, Daniels CJ, Aboulhosn JA, et al.

6个月前
29:12
420. Cardio-Rheumatology: Cardiovascular Multimodality Imaging & Systemic Inflammation with Dr. Monica Mukherjee

420. Cardio-Rheumatology: Cardiovascular Multimodality Imaging & Systemic Inflammation with Dr. Monica Mukherjee

In this episode, CardioNerds Dr. Gurleen Kaur, Dr. Richard Ferraro, and Dr. Jake Roberts are joined by Cardio-Rheumatology expert, Dr. Monica Mukherjee, to discuss the role of utilizing multimodal imaging for cardiovascular disease risk stratification, monitoring, and management in patients with chronic systemic inflammation. The team delves into the contexts for utilizing advanced imaging to assess systemic inflammation with cardiac involvement, as well as the role of imaging in monitoring various specific cardiovascular complications that may develop due to inflammatory diseases. Audio editing by CardioNerds academy intern, Christiana Dangas. CardioNerds Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Cardiovascular Multimodality Imaging & Systemic Inflammation Systemic inflammatory diseases are associated with an elevated CVD risk that has significant implications for early detection, risk stratification, and implementation of therapeutic strategies to address these risks and disease-specific complications. As an example, patients with SLE have a 48-fold increased risk for developing ASCVD compared to the general population. They may also develop disease-specific complications, such as pericarditis, that require focused imaging approaches to detect. In addition to increasing the risk for CAD, systemic inflammatory diseases can also result in cardiac complications, including myocardial, pericardial, and valvular involvement. Assessment of these complications requires the use of different imaging techniques, with the modality and serial studies selected based on the suspected disease process involved. In most contexts, echocardiography remains the starting point for evaluating cardiac involvement in systemic inflammatory diseases and can inform the next steps in terms of diagnostic study selection for the assessment of specific cardiac processes. For example, if echocardiography is completed in an SLE patient and demonstrates potential myocardial or pericardial inflammation, the next steps in evaluation may include completing a cardiac MRI for better characterization. While no current guidelines or standards of care directly guide our selection of advanced imaging studies for screening and management of CVD in patients with systemic inflammatory diseases, our understanding of cardiac involvement in these patients continues to improve and will likely lead to future guideline development. Due to the vast heterogeneity of cardiac involvement both across and within different systemic inflammatory diseases, a personalized approach to caring for each individual patient remains central to CVD evaluation and management in these patients. For example, patients with systemic sclerosis and symptoms of shortness of breath may experience these symptoms due to a range of causes. Echocardiography can be a central guiding tool in assessing these patients for potential concerns related to pulmonary hypertension or diastolic dysfunction. Based on the initial echocardiogram, the next steps in evaluation may involve further ischemic evaluation or right heart catheterization, depending on the pathology of concern. Show notes - Cardiovascular Multimodality Imaging & Systemic Inflammation Episode notes drafted by Dr. Jake Roberts. What are the contexts in which we should consider pursuing multimodal cardiac imaging, and are there certain inflammatory disorders associated with systemic inflammation and higher associated CVD risk for which advanced imaging can help guide early intervention? Systemic inflammatory diseases are associated with elevated CVD risk, which has significant implications for early detection, risk stratification, prognostication, and implementation of therapeutic strategies to address CVD risk and complications in these patient populations.The most well-characterized autoimmune diseases with an association between systemic inflammation and CVD risk are inflammatory arthritic conditions such as rheumatoid arthritis. Additional inflammatory diseases with elevated CVD risk include spondyloarthropathies and psoriatic arthritis.Patients with rheumatoid arthritis have a 1.5- 2x risk of developing coronary artery disease compared to the general population.The mechanism of elevated CVD risk in inflammatory disease patients is likely related to a combination of abnormalities in lipid metabolism, endothelial dysfunction, and vascular inflammation. Conditions including systemic lupus erythematosus (SLE), myositis, vasculitis disorders, and systemic sclerosis may have additional cardiovascular complications beyond CAD, including pericarditis, myocarditis, electrical, and valvular complications. Are there any established or emerging technologies to help with improving early detection or characterization of cardiac involvement in systemic inflammatory diseases? Echocardiography remains the most common and useful starting point for screening and early detection of cardiac involvement in systemic inflammatory diseases due to its widespread availability, real-time interpretation, low cost, and noninvasive nature. Furthermore, echocardiography remains a crucial tool in serial monitoring for disease progression and the detection of therapeutic effects. This modality additionally provides significant utility for early detection and screening of pericardial and valvular involvement. Given that patients with inflammatory disorders have an elevated risk for developing CAD, utilizing CAC scores and CCTA are often additionally helpful for CAD detection in these patient populations. Are there different imaging techniques that should be used to assess complications specific to different systemic inflammatory diseases? Based on the specific disease involved, the choice of imaging technique may vary depending on the clinical context and the cardiovascular complication requiring further investigation. As an example, in systemic sclerosis, there can be a wide range of variable cardiac manifestations that emerge depending on the subtype of the disease, with the cardiac complications developing either because of the fibrotic disease process or from other secondary effects of the disease. Specifically, if the patient's phenotype involves interstitial lung disease, the right ventricle of the heart will encounter chronic increased afterload, which can lead to adverse adaptive responses and remodeling over time. As a result, screening tools such as echocardiography can be very useful in this patient population, with these patients often requiring regular annual screening echocardiograms coupled with pulmonary function testing to screen for coupled changes in individual patients’ physiology. When these patients develop complications of their disease, including pulmonary hypertension, echocardiography can help evaluate the underlying cause of this complication and inform subsequent diagnostic steps. In terms of assessing myocardial disease and inflammation in myocardial tissue, cardiac MRI remains a valuable tool in detecting subclinical myocardial disease and can identify areas of low-grade myocardial inflammation. One of the advantages of cardiac MRI over other imaging techniques involves its ability to allow for noninvasive tissue characterization. For disease complications such as pericarditis, which can commonly develop in SLE, 2D echocardiography remains the first-line imaging modality of choice to detect pericardial disease involvement. In SLE patients who have long-standing pericardial disease with progression, they can also develop constrictive symptoms resulting from this process. In those cases, either CT or cardiac MRI can assist in defining the pericardial or myocardial anatomy. As an example, what would be the approach to utilizing advanced imaging to assess for CVD detection and monitoring in a patient with SLE with relatively well-controlled symptoms on chronic immunosuppressive agents and no prior history of heart failure or CVD? As a starting point, all patients with systemic inflammatory diseases should undergo comprehensive ASCVD risk assessment. Initial stratification involves completing a laboratory assessment with a standard lipid panel and diabetes screening studies. Further evaluation of any symptoms that a patient may describe, which could indicate potential early cardiovascular disease processes, should also be thoroughly assessed and may influence the next steps in screening. In the context of SLE, pericardial disease is common, and therefore, obtaining a baseline echocardiogram to assess for any early pericardial involvement should be the initial step in evaluation. If the patient also has an elevated ASCVD risk, they should also undergo assessment for coronary artery disease. What should be the approach to the sequence of imaging technique selection, serial imaging, monitoring, and follow-up in patients with systemic inflammatory disorders undergoing evaluation of CVD screening and monitoring? The initial selection of imaging modality should be based on what is suspected to be the primary driver of the patient’s symptoms or as the primary underlying process of concern that requires further evaluation. As an important consideration in the context of systemic inflammatory diseases such as SLE, ischemic disease may involve atypical presentations due to underlying myocardial dysfunction and microvascular disease. Therefore, imaging and other diagnostic studies may be warranted to assess for reversible ischemia. There is emerging evidence that cardiac PET perfusion and cardiac MRI may be particularly useful in this patient population to assess coronary flow reserve to evaluate for coronary microvascular disease.

6个月前
17:54
419. HFpEF in Women with Dr. Anu Lala and Dr. Martha Gulati

419. HFpEF in Women with Dr. Anu Lala and Dr. Martha Gulati

In this episode, CardioNerds Dr. Anna Radakrishnan and Dr. Apoorva Gangavelli are joined by prevention expert Dr. Martha Gulati and heart failure expert Dr. Anu Lala to discuss heart failure with preserved ejection fraction (HFpEF), a multifactorial, evolving challenge, particularly in women. In this episode, we delve into the distinctive clinical presentation and pathophysiology of HFpEF among women, exploring both traditional and gender-specific risk factors, from metabolic and inflammatory processes to the impact of obesity, sleep apnea, and gender-specific conditions. We also discussed the latest evidence on prevention strategies and emerging therapies that not only target HFpEF symptoms but also address underlying risk factors. This conversation highlights the importance of multidisciplinary, holistic care to advance diagnosis, management, and ultimately, patient outcomes for women with HFpEF. Audio editing by CardioNerds academy intern, Christiana Dangas.  Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Heart Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - HFpEF in Women HFpEF Is a Multisystem Syndrome:HFpEF in women involves more than just diastolic dysfunction—it represents a convergence of metabolic, inflammatory, and hormonal factors that make its diagnosis and management uniquely challenging. Visceral Adiposity Drives Risk:Obesity isn’t just excess weight; central or visceral adiposity actively promotes inflammation, insulin resistance, and microvascular dysfunction, which are crucial in triggering HFpEF in women. Early Identification Is Key:Recognizing—and treating—subtle risk factors such as sleep-disordered breathing, hypertension, and subtle metabolic dysfunction early, especially in women who may underreport symptoms, can prevent progression to HFpEF. Holistic, Lifespan Approach Matters:Effective HFpEF care involves managing the whole cardiometabolic profile with tailored lifestyle interventions, advanced medications (e.g., SGLT2 inhibitors, GLP-1 agonists), and even cardiac rehabilitation, which remain critical at every stage, even after diagnosis. Tailoring Prevention to Unique Risks in Women:Gender-specific factors such as postmenopausal hormonal changes, pregnancy-related complications, and autoimmune conditions demand a customized prevention strategy, reminding us that prevention isn’t one-size-fits-all. Show notes - HFpEF in Women Notes drafted by Dr. Apoorva Gangavelli 1. What are the gender-based differences in HFpEF presentation? HFpEF in women often presents with more subtle symptoms such as exertional dyspnea and fatigue, which may be mistakenly attributed to aging or obesity. Women tend to have a higher prevalence of preserved ejection fraction despite a similar heart failure symptom burden to men. The diagnostic challenge is compounded by lower natriuretic peptide levels influenced by hormonal factors, particularly postmenopausal estrogen deficiency, leading to false negatives and underdiagnosis. 2. How do traditional and gender-specific risk factors contribute to the development of HFpEF in women? Traditional risk factors include obesity, hypertension, diabetes, and metabolic syndrome. Gender-specific risk factors encompass pregnancy-related complications, menopause, and autoimmune diseases, which may uniquely affect cardiovascular structure and function in women. The interaction between visceral adiposity and systemic inflammation is central in predisposing women to HFpEF. 3. What underlying pathophysiological mechanisms make women more susceptible to HFpEF? Chronic inflammation and endothelial dysfunction contribute to myocardial stiffness and diastolic dysfunction. Insulin resistance results in impaired myocardial metabolism and lipotoxicity. Microvascular dysfunction, with reduced nitric oxide bioavailability, is more pronounced in women, exacerbating cardiac remodeling and fibrosis. 4. What prevention strategies can be tailored across different life stages to reduce HFpEF risk in women? Early detection and aggressive management of traditional risk factors (e.g., blood pressure control, weight management) during perimenopause and early adulthood. Incorporating lifestyle modifications such as structured exercise programs, improved dietary habits, and sleep optimization. Preventive interventions might also include screening for gender-specific risk factors like pregnancy complications and autoimmune conditions early in life. 5. What current and emerging therapeutic approaches are used in the management of HFpEF in women? Use of mineralocorticoid receptor antagonists and nonsteroidal alternatives shows promise, particularly in reducing hospitalizations. Novel pharmacologic agents such as SGLT2 inhibitors and GLP-1 receptor agonists address both heart failure symptoms and metabolic dysfunction. Cardiac rehabilitation is advocated to improve functional capacity and quality of life despite challenges with insurance coverage. References - HFpEF in Women Borlaug BA, Sharma K, Shah SJ, Ho J. Heart Failure With Preserved Ejection Fraction. Journal of the American College of Cardiology. 2023;81(18). doi:https://doi.org/10.1016/j.jacc.2023.01.049 ‌Kittleson MM, Gurusher Panjrath, Kaushik Amancherla, et al. 2023 ACC Expert Consensus Decision Pathway on Management of Heart Failure With Preserved Ejection Fraction. Journal of the American College of Cardiology. 2023;81(18). doi:https://doi.org/10.1016/j.jacc.2023.03.393 Radakrishnan A, Agrawal S, Singh N, et al. Underpinnings of Heart Failure With Preserved Ejection Fraction in Women - From Prevention to Improving Function. A Co-publication With the American Journal of Preventive Cardiology and the Journal of Cardiac Failure. Journal of Cardiac Failure. Published online February 2025. doi:https://doi.org/10.1016/j.cardfail.2025.01.008

7个月前
24:40
418. CardioNerds x CSWG – LV Unloading in AMI-Shock with Dr. Navin Kapur, Dr. Shashank Sinha & Dr. Rachna Kataria

418. CardioNerds x CSWG – LV Unloading in AMI-Shock with Dr. Navin Kapur, Dr. Shashank Sinha & Dr. Rachna Kataria

In this webinar, the CardioNerds collaborated with the Cardiogenic Shock Working Group (CSWG) to discuss LV unloading and the updated AMI guidelines, which upgraded transvalvular flow pumps to a Class 2A recommendation in AMI shock. Dr. Rachel Goodman and Dr. Gurleen Kaur from CardioNerds were joined by Dr. Navin Kapur (Tufts Medical Center), Dr. Shashank Sinha (INOVA Fairfax Hospital), and Dr. Rachna Kataria (Brown University) from the CSWG. Together, they explore a case of an older woman who presented with inferior STEMI and was found to have complete occlusion of an anomalous single coronary artery originating from the right coronary cusp and supplying the entire left ventricle. She was treated with DES to the anomalous RCA. Her course was complicated by AMI shock with re-occlusion of the DES, which was treated with thrombectomy and balloon angioplasty. An IABP was placed. After transfer to a tertiary care center, a pulmonary artery catheter revealed a CI of 0.96. With worsening shock, rising lactate, and end organ dysfunction, the team proceeded with VA-ECMO and Impella CP for LV unloading. Her lactate subsequently normalized. Produced by CardioNerds in collaboration with the Cardiogenic Shock Working Group. CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

8个月前
23:25
417. Case Report: Clear Vision, Clouded Heart: Ocular Venous Air Embolism with Pulmonary Air Embolism, RV Failure, and Cardiac Arrest – Trinity Health Ann Arbor

417. Case Report: Clear Vision, Clouded Heart: Ocular Venous Air Embolism with Pulmonary Air Embolism, RV Failure, and Cardiac Arrest – Trinity Health Ann Arbor

CardioNerds Critical Care Cardiology Council members Dr. Gurleen Kaur and Dr. Katie Vanchiere meet with Dr. Yash Patel, Dr. Akanksha, and Dr. Mohammed El Nayir from Trinity Health Ann Arbor. They discuss a case of pulmonary air embolism, RV failure, and cardiac arrest secondary to an ocular venous air embolism. Expert insights provided by Dr. Tanmay Swadia. Audio editing by CardioNerds Academy intern, Grace Qiu. A 36-year-old man with a history of multiple ocular surgeries, including a complex retinal detachment repair, suffered a post-vitrectomy collapse at home. He was found hypoxic, tachycardic, and hypotensive, later diagnosed with a pulmonary embolism from ocular venous air embolism leading to severe right heart failure. Despite a mild embolic burden, the cardiovascular response was profound, requiring advanced hemodynamic support, including an Impella RP device (Abiomed, Inc.). Multidisciplinary management, including fluid optimization, vasopressors and mechanical support to facilitate recovery. This case underscores the need for early recognition and individualized intervention in cases of ocular venous air embolism. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls- Clear Vision, Clouded Heart: Ocular Venous Air Embolism with Pulmonary Air Embolism, RV Failure, and Cardiac Arrest Hypoxia, hypotension and tachycardia in a patient following ocular instrumentation are classic findings suggestive of pulmonary embolism from possible air embolism. The diagnosis of RV failure is based on clinical presentation, echocardiographic findings (such as McConnell’s sign), and invasive hemodynamic assessment via right heart catheterization. Mechanical circulatory support can be considered as a temporary measure for patients with refractory RV failure. Central Figure: Approach to Pulmonary Embolism with Acute RV Failure Notes - Clear Vision, Clouded Heart: Ocular Venous Air Embolism with Pulmonary Air Embolism, RV Failure, and Cardiac Arrest 1. What is an Ocular Venous Air Embolism (VAE), and how can it be managed in critically ill patients? An Ocular Venous Air Embolism is defined as the entry of air into the systemic venous circulation through the ocular venous circulation, often during vitrectomy procedures. Early diagnosis is key to preventing cardiovascular collapse in cases of Ocular Venous Air Embolism (VAE).  The goal is to stop further air entry. This can be done by covering the surgical site with saline-soaked dressings and checking for air entry points. Adjusting the operating table can help, especially with a reverse Trendelenburg position for lower-body procedures. The moment VAE is suspected, discontinue nitrous oxide and switch to 100% oxygen. This helps with oxygenation, speeds up nitrogen elimination, and shrinks air bubbles. Hyperbaric Oxygen Therapy can reduce bubble size and improve oxygenation, especially in cases of cerebral air embolism, when administered within 6 hours of the incident. Though delayed hyperbaric oxygen therapy can still offer benefits, the evidence is mixed. VAE increases right heart strain, so inotropic agents like dobutamine can help boost cardiac output, while norepinephrine supports ventricular function and systemic vascular resistance, but this may also worsen pulmonary resistance.  Aspiration of air via multi-orifice or Swan-Ganz catheters has limited success, with success rates ranging from 6% to 16%. In contrast, the Bunegin-Albin catheter has shown more promise, with a 30-60% success rate. Catheterization for acute VAE-induced hemodynamic compromise is controversial, and there's insufficient evidence to support its widespread emergency use. 2. What are the key hemodynamic parameters used to assess RV function? On echocardiogram, there are a number of parameters that can assess RV function: Tricuspid Annular Plane Systolic Excursion (TAPSE): Measures the lateral tricuspid annulus’ movement during systole. A TAPSE value below 1.6 cm is associated with poor prognosis.RV Outflow Tract (RVOT) Acceleration Time: Measured via pulsed wave Doppler, an acceleration time of <100 ms is abnormal, with values ≤60 ms indicating a worse prognosis.Global RV Longitudinal Strain: Assessed via speckle tracking, with a strain value of −20% being highly predictive of RV dysfunction (normal values typically range -24.5 to -28.5%).Tricuspid Regurgitation (TR) Jet Velocity: Helps estimate pulmonary systolic pressure and provides prognostic information.Inferior Vena Cava (IVC) Collapsibility: Useful in estimating right atrial pressure and guiding volume resuscitation, though it lacks prognostic significance. The RV:LV diameter ratio offers prognostic value, with a ratio greater than 0.9  linked to worse outcomes. Invasive Hemodynamic Monitoring (Right heart catheterization, PA Catheter) The Pulmonary Artery Pulsatility Index (PAPI) is an invasive hemodynamic parameter used to assess right ventricular (RV) function, particularly in cases of RV failure and cardiogenic shock. PAPi is the pulmonary arterial pulse pressure divided by the RA pressure. A PAPi of <0.9 is a poor indicator, especially in the acute myocardial infarction population. 3. What are the core principles in managing a patient with RV failure?  The management to optimize RV function is centered around optimizing preload, afterload, and contractility.Optimizing preload - Optimizing preload is one of the most important aspects in the management of acute decompensated RV failure. The majority of us are taught that the RV is “preload dependent” and patients should be fluid resuscitated. However, many patients are actually volume overloaded and may benefit from diuresis. Overall, this is a patient-to-patient decision, depending on the clinical picture, to optimize preload; though the use of pulmonary artery (PA) catheters in this setting is not well supported.Reducing afterload - Avoid intubation if clinically feasible, as they may increase PVR; however, if essential, ideally, oxygen saturation (SaO₂) should be maintained above 92%, and ventilator settings should be adjusted to optimize lung volume and maintain a normal pH and PCO₂. Nitric oxide has also been beneficial in improving oxygenation and reducing PVR with its vasodilatory effects. Support cardiac output May support with the use of inotropes as well as mechanical circulatory support.Pressors: The ideal vasopressor increases systemic arterial pressure and RV contractility without raising pulmonary vascular resistance.Norepinephrine: Primarily an α1 agonist, it improves systemic blood pressure with some β1 stimulation. It has shown benefits in maintaining RV-PA coupling.Dobutamine: A β1 agonist that improves myocardial contractility and RV-PA coupling, though it can cause vasodilation at higher doses.In general, dobutamine is considered the best for acute RVF with PH, unless hypotension is a significant concern, in which case norepinephrine might be preferred. Milrinone is another option. MCS: short-term MCS should be considered in patients with cardiogenic shock as a bridge to recovery, a bridge to decision, or a bridge to bridge whilst the underlying causes for cardiogenic shock are addressed further described below Options include:Venous-arterial extracorporeal membranous oxygenation (V-A ECMO)RA to PA extracorporeal pump. (surgical RVAD) Flow device with an intake in the RA and an output in the PA. (Impella RP, Protek Duo) 4. When should we consider mechanical circulatory support for right ventricular (RV) failure? Short-term MCS should be considered in patients with cardiogenic shock as a bridge to recovery, a bridge to decision, or a bridge to bridge whilst the underlying causes for cardiogenic shock are addressed. Clinical parameters that suggest acute MCS use include signs of relative hypoperfusion plus hemodynamic features suggestive of RV failure, which were present in our patient. A specific additional consideration relates to where acute left-sided MCS reveals acute RV failure. Discerning whether this is intrinsic RV failure or due to persistently elevated RV afterload from inadequate LV support is also essential, as it will define management.  The goal of percutaneous mechanical support is to bypass the right ventricle and improve hemodynamics, while allowing time for optimization of the patient and recovery of the RV.  References Arrigo, Mattia, et al. “Diagnosis and Treatment of Right Ventricular Failure Secondary to Acutely Increased Right Ventricular Afterload (Acute Cor Pulmonale). A Clinical Consensus Statement of the Association for Acute CardioVascular Care (ACVC) of the ESC.” European Heart Journal. Acute Cardiovascular Care, vol. 13, no. 3, 22 Dec. 2023, pp. 304–312, https://doi.org/10.1093/ehjacc/zuad157. Accessed 17 May 2024. Chen, Guohai, et al. “INCIDENCE of ENDOPHTHALMITIS after VITRECTOMY: A Systematic Review and Meta-Analysis.” Retina (Philadelphia, Pa.), vol. 39, no. 5, May 2019, pp. 844–852, pubmed.ncbi.nlm.nih.gov/29370034/, https://doi.org/10.1097/IAE.0000000000002055. Fakkert, Raoul A, et al. “Early Hyperbaric Oxygen Therapy Is Associated with Favorable Outcome in Patients with Iatrogenic Cerebral Arterial Gas Embolism: Systematic Review and Individual Patient Data Meta-Analysis of Observational Studies.” Critical Care, vol. 27, no. 1, 12 July 2023, https://doi.org/10.1186/s13054-023-04563-x. Accessed 7 June 2024. Flaxel, Christina J., et al. “Idiopathic Epiretinal Membrane and Vitreomacular Traction Preferred Practice Pattern®.” Ophthalmology, vol. 127, no. 2, Feb. 2020, pp. P145–P183,

8个月前
19:47
416. Hearts Over Time: Navigating Grief and Growth in Adult Congenital Cardiology

416. Hearts Over Time: Navigating Grief and Growth in Adult Congenital Cardiology

CardioNerds ACHD Council members Dr. Rawan Amir and Dr. Claire Cambron lead a profound conversation with ACHD faculty Dr. Allison Tsao, Dr. Jill Steiner, and Dr. Katherine Salciccioli. Together, they explore the emotional and professional challenges that ACHD providers face across the lifespan of congenital heart disease. Topics discussed include navigating challenging case scenarios, empowering patients through tough decisions, leveraging multi-subspecialty expertise, celebrating the successes, preparing for and grieving loss, and more. This episode was planned by the CardioNerds ACHD Council. CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

8个月前
28:48
415. Case Report: Unraveling MINOCA: Role of Cardiac MRI and Functional Testing in Diagnosing Coronary Vasospasm – The Christ Hospital

415. Case Report: Unraveling MINOCA: Role of Cardiac MRI and Functional Testing in Diagnosing Coronary Vasospasm – The Christ Hospital

CardioNerds (Drs. Daniel Ambinder and Eunice Dugan) are joined by Namrita Ashokprabhu, incoming medical student, along with Drs. Yulith Roca Alvarez and Mehmet Yildiz from The Christ Hospital. Expert insights provided by Dr. Odayme Quesada. Audio editing by CardioNerds intern Christiana Dangas. This episode explores how cardiac MRI and coronary function testing revealed coronary vasospasm in a case of MINOCA. Cardiac MRI is crucial in evaluating myocardial infarction with nonobstructive coronary arteries (MINOCA) and diagnosing myocarditis, but findings must be interpreted within clinical context. A 58-year-old man with hypertension, hyperlipidemia, diabetes, a family history of cardiovascular disease, and smoking history presented with sudden chest pain, non-ST-elevation on EKG, and elevated troponin I (0.64 µg/L). Cardiac angiography revealed nonobstructive coronary disease, including a 40% stenosis in the LAD, consistent with MINOCA. Eight weeks later, another event (troponin I 1.18 µg/L) led to cardiac MRI findings suggesting myocarditis. Further history revealed episodic chest pain and coronary vasospasm, confirmed by coronary functional angiography showing severe vasoconstriction, resolved with nitroglycerin. Management included calcium channel blockers and long-acting nitrates, reducing symptoms. Coronary vasospasm is a frequent MINOCA cause and can mimic myocarditis on CMRI. Invasive coronary functional testing, including acetylcholine provocation testing, is indicated in suspicious cases.  US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Notes - Coronary Vasospasm What are the potential underlying causes of MINOCA (Myocardial Infarction with Non-Obstructive Coronary Arteries)?  Plaque Rupture: Plaque disruption, which includes plaque rupture, erosion, and calcified nodules, occurs as lipids accumulate in coronary arteries, leading to inflammation, necrosis, fibrosis, and calcification. Plaque rupture exposes the plaque to the lumen, causing thrombosis and thromboembolism, while plaque erosion results from thrombus formation without rupture and is more common in women and smokers. Intravascular imaging, such as IVUS and OCT, can detect plaque rupture and erosion, with studies showing plaque disruption as a frequent cause of MINOCA, particularly in women, though the true prevalence may be underestimated due to limited imaging coverage.  Coronary Vasospasm: Coronary vasospasm is characterized by nitrate-responsive chest pain, transient ischemic EKG changes, and >90% vasoconstriction during provocative testing with acetylcholine or ergonovine, due to hyper-reactivity in vascular smooth muscle. It is a common cause of MINOCA, with approximately half of MINOCA patients testing positive in provocative tests, and Asians are at a significantly higher risk than Whites. Smoking is a known risk factor for vasospasm. In contrast, traditional risk factors like sex, hypertension, and diabetes do not increase the risk, and vasospasm is associated with a 2.5–13% long-term risk of major adverse cardiovascular events (MACE).  Spontaneous Coronary Artery Dissection: Spontaneous coronary artery dissection (SCAD) involves the formation of a false lumen in epicardial coronary arteries without atherosclerosis, caused by either an inside-out tear or outside-in intramural hemorrhage. SCAD is classified into four types based on angiographic features, with coronary angiography being the primary diagnostic tool. However, in uncertain cases, advanced imaging like IVUS or OCT may be used cautiously. While the true prevalence is unclear due to missed diagnoses, SCAD is more common in women and is considered a cause of MINOCA when it results in non-obstructive lesions, with various predisposing factors including genetics, fibromuscular dysplasia, and emotional stress.   Coronary Embolism/Thrombosis: Coronary embolism, often underdiagnosed, can be classified based on thrombus origin as direct, paradoxical, or iatrogenic, with atrial fibrillation being the most common cause. A Japanese study found that only 2.9% of AMI patients were related to coronary embolism, and 73% of these cases were due to atrial fibrillation, with recurrent thromboembolic events occurring in 10% of patients during follow-up. Risk factors for coronary thromboembolism include hereditary thrombophilia, with 14% of MINOCA patients having hereditary thrombophilia, and an extensive evaluation, including a hypercoagulable workup and screening for atrial fibrillation or patent foramen ovale, is crucial to determine the underlying cause.  Coronary Microvascular Dysfunction: The role of microvascular dysfunction in MINOCA remains uncertain due to limited data, though it is characterized by impaired vasodilation, increased vasoconstriction, and abnormal microcirculation remodeling, which affects coronary flow reserve without epicardial disease. Microvascular dysfunction is often underdiagnosed because it requires invasive functional testing, and studies in patients with ischemia but no obstructive coronary disease (INOCA) show a prevalence of up to 41%. A small study of MINOCA patients found that 25% had low myocardial perfusion reserve, suggesting potential involvement, but further research is needed to establish its role as a cause of MINOCA.  MINOCA mimickers:  Myocarditis: Myocarditis, often caused by viral infections, can also result from bacterial infections, toxic substances, or autoimmune disorders, and is more common in younger patients, though it can affect all ages. Fulminant myocarditis, though rare, can lead to life-threatening cardiogenic shock, and is diagnosed through CMR showing diffuse myocardial edema on T2 and myocardial biopsy. A meta-analysis found that one-third of MINOCA patients had myocarditis, particularly younger patients and those with elevated C-reactive protein levels.  Non-ischemic Cardiomyopathy: Non-ischemic cardiomyopathy encompasses conditions like dilated, hypertrophic, restrictive, and arrhythmogenic cardiomyopathy, with dilated cardiomyopathy being the most common. A longitudinal study found that 25% of MINOCA patients had non-ischemic cardiomyopathy, which was associated with the highest mortality compared to other MINOCA mechanisms. Stress CMR has also identified underlying microvascular dysfunction in patients with dilated cardiomyopathy.  Takotsubo Cardiomyopathy: Takotsubo cardiomyopathy, or stress-induced cardiomyopathy, is characterized by reversible wall motion abnormalities without obstructive CAD. It is often triggered by emotional or physical stress and is associated with a catecholamine surge. The condition is more common in postmenopausal women and has four main anatomical variants, with apical ballooning being the most common. Diagnosis typically involves coronary angiography, ventriculography, and CMRI to rule out other causes of AMI, with risks of cardiogenic shock and death comparable to those of AMI patients with CAD.  What are the key diagnostic tests to evaluate MINOCA, and how are they applied in this case?  Coronary Intravascular Imaging: Coronary intravascular imaging with IVUS and OCT is essential for diagnosing plaque disruption in MINOCA and should be performed during coronary angiography of all three major epicardial arteries. IVUS identifies plaque disruption in up to 40% of MINOCA cases, while OCT detects the culprit lesion in about 50%. These imaging techniques are also valuable for evaluating SCAD in cases of diagnostic uncertainty.  Cardiac Imaging: Transthoracic echocardiography is valuable for assessing cardiac function after MINOCA, diagnosing Takotsubo and non-ischemic cardiomyopathy, and monitoring recovery of left ventricular function. Transesophageal echocardiography may be considered when coronary embolism is suspected. CMR is recommended for uncertain MINOCA diagnoses, providing accurate results in 74–87% of cases. It can differentiate between ischemic and non-ischemic MI, diagnose myocarditis, and detect coronary microvascular dysfunction through perfusion imaging. CMR's diagnostic accuracy improves when performed closer to the event and also serves as a prognostic tool for long-term cardiovascular outcomes.  Invasive Coronary Functional Testing: Provocative spasm testing with intracoronary acetylcholine helps diagnose coronary vasospasm (epicardial or microvascular) and endothelial-dependent microvascular dysfunction, with a low complication rate (0.5%). In MINOCA patients, spasm testing is positive in about half, with epicardial spasm in 65% and microvascular spasm in 35%. CFR assessed by doppler flow velocity or thermodilution (with values 25) are used to assess microvascular dysfunction, though CFR is more sensitive. While coronary microvascular dysfunction is linked to worse outcomes in INOCA, its prognostic impact in MINOCA is less clear. However, low CFR has been associated with increased mortality across various patient populations.  How is MINOCA treated based on its underlying etiology?  Plaque Rupture: Patients with plaque disruption should be treated with aspirin and high-intensity statin therapy. Additionally, for those with plaque disruption who do not require stenting, dual antiplatelet therapy with ticagrelor for up to 1 month may be considered, given the low revascularization rates at 1 year (5.7%) and 4 years (21.1%) follow-up.   Coronary Vasospasm: Long-acting calcium channel blockers (both dihydropyridine and non-dihydropyridine) are commonly used in MINOCA patients with epicardial coronary vasospasm.

9个月前
42:33
414. Case Report: Got Milky Blood? Hypertriglyceridemia Unveiled in a Case of Abdominal Pain – National Lipid Association

414. Case Report: Got Milky Blood? Hypertriglyceridemia Unveiled in a Case of Abdominal Pain – National Lipid Association

CardioNerds co-founders Dr. Daniel Ambinder and Dr. Amit Goyal are joined by Dr. Spencer Weintraub, Chief Resident of Internal Medicine at Northwell Health, Dr. Michael Albosta, third-year Internal Medicine resident at the University of Miami, and Anna Biggins, Registered Dietitian Nutritionist at the Georgia Heart Institute. Expert commentary is provided by Dr. Zahid Ahmad, Associate Professor in the Division of Endocrinology at the University of Texas Southwestern. Together, they discuss a fascinating case involving a patient with a new diagnosis of hypertriglyceridemia. Episode audio was edited by CardioNerds Intern Student Dr. Pacey Wetstein. A woman in her 30s with type 2 diabetes, HIV, and polycystic ovarian syndrome presented with one day of sharp epigastric pain, non-bloody vomiting, and a new lower extremity rash. She was diagnosed with hypertriglyceridemia-induced pancreatitis, necessitating insulin infusion and plasmapheresis.   The CardioNerds discuss the pathophysiology of hypertriglyceridemia-induced pancreatitis, potential organic and iatrogenic causes, and the cardiovascular implications of triglyceride disorders. We explore differential diagnoses for cardiac and non-cardiac causes of epigastric pain, review acute and long-term management of hypertriglyceridemia, and discuss strategies for the management of the chylomicronemia syndrome, focusing on lifestyle changes and pharmacotherapy.  This episode is part of a case reports series developed in collaboration with the National Lipid Association and their Lipid Scholarship Program, with mentorship from Dr. Daniel Soffer and Dr. Eugenia Gianos. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Hypertriglyceridemia Cardiac sarcoidosis can present with a variety of symptoms, including arrhythmias, heart block, heart failure, or sudden cardiac death. The acute management of hypertriglyceridemia-induced pancreatitis involves prompt recognition and initiation of therapy to lower triglyceride levels using either plasmapheresis or intravenous insulin infusion +/- heparin infusion. Insulin infusion is used more commonly, while plasmapheresis is preferred in pregnancy.   Medications such as fibrates and omega-3 fatty acids can be used to maintain long-term triglyceride reduction to prevent the recurrence of pancreatitis, especially in patients with persistent triglyceride elevation despite lifestyle modifications. Statins can be used in patients for ASCVD reduction in patients with a 10-year ASCVD risk > 5%, age > 40 years old, and diabetes or diabetes with end-organ damage or known atherosclerosis. Consider preferential use of icosapent ethyl as an omega-3 fatty acid for triglyceride lowering if the patients fit the populations that appeared to benefit in the REDUCE IT trial.   Apply targeted dietary interventions within the context of an overall healthy dietary pattern, such as a Mediterranean or DASH diet. Limit full-fat dairy, fatty meats, refined starches, added sugars, and alcohol. Encourage high-fiber vegetables, whole fruits, low-fat or fat-free dairy, plant proteins, lean poultry, and fish. Pay special attention to the cooking oils to ensure the patient is not using palm oil, coconut oil, or butter when cooking. Instead, use liquid non-tropical plant oils. Initiate a very low-fat diet ( 750 mg/dL.  Recommend and encourage patients to exercise regularly, with a minimum goal of 150 minutes/week of moderate-intensity aerobic activity. If weight loss is required, aim for more than >225 - 250 minutes/week.   Develop patient-centered and multidisciplinary strategies for preventing hypertriglyceridemia-induced pancreatitis by incorporating patient education on the importance of medication adherence, specialist follow-up, regular monitoring of triglyceride levels, and lifestyle modifications to maintain optimal lipid profiles and reduce the future risk of pancreatitis.  Notes - Hypertriglyceridemia Who is at risk for hypertriglyceridemia and what are the key pathophysiological mechanisms by which elevated triglycerides may lead to pancreatitis?   The exact mechanism is not clear. The proposed mechanism is that when serum triglycerides exceed 1000 mg/dL, blood flow is impaired through the capillary beds supplying the pancreas, resulting in ischemia. The ischemic injury resulting from this disruption of microcirculation disrupts the acinar structure of pancreatic cells and exposes pancreatic enzymes to triglyceride-rich particles. This results in activation of enzymatic activity with degradation of the chylomicron-triglycerides particles, which causes inflammation, subsequently leading to hemorrhage, edema, and necrosis of the pancreatic tissue.   Chylomicronemia syndrome can be multifactorial or familial. Familial chylomicronemia syndrome (FCS) is often discovered very early in life, and patients have a loss of function in one of the several genes involved in regulating triglyceride metabolism. These genes include LPL, APOC2, APOA5, LMF1, and GPIHBP1.  Multifactorial chylomicronemia syndrome is the most common cause of chylomicronemia syndrome. It is usually the result of a clustering of genetic variants, including heterozygosity of one of the five genes previously mentioned, as well as more frequent variants with small effects in more than 40 additional genes that have been implicated. Having a genetic variant plus an aggravating factor will often exacerbate the metabolic defect and lead to chylomicronemia syndrome. There are many potential aggravating factors, but some of the more common ones include a diet high in refined sugars, heavy alcohol consumption, obesity with or without metabolic syndrome, medications, renal disease, HIV, and pregnancy.   What are the acute treatment strategies for hypertriglyceridemia-induced pancreatitis, and how are they similar and different to treating pancreatitis from other etiologies?   All patients should be assessed for hemodynamic compromise, the severity of illness with or without scoring systems, and end-organ damage to determine the need for intensive care resources. Initially, patients usually require aggressive fluid resuscitation and pain management, which are standard across all types of acute pancreatitis. Delayed fluid resuscitation has been associated with worse outcomes. Multiple trials have been performed evaluating the best amount of fluid. Although there is not an exact answer to this, as all patients are different, all patients should be resuscitated until euvolemic. The WATERFALL trial showed that administration of 10 mL/kg bolus followed by 1.5 mL/kg maintenance until the patient reaches euvolemia was a superior approach to more aggressive fluid resuscitation. A patient's volume status should be reassessed every 6 hours for 24 – 48 hours, and fluids should be discontinued once euvolemia has been achieved. There is no guideline consensus on the preferred analgesic management, but it is generally recommended to administer medication to mitigate symptoms of pain and nausea for all patients.   For hypertriglyceridemia-induced pancreatitis, it is key to initiate fasting to decrease chylomicron production and further increasing triglyceride levels. Although historically, this was the same approach for other causes of pancreatitis, more recent data shows that early enteral feeding reduces the risk of complications such as pancreatic necrosis. However, these studies were not performed in patients with pancreatitis from hypertriglyceridemia and should not be extrapolated to this distinct population. Currently, it is recommended that patients be kept NPO until triglycerides are below 500 mg/dL, which is the point at which LPL activity becomes saturated. When feeding is initiated, it should be with a very low-fat diet with no refined carbohydrates.   Hypertriglyceridemia differs from other causes of pancreatitis as the management is centered around the rapid reduction of triglyceride content in the blood. Generally, these patients are admitted to the intensive care unit to undergo either insulin infusion +/- heparin drip or plasmapheresis. Although there has never been a clinical trial comparing these two approaches, a recent comprehensive meta-analysis showed no significant difference in mortality or clinical outcomes. Insulin infusion had a lower number of deaths, but a higher rate of acute renal failure, hypoglycemia, and hypotension, neither of which reached statistical significance. Insulin is more commonly used and generally preferred given that it is more cost-effective, less invasive, and can have utility in treating underlying diabetes exacerbation, which is common amongst these patients. Insulin infusion works by increasing the activity of lipoprotein lipase (LPL), resulting in increased clearance of chylomicron particles. Although in some countries, insulin is combined with heparin, given heparin's ability to increase LPL release, this is rarely done as heparin can deplete endothelial LPL, increase bleeding events, and potentially cause heparin-induced thrombocytopenia. Plasmapheresis, on the other hand, works by removing the triglycerides directly from the bloodstream, which can rapidly reduce levels. It does require central venous access, which is more invasive. Plasmapheresis is preferred in pregnancy as data in case series supports it reduces the risk of a systemic inflammatory response.   What are the proposed mechanisms by which high triglycerides may contribute to atherosclerosis?

9个月前
1小时17分钟
413. Case Report: Cardiac Sarcoidosis Presenting as STEMI – Mount Sinai Medical Center in Miami

413. Case Report: Cardiac Sarcoidosis Presenting as STEMI – Mount Sinai Medical Center in Miami

CardioNerds (Dr. Rick Ferraro and Dr. Dan Ambinder) join Dr. Sri Mandava, Dr. David Meister, and Dr. Marissa Donatelle from the Columbia University Division of Cardiology at Mount Sinai Medical Center in Miami. Expert commentary is provided by Dr. Pranav Venkataraman. They discuss the following case involving a patient with cardiac sarcoidosis presenting as STEMI. A 57-year-old man with a history of hyperlipidemia presented with sudden onset chest pain. On admission, he was vitally stable with a normal cardiorespiratory exam but appeared in acute distress and was diffusely diaphoretic. His ECG revealed sinus rhythm, a right bundle branch block (RBBB), and ST elevation in the inferior-posterior leads. He was promptly taken for emergent cardiac catheterization, which identified a complete thrombotic occlusion of the mid-left circumflex artery (LCX) and large obtuse marginal (OM) branch, with no underlying coronary atherosclerotic disease. Aspiration thrombectomy and percutaneous coronary intervention (PCI) were performed, with one drug-eluting stent placed. An echocardiogram showed a left ventricular ejection fraction (EF) of 31%, hypokinesis of the inferior, lateral, and apical regions, and an apical left ventricular thrombus. The patient was started on triple therapy. A hypercoagulable workup was negative. A cardiac MRI was obtained to further evaluate non-ischemic cardiomyopathy. In conjunction with a subsequent CT chest, the results raised suspicion for cardiac sarcoidosis with systemic involvement. In view of a reduced EF and significant late-gadolinium enhancement, electrophysiology was consulted to evaluate for ICD candidacy. A decision was made to delay ICD implantation until a definitive diagnosis of cardiac sarcoidosis could be established by tissue biopsy. The patient was started on HF-GDMT and discharged with a LifeVest. Close outpatient follow-up with cardiology and electrophysiology was arranged.  US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Cardiac Sarcoidosis Presenting as STEMI Cardiac sarcoidosis can present with a variety of symptoms, including arrhythmias, heart block, heart failure, or sudden cardiac death. Symptoms can be subtle or mimic other cardiac conditions.  Conduction abnormalities, particularly AV block or ventricular arrhythmias, are common and may be the initial indication of cardiac involvement with sarcoidosis.  The additive value of Echocardiography, FDG-PET, and cardiac MR is indispensable in the diagnostic workup of suspected cardiac sarcoidosis.  Specific role of MRI/PET: Both cardiac MRI and FDG-PET provide a complementary role in the diagnosis of cardiac sarcoidosis. Cardiac MRI is an effective diagnostic screening tool with fairly high sensitivity but is limited by its inability to decipher inflammatory (“active” disease) versus fibrotic myocardium. FDG-PT helps to make this discrimination, refine the diagnosis, and guide clinical management. Ultimately, these studies are most useful when interpreted in the context of other clinical information.  Primary prevention of sudden cardiac death in cardiac sarcoidosis focuses on risk stratification, with ICD placement for high-risk patients. For patients awaiting definitive diagnosis, a LifeVest may be used as a temporary measure to protect from sudden arrhythmic events until an ICD is placed.  Notes - Cardiac Sarcoidosis Presenting as STEMI 1. Is STEMI always a result of coronary artery disease?  By definition, a STEMI is an acute S-T segment elevation myocardial infarction. This occurs when there is occlusion of a major coronary artery, which results in transmural ischemia and damage, resulting in electrical changes seen on the ECG. The most common cause of coronary artery occlusion is coronary artery disease (CAD) from plaque rupture and thrombus formation; however, many other causes of coronary artery occlusion are not related to CAD. These include vasospasm (isolated and recurrent), in-situ thrombotic occlusion, spontaneous coronary artery dissection, and supply-demand mismatch, such as in the setting of severe anemia. DDx includes other causes of injury current, such as myocarditis. It is important to keep these other differentials in mind while preparing for coronary angiography, as it may help guide intra-catheterization and post-catheterization management.  2. What are the most common causes of LV thrombus?  When considering the causes of thrombus formation, think of Virchow’s triad. As with any other location, thrombus formation in the LV may be caused by injury/inflammation, systemic thrombophilia, and stasis.   Acute myocardial infarction (especially anterior MI) - damaged myocardium and impaired LV function lead to blood stasis and thrombus formation.  Heart failure with reduced ejection fraction (HFrEF) - severely impaired contractility increases the risk of thrombus development  Non-Ischemic cardiomyopathies - dilated or hypertrophic cardiomyopathies may cause abnormal blood flow, promoting thrombus formation.   Arrhythmias - although more associated with atrial thrombus, atrial fibrillation can also contribute to LVT in cases of significant LV dysfunction. Ventricular arrhythmias can also cause LV thrombus.  Hypercoagulable conditions - Conditions such as antiphospholipid antibody syndrome, inherited thrombophilias, malignancy-associated hypercoagulability, polycythemia vera, hyperhomocysteinemia, nephrotic syndrome or systemic lupus erythematous may predispose to LV thrombus formation  Inflammatory conditions - conditions like myocarditis or cardiac sarcoidosis can lead to inflammation along with focal stasis from aneurysmal changes, contributing to thrombus formation   3. What is the clinical presentation of cardiac sarcoidosis?  Chest pain: can arise from several mechanisms such as myocardial inflammation, pericarditis, coronary artery involvement, or arrhythmias.   Heart Failure: symptoms such as dyspnea, fatigue, and peripheral edema may result from left ventricular dysfunction or restrictive cardiomyopathy.  Arrhythmias: palpitations, dizziness or syncope may occur due to ventricular tachycardia or ventricular fibrillation.  Conduction abnormalities: Heart block, especially complete AV block, is a common early manifestation. Some studies have found that AV block is the presenting symptom in more than 40% of patients with cardiac sarcoidosis.  Sudden cardiac death (SCD): sudden death can occur due to ventricular arrhythmias or severe heart block.  Asymptomatic: in some cases, cardiac sarcoidosis is discovered incidentally during imaging or evaluation for systemic sarcoidosis.  4. What are the key imaging modalities used in the diagnosis of cardiac sarcoidosis?  Echocardiography, FDG-PET, and cardiac MRI are the key imaging modalities used to diagnose cardiac sarcoidosis.  The echocardiogram is often normal in clinically silent disease, but several key features may be seen in clinically active disease. The most specific findings are basal interventricular thinning and LV aneurysm. Other less specific findings include increased LV wall thickness, LV/RV diastolic and/or systolic dysfunction, and wall motion abnormalities (non-coronary distribution). Strain imaging is promising for use in earlier stages of disease, but this is not well established yet. FDG-PET is crucial in the initial diagnosis of cardiac sarcoidosis, allowing active inflammatory disease to be detected. There is no pathognomonic PET finding; however, focal or focal-on-diffuse FDG uptake patterns are highly suggestive of active disease. It should be noted that FDG-PET is also useful in guiding treatment or response to immunosuppressive therapy, as it can track the degree of inflammation over time. The role of cardiac MRI is discussed below.  5. What is the specific role of cardiac MRI in the diagnosis of cardiac sarcoidosis?  This depends on the specific clinical setting. A patient with established extra-cardiac sarcoidosis but asymptomatic from a cardiac standpoint should be appropriately screened for cardiac involvement by clinical history, ECG, echocardiography, and cardiac monitoring (e.g. Holter monitor, etc). If any of the aforementioned “screening” tests are abnormal, a cardiac MRI is then indicated to assess for evidence of cardiac sarcoidosis. More specifically, cardiac MRI detects inflammation and edema at earlier stages of disease and scar tissue at later stages. The classical finding specific for cardiac sarcoidosis is patchy late gadolinium enhancement, with a predilection for the basal septum and basal inferolateral wall. The enhancement is either subepicardial or mid-wall and rarely transmural. It should be noted that once cardiac sarcoidosis is diagnosed, FDG-PET imaging should be utilized in conjunction with, or complementary to MRI, to assess for “active sarcoid” (i.e. myocardial inflammation).  On the other hand, a patient with no known extracardiac sarcoidosis but with suggestive cardiac findings should have a cardiac MRI to assess for typical features as mentioned above, in addition to assessment for non-cardiac involvement.  It should be noted that cardiac MRI can also provide significant prognostic information.  The presence of LGE portends a worse prognosis due to increased CV death and ventricular arrhythmias. It should also be noted that LGE does not discriminate between active inflammation and fibrosis. Tissue characterization with T1 and T2 mapping techniques or PET imaging, as described above, can be more useful in this sense.  References 1.) Cheng RK, Kittleson MM,

10个月前
25:23
412: The Biology of Transthyretin amyloid cardiomyopathy (ATTR-CM) with Dr. Daniel Judge

412: The Biology of Transthyretin amyloid cardiomyopathy (ATTR-CM) with Dr. Daniel Judge

CardioNerds Cardiac Amyloidosis Series Chair Dr. Rick Ferraro and Episode Lead Dr. Anna Radakrishnan discuss the biology of transthyretin amyloid cardiomyopathy (ATTR-CM ) with Dr. Daniel Judge.  Notes were drafted by Dr. Anna Radakrishnan. The audio was engineered by student Dr. Julia Marques.  This episode provides a comprehensive overview of transthyretin (ATTR) cardiac amyloidosis, a complex and rapidly evolving disease process. The discussion covers the key red flags for cardiac amyloidosis, the diagnostic pathway, and the implications of hereditary versus wild-type ATTR. Importantly, the episode delves into the current and emerging therapies for ATTR, including stabilizers, gene silencers, and promising treatments like CRISPR-Cas9 and antibody-based approaches. Dr. Judge shares his insights and excitement about the rapidly advancing field, highlighting the need for early diagnosis and the potential to improve long-term outcomes for patients with this condition.  Enjoy this Circulation Paths to Discovery article to learn more about the CardioNerds mission and journey.  US Cardiology Review is now the official journal of CardioNerds! Submit your manuscripts here.  CardioNerds Cardiac Amyloid PageCardioNerds Episode Page Pearls: - Biology of Transthyretin amyloid cardiomyopathy Maintain a high index of suspicion! Look for subtle (yet telling) signs like ventricular hypertrophy, discordant EKG findings, bilateral carpal tunnel syndrome, and spontaneous biceps tendon rupture.  Utilize the right diagnostic tests. Endomyocardial biopsy remains the gold standard, but non-invasive tools like PYP scan with SPECT imaging and genetic testing are essential for accurate diagnosis.  Differentiating hereditary from wild-type ATTR is critical, as genetic forms may have a more aggressive course and familial implications.  Early diagnosis and intervention significantly improve prognosis, making vigilance in screening and prompt treatment initiation essential.  The future is now! Cutting-edge therapies are transforming the treatment landscape, including TTR stabilizers, gene silencers, and emerging technologies like CRISPR-Cas9 and antibody-based treatments.  Notes - Biology of Transthyretin amyloid cardiomyopathy What is transthyretin amyloid (aTTR) and how is it derived?  Transthyretin (TTR) is a transport protein primarily synthesized by the liver, responsible for carrying thyroid hormones (thyroxine) and retinol (vitamin A) in the blood. It circulates as a tetramer, composed of four identical monomers, which is essential for its stability and function.  In transthyretin amyloid (ATTR) amyloidosis, the TTR protein becomes unstable, leading to its dissociation into monomers. These monomers misfold and aggregate into insoluble amyloid fibrils, which deposit extracellularly in tissues such as the heart, nerves, and gastrointestinal tract. This progressive amyloid deposition leads to organ dysfunction, including restrictive cardiomyopathy and neuropathy.  There are two main forms of ATTR amyloidosis: hereditary (variant) and wild-type (senile) ATTR.  Hereditary ATTR (ATTRv) is caused by mutations in the TTR gene. These mutations destabilize the TTR tetramer, making it more prone to dissociation. This increases misfolding and amyloid fibril formation, resulting in systemic amyloid deposition.   Wild-type ATTR (ATTRwt) occurs without genetic mutations and is primarily age-related. Over time, even normal TTR tetramers can become unstable, leading to gradual misfolding and amyloid deposition, particularly in the heart. ATTRwt is a common but often underdiagnosed cause of heart failure with preserved ejection fraction (HFpEF) in elderly individuals.  How does aTTR lead to deleterious effects in the heart and other organ systems?    Transthyretin amyloidosis leads to organ dysfunction through the deposition of misfolded TTR protein as amyloid fibrils, which accumulate extracellularly and disrupt normal tissue architecture and function. These deposits cause progressive damage by increasing stiffness, inducing oxidative stress, and impairing normal cellular function.  Cardiac manifestations include amyloid deposition in the myocardial interstitium, leading to increased stiffness, diastolic dysfunction, and restrictive cardiomyopathy. As the disease progresses, systolic dysfunction may develop. Amyloid infiltration can also cause arrhythmia, conduction abnormalities such as atrioventricular block and atrial fibrillation, valvular thickening, coronary ischemia, and pericardial effusion. Disruption of transverse tubules in cardiomyocytes contributes to heart failure and arrhythmia.  Systemic involvement depends on the culprit amylodogenic protein. AL amyloidosis caused by deposition of immunoglobulin light chains may deposit in and disrupt the function of any tissue/organ except for the central nevous system. ATTR amyloidosis primarily affects the heart, peripheral nerves, and the musculoskeletal system.   Peripheral neuropathy can cause sensory loss, pain, and motor weakness, while autonomic dysfunction may lead to orthostatic hypotension, gastroparesis, and urinary retention. Carpal tunnel syndrome is a common early sign. Gastrointestinal amyloid deposits (specifically for AL but not ATTR) can cause gastroparesis, diarrhea, constipation, and malabsorption, leading to weight loss and malnutrition. Renal involvement (specifically for AL but not ATTR), though less common, can present as proteinuria and renal dysfunction. Amyloid deposition in soft tissues and the lungs may lead to hoarseness and musculoskeletal stiffness.  As the disease progresses, continued amyloid accumulation leads to worsening organ dysfunction and failure. Early diagnosis and intervention are essential to slowing disease progression and managing symptoms effectively.  When and why is aTTR cardiac amyloidosis hereditary versus obtained sporadically?  Hereditary aTTR is caused by genetic mutations in the TTR gene, which are often autosomal dominant.   Common mutations include V122I (more common in African Americans) and V30M (more common in certain regions like Portugal).   Hereditary aTTR typically presents at an earlier age and may have a more aggressive course, with a higher likelihood of neuropathic involvement.   Wild-type aTTR, or senile systemic amyloidosis, occurs sporadically and is more common in older individuals, typically without a family history.   The exact reasons for the development of wild-type aTTR are not fully understood, but factors like chronic inflammation and exercise may play a role in the misfolding and aggregation of the normal TTR protein.  References: Biology of Transthyretin amyloid cardiomyopathy Ruberg FL, Maurer MS. Cardiac Amyloidosis Due to Transthyretin Protein. JAMA. 2024;331(9):778-778. https://doi.org/10.1001/jama.2024.0442   Ruberg FL, Grogan M, Hanna M, Kelly JW, Maurer MS. Transthyretin Amyloid Cardiomyopathy. Journal of the American College of Cardiology. 2019;73(22):2872-2891. https://doi.org/10.1016/j.jacc.2019.04.003   ‌Maurer MS, Bokhari S, Damy T, et al. Expert Consensus Recommendations for the Suspicion and Diagnosis of Transthyretin Cardiac Amyloidosis. Circulation: Heart Failure. 2019;12(9). https://doi.org/10.1161/circheartfailure.119.006075   ‌Griffin JM, Rosenthal JL, Grodin JL, Maurer MS, Grogan M, Cheng RK. ATTR Amyloidosis: Current and Emerging Management Strategies. JACC: CardioOncology. 2021;3(4):488-505. https://doi.org/10.1016/j.jaccao.2021.06.006

10个月前
13:01
411. Journal Club: The VANISH2 Trial with Dr. Jeff Healey and Dr. Roderick Tung

411. Journal Club: The VANISH2 Trial with Dr. Jeff Healey and Dr. Roderick Tung

Join CardioNerds EP Council Chair Dr. Naima Maqsood and Episode Lead Dr. Jeanne De Lavallaz as they discuss the results of the VANISH2 Trial with expert faculty Dr. Jeff Healey and Dr. Roderick Tung. Audio editing by CardioNerds academy intern, Grace Qiu. The VANISH2 trial enrolled 416 patients with ischemic cardiomyopathy, an ICD in place, and recurrent episodes of sustained monomorphic ventricular tachycardia (VT) to receive either first-line VT catheter ablation or antiarrhythmic drug therapy with the primary composite outcome of death from any cause, appropriate ICD shock, ventricular tachycardia storm (meaning at least 3 ventricular tachycardia events within 24hrs) or treated ventricular tachycardia below the detection limit of the ICD. The study population had a mean age of 68 years, with 94% being men and predominantly of white ethnicity. On average, 14 years had elapsed since their last myocardial infarction, with approximately 60% having undergone percutaneous coronary intervention at the time. The mean ejection fraction was 34%. This episode was planned in collaboration with Heart Rhythm TV with mentorship from Dr. Daniel Alyesh and Dr. Mehak Dhande. CardioNerds Journal Club PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! References - VANISH2 Trial Sapp, J. L., Tang, A. S. L., Parkash, R., Stevenson, W. G., Healey, J. S., Gula, L. J., Nair, G. M., & the VANISH2 Study Team. (2025). Catheter ablation or antiarrhythmic drugs for ventricular tachycardia. The New England Journal of Medicine, 392, 737–747.

10个月前
30:05
410. Case Report: A Curious Case of Refractory Ventricular Tachycardia – Rutgers-Robert Wood Johnson

410. Case Report: A Curious Case of Refractory Ventricular Tachycardia – Rutgers-Robert Wood Johnson

CardioNerds (Dr. Colin Blumenthal and Dr. Saahil Jumkhawala) join Dr. Rohan Ganti, Dr. Nikita Mishra, and Dr. Jorge Naranjo from the Rutgers – Robert Wood Johnson program for a college basketball game, as the buzz around campus is high. They discuss the following case involving a patient with ventricular tachycardia:  The case involves a 61-year-old man with a medical history of hypothyroidism, hypertension, hyperlipidemia, seizure disorder on anti-epileptic medications, and major depressive disorder, who presented to the ER following an out-of-hospital cardiac arrest. During hospitalization, he experienced refractory polymorphic ventricular tachycardia (VT), requiring 18 defibrillation shocks. Further evaluation revealed non-obstructive hypertrophic cardiomyopathy (HCM). We review the initial management of electrical storm, special ECG considerations, diagnostic approaches once ischemia has been excluded, medications implicated in polymorphic VT, the role of multi-modality imaging in diagnosing hypertrophic cardiomyopathy, and risk stratification for implantable cardioverter-defibrillator (ICD) placement in patients with HCM.  Expert commentary is provided by Dr. Sabahat Bokhari.   Episode audio was edited by CardioNerds Intern and student Dr. Pacey Wetstein.   US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - A Curious Case of Refractory Ventricular Tachycardia - Rutgers-Robert Wood Johnson Diagnostic Uncertainty in VT Storm: In VT storm, ischemia is a primary consideration; when coronary angiography excludes significant epicardial disease, alternative causes such as cardiomyopathies, channelopathies, myocarditis, electrolyte disturbances, or drug-induced arrhythmias must be explored.  ST elevations in ECG lead aVR:  ST elevations in lead aVR and diffuse ST depressions can sometimes represent post-arrest oxygen demand and myocardial mismatch rather than an acute coronary syndrome. This pattern may occur in the context of polymorphic VT (PMVT), where myocardial oxygen demands outstrip supply, especially after an arrest. While these ECG changes could suggest myocardial ischemia, caution is needed, as they might not always indicate coronary pathology. However, PMVT generally should raise suspicion for underlying coronary disease and may warrant a coronary angiogram for further evaluation.  Medication Implications in PMVT and HCM: Certain medications, including psychotropic drugs (e.g., antidepressants, antipsychotics) and anti-epileptic drugs, can prolong the QT interval or interact with other drugs, thereby increasing the risk of polymorphic VT in patients with underlying conditions like HCM. Careful management of these medications is critical to avoid arrhythmic events in predisposed individuals.  Multi-Modality Imaging in HCM: Cardiac MRI with late gadolinium enhancement (LGE) is invaluable in assessing myocardial fibrosis, a key predictor of arrhythmic risk, and can guide decisions regarding ICD implantation. Echocardiography and contrast-enhanced CT can provide additional insights into structural abnormalities and risk assessment.  Polymorphic VT in Nonobstructive HCM: Polymorphic ventricular tachycardia (PMVT) can occur in nonobstructive hypertrophic cardiomyopathy due to myocardial fibrosis and disarray, even in the absence of significant late gadolinium enhancement and left ventricular outflow tract obstruction.  ICD Risk Stratification in HCM: Risk stratification for ICD placement in HCM includes assessment of clinical features such as family history of sudden cardiac death, history of unexplained syncope, presence of nonsustained VT on ambulatory monitoring, massive left ventricular hypertrophy (wall thickness ≥30 mm), and evidence of extensive myocardial fibrosis on cardiac MRI.  Notes - A Curious Case of Refractory Ventricular Tachycardia - Rutgers-Robert Wood Johnson Is there a benefit of starting antiarrhythmic medications for patients presenting with an out-of-hospital cardiac arrest with shock-refractory VT or VF?  There is likely no benefit. An RCT published by Kudenchuk et al in 2016 in which patients who had a non-traumatic out-of-hospital cardiac arrest with shock-refractory VF or pulseless VT were randomly assigned to receive lidocaine, amiodarone, or saline placebo, in addition to standard care, showed that neither antiarrhythmic drug had a significantly higher rate of survival or favorable neurologic outcome compared to placebo6.  What is the differential diagnosis and empiric management for a patient with polymorphic ventricular tachycardia?   The differential diagnosis for ventricular tachycardia includes myocardial ischemia, electrolyte derangements, medications that may cause QT prolongation, congenital long QT syndrome, Brugada syndrome, myocarditis, dilated cardiomyopathy, arrhythmic cardiomyopathies, and infiltrative or structural heart disease.  Standard BLS and ACLS measures are first-line treatment for pulseless VT.   For stable patients, the 2017 AHA/ACC/HRS0 guidelines list beta-blockers as first-line antiarrhythmic therapy because they have been shown to reduce mortality and suppress ventricular arrhythmias in structurally normal hearts3. Amiodarone is also listed, though its long-term effect on survival is unclear, with most studies showing no clear benefit over placebo 3. Lidocaine and mexiletine are also commonly used, but because they are less efficacious compared to amiodarone, they are usually used as combination therapy for refractory patients4. Multiple trials have demonstrated the efficacy of procainamide as an adjunct medication in patients with ongoing ventricular arrhythmias, despite amiodarone and lidocaine4. Quinidine has also been used for patients as a salvage therapy for patients with structural heart disease for recurrent ventricular arrhythmias despite antiarrhythmic drug treatment 4.   What medications can be associated with polymorphic VT?  Medications that are commonly associated with QT prolongation, therefore making patients more susceptible to developing VT, include Class I and Class III antiarrhythmics; fluoroquinolone and macrolide antibiotics, as well as antifungals; tricyclic antidepressants as well as certain SSRI’s and SNRI’s; and antipsychotics, among others5.  In this video, Dr. Nino Isakadze explains the proper way to measure the QT interval.   How can multimodal imaging help reach a diagnosis in patients with PMVT with a relatively normal echocardiogram and no coronary artery disease?  Multimodal imaging, specifically cardiac MRI, is useful for reaching a diagnosis in patients with PMVT due to improved myocardial tissue characterization.  Improved definition of the myocardium allows for the detection of structural abnormalities that may not be as easily visualized on TTE, such as LV non-compaction, now called excessive trabeculation of the left ventricle, and to more accurately measure left ventricular wall thickness, which is useful for diagnosing and risk stratifying patients with hypertrophic cardiomyopathy.  Improved tissue characterization by measuring T1 relaxation time, T2 relaxation time, extracellular volume, and late gadolinium enhancement (LGE) pattern is also useful for diagnosing infiltrative disease. Certain LGE patterns are associated with different cardiac conditions and play a role in determining prognosis. For example, the detection of mid-wall LGE in patients with dilated cardiomyopathy portends an increased risk of adverse events.   What are the risk factors for sudden cardiac death in patients with HCM?  The updated 2024 HCM guidelines have outlined several risk factors for sudden cardiac death 1  Family history of sudden cardiac death   Unexplained syncope  NSVT episodes on ambulatory monitoring when runs are frequent (≥ 3), longer (≥ 10 beats), and faster (≥ 200 bpm)    Increased LV wall thickness, with elevated risk greater than 30 mm  Other risk stratification markers include extensive LGE seen on cardiac MRI, apical aneurysm, and EF < 50% in patients without high-risk features 1  The AHA HCM SCD Calculator can be used to risk stratify patients to assist with decision-making in ICD implantation in these patients2  References Ommen SR, Ho CY, Asif IM, et al. 2024 AHA/ACC/AMSSM/HRS/PACES/SCMR Guideline for the Management of Hypertrophic Cardiomyopathy: A Report of the American Heart Association/American College of Cardiology Joint Committee on Clinical Practice Guidelines [published correction appears in Circulation. 2024 Aug 20;150(8):e198. doi: 10.1161/CIR.0000000000001277]. Circulation. 2024;149(23):e1239-e1311. doi:10.1161/CIR.0000000000001250  AHA HCM SCD Calculator   Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society [published correction appears in Circulation. 2018 Sep 25;138(13):e419-e420. doi: 10.1161/CIR.0000000000000614]. Circulation. 2018;138(13):e272-e391. doi:10.1161/CIR.0000000000000549  Larson J, Rich L, Deshmukh A, Judge EC, Liang JJ. Pharmacologic Management for Ventricular Arrhythmias: Overview of Anti-Arrhythmic Drugs. J Clin Med. 2022;11(11):3233. Published 2022 Jun 6. doi:10.3390/jcm11113233  Nachimuthu S, Assar MD, Schussler JM. Drug-induced QT interval prolongation: mechanisms and clinical management. Ther Adv Drug Saf. 2012;3(5):241-253.

10个月前
40:13
409. Journal Club: The ARREST-AF Trial with Drs. Prashanthan Sanders and Mehak Dhande

409. Journal Club: The ARREST-AF Trial with Drs. Prashanthan Sanders and Mehak Dhande

Join CardioNerds EP Council Chair Dr. Naima Maqsood and Episode Lead Dr. Jeanne De Lavallaz as they discuss the results of the ARREST-AF Trial with expert faculty Dr. Prashanthan Sanders and Dr. Mehak Dhande. Audio editing by CardioNerds intern Bhavya Shah. The ARREST-AF trial enrolled 122 patients with a BMI of 27 kg/m2 or greater and at least one cardiovascular risk factor with either paroxysmal or persistent AF and were scheduled to undergo de novo AF ablation. They were randomized to an intensive risk factor management (RFM) program versus usual care. The RFM program addressed obesity, sleep apnea, HTN, HLD, tobacco, and alcohol abuse, whereas the usual care arm had a discussion of risk factors but without an extensive risk factor modification or follow-up program. The study population had a mean age of 60 years, a mean BMI of 33 kg/m2, and 56-60% of patients with persistent AF. A third of the study population was female. The trial showed a significant improvement in the primary endpoint of the percentage of patients free from atrial fibrillation after ablation in those receiving the intensive lifestyle RFM program. At the end of the 12.3-month follow-up period, 66% percent of patients in the RFM group were free from AF compared to 42% in the usual care group (HR 0.53, p = 0.03). The RFM group also showed significant improvement in AF symptom severity, decline in body weight, systolic blood pressure, glycemic control, and exercise capacity. On average, patients in the RFM arm lost 9 kg of weight compared to 1 kg in the control group. Similarly, systolic blood pressure decreased by 13.1 mmHg in the RFM group but increased by four mmHg in the control group. This episode was planned in collaboration with Heart Rhythm TV with mentorship from Dr. Daniel Alyesh and Dr. Mehak Dhande. CardioNerds Journal Club PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! References - The SUMMIT Trial Pathak, Rajeev K., et al. "Aggressive Risk Factor Reduction Study for Atrial Fibrillation and Implications for the Outcome of Ablation: The ARREST-AF Cohort Study." Journal of the American College of Cardiology, vol. 64, no. 21, 2014, pp. 2222–2231.

11个月前
36:04
408. Journal Club: The SUMMIT Trial with Dr. Milton Packer

408. Journal Club: The SUMMIT Trial with Dr. Milton Packer

Join CardioNerds Heart Failure Section Chair Dr. Jenna Skowronski, episode lead Dr. Merna Hussein, and expert faculty Dr. Milton Packer as they discuss the SUMMIT trial. The SUMMIT trial randomized 731 patients with HFpEF with LVEF ≥ 50% and obesity with BMI ≥ 30 kg/m2 to receive tirzepatide or placebo for at least 52 weeks. The two co-primary endpoints were a composite of time to cardiovascular death or a worsening heart failure event and quality of life measured by the Kansas City Cardiomyopathy Questionnaire clinical summary score (KCCQ-CSS). Treatment with tirzepatide led to a lower risk of the composite of cardiovascular death or worsening heart failure as well as improved quality of life. This episode was planned in collaboration with the American College of Cardiology Section of the Prevention of Cardiovascular Disease with mentorship from Section Chair Dr. Eugenia Gianos. CardioNerds Journal Club PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! References - The SUMMIT Trial Packer, M., Zile, M. R., Kramer, C. M., Baum, S. J., Litwin, S. E., Menon, V., Ge, J., Weerakkody, G. J., Ou, Y., Bunck, M. C., Hurt, K. C., Murakami, M., Borlaug, B. A., & SUMMIT Trial Study Group. (2024). Tirzepatide for Heart Failure with Preserved Ejection Fraction and Obesity. The New England Journal of Medicine. https://doi.org/10.1056/NEJMoa2410027

11个月前
18:42