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. 









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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 ...

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.  















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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 w...

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. Mohammed 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. 











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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 r...

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. 

















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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...

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.





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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.  











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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,

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.

















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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.  

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.  











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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,

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.













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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 individ...

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. 



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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

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.









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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.







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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?

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.











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CardioNerds (Drs. Daniel Ambinder and Eunice Dugan) join Dr. Namrita Ashokprabhu, Dr. Yulith Roca Alvarez, and Dr. Mehmet Yildiz from The Christ Hospital. Expert commentary by Dr. Odayme Quesada. Audio editing by CardioNerds intern, Christiana Dangas. This episode highlights the pivotal role of cardiac MRI and functional testing in uncovering coronary vasospasm as an underlying cause 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. 







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*




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,

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.







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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,

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. 







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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,

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. 



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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,

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.









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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.

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.  







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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...

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.













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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.

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.













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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