Cardionerds: A Cardiology Podcast

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

  CardioNerds (Dr. Rick Ferraro and Dr. Dan Ambinder) join Dr. Sri Mandava, Dr. David Meister, and Dr. Marissa Donatelle from the Columbia University Division of Cardiology at Mount Sinai Medical Center in Miami. Expert commentary is provided by Dr. Pranav Venkataraman.   They discuss the following case involving a patient with cardiac sarcoidosis presenting as STEMI:  A 57-year-old man with a history of hyperlipidemia presented with sudden onset chest pain. On admission, he was vitally stable with a normal cardiorespiratory exam but appeared in acute distress and was diffusely diaphoretic. His ECG revealed sinus rhythm, a right bundle branch block (RBBB), and ST elevation in the inferior-posterior leads. He was promptly taken for emergent cardiac catheterization, which identified a complete thrombotic occlusion of the mid-left circumflex artery (LCX) and large obtuse marginal (OM) branch, with no underlying coronary atherosclerotic disease. Aspiration thrombectomy and percutaneous coronary intervention (PCI) were performed, with one drug-eluting stent placed. An echocardiogram showed a left ventricular ejection fraction (EF) of 31%, hypokinesis of the inferior, lateral, and apical regions, and an apical left ventricular thrombus. The patient was started on triple therapy. A hypercoagulable workup was negative. A cardiac MRI was obtained to further evaluate non-ischemic cardiomyopathy. In conjunction with a subsequent CT chest, the results raised suspicion for cardiac sarcoidosis with systemic involvement. In view of a reduced EF and significant late-gadolinium enhancement, electrophysiology was consulted to evaluate for ICD candidacy. A decision was made to delay ICD implantation until a definitive diagnosis of cardiac sarcoidosis could be established by tissue biopsy. The patient was started on HF-GDMT and discharged with a LifeVest. Close outpatient follow-up with cardiology and electrophysiology was arranged.  US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Cardiac Sarcoidosis Presenting as STEMI Cardiac sarcoidosis can present with a variety of symptoms, including arrhythmias, heart block, heart failure, or sudden cardiac death. Symptoms can be subtle or mimic other cardiac conditions.  Conduction abnormalities, particularly AV block or ventricular arrhythmias, are common and may be the initial indication of cardiac involvement with sarcoidosis.  The additive value of Echocardiography, FDG-PET, and cardiac MR is indispensable in the diagnostic workup of suspected cardiac sarcoidosis.  Specific role of MRI/PET: Both cardiac MRI and FDG-PET provide a complementary role in the diagnosis of cardiac sarcoidosis. Cardiac MRI is an effective diagnostic screening tool with fairly high sensitivity but is limited by its inability to decipher inflammatory (“active” disease) versus fibrotic myocardium. FDG-PT helps to make this discrimination, refine the diagnosis, and guide clinical management. Ultimately, these studies are most useful when interpreted in the context of other clinical information.  Primary prevention of sudden cardiac death in cardiac sarcoidosis focuses on risk stratification, with ICD placement for high-risk patients. For patients awaiting definitive diagnosis, a LifeVest may be used as a temporary measure to protect from sudden arrhythmic events until an ICD is placed.  Notes - Cardiac Sarcoidosis Presenting as STEMI 1. Is STEMI always a result of coronary artery disease?  By definition, a STEMI is an acute S-T segment elevation myocardial infarction. This occurs when there is occlusion of a major coronary artery, which results in transmural ischemia and damage,

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

  CardioNerds Cardiac Amyloidosis Series Chair Dr. Rick Ferraro and Episode Lead Dr. Anna Radakrishnan discuss the biology of transthyretin amyloid cardiomyopathy (ATTR-CM ) with Dr. Daniel Judge.  Notes were drafted by Dr. Anna Radakrishnan. The audio was engineered by student Dr. Julia Marques.  This episode provides a comprehensive overview of transthyretin (ATTR) cardiac amyloidosis, a complex and rapidly evolving disease process. The discussion covers the key red flags for cardiac amyloidosis, the diagnostic pathway, and the implications of hereditary versus wild-type ATTR. Importantly, the episode delves into the current and emerging therapies for ATTR, including stabilizers, gene silencers, and promising treatments like CRISPR-Cas9 and antibody-based approaches. Dr. Judge shares his insights and excitement about the rapidly advancing field, highlighting the need for early diagnosis and the potential to improve long-term outcomes for patients with this condition.  Enjoy this Circulation Paths to Discovery article to learn more about the CardioNerds mission and journey.  US Cardiology Review is now the official journal of CardioNerds! Submit your manuscripts here.  CardioNerds Cardiac Amyloid PageCardioNerds Episode Page Pearls: - Biology of Transthyretin amyloid cardiomyopathy Maintain a high index of suspicion! Look for subtle (yet telling) signs like ventricular hypertrophy, discordant EKG findings, bilateral carpal tunnel syndrome, and spontaneous biceps tendon rupture.  Utilize the right diagnostic tests. Endomyocardial biopsy remains the gold standard, but non-invasive tools like PYP scan with SPECT imaging and genetic testing are essential for accurate diagnosis.  Differentiating hereditary from wild-type ATTR is critical, as genetic forms may have a more aggressive course and familial implications.  Early diagnosis and intervention significantly improve prognosis, making vigilance in screening and prompt treatment initiation essential.  The future is now! Cutting-edge therapies are transforming the treatment landscape, including TTR stabilizers, gene silencers, and emerging technologies like CRISPR-Cas9 and antibody-based treatments.  Notes - Biology of Transthyretin amyloid cardiomyopathy What is transthyretin amyloid (aTTR) and how is it derived?  Transthyretin (TTR) is a transport protein primarily synthesized by the liver, responsible for carrying thyroid hormones (thyroxine) and retinol (vitamin A) in the blood. It circulates as a tetramer, composed of four identical monomers, which is essential for its stability and function.  In transthyretin amyloid (ATTR) amyloidosis, the TTR protein becomes unstable, leading to its dissociation into monomers. These monomers misfold and aggregate into insoluble amyloid fibrils, which deposit extracellularly in tissues such as the heart, nerves, and gastrointestinal tract. This progressive amyloid deposition leads to organ dysfunction, including restrictive cardiomyopathy and neuropathy.  There are two main forms of ATTR amyloidosis: hereditary (variant) and wild-type (senile) ATTR.  Hereditary ATTR (ATTRv) is caused by mutations in the TTR gene. These mutations destabilize the TTR tetramer, making it more prone to dissociation. This increases misfolding and amyloid fibril formation, resulting in systemic amyloid deposition.   Wild-type ATTR (ATTRwt) occurs without genetic mutations and is primarily age-related. Over time, even normal TTR tetramers can become unstable, leading to gradual misfolding and amyloid deposition, particularly in the heart. ATTRwt is a common but often underdiagnosed cause of heart failure with preserved ejection fraction (HFpEF) in elderly individuals.  How does aTTR lead to deleterious effects in the heart and other organ systems?    Transthyretin amyloidosis leads to organ dysfunction through the deposition of misfolded TTR protein as amyloid fib...

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

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

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

  CardioNerds (Dr. Colin Blumenthal and Dr. Saahil Jumkhawala) join Dr. Rohan Ganti, Dr. Nikita Mishra, and Dr. Jorge Naranjo from the Rutgers – Robert Wood Johnson program for a college basketball game, as the buzz around campus is high. They discuss the following case involving a patient with ventricular tachycardia:  The case involves a 61-year-old man with a medical history of hypothyroidism, hypertension, hyperlipidemia, seizure disorder on anti-epileptic medications, and major depressive disorder, who presented to the ER following an out-of-hospital cardiac arrest. During hospitalization, he experienced refractory polymorphic ventricular tachycardia (VT), requiring 18 defibrillation shocks. Further evaluation revealed non-obstructive hypertrophic cardiomyopathy (HCM). We review the initial management of electrical storm, special ECG considerations, diagnostic approaches once ischemia has been excluded, medications implicated in polymorphic VT, the role of multi-modality imaging in diagnosing hypertrophic cardiomyopathy, and risk stratification for implantable cardioverter-defibrillator (ICD) placement in patients with HCM.  Expert commentary is provided by Dr. Sabahat Bokhari.   Episode audio was edited by CardioNerds Intern and student Dr. Pacey Wetstein.   US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - A Curious Case of Refractory Ventricular Tachycardia - Rutgers-Robert Wood Johnson Diagnostic Uncertainty in VT Storm: In VT storm, ischemia is a primary consideration; when coronary angiography excludes significant epicardial disease, alternative causes such as cardiomyopathies, channelopathies, myocarditis, electrolyte disturbances, or drug-induced arrhythmias must be explored.  ST elevations in ECG lead aVR:  ST elevations in lead aVR and diffuse ST depressions can sometimes represent post-arrest oxygen demand and myocardial mismatch rather than an acute coronary syndrome. This pattern may occur in the context of polymorphic VT (PMVT), where myocardial oxygen demands outstrip supply, especially after an arrest. While these ECG changes could suggest myocardial ischemia, caution is needed, as they might not always indicate coronary pathology. However, PMVT generally should raise suspicion for underlying coronary disease and may warrant a coronary angiogram for further evaluation.  Medication Implications in PMVT and HCM: Certain medications, including psychotropic drugs (e.g., antidepressants, antipsychotics) and anti-epileptic drugs, can prolong the QT interval or interact with other drugs, thereby increasing the risk of polymorphic VT in patients with underlying conditions like HCM. Careful management of these medications is critical to avoid arrhythmic events in predisposed individuals.  Multi-Modality Imaging in HCM: Cardiac MRI with late gadolinium enhancement (LGE) is invaluable in assessing myocardial fibrosis, a key predictor of arrhythmic risk, and can guide decisions regarding ICD implantation. Echocardiography and contrast-enhanced CT can provide additional insights into structural abnormalities and risk assessment.  Polymorphic VT in Nonobstructive HCM: Polymorphic ventricular tachycardia (PMVT) can occur in nonobstructive hypertrophic cardiomyopathy due to myocardial fibrosis and disarray, even in the absence of significant late gadolinium enhancement and left ventricular outflow tract obstruction.  ICD Risk Stratification in HCM: Risk stratification for ICD placement in HCM includes assessment of clinical features such as family history of sudden cardiac death, history of unexplained syncope, presence of nonsustained VT on ambulatory monitoring,

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

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

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