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404. Case Report: A Stressful Case of Cardiogenic Shock – Tufts Medical Center
CardioNerds (Dr. Dan Ambinder and Dr. Yoav Karpenshif – Chair of the CardioNerds Critical Care Cardiology Council) join Dr. Munim Khan, Dr. Shravani Gangidi, and Dr. Rachel Goodman from Tufts Medical Center’s general cardiology fellowship program for hot pot in China Town in Boston. They discuss a case involving a patient who presented with stress cardiomyopathy leading to cardiogenic shock. Expert commentary is provided by Dr. Michael Faulx from the Cleveland Clinic. Notes were drafted by Dr. Rachel Goodman. Audio editing by Dr. Diane Masket.
A young woman presents with de novo heart-failure cardiogenic shock requiring temporary mechanical circulatory support who is found to have basal variant takotsubo cardiomyopathy. We review the definition and natural history of takotsubo cardiomyopathy, discuss initial evaluation and echocardiographic findings, and review theories regarding pathophysiology of the clinical syndrome. We also highlight complications of takotsubo cardiomyopathy, with a focus on left ventricular outflow obstruction, cardiogenic shock, and arrythmias.
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Pearls
Takotsubo cardiomyopathy is defined as a reversible systolic dysfunction with wall motion abnormalities that do not follow a coronary vascular distribution.
Takotsubo cardiomyopathy is a diagnosis of exclusion; patients often undergo coronary angiography to rule out epicardial coronary artery disease given an overlap in presentation and symptoms with acute myocardial infarction.
There are multiple echocardiographic variants of takotsubo. Apical ballooning is the classic finding, but mid-ventricular, basal, and biventricular variants exist as well.
Patients with takotsubo cardiomyopathy generally recover, but there are important complications to be aware of. These include arrhythmia, left ventricular outflow tract (LVOT) obstruction related to a hyperdynamic base in the context of apical ballooning, and cardiogenic shock.
Patients with Impella devices are at risk of clot formation and stroke. Assessing the motor current can be a clue to what is happening at the level of the motor or screw.
Notes
What is Takotsubo Syndrome (TTS)?
TTS is a syndrome characterized by acute heart failure without epicardial CAD with regional wall motion abnormalities seen on echocardiography that do not correspond to a coronary artery territory (see below).1
TTS classically develops following an acute stressor—this can be an emotional or physical stressor.1
An important feature of TTS is that the systolic dysfunction is reversible. The time frame of reversibility is variable, though generally hours to weeks.2
Epidemiologically, TTS has a predilection for post-menopausal women, however anyone can develop this syndrome.1
TTS is a diagnosis of exclusion. Coronary artery disease (acute coronary syndrome, spontaneous coronary artery dissection, coronary embolus, etc) should be excluded when considering TTS. Myocarditis is on the differential diagnosis.
What are the echocardiographic findings of takotsubo cardiomyopathy?
The classic echocardiographic findings of TTS is “apical ballooning,” which is a way of descripting basal hyperkinesis with mid- and apical hypokinesis, akinesis, or dyskinesis.3
There are multiple variants of TTS. The four most common are listed below:3(1) Apical ballooning (classic TTS)(2) Mid-ventricular variant(3) Basal variant
(4) Focal variant
Less common variants include the biventricular variant and the isolated right ventricular variant.3
Do patients with TTS generally have EKG changes or biomarker elevation?
Patients often have elevated troponin,
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403. Cardio-Rheumatology: Treating Inflammation and Real-World Implementation of Therapies with Dr. Brittany Weber and Dr. Michael Garshick
In this episode, CardioNerds Dr. Gurleen Kaur and Dr. Akiva Rosenzveig are joined by Cardio-Rheumatology experts, Dr. Brittany Weber and Dr. Michael Garshick to discuss treating inflammation, delving into the pathophysiology behind the inflammatory hypothesis of atherosclerotic cardiovascular disease and the evolving data on anti-inflammatory therapies for reducing ASCVD risk, with insights on real-world implementation.
Show notes were drafted by. Dr. Akiva Rosenzveig.
This episode was produced in collaboration with the American Society of Preventive Cardiology (ASPC) with independent medical education grant support from Lexicon Pharmaceuticals.
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Pearls - Treating Inflammation
Our understanding of the pathophysiology of atherosclerosis has undergone a few iterations from the incrustation hypothesis to the lipid hypothesis to the response-to-injury hypothesis and culminating with our current understanding of the inflammation hypothesis.
Both the adaptive and innate immune systems play instrumental roles in the pathogenesis of atherosclerosis.
After adequately controlling classic modifiable risk factors such as blood pressure, dyslipidemia, glucose intolerance, and obesity, systemic inflammation as assessed by CRP can be ascertained as CRP is associated with ~1.8-fold increased risk of cardiovascular events
Although the most common side effect of colchicine is gastrointestinal intolerance, colchicine can induce lactose intolerance, so a lactose free diet may help ameliorate colchicine-induced GI symptoms.
Anti-inflammatory therapeutics have shown promise in reducing cardiovascular risk but much more is to be learned with ongoing and future basic, translational, and clinical research.
Show notes - Treating Inflammation
What are the origins of the inflammatory hypothesis?
The first hypothesis as to the pathogenesis of atherosclerosis was the incrustation hypothesis by Carl Von Rokitansky in 1852. He suggested that atherosclerosis begins in the intima with thrombus deposition.In 1856, Rudolf Virchow suggested the lipid hypothesis whereby high levels of cholesterol in the blood lead to atherosclerosis. He observed inflammatory changes in the arterial walls associated with atherosclerotic plaque growth, called endo-arteritis chronica deformans.In 1977, Russell Ross suggested the response-to-injury hypothesis, that atherosclerosis develops from injury to the arterial wall.In the 1990’s the role of inflammation in ASCVD became more recognized. Both the adaptive and innate immune system are critical in atherosclerosis. Lipids and inflammation are synergistic in that lipid exposure is required but they translocate through damaged endothelium which occurs by way of inflammatory cytokines, namely within the NLRP3 inflammasome (IL-1, IL-6 etc.).Smooth muscle cells are also involved. They migrate to the endothelial region and secrete collagen to create the fibrous cap. They can also transform into macrophage-like cells to take up lipids and become foam cells.
T, B, and K cells are also part of this milieu. In fact, neutrophils, macrophages and monocytes make up only a small portion of the cells involved in the atherosclerotic process.
What are ways to individually optimize one’s ASCVD risk?Ensure the patient is on appropriate antiplatelet therapy, lipid lowering therapy, blood pressure is well controlled, and the Hemoglobin A1c is well controlled. Smoking cessation is pivotal.If the patient has an elevated Lipoprotein (a), pursue more aggressive lipid lowering therapy. Targeted therapies may become available in the future.
Assess the patient’s systemic inflammatory risk as measured by C-Reactive Protein (CRP)
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402. Guidelines: 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure – Question #39 with Dr. Robert Mentz
The following question refers to Sections 7.3.3 and 7.3.6 of the 2022 ACC/AHA/HFSA Guideline for the Management of Heart Failure.The question is asked by Palisades Medical Center medicine resident & CardioNerds Academy Fellow Dr. Maryam Barkhordarian, answered first by UTSW AHFT Cardiologist & CardioNerds FIT Ambassador Dr. Natalie Tapaskar, and then by expert faculty Dr. Robert Mentz.Dr. Mentz is associate professor of medicine and section chief for Heart Failure at Duke University, a clinical researcher at the Duke Clinical Research Institute, and editor-in-chief of the Journal of Cardiac Failure. Dr. Mentz has been a mentor for the CardioNerds Clinical Trials Network as lead principal investigator for PARAGLIDE-HF and is a series mentor for this very Decipher the Guidelines Series. For these reasons and many more, he was awarded the Master CardioNerd Award during ACC22.The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
American Heart Association’s Scientific Sessions 2024As heard in this episode, the American Heart Association’s Scientific Sessions 2024 is coming up November 16-18 in Chicago, Illinois at McCormick Place Convention Center. Come a day early for Pre-Sessions Symposia, Early Career content, QCOR programming and the International Symposium on November 15. It’s a special year you won’t want to miss for the premier event for advancements in cardiovascular science and medicine as AHA celebrates its 100th birthday. Registration is now open, secure your spot here!When registering, use code NERDS and if you’re among the first 20 to sign up, you’ll receive a free 1-year AHA Professional Membership!
Question #39
Ms. Kay Lotsa is a 48-year-old woman with a history of CKD stage 2 (baseline creatinine ~1.2 mg/dL) & type 2 diabetes mellitus. She has recently noticed progressively reduced exercise tolerance, leg swelling, and trouble lying flat. This prompted a hospital admission with a new diagnosis of decompensated heart failure. A transthoracic echocardiogram reveals LVEF of 35%. Ms. Lotsa is diuresed to euvolemia, and she is started on carvedilol 25mg BID, sacubitril/valsartan 49-51mg BID, and empagliflozin 10mg daily, which she tolerates well. Her eGFR is at her baseline of 55 mL/min/1.73 m2 and serum potassium concentration is 3.9 mEq/L. Your team is anticipating she will be discharged home in the next one to two days and wants to start spironolactone. Which of the following is most important regarding her treatment with mineralocorticoid antagonists?ASpironolactone is contraindicated based on her level of renal impairment and should not be startedBSerum potassium levels and kidney function should be assessed within 1-2 weeks of starting spironolactoneCEplerenone confers a higher risk of gynecomastia than does spironolactoneDThe patient will likely not benefit from initiation of spironolactone if her cardiomyopathy is ischemic in origin
Answer #39
ExplanationThe correct answer is B – after starting a mineralocorticoid receptor antagonist (MRA), it is important to closely monitor renal function and serum potassium levels.MRA (also known as aldosterone antagonists or anti-mineralocorticoids) show consistent improvements in all-cause mortality, HF hospitalizations, and SCD across a wide range of patients with HFrEF.
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401. Guidelines: 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure – Question #38 with Dr. Randall Starling
The following question refers to Sections 7.4 and 7.5 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.The question is asked by the Director of the CardioNerds Internship Dr. Akiva Rosenzveig, answered first by Vanderbilt AHFT cardiology fellow Dr. Jenna Skowronski, and then by expert faculty Dr. Randall Starling.Dr. Starling is Professor of Medicine and an advanced heart failure and transplant cardiologist at the Cleveland Clinic where he was formerly the Section Head of Heart Failure, Vice Chairman of Cardiovascular Medicine, and member of the Cleveland Clinic Board of Governors. Dr. Starling is also Past President of the Heart Failure Society of America in 2018-2019. Dr. Staring was among the earliest CardioNerds faculty guests and has since been a valuable source of mentorship and inspiration. Dr. Starling’s sponsorship and support was instrumental in the origins of the CardioNerds Clinical Trials Program.The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
American Heart Association’s Scientific Sessions 2024As heard in this episode, the American Heart Association’s Scientific Sessions 2024 is coming up November 16-18 in Chicago, Illinois at McCormick Place Convention Center. Come a day early for Pre-Sessions Symposia, Early Career content, QCOR programming and the International Symposium on November 15. It’s a special year you won’t want to miss for the premier event for advancements in cardiovascular science and medicine as AHA celebrates its 100th birthday. Registration is now open, secure your spot here!When registering, use code NERDS and if you’re among the first 20 to sign up, you’ll receive a free 1-year AHA Professional Membership!
Question #38
Mrs. M is a 65-year-old woman with non-ischemic dilated cardiomyopathy (LVEF 40%) and moderate to severe mitral regurgitation (MR) presenting for outpatient follow-up. Despite improvement overall, she continues to experience dyspnea on exertion with two flights of stairs and occasional PND. She reports adherence with her medication regimen of sacubitril-valsartan 97-103mg twice daily, metoprolol succinate 200mg daily, spironolactone 25mg daily, empagliflozin 10mg daily, and furosemide 80mg daily. A transthoracic echocardiogram today shows an LVEF of 35%, an LVESD of 60 mm, severe MR with a regurgitant fraction of 60%, and an estimated right ventricular systolic pressure of 40 mmHg. Her EKG shows normal sinus rhythm at 65 bpm and a QRS complex width of 100 ms. What is the most appropriate recommendation for management of her heart failure?AContinue maximally tolerated GDMT; no other changesBRefer for cardiac resynchronization therapy (CRT)CRefer for transcatheter mitral valve intervention
Answer #38
ExplanationChoice C is correct. The 2020 ACC/AHA Guidelines for the management of patients with valvular heart disease outline specific recommendations.In patients with chronic severe secondary MR related to LV systolic dysfunction (LVEF <50%) who have persistent symptoms (NYHA class II, III, or IV) while on optimal GDMT for HF (Stage D), M-TEER is reasonable in patients with appropriate anatomy as defined on TEE and with LVEF between 20% and 50%, LVESD ≤70 mm, and pulmonary artery systolic pressure ≤70 mmHg (Class 2a, LOE B-R).Conversely,
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400. Cardio-Rheumatology: Targeting Inflammation for Cardiovascular Risk Reduction with Dr. Paul Ridker
In this episode, Dr. Paul Ridker, a pioneer in the field of cardiovascular inflammation, joins the CardioNerds (Dr. Gurleen Kaur, Dr. Richard Ferraro, and Dr. Nidhi Patel) to discuss the evolving landscape of inflammation as a key factor in cardiovascular risk reduction. The discussion dives into the importance of biomarkers like high-sensitivity C-reactive protein (hs-CRP) in guiding treatment strategies, the insights gleaned from landmark trials like the JUPITER and CANTOS studies, and the future of targeted anti-inflammatory therapies in cardiology.
Show notes were drafted by Dr. Nidhi Patel. Audio editing by CardioNerds academy intern, Grace Qiu.
This episode was produced in collaboration with the American Society of Preventive Cardiology (ASPC) with independent medical education grant support from Lexicon Pharmaceuticals.
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Pearls - Targeting Inflammation for Cardiovascular Risk
"If you don’t measure it, you can’t treat it”: Incorporate hs-CRP into routine practice for patients at risk of cardiovascular events, as it provides crucial information for risk stratification and management.
Recognize the dual benefits of statins in lowering both LDL and inflammation, particularly in patients with elevated hs-CRP.
Encourage patients to adopt heart-healthy habits, as lifestyle changes remain foundational in reducing both cholesterol and inflammatory risk.
Reminder that most autoimmune or inflammatory diseases, from psoriasis to Addison’s disease to lupus to scleroderma to inflammatory bowel disease, have been shown to have elevated cardiovascular risk
Ongoing randomized trials including ZEUS, HERMES, and ARTEMIS will inform whether novel targeting of IL-6 can safely lower cardiovascular event rates or slow renal progression
Show notes - Targeting Inflammation for Cardiovascular Risk
Why is it important to measure both LDL and hs-CRP, and what factors increase hs-CRP?
Inflammation and hyperlipidemia are synergistic in promoting atherosclerosis. They interact to exacerbate plaque formation and instability, increasing the risk of cardiovascular events.
Just like we measure blood pressure and LDL to know what to treat, we should measure hs-CRP to guide targeted therapy.
Clinical Example: in Ms. Flame's case, despite achieving target LDL levels with statins, her elevated hs-CRP indicates ongoing inflammation and residual cardiovascular risk that should be assessed.
Residual inflammatory risk should be assessed in both primary and secondary prevention.
Increased BMI1, smoking2, a sedentary lifestyle3, and genetics4 (such as a higher risk of metabolic disease in South Asians) all raise hs-CRP levels.
SGLTi5 and GLP-1 agonists6 have also been shown to decrease hs-CRP levels.
What data do we have to support measuring hs-CRP?
Women’s Health Study7: an early study showing that hs-CRP predicted risk at least as well as LDL cholesterol and that models incorporating hs-CRP in addition to lipids were significantly better at predicting risk than models based on lipids alone.
JUPITER Trial8 (Primary Prevention): Among patients with normal LDL but elevated hs-CRP there was a 44% reduction in major cardiovascular events (>50% in MI and stroke) and a 20% reduction in all-cause mortality in patients treated with statins. These results led to changes in guidelines in recognizing the need to measure and treat inflammation.
CANTOS Trial9 (Secondary Prevention): Randomized >10K patients with previous MI and hs-CRP ≥ 2mg/L and found that canakinumab reduced hs-CRP level from baseline in a dose-dependent manner, without reduction in the LDL, ApoB, TG, or blood pressure.
What are the guidelines and supportive data on using Colchicine?
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