Cardionerds: A Cardiology Podcast

By CardioNerds

Welcome to CardioNerds, where we bring you in-depth discussions with leading experts, case reports, and updates on the latest advancements in the world of cardiology. Tune in to expand your knowledge... more

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The podcast currently has 388 episodes available.

Cardionerds: A Cardiology Podcast episodes:

July 19, 2024381. Narratives in Cardiology: Advocacy for Refugee Health and Empowering First-Generation Cardiologists with Dr. Heval Kelli
In this episode, Dr. Gurleen Kaur (Cardiology FIT at Brigham and Women’s Hospital and APD of the CardioNerds Academy) and Dr. Chelsea Amo-Tweneboah (Medicine Resident at Stonybrook and CardioNerds Academy Intern) discuss with Dr. Heval Kelli (Cardiologist at Northside Hospital Cardiovascular Institute) about his personal and professional journey in Cardiology. They discuss Dr. Kelli’s lifelong advocacy for serving those in need including refugee and immigrant communities, his character in the documentary Refuge, and fostering inclusivity within Cardiology. Audio editing and show notes were drafted by Dr. Chelsea Amo-Tweneboah.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza.
The PA-ACC & CardioNerds Narratives in Cardiology Page
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Video version – Advocacy for Refugee Health and Empowering First-Generation Cardiologists
https://youtu.be/hP8bLt9q2sY
Quoatables – Advocacy for Refugee Health and Empowering First-Generation Cardiologists
“I have always believed that if someone opened the door for you, you have to hold the door for the next generation. Because if you just walk through the door and close it, you just close the door for many people behind you.”
“Instead of making luck a matter of luck, just make an opportunity for everyone else.”
“Hate makes us realize that no matter how privileged you are, you are not protected.”
“It is very hard to hate something you know.”
“Compassion starts with the neighbor next to you, and then you go out to the world and show it.”
“Your best intern wasn’t the smartest intern. Your best intern was the person ready to go for rounds, took care of everything, sharp early in the morning, stays late, and gets the work done.”
“Intelligence is relative. Hard work and dedication [are] the most important thing.”
Notes – Advocacy for Refugee Health and Empowering First-Generation Cardiologists
Advocacy for refugee health and empowering first-generation cardiologists
Focusing on creating professionals from a given community can help increase their chances of returning to that community and helping to address health disparities.
Refugees and immigrants come from countries and communities where, by and large, prevention is lacking. Seeing a healthcare provider is more appropriate in dire situations.
When approaching immigrants, it is important to present medical information in ways in which they can understand and absorb properly.
For many refugee families, there exists a language barrier and the children are most often the advocates for the family because they are most likely to understand the language of the community they live in.
The vast number of students in the US medical school system come from privileged backgrounds; however, this same statistic is not true for the populations they end up serving.
It is important to have health professionals reflect the populations they serve, and one of the methods to achieve this is through introducing as many individuals as possible to the field of medicine; one of the ways to overcome a leaky pipeline is to pack the pipeline. Strategies include encouraging medical students to serve as mentors for those junior to them.
It is important to build more sustainable relationships with communities because it leads to more trust and success.
Advocating for mental health in these communities is very important because they face these issues at an increased level. However, it is unfortunately under-addressed.
Resource avenues such as the CDC provide substantial information regarding different refugee and immigrant profiles and the issues most pertinent to these communities.
Inclusivity in Cardiology
It is important to normalize people feeling comfortable in having a discourse about differences and recognizing the challenges individuals face when pursuing a career in medicine or cardiology in order to promote inclusivity in this field. This is a major goal for the CardioNerds Narratives in Cardiology program.
Within Cardiology, structural racism and hate are present.
It is important to place yourself in a challenging environment or one different from what you are used to and attempt to find common ground with other individuals.
The Bridge Between Social Issues and Cardiology
As a physician, it is important to create boundaries and choose what social issues you wish to engage in.
If groups of people do not see eye to eye, steps should be taken to reach out to one another and establish and try to understand what these differences are.
Physicians are the best advocates in the world because, for the most part, they are trusted by their patients. Recognizing the importance of the influence that physicians have and realizing this influence can extend beyond the medical space.
Humor can be another means by which to make it easier to bring up important conversations that may otherwise be difficult.
Technology to Help Bridge the Gap
Technology can serve as a means of being able to communicate with refugee families because they are likely to have access to a smartphone.
Refugee families most often don’t understand the information given to them in paper or pamphlet form, and often important medical advice can be lost that way.
Technology provides increased access to medicine and allows patients more individuality and control in keeping on top of their health.
Artificial intelligence technology is the direction that health and medicine are heading in; thus, health professionals and patients must learn how to use this technology to their advantage.
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21min
July 12, 2024380. Case Report: Tearing Up My Heart – A Case of Papillary Muscle Rupture – University of Rochester
CardioNerds co-founder Dan Ambinder joins Dr. Lefan He, Dr. Sina Salehi Omran, and Dr. Neil Gupta from the University of Rochester Cardiovascular Disease Fellowship Program for a day sailing on Lake Ontario. Expert commentary is provided by Dr. Jeffrey Bruckel, and CV Fellowship Program Director Dr. Burr Hall shares insights on the University of Rochester fellowship. The episode audio was edited by CardioNerds intern Dr. Atefeh Ghorbanzadeh. They discuss the following case involving a patient with papillary muscle rupture.
This is a 63-year-old man with hypertension, hyperlipidemia, and active tobacco smoking who presented with acute dyspnea. He was tachycardic but otherwise initially hemodynamically stable. The physical exam demonstrated warm extremities with no murmurs or peripheral edema. Chest X-ray revealed diffuse pulmonary edema, and the ECG showed sinus tachycardia with T-wave inversions in the inferior leads. A bedside echocardiogram revealed a flail anterior mitral valve leaflet. The patient was taken for cardiac catheterization that revealed nonobstructive mid-RCA atheroma with a distal RCA occlusion, which was felt to reflect embolic occlusion from recanalized plaque. PCI was not performed. Right heart catheterization then demonstrated a low cardiac index as well as elevated PCWP and PA pressures. An intra-aortic balloon pump was placed at that time. A TEE was performed soon after which showed the posteromedial papillary muscle was ruptured with flail segments of the anterior mitral leaflet as well as severe posteriorly directed mitral regurgitation. The patient ultimately underwent a successful tissue mitral valve replacement and CABG.
“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!
case Media
Pearls – A Case of Papillary Muscle Rupture
Most cases of papillary muscle rupture demonstrate only small areas of ischemia with preserved ventricular function, thus causing high shear force on the ischemic papillary muscle.
The posteromedial papillary muscle has a single blood supply from the posterior descending artery, while the anterolateral papillary muscle has a dual blood supply from the LAD and the circumflex. Therefore, the posteromedial papillary muscle is more vulnerable to ischemia and, hence, rupture.
A murmur may be absent in cases of papillary muscle rupture due to the rapid equalization of left atrial and left ventricular pressures caused by the acuteness of the severe MR. Papillary muscle rupture should always be on the differential for acute dyspnea when ACS is suspected.
While mostly associated with STEMIs, mechanical complications of acute myocardial infarctions can also occur after NSTEMIs. Always auscultate patients carefully after a myocardial infarction!
When evaluating patients with chest pain presenting with acute or rapidly progressive heart failure and a hypercontractile LVEF should raise suspicion for mechanical complications of MI.
Once a papillary muscle rupture is diagnosed, cardiac surgery should be immediately contacted. Temporizing measures prior to surgery include positive pressure ventilation, IV nitroglycerin/nitroprusside, and temporary mechanical circulatory support.
Notes – A Case of Papillary Muscle Rupture
What is the clinical presentation of acute mitral regurgitation from papillary muscle rupture?
Patients typically present 3-5 days after a transmural infarct. Roughly half of these patients present with pulmonary edema that may quickly progress to cardiogenic shock.
Most cases are associated with STEMIs, but papillary muscle rupture is also possible with an NSTEMI.
The classic murmur is a mid-, late-, or holosystolic murmur. However, due to the rapid equalization of pressures between the LA and LV, many patients may not present with a murmur!
What is the pathophysiology of papillary muscle rupture?
The most common etiology is acute occlusion of the RCA causing infarct of the posteromedial papillary muscle, which then leads to a partial or complete tear 2-7 days later.
The posteromedial papillary muscle has a single blood supply from the posterior descending artery, while the anterolateral papillary muscle has a dual blood supply from the LAD and the circumflex. Therefore, the posteromedial papillary muscle is more vulnerable to ischemia and, hence, rupture.
What are the echocardiographic features of acute mitral regurgitation?
Typically, acute mitral regurgitation is caused by acute insult to the mitral valve or mitral valve apparatus. Examples include endocarditis with leaflet perforation, acute flail leaflet in the setting of mitral valve prolapse, and infarct-related papillary muscle rupture. Also, the LVEF can be hypercontractile.
Left ventricular and left atrial dimensions tend to be normal in acute MR as the heart has not had time to remodel. This also leads to rapid equalization of the LV-LA pressure during systole, blunting both the Doppler signal and the audible murmur which may under-appreciate acute severe mitral regurgitation.
Severe mitral regurgitation typically has a regurgitant volume of ≥60 mL or a regurgitant fraction of at least 50%. Additionally, an effective regurgitant orifice area of 0.4 cm^2 is typically indicative of severe mitral regurgitation. A complete multiparametric assessment is more important than any single parameter.
Systolic flow reversal in the pulmonary veins is pathognomonic for severe mitral regurgitation. This may not be apparent in all pulmonary veins if the MR is eccentric, as is usually the case of papillary muscle or acute leaflet flail.
How should acute mitral regurgitation due to papillary muscle rupture be managed?
Afterload reduction may help, but this may be limited by hypotension in the acute setting.
Temporary mechanical circulatory support may be necessary, often with an intra-aortic balloon pump which can be effective in improving forward flow.
The ultimate and definitive treatment is urgent cardiac surgery along with concomitant bypass grafting as appropriate. Transcatheter edge-to-edge repair may be considered sparingly when surgery is deemed very high risk.
What are the other mechanical complications of acute myocardial infarction?
Ventricular septal rupture typically occur 3-5 days after an infarct but there is a bimodal distribution. The presentation can vary from an isolated systolic murmur all the way to cardiogenic shock. Echocardiography will show a left to right shunt and right heart cath will show a step-up in oxygenation between the RA and PA as well as an elevated Qp/Qs. VSRs require urgent surgical or percutaneous repair.
Ventricular free wall rupture also occurs 3-5 days after an infarct and presents with elevated jugular venous distension, muffled heart sounds, and pulsus paradoxus. As blood irritates the pericardium, the patient’s ECG can show new ST-elevations. Management is emergent surgery.
Pseudoaneurysms present weeks to years after an infarct. These occur when a cardiac rupture is contained by pericardial adhesions and typically involve the inferior or lateral walls. Patients may be asymptomatic, but once diagnosed, pseudoaneurysms should be urgently repaired, lest they expand or become unstable.
References
Damluji AA, van Diepen S, Katz JN, Menon V, Tamis-Holland JE, Bakitas M, Cohen MG, Balsam LB, Chikwe J; on behalf of the American Heart Association Council on Clinical Cardiology; Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Cardiovascular Surgery and Anesthesia; and Council on Cardiovascular and Stroke Nursing. Mechanical complications of acute myocardial infarction: a scientific statement from the American Heart Association. Circulation. 2021;144:e16–e35. doi: 10.1161/CIR.0000000000000985
Chang C et al. Transcatheter Edge-to-Edge Repair for Acute Mitral Regurgitation due to Postinfarction Papillary Muscle Rupture. JSCAI (2022) 100431.
Kilic A et al. Mitral Valve Surgery for Papillary Muscle Rupture: Outcomes in 1342 Patients From The Society of Thoracic Surgeons Database. The Annals of Thoracic Surgery Volume 110, Issue 6, December 2020, Pages 1975-1981
van Diepen S, Katz JN, Albert NM, Henry TD, Jacobs AK, Kapur NK, Kilic A, Menon V, Ohman EM, Sweitzer NK, Thiele H, Washam JB, Cohen MG; on behalf of the American Heart Association Council on Clinical Cardiology; Council on Cardiovascular and Stroke Nursing; Council on Quality of Care and Outcomes Research; and Mission: Lifeline. Contemporary management of cardiogenic shock: a scientific statement from the American Heart Association. Circulation. 2017;136:e232–e268. doi: 10.1161/CIR.0000000000000525
Zoghbi, W. A., Adams, D., Bonow, R. O., Enriquez-Sarano, M., Foster, E., Grayburn, P. A., Hahn, R. T., Han, Y., Hung, J., Lang, R. M., Little, S. H., Shah, D. J., Shernan, S., Thavendiranathan, P., Thomas, J. D., & Weissman, N. J. (2017). Recommendations for noninvasive evaluation of native valvular regurgitation. Journal of the American Society of Echocardiography, 30(4), 303–371. https://doi.org/10.1016/j.echo.2017.01.007
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48min
July 09, 2024379. SGLT Inhibitors: The Biology of SGLT Inhibition with Dr. Katherine Tuttle
CardioNerds (Drs. Gurleen Kaur and Richard Ferraro) and episode FIT Lead Dr. Saahil Jumkhawala (Cardiology Fellow at the University of Miami) discuss SGLT inhibitors, focusing on the biology of SGLT and its inhibition, with Dr. Katherine Tuttle (Executive Director for Research at Providence Healthcare, Co-Principal Investigator of the Institute of Translational Health Sciences, and Professor of Medicine at the University of Washington). Show notes were drafted by Dr. Saahil Jumkhawala. The episode audio was engineered by CardioNerds intern Christiana Dangas.
This episode was produced in collaboration with the American Society of Preventive Cardiology (ASPC) with independent medical education grant support from Lexicon Pharmaceuticals.
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 – The Biology of SGLT Inhibition with Dr. Katherine Tuttle
SGLT inhibitors, while initially developed as antidiabetic medications, have been shown to be beneficial for cardiovascular and renal outcomes. These benefits result from their on-target glucosuric effects and additional off-target effects.
The side effect profiles of SGLTis are primarily mediated by glucose reabsorption in their target tissues. The side effect profile of SGLTis must be considered when prescribing these medications and is generally favorable for SGLT2is versus SGLT1is.
Once SGLTis are prescribed, patients should be given specific attention to their eGFR, serum potassium, and clinical evaluations of volume status and blood pressure.
Strategies to increase implementation of and reduce clinical inertia for these important class of medication remain an area of active investigation
Show notes – The Biology of SGLT Inhibition with Dr. Katherine Tuttle
What should prompt consideration of starting an SGLT inhibitor?
Considerations for SGLT inhibitor initiation are based on a history of heart failure, kidney disease, and diabetes status.
In the EMPA-KIDNEY trial, empagliflozin improved cardiovascular and kidney outcomes in those with low GFR (regardless of level of albuminuria).
What is the mechanism of action of SGLT2 inhibitors?
SGLT2 inhibitors improve glycemic control by blocking SGLT2 receptor-mediated reabsorption of glucose in the proximal convoluted tubule, where 80-90% of this reuptake occurs, and increased downstream excretion of glucose and sodium chloride. SGLT2 inhibitors provide only a modest glucose-lowering effect, particularly for patients with GFR <45.
How do SGLT2 inhibitors improve cardiac function?
Through corrected glomerular hyperfiltration, there is a reduction in blood pressure, a reduction in sympathetic neural activity, and increased glucosuria, improving diuresis. Systemically, there is an increase in erythropoietin, which raises red blood cell mass and oxygen-carrying capacity.
Beyond inhibition of the SGLT2 receptor, which is isolated to the proximal convoluted tubule, there are additional off-target effects. Through non-receptor-mediated mechanisms, glucose transport is blocked into cells by blocking GLUT1 and GLUT4 receptors. They also reduce the mTORC signal transduction pathway, thereby reducing inflammation and glycolysis, leading to a cardioprotective effect in myocytes.
In the DAPA-CKD and CREDENCE trials, GFR decreases of up to 30% were correlated with improved renal and cardiovascular outcomes.
The cardiovascular benefit of SGLT2 inhibitors is not dose-dependent.
Where are SGLT1 receptors located?
SGLT1 receptors are found primarily in small and large bowel enterocytes, as well as the kidney proximal tubule, beyond the convoluted segment.
Around 10% of glucose re-uptake is mediated by SGLT1 receptors in the proximal tubule.
What are some common side effects of SGLT inhibitors?
Given SGLT1 receptors’ presence in the gastrointestinal tract, the side effects of SGLT1 inhibition are primarily gastrointestinal upset through decreased glucose reabsorption in the gut.
SGLT2 inhibitors’ side effects are primarily sequelae of glucosuria, particularly those of genitourinary infections, volume depletion, and euglycemic ketoacidosis (most commonly in patients with diabetes who are longstanding insulin users).
Additionally, a GFR decline of >30% should be suggestive of other issues for patients taking these medications, most commonly volume depletion or hypotension.
References – The Biology of SGLT Inhibition with Dr. Katherine Tuttle
Cowie M.R., Fisher M. SGLT2 inhibitors: mechanisms of cardiovascular benefit beyond glycaemic control. Nat Rev Cardiol. 2020 Dec; 17(12):761-722.
Kuboto Y, Shimizu W. Clinical Benefits of Sodium-Glucose Cotransporter 2 Inhibitors and the Mechanisms Underlying their Cardiovascular Effects. JACC: Asia. 2022 Jun; 2:287-293.
Lopaschuk G.D., Verma S. Mechanisms of Cardiovascular Benefits of Sodium Glucose Co-Transporter 2 (SGLT2) Inhibitors. JACC Basic Trans Sci. 2020 Jun; 5(6):632-644.
Harrington J., Udell J.A., Jones W.S., Anker S.D., Bhatt D.L., Petrie M.C., & Butler J. Empagliflozin in patients post myocardial infarction: rationale and design of the EMPACT-MI trial. American Heart Journal. 2022; 253:86-98.
Talha K.M., Anker S.D., & Butler J. SGLT-2 inhibitors in heart failure: a review of current evidence. International Journal of Heart Failure. 2023; 5(2):82.
Tuttle K.R. Digging deep into cells to find mechanisms of kidney protection by SGLT2 inhibitors. J Clin Invest. 2023; 133(5).
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34min
June 26, 2024 378. Case Report: Severe Mitral Paravalvular Regurgitation Complicated by Hemolytic Anemia – Duke University
CardioNerds cofounder, Amit Goyal joins Dr. Belal Suleiman, Dr. Nkiru Osude, and Dr. David Elliott from Duke University. They discuss a case of severe mitral paravalvular regurgitation complicated by hemolytic anemia. Expert commentary is provided by Dr. Andrew Wang. Audio editing by CardioNerds Academy Intern, student doctor Adriana Mares.
“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!
Case Media – Severe Mitral Paravalvular Regurgitation Complicated by Hemolytic Anemia – Duke University
...more
20min
June 24, 2024377. CardioOncology: Multi-modality Imaging in Cardio-Oncology with Dr. Nausheen Akhter
CardioNerds Co-Founder Dr. Daniel Ambinder, Series Co-Chair Dr. Giselle Suero Abreu (FIT at MGH), and Episode Lead Dr. Iva Minga (FIT at the University of Chicago) discuss the use of multi-modality cardiovascular imaging in cardio-oncology with expert faculty Dr. Nausheen Akhter (Northwestern University). Show notes were drafted by Dr. Sukriti Banthiya and episode audio was edited by CardioNerds Intern and student Dr. Diane Masket.
They use illustrative cases to discuss:
Recommendations on the use of multimodality imaging, including advanced echocardiographic techniques and cardiac MRI, in patients receiving cardiotoxic therapies and long-term surveillance.
Role of nuclear imaging (MUGA scan) in monitoring left ventricular ejection fraction.
Use of computed tomography to identify and/or monitor coronary disease.
Imaging diagnosis of cardiac amyloidosis.
This episode is supported by a grant from Pfizer Inc.
This CardioNerds Cardio-Oncology series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Giselle Suero Abreu, Dr. Dinu Balanescu, and Dr. Teodora Donisan.
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 Cardio-Oncology 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!
References – Multi-modality Imaging in Cardio-Oncology
Baldassarre L, Ganatra S, Lopez-Mattei J, et al. Advances in Multimodality Imaging in Cardio-Oncology. J Am Coll Cardiol. 2022 Oct, 80 (16) 1560–1578.
Meet Our Collaborators
International Cardio-Oncology Society ( IC-OS). IC-OS exits to advance cardiovascular care of cancer patients and survivors by promoting collaboration among researchers, educators and clinicians around the world. Learn more at https://ic-os.org/.
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16min
June 21, 2024376. Case Report: Tamponade or Cardiovascular Support? A case of Pericardial Decompression Syndrome – University of Michigan
CardioNerds cofounders, Dan Ambinder joins Drs. Aishwarya Pastapur, Oyinkansola Osobamiro, and Rafik Issa from the University of Michigan for drinks in Ann Arbor. They discuss the following case of pericardial decompression syndrome. Expert commentary is provided by Dr. Brett Wanamaker. Notes were drafted by Dr. Aishwarya Pastapur and Dr. Rafik Issa. The episode audio was engineered by CardioNerds Intern student Dr. Atefeh Ghorbanzadeh.
A woman in her 50s with a past medical history of stage IV lung cancer (with metastatic involvement of the liver, bone, and brain), previous saddle pulmonary emboli, pericardial effusion, and malignant pleural effusions presents with dyspnea. She was found to have a pericardial effusion with tamponade physiology relieved by pericardiocentesis. We discuss the management of cardiac tamponade, indications for pericardiocentesis, how to monitor for post-pericardiocentesis complications, and what to keep on your differential diagnosis for decompensation after pericardiocentesis. We discuss the epidemiology, pathophysiology, diagnosis, and management of pericardial decompression syndrome.
“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!
Case Media – Pericardial Decompression Syndrome
Pearls – Pericardial Decompression Syndrome
Diminished heart sounds, a low-voltage EKG with electrical alternans, elevated jugular venous pressure/pulsations (JVP), and the presence of pulses paradoxes are important findings that could suggest tamponade.
McConnell sign is strongly concerning for right ventricular failure and pulmonary hypertension, potentially due to acute pulmonary embolism.
Mechanical thrombectomy for pulmonary embolism is not feasible if the emboli are diffusely scattered without a central lesion to target.
For patients who experience decompensation following pericardiocentesis, consider perforation, tamponade re-accumulation, or pericardial decompression syndrome (PDS).
When possible, avoid draining more than 1L of pericardial fluid at once to minimize the risk of PDS.
Notes – Pericardial Decompression Syndrome
What is Pericardial Decompression Syndrome (PDS), and how does it present?
Pericardial decompression syndrome is a rare, life-threatening syndrome occurring in about 5-10% of cases with paradoxical worsening of hemodynamics after pericardial drainage.
The clinical presentation ranges from pulmonary edema to cardiogenic shock to death, occurring a few hours to days after a successful pericardiocentesis.
What is the underlying mechanism for PDS?
The pathophysiology behind PDS is debated, but there are three proposed mechanisms:
Paradoxical Hemodynamic Derangement: After pericardiocentesis, venous return to the RV rapidly increases, resulting in RV expansion and potentially septal deviation towards the LV. Subsequently, the LV experiences decreased preload while still facing increased afterload as a compensatory response to obstructive shock, leading to decompensation.
Myocardial Ischemia: Increased intrapericardial pressure may impair coronary perfusion, leading to myocardial ischemia. Upon pericardiocentesis, there is myocardial stunning with increased demand due to increased venous return and cardiac output
Sympathetic Withdrawal: Withdrawal of sympathetic activation after drainage of pericardial fluid can trigger cardiovascular collapse
What are the risk factors for developing PDS, and how can we mitigate those risks for prevention?
Generally, patients with long-standing pericardial effusion with chronic compression of the heart, such as those with malignant pericardial effusions, are more vulnerable to developing PDS after pericardiocentesis.
Additionally, rapid fluid removal increases the risk. In terms of prevention, removing fluid to normalize CVP and MAP and letting the rest of the fluid drain slowly may mitigate the risk.
How do we manage a patient with PDS?
The management of PDS is supportive, focusing on addressing hemodynamic and respiratory derangements.
The underlying pathophysiology should resolve in 24-48 hours.
What is the prevalence and prognosis of PDS?
PDS affects 5-10% of pericardiocentesis procedures, although the exact frequency is difficult to ascertain.
It is a self-resolving process as the heart re-adapts to the new hemodynamics.
However, during the episode of PDS, mortality can be as high as 30% per some studies.
References – Pericardial Decompression Syndrome
Schnur M. Understanding Pulsus Paradoxus. Accessed February 27, 2024. https://nursingcenter.com/ncblog/august-2021/understanding-pulsus-paradoxus
Carlini’ ’Caterina Chiara De, Maggiolini’ ’Stefano. Pericardiocentesis in cardiac tamponade: indications and practical aspects. Accessed February 27, 2024. https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-15/Pericardiocentesis-in-cardiac-tamponade-indications-and-practical-aspects
Angouras DC, Dosios T. Pericardial Decompression Syndrome: A Term for a Well-Defined but Rather Underreported Complication of Pericardial Drainage. The Annals of Thoracic Surgery. 2010;89(5):1702-1703. doi:10.1016/j.athoracsur.2009.11.073
Imazio M. Pericardial decompression syndrome: A rare but potentially fatal complication of pericardial drainage to be recognized and prevented. European Heart Journal Acute Cardiovascular Care. 2015;4(2):121-123. doi:10.1177/2048872614557771
Prabhakar Y, Goyal A, Khalid N, et al. Pericardial decompression syndrome: A comprehensive review. World Journal of Cardiology. 2019;11(12):282-291. doi:10.4330/wjc.v11.i12.282
Sobieski C, Herner M, Goyal N, et al. Pericardial Decompression Syndrome After Drainage of Chronic Pericardial Effusions. JACC: Case Reports. 2022;4(22):1515-1521. doi:10.1016/j.jaccas.2022.08.023
Chhabra L. Pericardial Decompression Syndrome. American College of Cardiology. Accessed February 27, 2024. https://www.acc.org/Latest-in-Cardiology/Articles/2020/04/13/09/05/http%3a%2f%2fwww.acc.org%2fLatest-in-Cardiology%2fArticles%2f2020%2f04%2f13%2f09%2f05%2fPericardial-Decompression-Syndrome
Pradhan R, Okabe T, Yoshida K, Angouras DC, DeCaro MV, Marhefka GD. Patient characteristics and predictors of mortality associated with pericardial decompression syndrome: a comprehensive analysis of published cases. European Heart Journal Acute Cardiovascular Care. 2015;4(2):113-120. doi:10.1177/2048872614547975
Amro A, Mansoor K, Amro M, et al. A Comprehensive Systemic Literature Review of Pericardial Decompression Syndrome: Often Unrecognized and Potentially Fatal Syndrome. Current Cardiology Reviews. 17(1):101-110.
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18min
June 06, 2024375. Beyond the Boards: Foundations of Cardiovascular Prevention with Dr. Stephen Kopecky
CardioNerds (Amit Goyal and Dan Ambinder), Dr. Jaya Kanduri, and Dr. Jason Feinman discuss foundations of cardiovascular prevention with Dr. Stephen Kopecky. In this episode, the CardioNerds and topic expert Dr. Stephen Kopecky tackle cardiovascular prevention. They focus on how to identify patients at risk for cardiovascular disease by using the pooled cohort equation and discuss how to incorporate additional risk-enhancing factors in risk estimation. Later, they discuss the role of non-invasive imaging and testing for further patient risk stratification. Last, they discuss the appropriate pharmacologic interventions for patient care, how to determine what LDL-c to target for each patient, and how to modify your treatment modalities in response to side effects or the need for further lipid-lowering therapies.
Notes were drafted by Dr. Jason Feinman. Audio was engineered by CardioNerds Intern Christiana Dangas.
The CardioNerds Beyond the Boards Series was inspired by the Mayo Clinic Cardiovascular Board Review Course and designed in collaboration with the course directors Dr. Amy Pollak, Dr. Jeffrey Geske, and Dr. Michael Cullen.
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 Beyond the Boards Series
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Pearls and Quotes – Foundations of Cardiovascular Prevention
The 2018 cardiovascular prevention guidelines indicate that a single equation, like the pooled risk equation, does not fit everyone. There are additional risk enhancers that are not factored into the pooled risk equation that can impact an individual’s risk
These factors are often conditions that increase inflammation but can also include family history, ethnicity, chronic kidney disease, metabolic syndrome, premature menopause or gestational diabetes, and rheumatologic conditions
Data from Get With The Guidelines demonstrates that the average LDL at the time of the first myocardial infarction is 105 mg/dL.
Coronary artery calcium scores or a carotid ultrasound can be used to further risk stratify patients. However, CAC is likely to be negative in young women. A CAC of zero can be used to “de-risk” some patients but should not be used to guide therapy in the setting of tobacco usage, diabetes mellitus, or familial hypercholesterolemia.
Strategies to mitigate risk include healthy lifestyle habits and selectively targeting key risk factors including LDL, hypertriglyceridemia, inflammation, and the GLP1-pathway. Upcoming medications may address elevated Lp(a).
Notes – Foundations of Cardiovascular Prevention
Notes: Notes drafted by Dr. Jason Feinman.
How do you assess an individual’s risk for cardiovascular disease?
The paramount role of primary prevention is the assessment and mitigation of an individual’s risk for ASCVD event.1
The 10-year ASCVD risk calculator is a commonly used tool to assess an individual’s risk and to guide shared decision-making conversations and recommendations.2
Individuals can be characterized as having low (less than 5%), borderline (5%-7.5%), intermediate (7.5%-20%), or high (greater than 20%) risk.2
The 10-year ASCVD risk calculator has varying validation in ethnic minorities, and other risk calculators, such as the Framingham CVD risk score, may be considered in those groups.3-5
Additional risk enhancers may be used to guide recommendations for individuals at borderline or intermediate risk.1
What additional imaging testing may be beneficial in the assessment of an individual’s risk?
Individuals with intermediate or borderline risk may benefit from further non-invasive imaging to help guide therapeutic recommendations.2
Coronary artery calcification is a marker of underlying atherosclerosis, which can help to reclassify patients to be at higher risk for ASCVD events and support interventions to help lower this risk.6
Conversely, a score of zero can help to reclassify individuals into lower-risk groups
A score of zero should be used with caution in young women who are more likely to have non-calcified plaque and should not be used as a marker of low risk in individuals with other risk factors, including diabetes mellitus and tobacco usage.1
What non-pharmacological interventions may be considered to lower an individual’s ASCVD risk?
The 2019 guidelines give a class I recommendation for a diet of vegetables, fruits, nuts, whole grains, and fish to lower ASCVD risk factors.1
Increased intake of sugar has been demonstrated to correlate with increased rates of type 2 diabetes mellitus and subsequent increased risk for cardiovascular events.7
At least 150 minutes per week of moderate-intensity or 75 minutes of vigorous intensive is recommended to reduce the risk of ASCVD events.1
What pharmacological interventions can be considered for individuals with prior ASCVD events or at high risk for ASCVD?
A moderate-intensity statin is recommended for individuals at intermediate risk of ASCVD events with risk enhancers with a goal reduction in LDL-c of 30% or more.1
For individuals at a high 10-year risk for ASCVD events, a 50% reduction in LDL-C is recommended.1
A doubling of a statin dose can be predicted to lead to a 6% further reduction in LDL-C
Ezetimibe can be considered as adjunct therapy for individuals receiving statin therapy who do not reach their target LDL-C.2
How do you determine the goal LDL-c?
LDL goal is based on a history of prior ASCVD events and the risk of future ASCVD events.
For secondary prevention, especially for individuals at high risk for ASCVD events, an LDL goal of at least less than 70 mg/dL is recommended2
References – Foundations of Cardiovascular Prevention
Arnett DK, Blumenthal RS, Albert MA, et al. 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines [published correction appears in Circulation. 2019 Sep 10;140(11):e649-e650] [published correction appears in Circulation. 2020 Jan 28;141(4):e60] [published correction appears in Circulation. 2020 Apr 21;141(16):e774]. Circulation. 2019;140(11):e596-e646. doi:10.1161/CIR.0000000000000678
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 [published correction appears in Circulation. 2019 Jun 18;139(25):e1182-e1186] [published correction appears in Circulation. 2023 Aug 15;148(7):e5]. Circulation. 2019;139(25):e1082-e1143. doi:10.1161/CIR.0000000000000625
Yang X, Li J, Hu D, et al. Predicting the 10-Year Risks of Atherosclerotic Cardiovascular Disease in Chinese Population: The China-PAR Project (Prediction for ASCVD Risk in China). Circulation. 2016;134(19):1430-1440. doi:10.1161/CIRCULATIONAHA.116.022367
Jung KJ, Jang Y, Oh DJ, et al. The ACC/AHA 2013 pooled cohort equations compared to a Korean Risk Prediction Model for atherosclerotic cardiovascular disease. Atherosclerosis. 2015;242(1):367-375. doi:10.1016/j.atherosclerosis.2015.07.033
D’Agostino RB Sr, Vasan RS, Pencina MJ, et al. General cardiovascular risk profile for use in primary care: the Framingham Heart Study. Circulation. 2008;117(6):743-753. doi:10.1161/CIRCULATIONAHA.107.699579
DeFilippis AP, Young R, Carrubba CJ, et al. An analysis of calibration and discrimination among multiple cardiovascular risk scores in a modern multiethnic cohort. Ann Intern Med. 2015;162(4):266-275. doi:10.7326/M14-1281
Löfvenborg JE, Andersson T, Carlsson PO, et al. Sweetened beverage intake and risk of latent autoimmune diabetes in adults (LADA) and type 2 diabetes. Eur J Endocrinol. 2016;175(6):605-614. doi:10.1530/EJE-16-0376
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16min
May 31, 2024374. Case Report: Unraveling the Mystery – When Childhood Chest Pain Holds the Key to a Genetic Heart Condition – Wayne State University
This case report explores the intricacies of familial hypercholesterolemia (FH), delving into its genetic basis, atherosclerotic cascade, and early-onset cardiovascular complications. It examines established diagnostic criteria and emphasizes personalized management, including statins, novel therapies, and lifestyle modifications.
CardioNerds cofounders (Drs. Amit Goyal and Danial Ambinder) join Dr. Irfan Shafi, Dr. Preeya Prakash, and Dr. Rebecca Theisen from the Wayne State University/DMC and Central Michigan University at Campus Martius in Downtown Detroit for some holiday ice-skating! They discuss an interesting pediatric case (see case synopsis below). Dr. Luis C Afonso provides the Expert CardioNerd Perspectives & Review segment for this episode. Audio editing by CardioNerds academy intern, Pace Wetstein.
“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.
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Case Synopsis
FH, a 9-year-old female with no previous medical history, recently moved back to the US from Iraq. She presented to establish care and discuss new-onset chest pain and dyspnea. A systolic ejection murmur was noted during her initial visit to the pediatrician, prompting cholesterol testing and a cardiology referral. Testing revealed, alarming cholesterol levels (Total Cholesterol: 802 mg/dL, LDL: 731 mg/dL, Triglycerides: 123 mg/dL) prompted concern for cardiac involvement.
Due to persistent symptoms, FH was transferred to Children’s Hospital of Michigan. Despite normal findings on EKG and chest x-ray, a 2/6 systolic murmur was noted. She was discharged with a cardiology clinic follow-up.
However, two days later, FH experienced severe chest pain at rest, sweating, and difficulty breathing. She was transported to Children’s Hospital again, and her troponin level measured 3000, and her total cholesterol was 695 mg/dL. An echocardiogram revealed valvar and supravalvar aortic stenosis, necessitating collaboration between Pediatric and Adult cardiology teams.
CTA thorax revealed severe supravalvular stenosis, a hypoplastic right coronary artery, and significant coronary artery obstructions. Diagnostic cardiac catheterization confirmed severe aortic stenosis and coronary artery disease, leading to the decision for surgical intervention.
FH underwent the Ross operation, left main coronary artery augmentation, and right coronary artery reimplantation. Intraoperatively, atherosclerotic plaques were observed in multiple cardiac structures.
FH’s recovery was uneventful, discharged on a regimen including Atorvastatin, Ezetimibe, evolocumab, and antiplatelet therapy. Persistent high LDL levels required regular plasmapheresis. Plans for evaluations in Genetics, Lipid Clinic, Endocrine, and Gastroenterology were made, potentially leading to a liver transplant assessment. Given the severity of her condition, a heart/liver transplant might be considered in the future.
Conclusion:
This case of FH highlights the complex presentation of severe aortic stenosis and coronary artery disease in a pediatric patient. Urgent diagnosis, interdisciplinary collaboration, and aggressive management were crucial. The case underscores the importance of comprehensive care for pediatric patients with rare cardiac conditions, emphasizing collaboration between specialties for optimal outcomes and long-term well-being.
Case Media
Pearls – Familial Hypercholesterolemia
Mutations in LDLR, ApoB, or PCSK9 genes disrupt LDL-C clearance, leading to a cascade of events culminating in accelerated atherosclerosis and early-onset cardiovascular complications (e.g., CAD, aortic stenosis, PAD, stroke).
Diagnosis of familial hypercholesterolemia relies on a combination of clinical features (xanthomas, corneal arcus, high LDL-C), family history, and genetic testing guided by established criteria like DCLN or NLA recommendations.
Supravalvular aortic stenosis, while common in many congenital cases, should raise suspicion of homozygous familial hypercholesterolemia in the setting of extensively elevated LDL and unexpected coronary artery disease.
A multidisciplinary approach, including involvement of pediatric and adult cardiology teams, lipid specialists and cardiothoracic surgeons, should be involved in the overall evaluation and management of these patients, both at initiation of diagnosis, and in an outpatient setting.
In patients with FH, it is important to delineate between homozygous and heterozygous manifestations, as this can have extensive implications on treatment, management and the overall clinical prognosis and further disease sequelae that the patient may experience.
References – Familial Hypercholesterolemia
Shah, N. (2020). Familial hypercholesterolemia: Early diagnosis and treatment is key for cardiovascular prevention.Cleveland Clinic Journal of Medicine, 87(5), 109-120. https://pubmed.ncbi.nlm.nih.gov/23469913/
Turgeon, R. D., Barry, A. R., & Pearson, G. J. (2023). Familial hypercholesterolemia: Review of diagnosis,screening, and treatment. American Journal of Health-System Pharmacy, 80(11), 917-929.https://pubmed.ncbi.nlm.nih.gov/26796832/
Collins, R. T. (2018). Cardiovascular disease in Williams syndrome. Current Opinion in Pediatrics, 30(5), 609-615. https://www.ncbi.nlm.nih.gov/books/NBK544278/
Collins, R. T., Kaplan, P., Somes, G. W., & Rome, J. J. (2010). Long-term outcomes of patients with cardiovascular abnormalities and Williams syndrome. American Journal of Cardiology, 105(6), 874-878.https://pubmed.ncbi.nlm.nih.gov/30045083/
Honjo, R. S., Monteleone, V. F., Aiello, V. D., Wagenfuhr, J., Issa, V. S., Pomerantzeff, P. M. A., Furusawa, E. A.,Zanardo, E. A., Kulikowski, L. D., Bertola, D. R., & Kim, C. A. (2022). Cardiovascular findings in Williams-Beuren Syndrome: Experience of a single center with 127 cases. American Journal of Medical Genetics. Part A,188(3), 676-682. https://www.ncbi.nlm.nih.gov/books/NBK544278/
Pham, P. P., Moller, J. H., Hills, C., Larson, V., & Pyles, L. (2009). Cardiac catheterization and operative outcomes from a multicenter consortium for children with Williams syndrome. Pediatric Cardiology, 30(1), 9-14.https://pubmed.ncbi.nlm.nih.gov/19052807/
Olsen, M., Fahy, C. J., Costi, D. A., Kelly, A. J., & Burgoyne, L. L. (2014). Anaesthesia-related haemodynamic complications in Williams syndrome patients: A review of one institution’s experience. Anaesthesia and Intensive Care, 42(6), 619-624. https://pubmed.ncbi.nlm.nih.gov/25233176/
Harada-Shiba, M., Arai, H., Ishigaki, Y., Ishibashi, S., Okamura, T., Ogura, M., Dobashi, K., Nohara, A., Bujo, H.,Miyauchi, K., Yamashita, S., & Yokote, K. (2018). Guidelines for diagnosis and treatment of familial hypercholesterolemia 2017. Journal of Atherosclerosis and Thrombosis, 25(8), 751-770.https://pubmed.ncbi.nlm.nih.gov/29877295/
Alnouri, F., & Santos, R. D. (2022). New trends and therapies for familial hypercholesterolemia. Journal of Clinical Medicine, 11(22), 6638. https://pubmed.ncbi.nlm.nih.gov/36431115/
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29min
May 30, 2024373. Narratives in Cardiology: Becoming a “Big E” Medical Educator as a Cardiologist with Dr. James Arrighi
In this episode, Dr. Katie Fell (General Cardiology Fellow at University of Michigan and CardioNerds Academy Fellow) and Dr. Gurleen Kaur (incoming General Cardiology fellow at Brigham and Women’s Hospital and Director of CardioNerds Internship) discuss with Dr. James Arrighi (General Cardiologist and CEO of ACGME-International) about developing as a clinician educator and the concept of competency-based education.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza.
The PA-ACC & CardioNerds Narratives in Cardiology Page
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Video version – Becoming a “Big E” Medical Educator as a Cardiologist with Dr. James Arrighi
https://youtu.be/xcrwnz6_9Qg
Quoatables – Becoming a “Big E” Medical Educator as a Cardiologist with Dr. James Arrighi
“You really have to have a passion or a love for what you do…that’s probably responsible for most of the success one has in life” (time 4:43)
“Sub-subspecialty societies in Cardiology represent [a] great opportunity for junior faculty or even trainees to get involved, even before getting involved in ACC.” (time 5:30)
“Competency-based medical education and time variable training are not synonymous.” (time 16:43)
“As Cardiology evolves into more and more subspecialties…it begs the question… ‘Is Cardiology a primary specialty?’” (time 27:30)
“We need to think about [a] more efficient ways for training.” (time 31:55)
“As a clinician educator, there’s variety, there’s innovation!” (time 41:22)
Notes – Becoming a “Big E” Medical Educator as a Cardiologist with Dr. James Arrighi
How might one develop as a clinician educator on a national level?
Junior faculty and trainees should consider taking advantage of education opportunities in various Cardiology sub-specialty societies (ex: American Society of Nuclear Cardiology, ASNC). This may include involvement in different committees. These opportunities are great ways to build connections and establish a reputation on a national level. This can help lead to other opportunities with larger national organizations (ex: ACC, AHA).
Cardiology Training Oversight
The Accreditation Council for Graduate Medical Education (ACGME) and American Board of Internal Medicine (ABIM) both have regulatory power over Cardiology training, providing the minimum clinical experience standards for Cardiology fellowship training programs.
The ACGME oversees accreditation for Cardiology fellowships.
The ABIM defines the requirements for eligibility for certification of individuals.
Over time, the ACGME has transitioned to placing an emphasis on quality improvement, with a particular focus on continuous programmatic improvement.
The American College of Cardiology (ACC) helps define more granular recommendations for Cardiology training programs and their curriculum.
Periodically the ACC releases training guidelines for Cardiology fellowship programs, called Core Cardiovascular Training Statements, or COCATS. This document provides more contemporary, detailed, and specialty-specific recommendations for Cardiology training as compared to ACGME.
While ACC has no regulatory authority over Cardiology training programs, COCATS documents provide a roadmap for program directors on how to structure training.
The most recent version of the document, COCATS 4, incorporated in the concept of competency-based education (CBME).
What is Competency-Based Education (CBME)?
Medical education has evolved to focus more on outcome-based assessments of trainees structured around competency evaluations.
In 2002, the ACGME defined competencies by which training programs should evaluate their trainees. As a result, training shifted from a time-based structure to one in which trainees must demonstrate specific competencies within a specific time frame.
ACC further defined competencies for Cardiology training in the Core Cardiovascular Training Statement 4 (COCATS 4). This is the first COCATs document introducing aspects of CBME, including defining competencies, milestones, and tools to assess a Cardiology trainee’s performance.
Each of these documents focuses on optimizing fellow time while in training, targeting education to the learner’s goals and their future career trajectory.
Moving to a competency-based, time-variable training program in the U.S. would be challenging and would require significant restructuring of our current GME training system, including Medicare funding.
What is ACGME-International (ACGME-I)?
Group within the ACGME dedicated to improving health care internationally by assessing and advancing the quality of resident physicians’ education through accreditation.
The organization is currently present in 12 countries at 23 sponsoring institutions (as of April 2024).
ACGME-I provides postgraduate medical education programs with standardized frameworks on how to improve the quality of teaching, learning, research, and clinical practice for their trainees.
References
Weissman G, Auseon AJ, Arrighi JA, et al. Perceptions and Utilization of the U.S. Core Cardiovascular Training Statement. J Am Coll Cardiol. 2019;73(22):2896-2899.
Halperin JL, Williams ES, Fuster V. COCATS 4 Introduction. J Am Coll Cardiol. 2015;65(17):1724-1733.
Arrighi JA, Kilic S, Haines PG. Perspectives on Current Training Guidelines for Cardiac Imaging and Recommendations for the Future. Curr Cardiol Rep. 2018;20(6):43. Published 2018 Apr 23.
ACGME Program Requirements for Graduate Medical Education in Cardiovascular Disease. Accessed February 2, 2024.
Mendes LA, Weissman G, Berlacher K, et al. Competency-Based Alternative Training Pathway in Cardiovascular Disease and Clinical Cardiac Electrophysiology. J Am Coll Cardiol. 2022;79(25):2540-2542.
Production Team
Dr. Gurleen Kaur
Amit Goyal, MD
Daniel Ambinder, MD
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22min
May 23, 2024372. Case Report: Chronic Chagas Cardiomyopathy with Recurrent Ventricular Tachyarrhythmia – Georgetown University
CardioNerds (Dr. Jessie Holtzman, Chair for the CardioNerds Women’s Heart Disease Committee, and Dr. Naima Maqsood, Chair for the CardioNerds Electrophysiology Committee) join Dr. Ritika Gadodia, Dr. Namratha Meda, and Dr. Tsion Aberra from the Medstar Washington Hospital Center/Georgetown University Program for the National Cherry Blossom Festival. They discuss involving a patient with Chagas cardiomyopathy. Dr. Rachel Marcus provides the Expert CardioNerd Perspectives & Review segment for this episode. Episode audio was edited by Dr. Diane Masket.
A 79-year-old male with a history of cardiomyopathy presented with recurrent ventricular tachycardia (VT) post-CRT-D placement. On arrival, the patient was in cardiogenic shock. Initial treatment with amiodarone and milrinone failed, necessitating the addition of mexiletine. Imaging was suggestive of a left ventricular ejection fraction of 20-25% with severe global hypokinesis. Prior coronary angiogram had shown nonobstructive coronary artery disease. Further non-ischemic cardiomyopathy evaluation was unrevealing. Given his El Salvadorian origins, Chagas serology results revealed Chronic Chagas Cardiomyopathy (CCM) confirmed by CDC testing. This case underscores the importance of suspecting CCM in patients with risk factors. An early diagnosis of CCM, can prevent catastrophic events (heart blocks, ventricular arrhythmias, thromboembolic events).
In summary, this case takes the learner through the journey of a patient with non-ischemic cardiomyopathy and emphasizes the importance of approaching it with a wide range of differentials.
“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
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Case Media
Pearls – Chronic Chagas Cardiomyopathy with Recurrent Ventricular Tachyarrhythmia
Always consider Chagas cardiomyopathy when you have a patient from Latin America who presents with non-ischemic cardiomyopathy.
Chagas cardiomyopathy is associated with an unfavorable prognosis and serves as an independent predictor of mortality.
Chagas cardiomyopathy is arrhythmogenic and requires consideration for ICD and, when appropriate, catheter based ventricular tachycardia ablation.
It is crucial to treat patients with nifurtimox and benznidazole when appropriate.
Provide screening for first-degree family members or close relatives who may have lived in the same environment.
Show Notes – Chronic Chagas Cardiomyopathy with Recurrent Ventricular Tachyarrhythmia
What is the disease progression in Chagas disease5?
Acute Stage:
Initial infection occurs through contact with infected triatomine bug feces or contaminated blood products.
Symptoms may be mild or absent but can include fever, fatigue, body aches, and swelling at the injection site (chagoma).
Parasitemia is high during this stage.
Intermediate/Indeterminate Stage:
The infection becomes chronic if left untreated.
Many individuals enter this stage with no noticeable symptoms.
Parasitemia levels decrease, but the parasite remains in the body, mainly in muscle and cardiac tissue.
This stage can last for years to decades.
Chronic Stage:
Some individuals will remain asymptomatic throughout their lives.
Cardiac complications (chronic Chagas cardiomyopathy) can lead to arrhythmias, congestive heart failure, and sudden death.
Digestive complications can result in enlarged esophagus (megaesophagus) and colon (megacolon), leading to difficulties in swallowing and digestion.
When do we suspect, and who do we screen, for Chagas disease?
The seroprevalence of CCM in the USA is as high as 19%16. Among patients with LVEF<50%, the rate of positive serology was 28%. Similarly, the seropositivity among patients who reported recognizing the reduviid bug was 31%.
Individuals who have lived in endemic countries of Mexico, Central and South America, excluding the Caribbean islands.
T. cruzi seroprevalence is highest in Bolivia, Argentina, Paraguay, Ecuador, El Salvador, and Guatemala6.
Close relatives and those born to women from endemic countries7.
Persons with a history of bite/exposure to the vector responsible for transmission.
EKG abnormalities suggestive of infection even in the absence of symptoms.
TTE changes: regional wall motion abnormalities (particularly basal inferolateral, apical aneurysm)4
What diagnostic tests can confirm the diagnosis of chronic Chagas cardiomyopathy?
Serologic testing: no available assay has sufficient sensitivity and specificity to be used alone. Two serologic tests based on different antigens and/or techniques (e.g., ELISA and IFA) are used in parallel to increase the accuracy of the diagnosis8.
EKG: RBBB, LAFB, AV block, atrial fibrillation, ventricular tachycardias
TTE: dilated cardiomyopathy, reduced ejection fracture, regional wall motion abnormalities, left ventricular apical aneurysm
Cardiac MRI: myocardial fibrosis is a striking feature of CCM and LGE is used to detect and qualify the extent. Myocardial fibrosis also plays a role in risk stratification of CCM9.
What are the indications for treatment of Chagas disease?
Acute phase.
Early chronic phase, including women of childbearing age.
Reactivated infection (e.g., after immunosuppression).
Adults <50 years of age who do not have advanced cardiomyopathy (stage B1)10.
In all other cases, the potential benefit of medication in delaying the development of Chagas disease should be weighed against potential adverse reactions- benznidazole and nifurtimox should not be taken by pregnant women or people with kidney or liver failure.
What are the benefits of screening and early diagnosis?
Effective treatment, particularly in the acute phase.
The BENEFIT trial showed that Trypanocidal therapy with benznidazole in patients with CCM did not significantly reduce cardiac deterioration11.
Screening of family members/friends who grew up in the same environment.
Reduction of transmission due to blood transfusions and congenital transmission.
Early initiation of GDMT (guideline-directed medical therapy) for clinical heart failure 2/2 CCM.
Ongoing surveillance for cardiomyopathy can prevent catastrophic events (heart blocks, ventricular arrhythmias, thromboembolic events).
Cost effectiveness: Early diagnosis and treatment may reduce healthcare costs compared to the treatment of complications that arise from the chronic phase of the disease. Early diagnosis may also reduce the number of endomyocardial biopsies.
How is the management of VT unique in chronic Chagas cardiomyopathy?
In comparison to cardiomyopathies of other etiologies, CCM is associated with a higher risk of life-threatening ventricular arrhythmias and an unfavorable prognosis12,14.
Per ESC guidelines, the greatest benefit of ICD in CCM is in patients with an LVEF ≤40%15.
Per Gali et al, most patients with an ICD received appropriate ICD shocks/therapies regardless of their LV systolic function13.
Ablation of VT requires extensive mapping because multiple discrete circuits are typically present. The most common site of origin is the LV basal inferolateral wall. However, 1/3rd of the foci is located on the epicardial surface. This necessitates epicardial mapping to achieve successful ablation6.
References – Chronic Chagas Cardiomyopathy with Recurrent Ventricular Tachyarrhythmia
Ghzally Y, Mahajan K. Implantable Defibrillator. In: StatPearls. StatPearls Publishing; 2023. Accessed October 7, 2023. http://www.ncbi.nlm.nih.gov/books/NBK459196/
Vrettos A, Panoulas V. Diagnosing STEMI in the presence of paced rhythm: dispelling the myth of the ‘uninterpretable paced ECG.’ BMJ Case Rep. 2021;14(7):e242546. doi:10.1136/bcr-2021-242546
3. Bozkurt B, Colvin M, Cook J, et al. Current Diagnostic and Treatment Strategies for Specific Dilated Cardiomyopathies: A Scientific Statement From the American Heart Association. Circulation. 2016;134(23). doi:10.1161/CIR.0000000000000455
Forsyth CJ, Manne-Goehler J, Bern C, et al. Recommendations for Screening and Diagnosis of Chagas Disease in the United States. The Journal of Infectious Diseases. 2022;225(9):1601-1610. doi:10.1093/infdis/jiab513
CDC – Chagas Disease – Disease. Accessed October 7, 2023. https://www.cdc.gov/parasites/chagas/disease.html
Chagas Cardiomyopathy: An Update of Current Clinical Knowledge and Management: A Scientific Statement From the American Heart Association | Circulation. Accessed October 7, 2023. https://www.ahajournals.org/doi/10.1161/CIR.0000000000000599
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11. Morillo CA, Marin-Neto JA, Avezum A, et al. Randomized Trial of Benznidazole for Chronic Chagas’ Cardiomyopathy. N Engl J Med. 2015;373(14):1295-1306. doi:10.1056/NEJMoa1507574
12. Probability of Occurrence of Life‐Threatening Ventricular Arrhythmias in Chagas’ Disease versus Non‐Chagas’ Disease – FILHO – 2000 – Pacing and Clinical Electrophysiology – Wiley Online Library. Accessed October 7, 2023. https://onlinelibrary.wiley.com/doi/10.1111/j.1540-8159.2000.tb07058.x
13. Implantable cardioverter-defibrillators for treatment of sustained ventricular arrhythmias in patients with Chagas’ heart disease: comparison with a control group treated with amiodarone alone | EP Europace | Oxford Academic. Accessed October 7, 2023. https://academic.oup.com/europace/article/16/5/674/484618?login=fals
14. Barbosa MPT, Da Costa Rocha MO, De Oliveira AB, Lombardi F, Ribeiro ALP. Efficacy and safety of implantable cardioverter-defibrillators in patients with Chagas disease. EP Europace. 2013;15(7):957-962. doi:10.1093/europace/eut011
15. Requena-Méndez A, Aldasoro E, De Lazzari E, et al. Prevalence of Chagas Disease in Latin-American Migrants Living in Europe: A Systematic Review and Meta-analysis. Rodrigues MM, ed. PLoS Negl Trop Dis. 2015;9(2):e0003540. doi:10.1371/journal.pntd.0003540
16. Gadodia R, Kerai A, Aberra T, et al. SEROPREVALENCE OF CHAGAS CARDIOMYOPATHY IN LATIN AMERICAN IMMIGRANTS IN THE WASHINGTON DC METRO AREA. Journal of the American College of Cardiology. 2023;81(8):318. doi:10.1016/S0735-1097(23)00762-3
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