396. Case Report: Unmasking Constrictive Pericarditis Using Multimodality Imaging – University of Nebraska

Cardionerds: A Cardiology Podcast

#Medicine #Fitness #Health and Well-Being #Podcasting Education #Mental Health #Cardionerds #On Covid19

56:04

Growing up in a military family, Tristen Epps moved around a lot. But no matter where he was living, Friday nights were sacred. He got to dress up, go to a restaurant, not order from a kids menu, and feel like he was getting to know the place he was living — for now. At home, when his mom taught him to scramble an egg, he was mesmerized by the alchemy; one simple ingredient could transform into so many things. It's that wonder and curiosity that transformed him into the leader, visionary, and Top Chef winner he is today. He joined Tinfoil Swans at the Food & Wine Classic in Aspen to talk about his mission to “un-colonize colonized food,” the freedom he feels cooking in Air Jordans, why it's important to him to celebrate oxtails with Michelin-level finesse, and his belief that cooking has power to correct history. Sponsor: Old Fitzgerald® Kentucky Straight Bourbon Whiskey. Bardstown, KY. 50% Alc./Vol. Think Wisely. Drink Wisely. Learn more about your ad choices. Visit podcastchoices.com/adchoices…

about a year ago 37:19

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CardioNerds (Dr. Dan Ambinder and Dr. Rick Ferraro) join Dr. Mansi Oberoi and Dr. Mohan Gudiwada from the University of Nebraska Medical Center discuss a case of constrictive pericarditis. Expert commentary is provided by Dr. Adam Burdorf, who serves as the Program Director for the Cardiovascular Medicine Fellowship at the University of Nebraska Medical Center. The case discussed involves a 76-year-old woman with a history of monoclonal gammopathy of undetermined significance, chronic obstructive pulmonary disease, type 2 diabetes mellitus, and squamous cell carcinoma was admitted to the hospital for worsening shortness of breath, swelling in lower extremities, hyponatremia, and urinary tract infection. CT chest to evaluate for pulmonary embolism showed incidental pericardial calcifications; the heart failure team was consulted for the management of her decompensated heart failure. Echo images were nondiagnostic. Subsequent invasive hemodynamic monitoring showed elevated right and left-sided filling pressures, diastolic equalization of LV and RV pressures, and positive RV square root sign with ventricular interdependence. Cardiac MRI showed septal flattening on deep inspiration and septal bounce, suggestive of interventricular dependence. After a heart team discussion and with shared-decision making the patient opted for medical management owing to her comorbidities and frailty. Enjoy this 2024 JACC State-of-the-Art Review to learn more about pericardial diseases and best practices for pericardiectomy (Al-Kazac et al., JACC 2024) 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! Case Media - Constrictive Pericarditis Echo: Left Ventricular ejection fraction = 55-60%. Unclear septal motion in the setting of atrial fibrillation MRI: Diastolic septal flattening with deep inspiration as well as a septal bounce suggestive of interventricular dependence and constrictive physiology References Garcia, M. Constrictive Pericarditis Versus Restrictive Cardiomyopathy. Journal of the American College of Cardiology, vol. 67, no. 17, 2016, pp. 2061–2076. Pathophysiology and Diagnosis of Constrictive Pericarditis. American College of Cardiology, 2017. Geske, J., Anavekar, N., Nishimura, R., et al. Differentiation of Constriction and Restriction: Complex Cardiovascular Hemodynamics. Journal of the American College of Cardiology, vol. 68, no. 21, 2016, pp. 2329–2347. Constrictive Pericarditis. ScienceDirect. Constrictive Pericarditis. Journal of the American College of Cardiology, vol. 83, no. 12, 2024, pp. 1500-1512.

426 episodes

Cardionerds: A Cardiology Podcast

396. Case Report: Unmasking Constrictive Pericarditis Using Multimodality Imaging – University of Nebraska

Cardionerds: A Cardiology Podcast

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published about a year ago

MP3•Episode home

426 episodes

#Medicine #Fitness #Health and Well-Being #Podcasting Education #Mental Health #Cardionerds #On Covid19

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Cardionerds: A Cardiology Podcast

1
423. Case Report: The Malignant Murmur – More Than Meets the Echo in Nonbacterial Thrombotic Endocarditis – Baylor College of Medicine 16:03

2 days ago16:03

16:03

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

Cardionerds: A Cardiology Podcast

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422. Diagnosis of Transthyretin Amyloid Cardiomyopathy (ATTR-CM) with Dr. Venkatesh Murthy 13:38

12 days ago13:38

13:38

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

Cardionerds: A Cardiology Podcast

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421. Case Report: Switched at Birth: A Case of Congenital Heart Disease Presenting in Adulthood – New York Presbyterian Queens 29:12

27 days ago29:12

29:12

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. “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 Page CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron! Pearls- A Case of Congenital Heart Disease Presenting in Adulthood Congenitally Corrected Transposition of the Great Arteries (CCTGA) is a rare and unique structural heart disease which presents as an isolated combination of atrioventricular and ventriculoarterial discordance resulting in physiologically corrected blood flow. CCTGA occurs due to L looping of the embryologic heart tube. As a result, the morphologic right ventricle outflows into the systemic circulation, and the morphologic left ventricle outflows into the pulmonary circulation. CCTGA is frequently associated with ventricular septal defects, pulmonic stenosis, tricuspid valve abnormalities and dextrocardia. CCTGA is often asymptomatic in childhood and can present later in adulthood with symptoms of morphologic right ventricular failure, tricuspid regurgitation, or cardiac arrhythmias. Systemic atrioventricular valve (SAVV) intervention can be a valuable option for treating right ventricular failure and degeneration of the morphologic tricuspid valve. notes- A Case of Congenital Heart Disease Presenting in Adulthood Notes were drafted by Ayan Purkayastha. What is the pathogenesis of Congenitally Corrected Transposition of the Great Arteries? Occurs due to disorders in the development of the primary cardiac tube Bulboventricular part of the primary heart forms a left-sided loop instead of right-sided loop, leading to the normally located atria being connected to morphologically incompatible ventricles This is accompanied by abnormal torsion of the aortopulmonary septum (transposition of the great vessels) As a result, there is ‘physiologic correction’ of blood flow. Non-oxygenated blood flows into the right atrium and through the mitral valve into the morphologic left ventricle, which pumps blood into the pulmonary artery. Oxygenated blood from the pulmonary veins flows into the left atrium and through the tricuspid valve to the morphologic right ventricle, which pumps blood to the aorta. Compared with standard anatomy, the flow of blood is appropriate, but it is going through the incorrect ventricle on both sides. Frequent conditions associated with CCTGA include VSD, pulmonic stenosis and dextrocardia What is the presentation of Congenitally Corrected Transposition of the Great Arteries? In cases without concomitant deficits CCTA is asymptomatic early in life and often for several decades. Cyanosis and dyspnea are common presenting symptoms. Systemic right ventricular dysfunction due to high systemic pressures over time Arrythmias, commonly AV block, due to abnormal structure of the conduction system Tricuspid valve regurgitation resulting from dilation of the right ventricle and tricuspid valve annulus What is Dextrocardia and how is it associated with CCTGA? Dextrocardia is a cardiac positional anomaly where the heart is located in the right hemithorax with base to apex axis directed to the right and caudad Dextrocardia can occur in up to 20% cases of CCTGA Can be associated with both situs solitus (normal anatomic arrangement of chest and abdominal organs) or situs inversus (chest and abdominal organs are mirrored from their normal positions) How is CCTGA Diagnosed? Transthoracic echocardiography is the primary diagnostic tool in CCTGA Assessment of the systemic RV function is crucial but can be challenging. Techniques such as speckle tracking echocardiography and global longitudinal strain can help with assessment of systemic RV function Cardiac MRI can also provide accurate measurements of ventricular volumes as well as quantification of valvular regurgitation What is the long-term management of CCTGA in adults? Many patients with CCTGA and no associated lesions have long life expectancies with minimal or non-specific symptoms Symptoms of circulatory failure occur mainly in 5 th and 6 th decades of life The 2018 AHA/ACC Guidelines for the Management of Adults with Congenital Heart Disease recommends the following routine follow-up and testing intervals for CCTGA Physiologic stage A: Outpatient ACHD follow up every 12 months with ECG(12 months), TTE(12-24 months), Holter monitor(12-60 months), CMR/CCT and exercise test(36-60 months) Physiologic stage B: outpatient ACHD follow up every 12 months with ECG and TTE(12 months), Holter monitor(12-60 months), CMR/CCT and exercise test(36-60 months) Physiologic stage C: outpatient ACHD follow up every 6-12 months with ECG and TTE(12 months), pulse oximetry at each visit, Holter monitor(12-36 months), CMR/CCT and exercise test(12-24 months) Physiologic stage D: outpatient ACHD follow up every 3-6 months, ECG and TTE every 12 months, pulse oximetry at each visit, Holter monitor, CMR/CCT and exercise test every 12 months What is the role of Systemic Atrioventricular Valve Surgery (SAVV) for treatment of CCTGA as an adult? In CCTGA the morphologic tricuspid valve acts as the SAVV and is subject to functional deterioration from high systemic pressures Tricuspid valve regurgitation is a key prognostic overall survival determinant in CCTGA patients Studies have shown that 94% of patients with CCTGA suffered from intrinsic tricuspid valve abnormalities SAV surgery remains a valuable option with low early mortality and good long-term outcomes, especially with ejection fraction > 40%. The 2018 AHA/ACC Guidelines for the Management of Adults with Congenital Heart Disease recommends tricuspid valve replacement for symptomatic adults with CCTGA and severe TR and preserved or mildly depressed systemic ventricular function (class IB recommendation). References – A Case of Congenital Heart Disease Presenting in Adulthood 1. Baruteau AE, Abrams DJ, Ho SY, Thambo JB, McLeod CJ, Shah MJ. Cardiac Conduction System in Congenitally Corrected Transposition of the Great Arteries and Its Clinical Relevance. J Am Heart Assoc . 2017;6(12). doi:10.1161/JAHA.117.007759 2. Susheel Kumar TK. Congenitally corrected transposition of the great arteries. J Thorac Dis . 2020;12(3):1213-1218. doi:10.21037/jtd.2019.10.15 3. Osakada K, Ohya M, Waki K, Nasu H, Kadota K. Congenitally Corrected Transposition of the Great Arteries at Age 88 Years. CJC Open . 2020;2(6):726-728. doi:10.1016/j.cjco.2020.08.003 4. Munaf M, Farooqui S, Kazmi SK, Ul-Haque I. Congenitally Corrected Transposition of Great Arteries with Dextrocardia, Patent Ductus Arteriosus, Atrial Septal Defects and Ventricular Septal Defects in a 15-Year-Old Marfanoid Habitus Patient: A Case Study. Cureus . Published online July 1, 2020. doi:10.7759/cureus.8937 5. Abdelrehim AA, Stephens EH, Miranda WR, et al. Systemic Atrioventricular Valve Surgery in Patients With Congenitally Corrected Transposition of the Great Vessels. J Am Coll Cardiol . 2023;82(23):2197-2208. doi:10.1016/j.jacc.2023.09.822 6. Lippmann MR, Maron BA. The Right Ventricle: From Embryologic Development to RV Failure. Curr Heart Fail Rep . 2022;19(5):325-333. doi:10.1007/s11897-022-00572-z 7. Brida M, Diller GP, Gatzoulis MA. Systemic Right Ventricle in Adults with Congenital Heart Disease. Circulation . 2018;137(5):508-518. doi:10.1161/CIRCULATIONAHA.117.031544 8. Bevilacqua F, Pasqualin G, Ferrero P, et al. Overview of Long-Term Outcome in Adults with Systemic Right Ventricle and Transposition of the Great Arteries: A Review. Diagnostics . 2023;13(13). doi:10.3390/diagnostics13132205 9. Maldjian PD, Saric M. Approach to dextrocardia in adults: Review. American Journal of Roentgenology . 2007;188(6 SUPPL.). doi:10.2214/AJR.06.1179 10. Kandakure PR, Katta Y, Batra MJ, Timmanwar A, Lakka VK, Reddy B. Dextrocardia and corrected transposition of the great arteries with rheumatic tricuspid stenosis: a unique association. Indian J Thorac Cardiovasc Surg . 2019;35(2):230-232. doi:10.1007/s12055-018-0778-0 11. Stout KK, Daniels CJ, Aboulhosn JA, et al. 2018 AHA/ACC Guideline for the Management of Adults With Congenital Heart Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation . 2019;139(14):e698-e800. doi:10.1161/CIR.0000000000000603 12. Zubrzycki M, Schramm R, Costard-Jäckle A, et al. Pathogenesis and Surgical Treatment of Congenitally Corrected Transposition of the Great Arteries (ccTGA): Part III. J Clin Med . 2024;13(18). doi:10.3390/jcm13185461…

Cardionerds: A Cardiology Podcast

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420. Cardio-Rheumatology: Cardiovascular Multimodality Imaging & Systemic Inflammation with Dr. Monica Mukherjee 17:54

7 weeks ago17:54

17:54

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 . 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 Prevention Page CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron! Pearls – Cardiovascular Multimodality Imaging & Systemic Inflammation Systemic inflammatory diseases are associated with an elevated CVD risk that has significant implications for early detection, risk stratification, and implementation of therapeutic strategies to address these risks and disease-specific complications. As an example , patients with SLE have a 48-fold increased risk for developing ASCVD compared to the general population. They may also develop disease-specific complications, such as pericarditis, that require focused imaging approaches to detect. In addition to increasing the risk for CAD, systemic inflammatory diseases can also result in cardiac complications, including myocardial, pericardial, and valvular involvement. Assessment of these complications requires the use of different imaging techniques, with the modality and serial studies selected based on the suspected disease process involved. In most contexts, echocardiography remains the starting point for evaluating cardiac involvement in systemic inflammatory diseases and can inform the next steps in terms of diagnostic study selection for the assessment of specific cardiac processes. For example, if echocardiography is completed in an SLE patient and demonstrates potential myocardial or pericardial inflammation, the next steps in evaluation may include completing a cardiac MRI for better characterization. While no current guidelines or standards of care directly guide our selection of advanced imaging studies for screening and management of CVD in patients with systemic inflammatory diseases, our understanding of cardiac involvement in these patients continues to improve and will likely lead to future guideline development. Due to the vast heterogeneity of cardiac involvement both across and within different systemic inflammatory diseases, a personalized approach to caring for each individual patient remains central to CVD evaluation and management in these patients. For example, patients with systemic sclerosis and symptoms of shortness of breath may experience these symptoms due to a range of causes. Echocardiography can be a central guiding tool in assessing these patients for potential concerns related to pulmonary hypertension or diastolic dysfunction. Based on the initial echocardiogram, the next steps in evaluation may involve further ischemic evaluation or right heart catheterization, depending on the pathology of concern. Show notes – Cardiovascular Multimodality Imaging & Systemic Inflammation Episode notes drafted by Dr. Jake Roberts. What are the contexts in which we should consider pursuing multimodal cardiac imaging, and are there certain inflammatory disorders associated with systemic inflammation and higher associated CVD risk for which advanced imaging can help guide early intervention? Systemic inflammatory diseases are associated with elevated CVD risk, which has significant implications for early detection, risk stratification, prognostication, and implementation of therapeutic strategies to address CVD risk and complications in these patient populations. The most well-characterized autoimmune diseases with an association between systemic inflammation and CVD risk are inflammatory arthritic conditions such as rheumatoid arthritis. Additional inflammatory diseases with elevated CVD risk include spondyloarthropathies and psoriatic arthritis. Patients with rheumatoid arthritis have a 1.5- 2x risk of developing coronary artery disease compared to the general population. The mechanism of elevated CVD risk in inflammatory disease patients is likely related to a combination of abnormalities in lipid metabolism, endothelial dysfunction, and vascular inflammation. Conditions including systemic lupus erythematosus (SLE), myositis, vasculitis disorders, and systemic sclerosis may have additional cardiovascular complications beyond CAD, including pericarditis, myocarditis, electrical, and valvular complications. Are there any established or emerging technologies to help with improving early detection or characterization of cardiac involvement in systemic inflammatory diseases? Echocardiography remains the most common and useful starting point for screening and early detection of cardiac involvement in systemic inflammatory diseases due to its widespread availability, real-time interpretation, low cost, and noninvasive nature. Furthermore, echocardiography remains a crucial tool in serial monitoring for disease progression and the detection of therapeutic effects. This modality additionally provides significant utility for early detection and screening of pericardial and valvular involvement. Given that patients with inflammatory disorders have an elevated risk for developing CAD, utilizing CAC scores and CCTA are often additionally helpful for CAD detection in these patient populations. Are there different imaging techniques that should be used to assess complications specific to different systemic inflammatory diseases? Based on the specific disease involved, the choice of imaging technique may vary depending on the clinical context and the cardiovascular complication requiring further investigation. As an example, in systemic sclerosis, there can be a wide range of variable cardiac manifestations that emerge depending on the subtype of the disease, with the cardiac complications developing either because of the fibrotic disease process or from other secondary effects of the disease. Specifically, if the patient’s phenotype involves interstitial lung disease, the right ventricle of the heart will encounter chronic increased afterload, which can lead to adverse adaptive responses and remodeling over time. As a result, screening tools such as echocardiography can be very useful in this patient population, with these patients often requiring regular annual screening echocardiograms coupled with pulmonary function testing to screen for coupled changes in individual patients’ physiology. When these patients develop complications of their disease, including pulmonary hypertension, echocardiography can help evaluate the underlying cause of this complication and inform subsequent diagnostic steps. In terms of assessing myocardial disease and inflammation in myocardial tissue, cardiac MRI remains a valuable tool in detecting subclinical myocardial disease and can identify areas of low-grade myocardial inflammation. One of the advantages of cardiac MRI over other imaging techniques involves its ability to allow for noninvasive tissue characterization. For disease complications such as pericarditis, which can commonly develop in SLE, 2D echocardiography remains the first-line imaging modality of choice to detect pericardial disease involvement. In SLE patients who have long-standing pericardial disease with progression, they can also develop constrictive symptoms resulting from this process. In those cases, either CT or cardiac MRI can assist in defining the pericardial or myocardial anatomy. As an example, what would be the approach to utilizing advanced imaging to assess for CVD detection and monitoring in a patient with SLE with relatively well-controlled symptoms on chronic immunosuppressive agents and no prior history of heart failure or CVD? As a starting point, all patients with systemic inflammatory diseases should undergo comprehensive ASCVD risk assessment. Initial stratification involves completing a laboratory assessment with a standard lipid panel and diabetes screening studies. Further evaluation of any symptoms that a patient may describe, which could indicate potential early cardiovascular disease processes, should also be thoroughly assessed and may influence the next steps in screening. In the context of SLE, pericardial disease is common, and therefore, obtaining a baseline echocardiogram to assess for any early pericardial involvement should be the initial step in evaluation. If the patient also has an elevated ASCVD risk, they should also undergo assessment for coronary artery disease. What should be the approach to the sequence of imaging technique selection, serial imaging, monitoring, and follow-up in patients with systemic inflammatory disorders undergoing evaluation of CVD screening and monitoring? The initial selection of imaging modality should be based on what is suspected to be the primary driver of the patient’s symptoms or as the primary underlying process of concern that requires further evaluation. As an important consideration in the context of systemic inflammatory diseases such as SLE, ischemic disease may involve atypical presentations due to underlying myocardial dysfunction and microvascular disease. Therefore, imaging and other diagnostic studies may be warranted to assess for reversible ischemia. There is emerging evidence that cardiac PET perfusion and cardiac MRI may be particularly useful in this patient population to assess coronary flow reserve to evaluate for coronary microvascular disease. What evidence currently exists to demonstrate the impact on cardiovascular outcomes resulting from the utilization of advanced multimodality imaging for CVD detection and monitoring in patients with systemic inflammatory disorders? While there is limited evidence that has directly measured the impact of advanced imaging utilization on CVD outcomes in this patient population, there is growing recognition of the increased risk of cardiac complications in patients with systemic inflammatory diseases. With increasing recognition of the commonality of cardiac involvement in these diseases, we are now more often utilizing appropriate testing in these patients. Directly measuring outcomes in these patient populations is somewhat challenging in large part due to the wide heterogeneity of phenotypes both across and within specific inflammatory diseases. Much of the approach in cardio-rheumatology should emphasize personalized medicine specific to each patient, given the wide range of cardiovascular complications and unique presentations of cardiac involvement in individual patients. Providing care for patients with systemic inflammatory diseases further requires a collaborative approach across disciplines and subspecialties within medicine to provide appropriate comprehensive care. Is there a need for more standardized approaches for utilizing imaging in patients with systemic inflammatory diseases? Currently, there are no formal guidelines or standards of care to direct the use of multimodality imaging to assess CVD risk and direct management in patients with systemic inflammatory diseases. Many of the current standardized approaches are institution-dependent and often informed by clinical observations at individual medical centers. As we work to better understand the role of cardiac involvement in systemic inflammatory diseases and gain more experience in the evaluation of CVD and specific cardiovascular complications in these disorders, we will likely have ongoing development of standards of care and guidelines for management of CVD in these patients. References – Cardiovascular Multimodality Imaging & Systemic Inflammation Weber BN, Paik JJ, Ayaz Aghayev, et al. Novel Imaging Approaches to Cardiac Manifestations of Systemic Inflammatory Diseases. Journal of the American College of Cardiology. 2023;82(22):2128-2151. doi:https://doi.org/10.1016/j.jacc.2023.09.819 Mortensen MB, Jensen JM, Sand NP, et al. Association of Autoimmune Diseases with Coronary Atherosclerosis Severity and Ischemic Events. Journal of the American College of Cardiology. 2024;83(25):2643-2654. doi:https://doi.org/10.1016/j.jacc.2024.04.030 Thackeray JT, Lavine KJ, Liu Y. Imaging Inflammation Past, Present, and Future: Focus on Cardioimmunology. The Journal of Nuclear Medicine. 2023;64(Supplement 2):39S48S. doi:https://doi.org/10.2967/jnumed.122.264865 West HW, Katerina Dangas, Antoniades C. Advances in Clinical Imaging of Vascular Inflammation. JACC Basic to Translational Science. 2023;9(5):710-732. doi:https://doi.org/10.1016/j.jacbts.2023.10.007 Milner JJ, Kim AHJ. Cardiac Manifestations of Systemic Lupus Erythematosus. Rheumatic Disease Clinics of North America. 2024;40(1):51-60. https://doi.org/10.1016/j.rdc.2013.10.003 Lu J, Jani V, Mercurio V, et al. Stress Echocardiographic Prediction of Emerging Pulmonary Vascular Disease in Systemic Sclerosis. Journal of the American Society of Echocardiography. 2023;36(2):259-261. https://doi.org/10.1016/j.echo.2022.10.006 Gilotra NA, Griffin JM, Pavlovic N, et al. Sarcoidosis-Related Cardiomyopathy: Current Knowledge, Challenges, and Future Perspectives State-of-the-Art Review. Journal of Cardiac Failure. 2022;28(1):113-132. https://doi.org/10.1016/j.cardfail.2021.06.016 Trivieri MG, Spagnolo P, Birnie P, et al. Challenges in Cardiac and Pulmonary Sarcoidosis: JACC State-of-the-Art Review. 2020;76(16):1878-1901. https://doi.org/10.1016/j.jacc.2020.08.042…

Cardionerds: A Cardiology Podcast

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419. HFpEF in Women with Dr. Anu Lala and Dr. Martha Gulati 24:40

9 weeks ago24:40

24:40

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

Cardionerds: A Cardiology Podcast

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418. CardioNerds x CSWG – LV Unloading in AMI-Shock with Dr. Navin Kapur, Dr. Shashank Sinha & Dr. Rachna Kataria 23:25

12 weeks ago23:25

23:25

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 . Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Cardiac Critical Care Page CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!…

Cardionerds: A Cardiology Podcast

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417. Case Report: Clear Vision, Clouded Heart: Ocular Venous Air Embolism with Pulmonary Air Embolism, RV Failure, and Cardiac Arrest – Trinity Health Ann Arbor 19:47

13 weeks ago19:47

19:47

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. “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 Page CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron! Pearls- Clear Vision, Clouded Heart: Ocular Venous Air Embolism with Pulmonary Air Embolism, RV Failure, and Cardiac Arrest Hypoxia, hypotension and tachycardia in a patient following ocular instrumentation are classic findings suggestive of pulmonary embolism from possible air embolism. The diagnosis of RV failure is based on clinical presentation, echocardiographic findings (such as McConnell’s sign), and invasive hemodynamic assessment via right heart catheterization. Mechanical circulatory support can be considered as a temporary measure for patients with refractory RV failure. Central Figure : Approach to Pulmonary Embolism with Acute RV Failure Notes – Clear Vision, Clouded Heart: Ocular Venous Air Embolism with Pulmonary Air Embolism, RV Failure, and Cardiac Arrest 1. What is an Ocular Venous Air Embolism (VAE), and how can it be managed in critically ill patients? An Ocular Venous Air Embolism is defined as the entry of air into the systemic venous circulation through the ocular venous circulation, often during vitrectomy procedures. Early diagnosis is key to preventing cardiovascular collapse in cases of Ocular Venous Air Embolism (VAE). The goal is to stop further air entry. This can be done by covering the surgical site with saline-soaked dressings and checking for air entry points. Adjusting the operating table can help, especially with a reverse Trendelenburg position for lower-body procedures. The moment VAE is suspected, discontinue nitrous oxide and switch to 100% oxygen. This helps with oxygenation, speeds up nitrogen elimination, and shrinks air bubbles. Hyperbaric Oxygen Therapy can reduce bubble size and improve oxygenation, especially in cases of cerebral air embolism, when administered within 6 hours of the incident. Though delayed hyperbaric oxygen therapy can still offer benefits, the evidence is mixed. VAE increases right heart strain, so inotropic agents like dobutamine can help boost cardiac output, while norepinephrine supports ventricular function and systemic vascular resistance, but this may also worsen pulmonary resistance. Aspiration of air via multi-orifice or Swan-Ganz catheters has limited success, with success rates ranging from 6% to 16%. In contrast, the Bunegin-Albin catheter has shown more promise, with a 30-60% success rate. Catheterization for acute VAE-induced hemodynamic compromise is controversial, and there’s insufficient evidence to support its widespread emergency use. 2. What are the key hemodynamic parameters used to assess RV function? On echocardiogram, there are a number of parameters that can assess RV function: Tricuspid Annular Plane Systolic Excursion (TAPSE): Measures the lateral tricuspid annulus’ movement during systole. A TAPSE value below 1.6 cm is associated with poor prognosis. RV Outflow Tract (RVOT) Acceleration Time: Measured via pulsed wave Doppler, an acceleration time of <100 ms is abnormal, with values ≤60 ms indicating a worse prognosis. Global RV Longitudinal Strain: Assessed via speckle tracking, with a strain value of −20% being highly predictive of RV dysfunction (normal values typically range -24.5 to -28.5%). Tricuspid Regurgitation (TR) Jet Velocity: Helps estimate pulmonary systolic pressure and provides prognostic information. Inferior Vena Cava (IVC) Collapsibility: Useful in estimating right atrial pressure and guiding volume resuscitation, though it lacks prognostic significance. The RV:LV diameter ratio offers prognostic value, with a ratio greater than 0.9 linked to worse outcomes. Invasive Hemodynamic Monitoring (Right heart catheterization, PA Catheter) The Pulmonary Artery Pulsatility Index (PAPI) is an invasive hemodynamic parameter used to assess right ventricular (RV) function, particularly in cases of RV failure and cardiogenic shock. PAPi is the pulmonary arterial pulse pressure divided by the RA pressure. A PAPi of <0.9 is a poor indicator, especially in the acute myocardial infarction population. 3. What are the core principles in managing a patient with RV failure? The management to optimize RV function is centered around optimizing preload, afterload, and contractility. Optimizing preload – Optimizing preload is one of the most important aspects in the management of acute decompensated RV failure. The majority of us are taught that the RV is “preload dependent” and patients should be fluid resuscitated. However, many patients are actually volume overloaded and may benefit from diuresis. Overall, this is a patient-to-patient decision, depending on the clinical picture, to optimize preload; though the use of pulmonary artery (PA) catheters in this setting is not well supported. Reducing afterload – Avoid intubation if clinically feasible, as they may increase PVR; however, if essential, ideally, oxygen saturation (SaO₂) should be maintained above 92%, and ventilator settings should be adjusted to optimize lung volume and maintain a normal pH and PCO₂. Nitric oxide has also been beneficial in improving oxygenation and reducing PVR with its vasodilatory effects. Support cardiac output May support with the use of inotropes as well as mechanical circulatory support. Pressors: The ideal vasopressor increases systemic arterial pressure and RV contractility without raising pulmonary vascular resistance. Norepinephrine: Primarily an α1 agonist, it improves systemic blood pressure with some β1 stimulation. It has shown benefits in maintaining RV-PA coupling. Dobutamine: A β1 agonist that improves myocardial contractility and RV-PA coupling, though it can cause vasodilation at higher doses. In general, dobutamine is considered the best for acute RVF with PH, unless hypotension is a significant concern, in which case norepinephrine might be preferred. Milrinone is another option. MCS: short-term MCS should be considered in patients with cardiogenic shock as a bridge to recovery, a bridge to decision, or a bridge to bridge whilst the underlying causes for cardiogenic shock are addressed further described below Options include: Venous-arterial extracorporeal membranous oxygenation (V-A ECMO) RA to PA extracorporeal pump. (surgical RVAD) Flow device with an intake in the RA and an output in the PA. (Impella RP, Protek Duo) 4. When should we consider mechanical circulatory support for right ventricular (RV) failure? Short-term MCS should be considered in patients with cardiogenic shock as a bridge to recovery, a bridge to decision, or a bridge to bridge whilst the underlying causes for cardiogenic shock are addressed. Clinical parameters that suggest acute MCS use include signs of relative hypoperfusion plus hemodynamic features suggestive of RV failure, which were present in our patient. A specific additional consideration relates to where acute left-sided MCS reveals acute RV failure. Discerning whether this is intrinsic RV failure or due to persistently elevated RV afterload from inadequate LV support is also essential, as it will define management. The goal of percutaneous mechanical support is to bypass the right ventricle and improve hemodynamics, while allowing time for optimization of the patient and recovery of the RV. References Arrigo, Mattia, et al. “Diagnosis and Treatment of Right Ventricular Failure Secondary to Acutely Increased Right Ventricular Afterload (Acute Cor Pulmonale ). A Clinical Consensus Statement of the Association for Acute CardioVascular Care (ACVC) of the ESC.” European Heart Journal. Acute Cardiovascular Care , vol. 13, no. 3, 22 Dec. 2023, pp. 304–312, https://doi.org/10.1093/ehjacc/zuad157 . Accessed 17 May 2024. Chen, Guohai, et al. “INCIDENCE of ENDOPHTHALMITIS after VITRECTOMY: A Systematic Review and Meta-Analysis.” Retina (Philadelphia, Pa.) , vol. 39, no. 5, May 2019, pp. 844–852, pubmed.ncbi.nlm.nih.gov/29370034/, https://doi.org/10.1097/IAE.0000000000002055 . Fakkert, Raoul A, et al. “Early Hyperbaric Oxygen Therapy Is Associated with Favorable Outcome in Patients with Iatrogenic Cerebral Arterial Gas Embolism: Systematic Review and Individual Patient Data Meta-Analysis of Observational Studies.” Critical Care , vol. 27, no. 1, 12 July 2023, https://doi.org/10.1186/s13054-023-04563-x . Accessed 7 June 2024. Flaxel, Christina J., et al. “Idiopathic Epiretinal Membrane and Vitreomacular Traction Preferred Practice Pattern®.” Ophthalmology , vol. 127, no. 2, Feb. 2020, pp. P145–P183, https://doi.org/10.1016/j.ophtha.2019.09.022 . Accessed 16 July 2020. Frémont, Benoît, et al. “Prognostic Value of Echocardiographic Right/Left Ventricular End-Diastolic Diameter Ratio in Patients with Acute Pulmonary Embolism.” Chest , vol. 133, no. 2, Feb. 2008, pp. 358–362, https://doi.org/10.1378/chest.07-1231 . Huang, Ryan S, et al. “Pars Plana Vitrectomy with Silicone Oil or Gas Tamponade for Uncomplicated Retinal Detachment: A Systematic Review and Meta-Analysis.” American Journal of Ophthalmology , vol. 266, Oct. 2024, pp. 144–155, pubmed.ncbi.nlm.nih.gov/38815844/, https://doi.org/10.1016/j.ajo.2024.05.008 . Kanwar, Manreet K, et al. “Epidemiology and Management of Right Ventricular-Predominant Heart Failure and Shock in the Cardiac Intensive Care Unit.” European Heart Journal. Acute Cardiovascular Care , vol. 11, no. 7, 29 June 2022, pp. 584–594, https://doi.org/10.1093/ehjacc/zuac063 . Accessed 5 Mar. 2023. Lahm, Tim, et al. “Medical and Surgical Treatment of Acute Right Ventricular Failure.” Journal of the American College of Cardiology , vol. 56, no. 18, Oct. 2010, pp. 1435–1446, www.onlinejacc.org/content/56/18/1435, https://doi.org/10.1016/j.jacc.2010.05.046 . Accessed 30 Nov. 2019. Mirski, Marek A., et al. “Diagnosis and Treatment of Vascular Air Embolism.” Anesthesiology , vol. 106, no. 1, 1 Jan. 2007, pp. 164–177, pubs.asahq.org/anesthesiology/article/106/1/164/8884/Diagnosis-and-Treatment-of-Vascular-Air-Embolism, https://doi.org/10.1097/00000542-200701000-00026 . Accessed 13 Apr. 2021. Moon, Young Eun. “Venous Air Embolism during Vitrectomy: A Rare but Potentially Fatal Complication.” Korean Journal of Anesthesiology , vol. 67, no. 5, 1 Jan. 2014, pp. 297–297, pmc.ncbi.nlm.nih.gov/articles/PMC4252339/, https://doi.org/10.4097/kjae.2014.67.5.297 . Accessed 10 Mar. 2025. “Right Ventricular Failure.” Escardio.org , 2016, www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-14/Right-ventricular-failure . Stickel, Simone, et al. “The Practical Management of Fluid Retention in Adults with Right Heart Failure due to Pulmonary Arterial Hypertension.” European Heart Journal Supplements , vol. 21, 1 Dec. 2019, pp. 46–53, academic.oup.com/eurheartjsupp/article/21/Supplement_K/K46/5678698, https://doi.org/10.1093/eurheartj/suz207 . Ventetuolo, Corey E., and James R. Klinger. “Management of Acute Right Ventricular Failure in the Intensive Care Unit.” Annals of the American Thoracic Society , vol. 11, no. 5, 1 June 2014, pp. 811–822, www.ncbi.nlm.nih.gov/pmc/articles/PMC4225807/#:~:text=Abstract , https://doi.org/10.1513/AnnalsATS.201312-446FR . Accessed 10 Aug. 2020. What Is Vitrectomy. “What Is Vitrectomy?” American Academy of Ophthalmology , 15 May 2019, www.aao.org/eye-health/treatments/what-is-vitrectomy . Zhao, Steven, and Oren Friedman. “Management of Right Ventricular Failure in Pulmonary Embolism.” Critical Care Clinics , vol. 36, no. 3, July 2020, pp. 505–515, https://doi.org/10.1016/j.ccc.2020.02.006 . Accessed 29 Nov. 2020. 239. CCC: Approach to RV Predominant Cardiogenic Shock with Dr. Ryan Tedford…

Cardionerds: A Cardiology Podcast

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416. Hearts Over Time: Navigating Grief and Growth in Adult Congenital Cardiology 28:48

15 weeks ago28:48

28:48

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 . 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 Page CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!…

Cardionerds: A Cardiology Podcast

1
415. Case Report: Unraveling MINOCA: Role of Cardiac MRI and Functional Testing in Diagnosing Coronary Vasospasm – The Christ Hospital 42:33

17 weeks ago42:33

42:33

CardioNerds ( Drs. Daniel Ambinder and Eunice Dugan ) are joined by Namrita Ashokprabhu , incoming medical student, along with Drs. Yulith Roca Alvarez and Mehmet Yildiz from The Christ Hospital. Expert insights provided by Dr. Odayme Quesada . Audio editing by CardioNerds intern Christiana Dangas . This episode explores how cardiac MRI and coronary function testing revealed coronary vasospasm in a case of MINOCA. Cardiac MRI is crucial in evaluating myocardial infarction with nonobstructive coronary arteries (MINOCA) and diagnosing myocarditis, but findings must be interpreted within clinical context. A 58-year-old man with hypertension, hyperlipidemia, diabetes, a family history of cardiovascular disease, and smoking history presented with sudden chest pain, non-ST-elevation on EKG, and elevated troponin I (0.64 µg/L). Cardiac angiography revealed nonobstructive coronary disease, including a 40% stenosis in the LAD, consistent with MINOCA. Eight weeks later, another event (troponin I 1.18 µg/L) led to cardiac MRI findings suggesting myocarditis. Further history revealed episodic chest pain and coronary vasospasm, confirmed by coronary functional angiography showing severe vasoconstriction, resolved with nitroglycerin. Management included calcium channel blockers and long-acting nitrates, reducing symptoms. Coronary vasospasm is a frequent MINOCA cause and can mimic myocarditis on CMRI. Invasive coronary functional testing, including acetylcholine provocation testing, is indicated in suspicious cases. “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 Page CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron! Notes – Coronary Vasospasm What are the potential underlying causes of MINOCA (Myocardial Infarction with Non-Obstructive Coronary Arteries)? Plaque Rupture: Plaque disruption, which includes plaque rupture, erosion, and calcified nodules, occurs as lipids accumulate in coronary arteries, leading to inflammation, necrosis, fibrosis, and calcification. Plaque rupture exposes the plaque to the lumen, causing thrombosis and thromboembolism, while plaque erosion results from thrombus formation without rupture and is more common in women and smokers. Intravascular imaging, such as IVUS and OCT, can detect plaque rupture and erosion, with studies showing plaque disruption as a frequent cause of MINOCA, particularly in women, though the true prevalence may be underestimated due to limited imaging coverage. Coronary Vasospasm: Coronary vasospasm is characterized by nitrate-responsive chest pain, transient ischemic EKG changes, and >90% vasoconstriction during provocative testing with acetylcholine or ergonovine, due to hyper-reactivity in vascular smooth muscle. It is a common cause of MINOCA, with approximately half of MINOCA patients testing positive in provocative tests, and Asians are at a significantly higher risk than Whites. Smoking is a known risk factor for vasospasm. In contrast, traditional risk factors like sex, hypertension, and diabetes do not increase the risk, and vasospasm is associated with a 2.5–13% long-term risk of major adverse cardiovascular events (MACE). Spontaneous Coronary Artery Dissection: Spontaneous coronary artery dissection (SCAD) involves the formation of a false lumen in epicardial coronary arteries without atherosclerosis, caused by either an inside-out tear or outside-in intramural hemorrhage. SCAD is classified into four types based on angiographic features, with coronary angiography being the primary diagnostic tool. However, in uncertain cases, advanced imaging like IVUS or OCT may be used cautiously. While the true prevalence is unclear due to missed diagnoses, SCAD is more common in women and is considered a cause of MINOCA when it results in non-obstructive lesions, with various predisposing factors including genetics, fibromuscular dysplasia, and emotional stress. Coronary Embolism/Thrombosis: Coronary embolism, often underdiagnosed, can be classified based on thrombus origin as direct, paradoxical, or iatrogenic, with atrial fibrillation being the most common cause. A Japanese study found that only 2.9% of AMI patients were related to coronary embolism, and 73% of these cases were due to atrial fibrillation, with recurrent thromboembolic events occurring in 10% of patients during follow-up. Risk factors for coronary thromboembolism include hereditary thrombophilia, with 14% of MINOCA patients having hereditary thrombophilia, and an extensive evaluation, including a hypercoagulable workup and screening for atrial fibrillation or patent foramen ovale, is crucial to determine the underlying cause. Coronary Microvascular Dysfunction: The role of microvascular dysfunction in MINOCA remains uncertain due to limited data, though it is characterized by impaired vasodilation, increased vasoconstriction, and abnormal microcirculation remodeling, which affects coronary flow reserve without epicardial disease. Microvascular dysfunction is often underdiagnosed because it requires invasive functional testing, and studies in patients with ischemia but no obstructive coronary disease (INOCA) show a prevalence of up to 41%. A small study of MINOCA patients found that 25% had low myocardial perfusion reserve, suggesting potential involvement, but further research is needed to establish its role as a cause of MINOCA. MINOCA mimickers: Myocarditis: Myocarditis, often caused by viral infections, can also result from bacterial infections, toxic substances, or autoimmune disorders, and is more common in younger patients, though it can affect all ages. Fulminant myocarditis, though rare, can lead to life-threatening cardiogenic shock, and is diagnosed through CMR showing diffuse myocardial edema on T2 and myocardial biopsy. A meta-analysis found that one-third of MINOCA patients had myocarditis, particularly younger patients and those with elevated C-reactive protein levels. Non-ischemic Cardiomyopathy: Non-ischemic cardiomyopathy encompasses conditions like dilated, hypertrophic, restrictive, and arrhythmogenic cardiomyopathy, with dilated cardiomyopathy being the most common. A longitudinal study found that 25% of MINOCA patients had non-ischemic cardiomyopathy, which was associated with the highest mortality compared to other MINOCA mechanisms. Stress CMR has also identified underlying microvascular dysfunction in patients with dilated cardiomyopathy. Takotsubo Cardiomyopathy: Takotsubo cardiomyopathy, or stress-induced cardiomyopathy, is characterized by reversible wall motion abnormalities without obstructive CAD. It is often triggered by emotional or physical stress and is associated with a catecholamine surge. The condition is more common in postmenopausal women and has four main anatomical variants, with apical ballooning being the most common. Diagnosis typically involves coronary angiography, ventriculography, and CMRI to rule out other causes of AMI, with risks of cardiogenic shock and death comparable to those of AMI patients with CAD. What are the key diagnostic tests to evaluate MINOCA, and how are they applied in this case? Coronary Intravascular Imaging: Coronary intravascular imaging with IVUS and OCT is essential for diagnosing plaque disruption in MINOCA and should be performed during coronary angiography of all three major epicardial arteries. IVUS identifies plaque disruption in up to 40% of MINOCA cases, while OCT detects the culprit lesion in about 50%. These imaging techniques are also valuable for evaluating SCAD in cases of diagnostic uncertainty. Cardiac Imaging: Transthoracic echocardiography is valuable for assessing cardiac function after MINOCA, diagnosing Takotsubo and non-ischemic cardiomyopathy, and monitoring recovery of left ventricular function. Transesophageal echocardiography may be considered when coronary embolism is suspected. CMR is recommended for uncertain MINOCA diagnoses, providing accurate results in 74–87% of cases. It can differentiate between ischemic and non-ischemic MI, diagnose myocarditis, and detect coronary microvascular dysfunction through perfusion imaging. CMR’s diagnostic accuracy improves when performed closer to the event and also serves as a prognostic tool for long-term cardiovascular outcomes. Invasive Coronary Functional Testing: Provocative spasm testing with intracoronary acetylcholine helps diagnose coronary vasospasm (epicardial or microvascular) and endothelial-dependent microvascular dysfunction, with a low complication rate (0.5%). In MINOCA patients, spasm testing is positive in about half, with epicardial spasm in 65% and microvascular spasm in 35%. CFR assessed by doppler flow velocity or thermodilution (with values <2.0) and IMR (>25) are used to assess microvascular dysfunction, though CFR is more sensitive. While coronary microvascular dysfunction is linked to worse outcomes in INOCA, its prognostic impact in MINOCA is less clear. However, low CFR has been associated with increased mortality across various patient populations. How is MINOCA treated based on its underlying etiology? Plaque Rupture: Patients with plaque disruption should be treated with aspirin and high-intensity statin therapy. Additionally, for those with plaque disruption who do not require stenting, dual antiplatelet therapy with ticagrelor for up to 1 month may be considered, given the low revascularization rates at 1 year (5.7%) and 4 years (21.1%) follow-up. Coronary Vasospasm: Long-acting calcium channel blockers (both dihydropyridine and non-dihydropyridine) are commonly used in MINOCA patients with epicardial coronary vasospasm. They relax vascular smooth muscle by inhibiting calcium ion influx. For patients with refractory angina, nitrates may be added to calcium channel blockers to enhance smooth muscle relaxation through increased nitric oxide availability. SCAD: Conservative management is preferred over PCI in SCAD patients, as most dissections heal without intervention and PCI carries higher complication risks. PCI is reserved for STEMI, cardiogenic shock, or persistent ischemia. The use of antithrombotic agents during acute SCAD is debated, and secondary prevention (aspirin, beta-blockers, statins, and ACE inhibitors) should be tailored to individual risk factors. CMD: Treatment options for coronary microvascular dysfunction are limited and mainly based on data from INOCA patients. Statins and renin-angiotensin system inhibitors have been shown to improve coronary flow reserve (CFR). Antianginal therapies such as beta-blockers, calcium channel blockers, and ranolazine are commonly used for patients with chest pain. MINOCA Mimickers: Takotsubo Cardiomyopathy: Management of MINOCA mimickers mainly involves supportive care and guideline-directed medical therapy for heart failure, though evidence is limited. Most patients with Takotsubo cardiomyopathy recover normal cardiac function spontaneously, while those with left ventricular dysfunction are treated with beta-blockers and renin-angiotensin system inhibitors. In cases of progressive circulatory failure, mechanical circulatory support may be needed. Myocarditis: Myocarditis typically resolves within 2–4 weeks, but patients with arrhythmias or persistent cardiac dysfunction should receive guideline-directed therapy. Physical activity should be avoided in the acute phase for up to 6 months. Ongoing trials on antiviral and immunosuppressive treatments may offer targeted therapies in the future. References – Coronary Vasospasm Tamis-Holland JE, Jneid H, Reynolds HR, et al. Contemporary diagnosis and management of patients with myocardial infarction in the absence of obstructive coronary artery disease: a scientific statement from the American Heart Association. Circulation. 2019;139:e891–908. doi:10.1161/CIR.0000000000000670 Reynolds HR, Maehara A, Kwong RY, et al. Coronary optical coherence tomography and cardiac magnetic resonance imaging to determine underlying causes of myocardial infarction with nonobstructive coronary arteries in women. Circulation. 2021;143:624–40. doi:10.1161/CIRCULATIONAHA.120.052008 di Fusco SA, Rossini R, Zilio F, et al. Spontaneous coronary artery dissection: overview of pathophysiology. Trends Cardiovasc Med. 2022;32:92–100. doi:10.1016/j.tcm.2021.01.002 Zilio F, Muraglia S, Morat F, et al. Sex differences in clinical and angiographic characteristics in spontaneous coronary artery dissection. Future Cardiol. 2021;17:669–75. doi:10.2217/fca-2020-0124 Omerovic E, Citro R, Bossone E, et al. Pathophysiology of takotsubo syndrome – a joint scientific statement from the heart failure association takotsubo syndrome study group and myocardial function working group of the European society of cardiology – part 2: vascular pathophysiology, gender and sex hormones, genetics, chronic cardiovascular problems and clinical implications. Eur J Heart Fail. 2022;24:274–86. doi:10.1002/ejhf.2368 Agdamag AC, Patel H, Chandra S, et al. Sex differences in takotsubo syndrome: a narrative review. J Womens Health. 2020;29:1122–30. doi:10.1089/jwh.2019.7741 Bentzon JF, Otsuka F, Virmani R, Falk E. Mechanisms of plaque formation and rupture. Circ Res. 2014;114:1852–66. doi:10.1161/CIRCRESAHA.114.302721 Virmani R, Burke AP, Farb A, Kolodgie FD. Pathology of the vulnerable plaque. J Am Coll Cardiol. 2006;47:C13–8. doi:10.1016/j.jacc.2005.10.065 Montone RA, Niccoli G, Fracassi F, et al. Patients with acute myocardial infarction and non-obstructive coronary arteries: safety and prognostic relevance of invasive coronary provocative tests. Eur Heart J. 2017;39:91–8. doi:10.1093/eurheartj/ehx667 Raphael CE, Heit JA, Reeder GS, et al. Coronary embolus: an underappreciated cause of acute coronary syndromes. JACC Cardiovasc Interv. 2018;11:172–80. doi:10.1016/j.jcin.2017.08.057 Tschöpe C, Ammirati E, Bozkurt B, et al. Myocarditis and inflammatory cardiomyopathy: current evidence and future directions. Nat Rev Cardiol. 2021;18:169–93. doi:10.1038/s41569-020-00435-x Tornvall P, Gerbaud E, Behaghel A, et al. Myocarditis or “true” infarction by cardiac magnetic resonance in patients with a clinical diagnosis of myocardial infarction without obstructive coronary disease: a meta-analysis of individual patient data. Atherosclerosis. 2015;241:87–91. doi:10.1016/j.atherosclerosis.2015.04.816 Lintingre P-F, Nivet H, Clément-Guinaudeau S, et al. High-resolution late gadolinium enhancement magnetic resonance for the diagnosis of myocardial infarction with nonobstructed coronary arteries. JACC Cardiovasc Imaging. 2020;13:1135–48. doi:10.1016/j.jcmg.2019.11.020 AlBadri A, Bairey Merz CN, Johnson BD, et al. Impact of abnormal coronary reactivity on long-term clinical outcomes in women. J Am Coll Cardiol. 2019;73:684–93. doi:10.1016/j.jacc.2018.11.040 Kelshiker MA, Seligman H, Howard JP, et al. Coronary flow reserve and cardiovascular outcomes: a systematic review and meta-analysis. Eur Heart J. 2022;43:1582–93. doi:10.1093/EURHEARTJ/EHAB775 Slavich M, Patel RS. Coronary artery spasm: current knowledge and residual uncertainties. IJC Heart Vasculat. 2016;10:47–53. doi:10.1016/j.ijcha.2016.01.003 Samuels B, Shah S, Widmer R, et al. Comprehensive management of ANOCA, Part 1—definition, patient population, and diagnosis: JACC state-of-the-art review. JACC. 2023;82(12):1245–63. doi:10.1016/j.jacc.2023.06.043 Smilowitz N, Prasad M, Widmer R, et al. Comprehensive management of ANOCA, Part 2—program development, treatment, and research initiatives: JACC state-of-the-art review. JACC. 2023;82(12):1264–79. doi:10.1016/j.jacc.2023.06.044 Quesada O, Ashokprabhu ND, Tapp DN, et al. Utilizing invasive coronary functional testing in a coronary microvascular and vasomotor dysfunction program: methods and considerations. Catheter Cardiovasc Interv. 2024;104(7):1327–36. doi:10.1002/ccd.31282 Yildiz M, Ashokprabhu N, Shewale A, et al. Myocardial infarction with non-obstructive coronary arteries (MINOCA). Front Cardiovasc Med. 2022;9:1032436. doi:10.3389/fcvm.2022.1032436…

Cardionerds: A Cardiology Podcast

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414. Case Report: Got Milky Blood? Hypertriglyceridemia Unveiled in a Case of Abdominal Pain – National Lipid Association 1:17:42

19 weeks ago1:17:42

1:17:42

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. “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 Page CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron! Pearls – Hypertriglyceridemia Cardiac sarcoidosis can present with a variety of symptoms, including arrhythmias, heart block, heart failure, or sudden cardiac death. The acute management of hypertriglyceridemia-induced pancreatitis involves prompt recognition and initiation of therapy to lower triglyceride levels using either plasmapheresis or intravenous insulin infusion +/- heparin infusion. Insulin infusion is used more commonly, while plasmapheresis is preferred in pregnancy. Medications such as fibrates and omega-3 fatty acids can be used to maintain long-term triglyceride reduction to prevent the recurrence of pancreatitis, especially in patients with persistent triglyceride elevation despite lifestyle modifications. Statins can be used in patients for ASCVD reduction in patients with a 10-year ASCVD risk > 5%, age > 40 years old, and diabetes or diabetes with end-organ damage or known atherosclerosis. Consider preferential use of icosapent ethyl as an omega-3 fatty acid for triglyceride lowering if the patients fit the populations that appeared to benefit in the REDUCE IT trial. Apply targeted dietary interventions within the context of an overall healthy dietary pattern, such as a Mediterranean or DASH diet. Limit full-fat dairy, fatty meats, refined starches, added sugars, and alcohol. Encourage high-fiber vegetables, whole fruits, low-fat or fat-free dairy, plant proteins, lean poultry, and fish. Pay special attention to the cooking oils to ensure the patient is not using palm oil, coconut oil, or butter when cooking. Instead, use liquid non-tropical plant oils. Initiate a very low-fat diet (< 5% of total daily calories from fat) for 1-4 weeks when TG levels are > 750 mg/dL. Recommend and encourage patients to exercise regularly, with a minimum goal of 150 minutes/week of moderate-intensity aerobic activity. If weight loss is required, aim for more than >225 – 250 minutes/week. Develop patient-centered and multidisciplinary strategies for preventing hypertriglyceridemia-induced pancreatitis by incorporating patient education on the importance of medication adherence, specialist follow-up, regular monitoring of triglyceride levels, and lifestyle modifications to maintain optimal lipid profiles and reduce the future risk of pancreatitis. Notes – Hypertriglyceridemia Who is at risk for hypertriglyceridemia and what are the key pathophysiological mechanisms by which elevated triglycerides may lead to pancreatitis? The exact mechanism is not clear. The proposed mechanism is that when serum triglycerides exceed 1000 mg/dL, blood flow is impaired through the capillary beds supplying the pancreas, resulting in ischemia. The ischemic injury resulting from this disruption of microcirculation disrupts the acinar structure of pancreatic cells and exposes pancreatic enzymes to triglyceride-rich particles. This results in activation of enzymatic activity with degradation of the chylomicron-triglycerides particles, which causes inflammation, subsequently leading to hemorrhage, edema, and necrosis of the pancreatic tissue. Chylomicronemia syndrome can be multifactorial or familial. Familial chylomicronemia syndrome (FCS) is often discovered very early in life, and patients have a loss of function in one of the several genes involved in regulating triglyceride metabolism. These genes include LPL, APOC2, APOA5, LMF1, and GPIHBP1. Multifactorial chylomicronemia syndrome is the most common cause of chylomicronemia syndrome. It is usually the result of a clustering of genetic variants, including heterozygosity of one of the five genes previously mentioned, as well as more frequent variants with small effects in more than 40 additional genes that have been implicated. Having a genetic variant plus an aggravating factor will often exacerbate the metabolic defect and lead to chylomicronemia syndrome. There are many potential aggravating factors, but some of the more common ones include a diet high in refined sugars, heavy alcohol consumption, obesity with or without metabolic syndrome, medications, renal disease, HIV, and pregnancy. What are the acute treatment strategies for hypertriglyceridemia-induced pancreatitis, and how are they similar and different to treating pancreatitis from other etiologies? All patients should be assessed for hemodynamic compromise, the severity of illness with or without scoring systems, and end-organ damage to determine the need for intensive care resources. Initially, patients usually require aggressive fluid resuscitation and pain management, which are standard across all types of acute pancreatitis. Delayed fluid resuscitation has been associated with worse outcomes. Multiple trials have been performed evaluating the best amount of fluid. Although there is not an exact answer to this, as all patients are different, all patients should be resuscitated until euvolemic. The WATERFALL trial showed that administration of 10 mL/kg bolus followed by 1.5 mL/kg maintenance until the patient reaches euvolemia was a superior approach to more aggressive fluid resuscitation. A patient’s volume status should be reassessed every 6 hours for 24 – 48 hours, and fluids should be discontinued once euvolemia has been achieved. There is no guideline consensus on the preferred analgesic management, but it is generally recommended to administer medication to mitigate symptoms of pain and nausea for all patients. For hypertriglyceridemia-induced pancreatitis, it is key to initiate fasting to decrease chylomicron production and further increasing triglyceride levels. Although historically, this was the same approach for other causes of pancreatitis, more recent data shows that early enteral feeding reduces the risk of complications such as pancreatic necrosis. However, these studies were not performed in patients with pancreatitis from hypertriglyceridemia and should not be extrapolated to this distinct population. Currently, it is recommended that patients be kept NPO until triglycerides are below 500 mg/dL, which is the point at which LPL activity becomes saturated. When feeding is initiated, it should be with a very low-fat diet with no refined carbohydrates. Hypertriglyceridemia differs from other causes of pancreatitis as the management is centered around the rapid reduction of triglyceride content in the blood. Generally, these patients are admitted to the intensive care unit to undergo either insulin infusion +/- heparin drip or plasmapheresis. Although there has never been a clinical trial comparing these two approaches, a recent comprehensive meta-analysis showed no significant difference in mortality or clinical outcomes. Insulin infusion had a lower number of deaths, but a higher rate of acute renal failure, hypoglycemia, and hypotension, neither of which reached statistical significance. Insulin is more commonly used and generally preferred given that it is more cost-effective, less invasive, and can have utility in treating underlying diabetes exacerbation, which is common amongst these patients. Insulin infusion works by increasing the activity of lipoprotein lipase (LPL), resulting in increased clearance of chylomicron particles. Although in some countries, insulin is combined with heparin, given heparin’s ability to increase LPL release, this is rarely done as heparin can deplete endothelial LPL, increase bleeding events, and potentially cause heparin-induced thrombocytopenia. Plasmapheresis, on the other hand, works by removing the triglycerides directly from the bloodstream, which can rapidly reduce levels. It does require central venous access, which is more invasive. Plasmapheresis is preferred in pregnancy as data in case series supports it reduces the risk of a systemic inflammatory response. What are the proposed mechanisms by which high triglycerides may contribute to atherosclerosis? There are several proposed mechanisms for the association between elevated triglyceride levels and ASCVD. First, elevated triglyceride levels correspond with high circulating triglyceride-rich lipoprotein particles, also known as remnant cholesterol. This includes VLDL, IDL, and chylomicron remnants. These particles are thought to be at least as, if not more, atherogenic than LDL-C. Remnant particles readily penetrate the arterial wall, similar to LDL, but do not require oxidative modification for macrophage uptake and can be taken up unregulated, leading to foam cells and atherosclerosis. Second, having elevated levels of triglyceride-rich lipoproteins is pro-inflammatory. When triglyceride-rich lipoproteins are hydrolyzed by lipoprotein and endothelial lipases, the release of oxidized free fatty acids along the endothelial wall leads to the activation of pro-inflammatory signaling pathways that can increase vascular permeability and promote the migration of leukocytes and atherogenic lipoprotein particles into the arterial wall. This is mediated by cytokines and chemoattractant proteins. What long-term pharmacologic management strategies should be considered in patients with hypertriglyceridemia-induced pancreatitis? Fibrates are the first line pharmacotherapy when the goal of treatment is to prevent acute pancreatitis, especially when triglyceride levels are >1000. The ability of lipoprotein lipase to clear triglyceride-rich lipoproteins becomes saturated at TG levels of approximately 500-700 mg/dL. When the ability to clear TRL is impaired, dietary fat intake can lead to large increases in blood TG levels. Those with TG >1000 are at particularly high risk of acute pancreatitis. Fibrates stimulate PPAR alpha and primarily decrease TGs via the upregulation of LPL. The reduction of TGs from fibrates ranges from 25-50%. Some data suggests fenofibrate may be more effective at lowering TG then gemfibrozil. Gemfibrozil is the only Fibrate therapy that has shown a reduction in cardiovascular events in the VA-HIT and HHS trials. However, it is worth noting these trials were not performed on background statin therapy, which is now contraindicated in patients taking Gemfibrozil due to the increased risk of rhabdomyolysis. Prescription Omega-3 fatty acids lower TGs, possibly via decreased activity of SREBP1c. These are less potent reducers of triglycerides with reductions between 10-50%. While Icosapent Ethyl, a purified form of EPA, does have TG-lowering effects, it is primarily used for ASCVD risk reduction in individuals >age 50 with TG >150 and a history of ASCVD or those without ASCVD but with diabetes mellitus and multiple risk factors. This is based on the aforementioned REDUCE-IT trial. Briefly, REDUCE-IT randomized patients having moderate hypertriglyceridemia and a history of ASCVD or diabetes and other risk factors on background statin therapy to receive icosapent ethyl (pure EPA) or placebo. Patients in the icosapent ethyl group experienced an 18.3% reduction in triglyceride level compared to a 2.2% increase in the placebo group, as well as a 4.8% absolute risk reduction and 25% relative risk reduction in the primary endpoint, a composite of CV death, non-fatal MI, non-fatal stroke, coronary revascularization, or unstable angina with an NNT of 21. The therapy was associated with a slight, although significant, increase in risk of atrial fibrillation, which occurred in 5.3% of patients receiving IPE compared to 3.9% in the placebo group. There was also an increased risk of bleeding, which approached statistical significance. The use of biologically active mineral oil as the placebo has led to some controversy regarding the validity of REDUCE-IT results. In this case, our patient does not exactly fit this study population investigated in that clinical trial. Other Omega-3 fatty acids include mixtures of EPA/DHA such as Omega-3-acid ethyl esters and Omega-3-carboxylic acids, which are often used to reduce the risk of pancreatitis in those with triglyceride levels >500 mg/dL. Combined EPA/DHA products have been investigated in several trials, including but not limited to STRENGTH, VITAL, ASCEND, and OMEMI. However, none of these trials have shown any significant reduction in cardiovascular endpoints. Statins are primarily used for reducing ASCVD risk, although they do lower triglycerides primarily through increased clearance of VLDL via upregulation of the remnant receptor. The 2021 ACC Expert Consensus Decision Pathway for hypertriglyceridemia recommends initiating or intensifying statin therapy for patients aged 40-75 years, with triglycerides of 500-999 mg/dL and with either a 10-year ASCVD risk of ≥5% or diabetes mellitus. The 2018 ACC/AHA multisociety Guideline on the Management of Blood Cholesterol provides key groups that qualify for primary prevention of statin therapy, including those with ASCVD risk >7.5%, age between 40-75 with diabetes mellitus type 1 or 2, and low-density lipoprotein cholesterol (LDL-c) >190 mg/dL. These guidelines further elaborate that in adults 20 to 39 years of age with diabetes mellitus type 2, statin therapy can be considered if they have type 2 diabetes mellitus ≥10 years, albuminuria (≥30 mcg of albumin/mg creatinine), eGFR < 60 mL/min/1.73 m2, retinopathy, neuropathy, or ABI <0.9. What dietary management approaches are effective in preventing recurrent episodes of hypertriglyceridemia-induced pancreatitis, and how do they impact triglyceride levels? There are many ways to approach dietary interventions in the clinic. The National Lipid Association created a 2023 guideline called “Nutrition interventions for adults with dyslipidemia: A Clinical Perspective from the National Lipid Association,” which can be helpful in guiding clinical care. Always use a patient-centered approach and incorporate patients’ preferences, cultural backgrounds, financial resources, and food availability when applying the dietary guidelines. Start by identifying the food sources in a patient’s diet that can dramatically raise triglycerides: foods rich in added sugars, refined starches, saturated fats, and alcohol. Identifying and minimizing or eliminating these foods upfront (depending on the severity of the hypertriglyceridemia) will lead to substantial improvements in a patient’s lipid profile. The NLA guidelines created four categories based on the severity of hypertriglyceridemia and whether patients have FCS. These categories include patients with triglycerides >= 750 mg/dL with FCS, >= 750mg/dL with suspected MCS, >= 500 mg/dL and < 500 mg/dL. All patients with elevated triglycerides should be advised to strive for an overall healthy dietary pattern such as a Mediterranean or DASH Diet, maximize plant sources of protein, limit or eliminate beverages and foods with added sugars, limit full-fat dairy products, maximize intake of fibrous vegetables, and are encouraged to perform at least 150 minutes/week of moderate-intensity exercise or 75 minutes/week of vigorous exercise but increasing the exercise past this threshold will continue to have added benefits as recommended by the American College of Sports Medicine. The NLA recommends completely abstaining from alcohol for patients with triglycerides >500 mg/dL. For those below 500 mg/dL the recommendation is that men do not exceed two drinks/day and women do not exceed one drink/day. However, in general, it’s best to advise all patients to limit their alcohol as much as possible because it increases the secretion of VLDL, impairs lipolysis, and increases free fatty acid fluxes from adipose tissue to the liver. Dietary saturated fats can also raise both triglycerides and LDL-C and should be replaced with unsaturated fatty acids. Foods rich in saturated fats include those such as butter, beef, and tropical oils such as coconut oil, palm, and palm kernel oil. A thorough review of how patients prepare their food should be performed because making simple changes, such as cooking with olive oil rather than butter or tropical oils, can improve triglycerides and LDL-C. For those with TG levels > 750mg/dL: the goal should be initially to maintain a very low-fat diet with <5%, but after 4 weeks and improvement of triglyceride elevations, there can be liberalization of the patient’s diet. Depending on the patient’s risk profile, including whether they have FCS and current triglyceride levels, cautious relaxation of dietary restrictions can be allowed to improve quality of life and allow for more flexibility in food intake. Patients with FCS must maintain a very low-fat diet for life and should be referred to a registered dietitian specializing in lipid management. References – Hypertriglyceridemia Varbo A, Benn M, Tybjærg-Hansen A, Jørgensen AB, Frikke-Schmidt R, Nordestgaard BG. Remnant cholesterol as a causal risk factor for ischemic heart disease. J Am Coll Cardiol. 2013 Jan 29;61(4):427-436. doi:10.1016/j.jacc.2012.08.1026. https://www.sciencedirect.com/science/article/pii/S0735109712055222?via%3Dihub Nordestgaard BG. Triglyceride-Rich Lipoproteins and Atherosclerotic Cardiovascular Disease: New Insights From Epidemiology, Genetics, and Biology. Circ Res. 2016 Feb 19;118(4):547-563. doi:10.1161/circresaha.115.306249. https://www.ahajournals.org/doi/full/10.1161/CIRCRESAHA.115.306249 Toth PP. Triglyceride-rich lipoproteins as a causal factor for cardiovascular disease. Vasc Health Risk Manag. 2016;12:171-183. doi:10.2147/vhrm.S104369. https://www.dovepress.com/triglyceride-rich-lipoproteins-as-a-causal-factor-for-cardiovascular-d-peer-reviewed-fulltext-article-VHRM Goldberg RB, Chait A. A Comprehensive Update on the Chylomicronemia Syndrome. Front Endocrinol (Lausanne). 2020;11:593931. doi:10.3389/fendo.2020.593931. https://www.frontiersin.org/journals/endocrinology/articles/10.3389/fendo.2020.593931/full Kaur G, Gulati M. Considerations for treatment of lipid disorders during pregnancy and breastfeeding. Prog Cardiovasc Dis. 2022 Nov-Dec;75:33-39. doi:10.1016/j.pcad.2022.11.001. https://www.sciencedirect.com/science/article/abs/pii/S003306202200113X?via%3Dihub Donnelly JE, Blair SN, Jakicic JM, Manore MM, Rankin JW, Smith BK. American College of Sports Medicine Position Stand. Appropriate physical activity intervention strategies for weight loss and prevention of weight regain for adults. Med Sci Sports Exerc. 2009 Feb;41(2):459-471. doi:10.1249/MSS.0b013e3181949333. https://journals.lww.com/acsm-msse/fulltext/2001/12000/appropriate_intervention_strategies_for_weight.26.aspx Piplani S, Jain A, Singh K, Gulati S, Chaturvedi S, Bejugam VR, Brown D, Asuzu C, Kolli ST, Shah U, Reet J, Mihajlovic M, Jelic V, Jelic G, Roberts RS, Damania D, Radulovic M. Efficacy and adverse effects of insulin versus plasmapheresis in patients with hypertriglyceridemia-3-induced acute pancreatitis: a systematic review and meta-analysis. Ann Gastroenterol. 2024 Jan-Feb;37(1):109-116. doi: 10.20524/aog.2023.0849. Epub 2023 Dec 20. PMID: 38223249; PMCID: PMC10785016. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10785016/#:~:text=From%20this%20study’s%20analysis%2C%20insulin,%25CI%200.25%2D1.95 ). Atkinson FS, Brand-Miller JC, Foster-Powell K, Buyken AE, Goletzke J. International tables of glycemic index and glycemic load values 2021: a systematic review. Am J Clin Nutr. 2021 Nov 8;114(5):1625-1632. doi: 10.1093/ajcn/nqab233. PMID: 34258626. https://www.sciencedirect.com/science/article/pii/S0002916522004944?via%3Dihub Gouni-Berthold I, Schwarz J, Berthold HK. Updates in Drug Treatment of Severe Hypertriglyceridemia. Curr Atheroscler Rep. 2023 Oct;25(10):701-709. doi: 10.1007/s11883-023-01140-z. PMID: 37642858; PMCID: PMC10564803. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10564803/ Raal FJ, Rosenson RS, Reeskamp LF, Hovingh GK, Kastelein JJP, Rubba P, Ali S, Banerjee P, Chan KC, Gipe DA, Khilla N, Pordy R, Weinreich DM, Yancopoulos GD, Zhang Y, Gaudet D; ELIPSE HoFH Investigators. Evinacumab for Homozygous Familial Hypercholesterolemia. N Engl J Med. 2020 Aug 20;383(8):711-720. doi: 10.1056/NEJMoa2004215. PMID: 32813947. https://www.nejm.org/doi/full/10.1056/NEJMoa2004215 Rosenson RS, Gaudet D, Ballantyne CM, Baum SJ, Bergeron J, Kershaw EE, Moriarty PM, Rubba P, Whitcomb DC, Banerjee P, Gewitz A, Gonzaga-Jauregui C, McGinniss J, Ponda MP, Pordy R, Zhao J, Rader DJ. Evinacumab in severe hypertriglyceridemia with or without lipoprotein lipase pathway mutations: a phase 2 randomized trial. Nat Med. 2023 Mar;29(3):729-737. doi: 10.1038/s41591-023-02222-w. PMID: 36879129; PMCID: PMC10033404. https://www.nature.com/articles/s41591-023-02222-w Witztum JL, Gaudet D, Arca M, Jones A, Soran H, Gouni-Berthold I, Stroes ESG, Alexander VJ, Jones R, Watts L, Xia S, Tsimikas S. Volanesorsen and triglyceride levels in familial chylomicronemia syndrome: Long-term efficacy and safety data from patients in an open-label extension trial. J Clin Lipidol. 2023 May-Jun;17(3):342-355. doi: 10.1016/j.jacl.2023.03.007. PMID: 37100699. Erratum in: J Clin Lipidol. 2023 Oct 13;: PMID: 37100699. https://www.lipidjournal.com/article/S1933-2874(23)00065-X/fulltext Witztum JL, Gaudet D, Freedman SD, Alexander VJ, Digenio A, Williams KR, Yang Q, Hughes SG, Geary RS, Arca M, Stroes ESG, Bergeron J, Soran H, Civeira F, Hemphill L, Tsimikas S, Blom DJ, O’Dea L, Bruckert E. Volanesorsen and Triglyceride Levels in Familial Chylomicronemia Syndrome. N Engl J Med. 2019 Aug 8;381(6):531-542. doi: 10.1056/NEJMoa1715944. PMID: 31390500. https://www.nejm.org/doi/10.1056/NEJMoa1715944?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed Tardif JC, Karwatowska-Prokopczuk E, Amour ES, Ballantyne CM, Shapiro MD, Moriarty PM, Baum SJ, Hurh E, Bartlett VJ, Kingsbury J, Figueroa AL, Alexander VJ, Tami J, Witztum JL, Geary RS, O’Dea LSL, Tsimikas S, Gaudet D. Apolipoprotein C-III reduction in subjects with moderate hypertriglyceridaemia and at high cardiovascular risk. Eur Heart J. 2022 Apr 6;43(14):1401-1412. doi: 10.1093/eurheartj/ehab820. PMID: 35025993; PMCID: PMC8986458. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8986458/ Kirkpatrick CF, Sikand G, Petersen KS, Anderson CAM, Aspry KE, Bolick JP, Kris-Etherton PM, Maki KC. Nutrition interventions for adults with dyslipidemia: A Clinical Perspective from the National Lipid Association. J Clin Lipidol. 2023 Jul-Aug;17(4):428-451. doi: 10.1016/j.jacl.2023.05.099. PMID: 37271600. https://www.lipidjournal.com/article/S1933-2874(23)00185-X/fulltext Fialkow J. Omega-3 Fatty Acid Formulations in Cardiovascular Disease: Dietary Supplements are Not Substitutes for Prescription Products. Am J Cardiovasc Drugs. 2016 Aug;16(4):229-239. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4947114/ Skulas-Ray AC, Wilson PWF, Harris WS, Brinton EA, Kris-Etherton PM, Richter CK, Jacobson TA, Engler MB, Miller M, Robinson JG, Blum CB, Rodriguez-Leyva D, de Ferranti SD, Welty FK., American Heart Association Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Lifestyle and Cardiometabolic Health; Council on Cardiovascular Disease in the Young; Council on Cardiovascular and Stroke Nursing; and Council on Clinical Cardiology. Omega-3 Fatty Acids for the Management of Hypertriglyceridemia: A Science Advisory From the American Heart Association. Circulation. 2019 Sep 17;140(12) https://www.ahajournals.org/doi/full/10.1161/CIR.0000000000000709?rfr_dat=cr_pub++0pubmed&url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org Ito MK. A Comparative Overview of Prescription Omega-3 Fatty Acid Products. P T. 2015 Dec;40(12):826-857. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4671468/ Laufs U, Parhofer KG, Ginsberg HN, Hegele RA. Clinical review on triglycerides. Eur Heart J. 2020 Jan 1;41(1):99-109c. doi: 10.1093/eurheartj/ehz785. PMID: 31764986; PMCID: PMC6938588. https://academic.oup.com/eurheartj/article/41/1/99/5640489 Virani SS, Morris PB, Agarwala A, Ballantyne CM, Birtcher KK, Kris-Etherton PM, Ladden-Stirling AB, Miller M, Orringer CE, Stone NJ. 2021 ACC Expert Consensus Decision Pathway on the Management of ASCVD Risk Reduction in Patients With Persistent Hypertriglyceridemia: A Report of the American College of Cardiology Solution Set Oversight Committee. J Am Coll Cardiol. 2021 Aug 31;78(9):960-993. doi: 10.1016/j.jacc.2021.06.011. PMID: 34332805. https://www.jacc.org/doi/10.1016/j.jacc.2021.06.011 Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019 Jun 18;139(25). doi: 10.1161/CIR.0000000000000625. Epub 2018 Nov 10. Erratum in: Circulation. 2019 Jun 18;139(25). doi: 10.1161/CIR.0000000000000698. Erratum in: Circulation. 2023 Aug 15;148(7). doi: 10.1161/CIR.0000000000001172. PMID: 30586774; PMCID: PMC7403606.\ https://www.ahajournals.org/doi/10.1161/CIR.0000000000000625 Writing Committee; Lloyd-Jones DM, Morris PB, Ballantyne CM, Birtcher KK, Covington AM, DePalma SM, Minissian MB, Orringer CE, Smith SC Jr, Waring AA, Wilkins JT. 2022 ACC Expert Consensus Decision Pathway on the Role of Nonstatin Therapies for LDL-Cholesterol Lowering in the Management of Atherosclerotic Cardiovascular Disease Risk: A Report of the American College of Cardiology Solution Set Oversight Committee. J Am Coll Cardiol. 2022 Oct 4;80(14):1366-1418. doi: 10.1016/j.jacc.2022.07.006. Epub 2022 Aug 25. Erratum in: J Am Coll Cardiol. 2023 Jan 3;81(1):104. doi: 10.1016/j.jacc.2022.11.016. PMID: 36031461. https://www.jacc.org/doi/10.1016/j.jacc.2022.07.006…

Cardionerds: A Cardiology Podcast

1
413. Case Report: Cardiac Sarcoidosis Presenting as STEMI – Mount Sinai Medical Center in Miami 25:23

21 weeks ago25:23

25:23

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,…

Cardionerds: A Cardiology Podcast

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412: The Biology of Transthyretin amyloid cardiomyopathy (ATTR-CM) with Dr. Daniel Judge 13:01

22 weeks ago13:01

13:01

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...…

Cardionerds: A Cardiology Podcast

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411. Journal Club: The VANISH2 Trial with Dr. Jeff Healey and Dr. Roderick Tung 30:05

23 weeks ago30:05

30:05

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.…

Cardionerds: A Cardiology Podcast

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410. Case Report: A Curious Case of Refractory Ventricular Tachycardia – Rutgers-Robert Wood Johnson 40:13

25 weeks ago40:13

40:13

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,…

Cardionerds: A Cardiology Podcast

1
409. Journal Club: The ARREST-AF Trial with Drs. Prashanthan Sanders and Mehak Dhande 36:04

27 weeks ago36:04