Cardionerds: A Cardiology Podcast

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.  Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. 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.

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. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. 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, patients become dependent on pacing and lifelong pacemaker implantation, and the potential for device complications AVNA does not prevent progression or recurrence of AF The type of device is dependent on patient comorbidities but the advent of conduction system pacing may improve outcomes in these patients compared with RV pacing. What are some recommendations for managing atrial fibrillation in the perioperative period?  In patients with AF (excluding those with recent stroke or TIA, or a mechanical valve) and on oral anticoagulation with either warfarin or DOAC who are scheduled to undergo an invasive procedure or surgery, temporary cessation of oral anticoagulation without bridging anticoagulation is recommended (COR-LOE 1-B) In patients with AF on DOAC that has been interrupted for an invasive procedure or surgery, in general, resumption of anticoagulation the day after low bleeding risk surgery and between the evening of the second day and the evening of the third day after high bleeding risk surgery is reasonable, as long as hemostasis has been achieved and further bleeding is not anticipated (COR-LOE 2a-B) Preop prophylaxis to prevent AF after cardiac surgery with either beta blocker or amiodarone shows mixed benefit and carries a 2a-B recommendation; however, beta blocker is a class 1-A recommendation in patients who do develop AF in the postop period It should be noted that patients who develop AF in the setting of an acute illness or surgery are at risk of recurrence References Joglar, J, Chung, M. et al. 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. JACC. 2024 Jan, 83 (1) 109–279. https://doi.org/10.1016/j.jacc.2023.08.017 Fuster F, Rydén L, et al. ACC/AHA/ESC Guidelines for the Management of Patients With Atrial Fibrillation: Executive Summary A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to Develop Guidelines for the Management of Patients With Atrial Fibrillation) Developed in Collaboration With the North American Society of Pacing and Electrophysiology. Circulation. 2001 Oct, 104 (17). https://doi.org/10.1161/circ.104.17.2118 Kirchhof P, Camm A, et al. Early Rhythm-Control Therapy in Patients with Atrial Fibrillation. N Engl J Med. 2020 Aug, 383 (14) 1305-1416. DOI: 10.1056/NEJMoa2019422 Olshansky, B, Rosenfeld, L, Warner, A. et al. The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) study: Approaches to control rate in atrial fibrillation. JACC. 2004 Apr, 43 (7) 1201–1208.https://doi.org/10.1016/j.jacc.2003.11.032 Whitlock R, Belley-Cote E, et al. Left Atrial Appendage Occlusion during Cardiac Surgery to Prevent Stroke. N Engl J Med. 2021 May, 384 (22) 2081-2091. DOI: 10.1056/NEJMoa2101897 Kirchhof P, Toennis T, et al. Anticoagulation with Edoxaban in Patients with Atrial High-Rate Episodes. N Engl J Med. 2023 Aug, 389 (13) 1167-1179. DOI: 10.1056/NEJMoa2303062 Healey J, Lopes R, et al. Apixaban for Stroke Prevention in Subclinical Atrial Fibrillation. N Engl J Med. 2023 Nov, 390 (2) 107-117. DOI: 10.1056/NEJMoa2310234 Roy D, Talajic M, et al. Rhythm Control versus Rate Control for Atrial Fibrillation and Heart Failure. N Engl J Med. 2008 Jun, 358 (25) 2667-2677. DOI: 10.1056/NEJMoa0708789 Gillinov A, Bagiella E, et al. Rate Control versus Rhythm Control for Atrial Fibrillation after Cardiac Surgery. N Engl J Med. 2016 Mar, 374 (20) 1911-1921. DOI: 10.1056/NEJMoa1602002

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. We Were Thrilled to Join the American Heart Association’s Scientific Sessions 2025! AHA Scientific Sessions 2025 took place November 7–10 in New Orleans, LA — one of the premier annual gatherings in cardiovascular science and education. It was an incredible opportunity to connect with colleagues, hear cutting-edge research, and contribute to the ongoing conversations shaping the future of cardiovascular care. We’re grateful to everyone who joined us in New Orleans and made this year’s meeting so impactful. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. 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!

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. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. We Were Thrilled to Join the American Heart Association’s Scientific Sessions 2025! AHA Scientific Sessions 2025 took place November 7–10 in New Orleans, LA — one of the premier annual gatherings in cardiovascular science and education. It was an incredible opportunity to connect with colleagues, hear cutting-edge research, and contribute to the ongoing conversations shaping the future of cardiovascular care. We’re grateful to everyone who joined us in New Orleans and made this year’s meeting so impactful. 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, the fact that this patient has been in atrial fibrillation for several weeks with only prior paroxysmal episodes indicates that her arrhythmia is likely contributing to her decompensation and therefore should be addressed during hospitalization. This patient should be considered for AAD initiation and careful considerations should be made to ensure that this patient is appropriately anticoagulated. Once anticoagulation has been established, interventions including electrical cardioversion can be considered. For this patient with a reduced LVEF, AAD initiation should be considered prior to cardioversion with options limited to amiodarone or dofetilide. For patients with renal disease and concerns for QT prolongation, amiodarone can be used as a reasonable short-term solution to bridge the patient to more definitive long-term strategies for rhythm control. This patient can be initiated on AAD and, if she does not convert on medication, can be considered for electrical cardioversion. The timing of cardioversion would depend on when the patient is optimized from a heart failure standpoint, including when the patient has become more euvolemic. With dofetilide, electrical cardioversion is typically attempted after the fourth dose is given to ensure that the patient can stay in sinus rhythm after cardioversion. 7. A common scenario in which we often find ourselves managing atrial fibrillation is in the postoperative setting. What are some of the management strategies for postoperative atrial fibrillation and how does this vary between patients who underwent cardiac versus non-cardiac procedures? Compared to non-cardiac surgery, in cardiac surgery there is an increased risk for developing postoperative atrial fibrillation, with rates of occurrence ranging from 30-60%.4,5 While there are higher rates of post-operative atrial fibrillation in patients undergoing cardiac surgeries, there is no significant difference in the strategies used to treat patients who underwent cardiac versus non-cardiac surgeries. For patients who have no prior history of atrial fibrillation prior to developing post-operatively, historical teaching endorsed the idea that this arrhythmia developed in response to inflammation occurring during acute recovery and should not have long-term consequences; however, more recent data suggests that if a patient develops atrial fibrillation post-operatively, they are more likely to have recurrence of this arrhythmia in the future.6  Current guidelines support anticoagulation based on the CHADSVASc score for at least 60 days post-operatively while monitoring for persistence of the arrhythmia.7 Further, data suggest that rhythm approaches post-operatively lead to better long-term outcomes in terms of re-hospitalizations and mortality. In patients who underwent surgeries with high bleeding risk during recovery and have contraindications to anticoagulation, rate-control strategies are most appropriate initially. If a patient has new atrial fibrillation without a prior diagnosis, they will need monitoring for recurrence for 30-60 days post-operatively. 8. What are some of the considerations for a pill-in-the-pocket strategy for those patients who experience infrequent episodes of symptomatic atrial fibrillation? In this strategy, the patient takes medication when they are having symptoms with the intention of terminating the atrial fibrillation episode acutely.  When initiating this approach, it is essential to do so in a monitoring setting because of the effects that can result from giving high doses of these medications to treat acute episodes. For example, with flecainide, a dose of 300 mg may be given at one time compared to a dose of 50-150 mg twice daily to reach the maintenance dose. When medications such as flecainide are given in these loading doses, it is important to monitor for any acute toxicity. Given the potential toxicities and challenges inherent to a pill-in-the-pocket approach, the desire to prevent rather than reactively treat episodes of atrial fibrillation, and improvements in catheter ablation techniques, this strategy is now rarely used in practice, with patients managed either with a maintenance medication or ablation. References 1.         Van Gelder IC, Groenveld HF, Crijns HJGM, et al. Lenient versus Strict Rate Control in Patients with Atrial Fibrillation. New England Journal of Medicine. 2010;362(15). doi:10.1056/nejmoa1001337 2.         Kirchhof P, Camm AJ, Goette A, et al. Early Rhythm-Control Therapy in Patients with Atrial Fibrillation. New England Journal of Medicine. 2020;383(14). doi:10.1056/nejmoa2019422 3.          Rillig A, Magnussen C, Ozga AK, et al. Early Rhythm Control Therapy in Patients With Atrial Fibrillation and Heart Failure. Circulation. 2021;144(11). doi:10.1161/CIRCULATIONAHA.121.056323 4.         Gaudino M, Di Franco A, Rong LQ, Piccini J, Mack M. Postoperative atrial fibrillation: From mechanisms to treatment. Eur Heart J. 2023;44(12). doi:10.1093/eurheartj/ehad019 5.         Perezgrovas-Olaria R, Alzghari T, Rahouma M, et al. Differences in Postoperative Atrial Fibrillation Incidence and Outcomes After Cardiac Surgery According to Assessment Method and Definition: A Systematic Review and Meta-Analysis. J Am Heart Assoc. 2023;12(19). doi:10.1161/JAHA.123.030907 6.         Gilbers MD, Kawczynski MJ, Bidar E, et al. Determinants and impact of postoperative atrial fibrillation burden during 2.5 years of continuous rhythm monitoring after cardiac surgery: Results from the RACE V prospective cohort study. Heart Rhythm. 2024;22(3):647-660. doi:10.1016/j.hrthm.2024.08.014 7.          Joglar JA, Chung MK, Armbruster AL, et al. 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). doi:10.1161/CIR.0000000000001193

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. We Were Thrilled to Join the American Heart Association’s Scientific Sessions 2025! AHA Scientific Sessions 2025 took place November 7–10 in New Orleans, LA — one of the premier annual gatherings in cardiovascular science and education. It was an incredible opportunity to connect with colleagues, hear cutting-edge research, and contribute to the ongoing conversations shaping the future of cardiovascular care. We’re grateful to everyone who joined us in New Orleans and made this year’s meeting so impactful. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. 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!

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!

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.  We Were Thrilled to Join the American Heart Association’s Scientific Sessions 2025! AHA Scientific Sessions 2025 took place November 7–10 in New Orleans, LA — one of the premier annual gatherings in cardiovascular science and education. It was an incredible opportunity to connect with colleagues, hear cutting-edge research, and contribute to the ongoing conversations shaping the future of cardiovascular care. We’re grateful to everyone who joined us in New Orleans and made this year’s meeting so impactful. 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.  “To study the phenomena of disease without books is to sail an uncharted sea, while to study books without patients is not to go to sea at all.” – Sir William Osler. CardioNerds thank the patients and their loved ones whose stories teach us the Art of Medicine and support our Mission to Democratize Cardiovascular Medicine. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. 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, increasing the risk of dangerous heart rhythms and sudden cardiac death (SCD). Here’s how LGE refines risk assessment: 1. Predicting Sudden Cardiac Death (SCD) Major risk multiplier: Patients with LGE have 4.3× higher odds of life-threatening arrhythmia, regardless of their heart’s pumping ability (ejection fraction, EF). For every 1% increase in scar size (as % of heart muscle), SCD risk rises by 15%. Thresholds matter: In hypertrophic cardiomyopathy (HCM), LGE covering ≥5% of the heart muscle adds critical risk stratification, even in patients not initially flagged as high-risk by guidelines. Larger scars (≥10-15%) correlate with dramatically higher SCD risk, especially in HCM. 2. Mortality Signals Annual death rates: LGE+ patients: 4.7% annual mortality (similar to ischemic heart disease). LGE− patients: 1.7% annual mortality. Patterns and locations: Midwall scars (e.g., in dilated cardiomyopathy): 4.6× higher risk of SCD. Inferolateral scars (common in cardiac sarcoidosis): Linked to frequent ventricular tachycardia (VT). 3. Quantifying Scars: Methods Matter Full Width at Half Maximum (FWHM): Most reproducible method for measuring scar size. Reduces overestimation compared to other techniques. Standard Deviation (SD) thresholds: 5-SD method: Widely used but may overestimate scar size. 6-SD method: Best studied; 10% LGE is the optimal cutoff for predicting SCD in HCM. Dark-blood vs. bright-blood imaging: Dark-blood LGE improves scar visualization in ischemic heart disease but performs similarly to bright-blood LGE in non-ischemic conditions. 4. Guideline Gaps and Solutions Current ICD criteria fall short: Guidelines focus on EF ≤35%, missing high-risk patients with EF >35% but significant LGE. Example: A patient with EF 45% and 12% LGE has higher SCD risk than many with EF ≤35%. Emerging recommendations: Use LGE to guide ICD decisions in the “grey zone” (EF 36-50%). The 2022 ESC HCM model now integrates LGE for better risk prediction. 5. Tracking Changes Over Time Serial imaging: Repeat MRIs every 1-2 years monitor scar progression. Example: If LGE grows from 8% to 14%, ICD may be warranted even if EF remains normal. 6. Limitations Not all scars are equal: Ischemic scars (from blocked arteries) vs. non-ischemic scars (e.g., HCM) carry different risks. Technical challenges: Labs use different methods (e.g., FWHM vs. SD), causing variability in measurements. Contraindications: Severe kidney disease (risk of gadolinium toxicity) or implanted devices (e.g., older pacemakers) may limit MRI use. References – Malignant Ventricular Arrhythmias Al-Khatib, S. M., Stevenson, W. G., Ackerman, M. J., Bryant, W. J., Callans, D. J., Curtis, A. B., … & Page, R. L. (2018). 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. Journal of the American College of Cardiology, 72(14), e91-e220. https://www.ahajournals.org/doi/10.1161/CIR.0000000000000549  Di Marco, A., Anguera, I., Schmitt, M., Klem, I., Neilan, T. G., White, J. A., … & Cequier, A. (2017). Late gadolinium enhancement and the risk for ventricular arrhythmias or sudden death in dilated cardiomyopathy: systematic review and meta-analysis. JACC: Heart Failure, 5(1), 28-38. https://www.sciencedirect.com/science/article/pii/S2213177916305698?via%3Dihub  Kuruvilla, S., Adenaw, N., Katwal, A. B., Lipinski, M. J., Kramer, C. M., & Salerno, M. (2014). Late gadolinium enhancement on cardiac magnetic resonance predicts adverse cardiovascular outcomes in nonischemic cardiomyopathy: a systematic review and meta-analysis. Circulation: Cardiovascular Imaging, 7(2), 250-258.  https://pubmed.ncbi.nlm.nih.gov/24363358 Gulati, A., Jabbour, A., Ismail, T. F., Guha, K., Khwaja, J., Raza, S., … & Prasad, S. K. (2013). Association of fibrosis with mortality and sudden cardiac death in patients with nonischemic dilated cardiomyopathy. Jama, 309(9), 896-908. https://jamanetwork.com/journals/jama/fullarticle/1660382  Piers, S. R., Tao, Q., van Huls van Taxis, C. F., Schalij, M. J., van der Geest, R. J., & Zeppenfeld, K. (2013). Contrast-enhanced MRI–derived scar patterns and associated ventricular tachycardias in nonischemic cardiomyopathy: implications for the ablation strategy. Circulation: Arrhythmia and Electrophysiology, 6(5), 875-883. https://pubmed.ncbi.nlm.nih.gov/24036134/  Priori, S. G., Blomström-Lundqvist, C., Mazzanti, A., Blom, N., Borggrefe, M., Camm, J., … & Van Veldhuisen, D. J. (2015). ESC Scientific Document Group. 2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: The Task Force for the Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death of the European Society of Cardiology (ESC). Endorsed by: Association for European Paediatric and Congenital Cardiology (AEPC). Eur Heart J, 36(41), 2793-2867. https://pubmed.ncbi.nlm.nih.gov/26320108/  Wang, J., Yang, S., Ma, X., Zhao, K., Yang, K., Yu, S., … & Zhao, S. (2023). Assessment of late gadolinium enhancement in hypertrophic cardiomyopathy improves risk stratification based on current guidelines. European heart journal, 44(45), 4781-4792. https://pubmed.ncbi.nlm.nih.gov/37795986/  Kiaos, A., Daskalopoulos, G. N., Kamperidis, V., Ziakas, A., Efthimiadis, G., & Karamitsos, T. D. (2024). Quantitative late gadolinium enhancement cardiac magnetic resonance and sudden death in hypertrophic cardiomyopathy: a meta-analysis. Cardiovascular Imaging, 17(5), 489-497. https://pubmed.ncbi.nlm.nih.gov/37795986/  Case Media