CardioNerds co-founder Dr. Amit Goyal and episode leads Dr. Jaya Kanduri (FIT Ambassador from Cornell University) and Dr. Jenna Skowronski (FIT Ambassador from UPMC) discuss Complications of acute myocardial infarction with expert faculty Dr. Jeffrey Geske. They discuss various complications of acute MI such as cardiogenic shock, bradyarrythmias, left ventricular outflow tract obstruction, ruptures (papillary muscle rupture, VSD, free wall rupture), and more. Show notes were drafted by Dr. Jaya Kanduri. Audio editing by CardioNerds Academy Intern, student doctor Tina Reddy.

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.

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Pearls and Quotes - Complications of Acute Myocardial Infarction

Sinus tachycardia is a “harbinger of doom”!

The triad for RV infarction includes hypotension, elevated JVP, and clear lungs. These patients are preload dependent and may need fluid resuscitation despite having an elevated JVP.

Bradyarrythmias in inferior MIs are frequently vagally mediated. The focus should be on medical management before committing to a temporary transvenous pacemaker, such as reperfusion, maintaining RV preload and inotropy, avoiding hypoxia, and considering RV-specific mechanical circulator support (MCS).

Worsening hypotension with inotropic agents (e.g., dobutamine, epinephrine, dopamine, norepinephrine) after a large anterior-apical MI should raise suspicion for dynamic left ventricular outflow tract obstruction due to compensatory hyperdynamic basal segments.

The myocardium after a late presentation MI is as “mushy as mashed potatoes”! Need to look out for papillary muscle rupture, VSD, and free wall rupture as potential complications. Papillary muscle rupture can occur with non-transmural infarcts, and often presents with flash pulmonary edema. VSDs will have a harsh systolic murmur and are less likely to present with pulmonary congestion. Free wall rupture can present as a PEA arrest. All of these complications require urgent confirmation on imaging and early involvement of surgical teams.

Notes - Complications of Acute Myocardial Infarction

How should we approach cardiogenic shock (CS) in acute myocardial infarction (AMI)?

Only 10% of AMI patients present with CS, but CS accounts for up to 70-80% of mortality associated with AMI, usually due to extensive LV infarction with ensuing pump failure.

Physical examSinus tachycardia is considered a “harbinger of doom”, when the body compensates for low cardiac output by ramping up the heart rateThe presence of sinus tachycardia and low pulse and/or blood pressure in a patient with a large anterior MI should raise suspicion for cardiogenic shockBe wary of giving IV beta blockers in this situation as negative inotropes can precipitate cardiogenic shock (Commit Trial)

When interpreting a patient’s blood pressure in the acute setting, it is helpful to know their baseline blood pressure and if they have a significant history of hypertension.

Patients <75 years of age with CS have improved survival at 6 months and at 1 year with early revascularization (SHOCK trial)

Mechanical circulatory supportIntra-aortic balloon pump (IABP)No mortality benefit with IABP use in CS at 30 days and at 1 year (IABP-SHOCK II trial)ACC/AHA guidelines give IABP a class IIa recommendation for medically refractory AMI-CS in the USA, whereas the ESC guidelines give it a class III recommendation.Percutaneous left ventricular assist device (Impella)No difference in mortality between IABP or Impella use after 30 days or 6 months (IMPRESS trial)However, observational data like the Detroit & VAD registries show improvement in survival with Impella use in AMI-CS with the cost of excess complications (vascular injury, bleeding, etc)Upcoming trials (DanGer Shock and Recover IV) will hopefully have more promising data supporting the use of Impella in AMI-CS

In the setting of discrepant guidelines, the decision for MCS should be multidisciplinary and based on clinical expertise.  

For more on AMI-CS, enjoy CardioNerds #223. CCC: Approach to Acute Myocardial Infarction Cardiogenic Shock with Dr. Venu Menon

How does RV infarction present?

Physical examRV infarct triad: hypotension, elevated JVP, clear lungsHypotension precipitated by nitroglycerin administration highlights the preload dependent state of an infarcted RVGI symptoms (nausea and emesis) are common

Patients may actually need fluids despite an elevated JVP because of an underfilled left ventricle

EKG

Consider a right sided leads (ST elevation in V1 and V4R are the most sensitive EKG markers of RV injury), but this should not delay emergent coronary angiography +/- PCI if suspicion for AMI is high

RhythmAV synchrony plays an important role in RV infarct given the dependence on preloadIf a patient loses AV synchrony due to heart block or atrial fibrillation, they can become more unstable due to a further drop in RV preload and overall cardiac outputHowever, bradyarrythmias in inferior MIs are frequently vagally mediated, and therefore temporary

Strategy for management of an inferior MI with RV infarct should be to optimize all other aspects hemodynamically before placing a temporary transvenous pacemaker (risk of RV perforation)Prompt reperfusionMaintain RV preloadInotropesAvoid hypoxia (potent pulmonary vasoconstriction, can increase RV afterload)

MCS providing RV support (Protek-Duo, RP Impella, VA-ECMO)

For more on RV-predominant cardiogenic shock, enjoy CardioNerds #239. CCC: Approach to RV Predominant Cardiogenic Shock with Dr. Ryan Tedford

How does LVOT obstruction in a large anterior MI present?

Hypotension with dobutamine or norepinephrine in a patient with an anterior MI and apical infarct, should raise suspicion for dynamic left ventricular outflow tract obstruction due to compensatory hyperdynamic basal walls

Echocardiography is invaluable for diagnosis!

ManagementPrompt reperfusionIV fluids (preload dependent)Beta blockers (eg: esmolol quick on, quick off)Phenylephrine (can improve BP by increasing afterload)Avoid positive inotropes (e.g., norepinephrine, epinephrine, dopamine, dobutamine, milrinone)

Avoid IABP

What are the different types of ruptures which may complicate a late-presentating MI?

Papillary muscle rupturePosteromedial papillary more likely to be affected due to single coronary blood supplyPapillary muscles are subendocardial so rupture can occur with non-transmural infarctsPresents with acute dyspnea from flash pulmonary edema and hypotension from drop in cardiac outputExam with new systolic murmur which may not be audible due to rapid equalization of pressures. For the same reason, Doppler may also underestimate the degree of MR.

V wave from mitral regurgitation

Ventricular septal ruptureRisk factors: advanced age, female sex, first MI with lack of coronary collateralsPresents with hypotension, chest discomfort, dyspneaExam with harsh systolic murmur with palpable thrill; pulmonary congestion is unusual unusualV wave from increased flow through the pulmonary circuit (but not high enough to cause flash pulmonary edema)Step up in RV saturation during right heart catheterizationInferobasal VSD with RCA infarcts (near the valves and conduction tissue and with more serpentine lesions, leading to worse outcomes)

Apical VSD with LAD infarcts (can miss on TTE)

Free wall ruptureRisk factors: advanced age, female sex, first MI with lack of coronary collateralsPartial rupture may present as a vagal event that heralds the initial tear; TTE with new pericardial effusion should raise suspicion of an incomplete ruptureFull rupture can present as PEA arrest with abysmally low survival

May partially heal as a pseudo-aneurysm

How do we manage rupture complications?

For any of the three rupture scenarios (VSR, papillary muscle rupture, or free wall rupture), time is of the essence to confirm the site of rupture and to get the surgical team involved

Can have abrupt, unexpected, unpredictable progression so need to bring in surgical expertise early

Papillary muscle rupture will need mitral valve replacement

For VSR closure, can pursue surgical versus percutaneous options depending on anatomical features of the lesion and patient characteristicsIntervention is more challenging in inferobasal VSRs with higher operative mortality, but also less amenable to percutaneous closure (less likely to have appropriate rims for closure)If poor operative candidacy, more likely to opt for percutaneous options

If size of defect large, would more likely lean towards surgery

Can consider bridging with MCS if patient in CS (eg: IABP, Impella) as long as this will not delay the surgical intervention

References

Early intravenous then oral metoprolol in 45 852 patients with acute myocardial infarction: Randomised placebo-controlled trial. The Lancet. 2005;366(9497):1622-1632. doi:10.1016/s0140-6736(05)67661-1. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(05)67661-1/fulltext

Dzavik V. Early revascularization is associated with improved survival in elderly patients with acute myocardial infarction complicated by cardiogenic shock: A report from the Shock Trial Registry. European Heart Journal. 2003;24(9):828-837. doi:10.1016/s0195-668x(02)00844-8. https://www.nejm.org/doi/full/10.1056/nejm199908263410901

Thiele H, Zeymer U, Neumann F-J, et al. Intraaortic balloon support for myocardial infarction with Cardiogenic shock. New England Journal of Medicine....

The following question refers to Figures 6-8 from Sections 3.2 of the 2021 ESC CV Prevention Guidelines. The question is asked by student Dr. Hirsh Elhence, answered first by Ohio State University Cardiology Fellow Dr. Alli Bigeh, and then by expert faculty Dr. Eugene Yang.Dr. Yang is Professor of Medicine at the University of Washington where he is also the Medical Director of the Eastside Specialty Center and the co-Director of the Cardiovascular Wellness and Prevention Program. Dr. Yang is former Governor of the ACC Washington Chapter and as well as former Chair of the ACC Prevention of CVD Section.  The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #31

The 2021 ESC CV Prevention guidelines recommend a stepwise approach to risk stratification and treatment options. What is the first step in risk factor treatment regardless of past medical history, risk factors, or established ASCVD?AInitiate statin for goal LDL <100 mg/dlBAssess family history of premature CVDCCounsel on ketogenic dietDStop smoking and lifestyle recommendations

Answer #31

ExplanationThe correct answer is D – stop smoking and lifestyle recommendations. Smoking cessation and lifestyle modifications are recommended for everyone across the spectrum of ASCVD risk including for both primary and secondary prevention (Class 1). It is worth noting that many patients can move themselves towards a lower risk category without taking drugs just by stopping smoking.Option A is incorrect. While initiating statin therapy for goal LDL <100 mg/dL may be an appropriate treatment option for some patients, it is not the first step per the “stepwise approach” recommended in the ESC guidelines. Whether or not to initiate a statin depends on a multitude of factors including estimated 10-year CVD risk, age, comorbidities, established ASCVD, and patient preference. The first step for patients with established ASCVD includes LDL-C reduction to goal <70 mg/dL (class I) with intensification to a goal LDL-C <55mg/dL based on residual 10-year CVD risk, lifetime CVD risk and treatment benefit, comorbidities, frailty, and patient preference.  Primary prevention of ASCVD first targets LDL-C goal <100 (class IIa) in appropriately selected patients.Option B is incorrect. While assessing family history of premature CVD should be part of an initial evaluation and certainly considered a risk enhancing factor, it is not a modifiable risk factor with regards to treatment.Option C is incorrect. A ketogenic diet is not endorsed nor recommended by ACC/AHA or ESC.Studies have shown the benefit of a stepwise approach to treatment intensification. Attainment of treatment goals is similar, side effects are fewer, and patient satisfaction is significantly greater with such an approach. It is not recommended to stop assessment of treatment goals after the first step.Main TakeawayA stepwise approach to treatment intensification is recommended. The first steps for all patients are to stop smoking and institute lifestyle recommendations.Guideline Loc.·       3.2.3 Figures 6-8

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The following question refers to Sections 6.1 and 7.3 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by Keck School of Medicine USC medical student & former CardioNerds Intern Hirsh Elhence, answered first by Greater Baltimore Medical Center medicine resident and CardioNerds Academy Fellow Dr. Alaa Diab, and then by expert faculty Dr. Mark Drazner.

Dr. Drazner is an advanced heart failure and transplant cardiologist, Professor of Medicine, and Clinical Chief of Cardiology at UT Southwestern. He is the past President of the Heart Failure Society of America.

 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.

Question #25

A 50-year-old man with a history of type 2 diabetes mellitus, persistent atrial fibrillation, coronary artery disease with prior remote percutaneous coronary intervention, and ischemic cardiomyopathy with HFrEF (LVEF 38%) presents to your outpatient clinic. He denies dyspnea on exertion, orthopnea, bendopnea, paroxysmal nocturnal dyspnea, or peripheral edema. His heart rate is irregularly irregular at 112 beats per minute and blood pressure is 112/67 mmHg. Routine laboratory studies reveal a hemoglobin A1c of 7.7%. Which of the following medications should not be used to control this patient’s comorbidities?

A

Metoprolol succinate

B

Verapamil

C

Dapagliflozin

D

Pioglitizone

E

Both B and D

Answer #25

Explanation

The correct answer is E – both verapamil and pioglitazone should be avoided here.

Both verapamil and pioglitizone are associated with harm in patients with LVEF < 50% (Class 3: Harm). Verapamil and diltiazem are non-dihydropyridine calcium channel blockers. These medications can cause negative inotropic effects through inhibition of calcium influx and may be harmful in this patient population. Pioglitizone belongs to a class of diabetic medications known as the thiazolidinediones. This class of medications may increase the risk of fluid retention, heart failure, and hospitalization in patients with LVEF of less than 50%.

Metoprolol succinate, and other evidence-based beta blockers, have a Class 1 recommendation for patients with reduced ejection fraction ≤ 40% to prevent symptomatic heart failure and reduce mortality. It may additionally help with rate control in this patient with atrial fibrillation and rapid ventricular response.

SGLT2 inhibitors including dapagliflozin have a Class I recommendation for patients with symptomatic chronic HFrEF to reduce hospitalization for HF and cardiovascular mortality, irrespective of the presence of type 2 diabetes (Class 1, LOE A). They also have a Class I recommendation in patients with type 2 diabetes and either established CVD or at high cardiovascular risk to prevent hospitalization for HF (Class 1, LOE A). Our patient has asymptomatic, or pre-HF (Stage B) heart failure with poorly controlled diabetes, and so use of an SGLT2 inhibitor would be appropriate.

Main Takeaway

Non-dihydropyridine calcium channel blockers and thiozolidinediones

both have Class 3 recommendations for harm in patients with reduced LV systolic dysfunction.

Guideline Loc.

Section 6.1 and 7.3

 

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Stroke is a potentially devastating TAVR complication. In this episode, CardioNerds (Drs. Amit Goyal, Nikolaos Spilias, Ahmed Ghoneem, and Chelsea Amo-Tweneboah) discuss TAVR and stroke risk, stroke prevention strategies, and future directions with Dr. Samir Kapadia, Department chair and chief, Cardiovascular Medicine at Cleveland Clinic. They also discuss device innovation and randomized controlled trial implementation for testing device safety and efficacy. Audio editing by CardioNerds Academy Intern, Dr. Chelsea Amo Tweneboah.

As an adjunct to this episode and for a deeper review of cerebral embolic protection devices, read “Cerebral Embolic Protection Devices: Current State of the Art” by Agrawal, Kapadia et al., in US Cardiology Review.

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References - TAVR and Stroke

Leon MB, Smith CR, Mack M, et al. Transcatheter Aortic-Valve Implantation for Aortic Stenosis in Patients Who Cannot Undergo Surgery. New England Journal of Medicine. 2010;363(17):1597-1607.

Kapadia SR, Makkar R, Leon M, et al. Cerebral Embolic Protection during Transcatheter Aortic-Valve Replacement. New England Journal of Medicine. 2022;387(14):1253-1263.

Kapadia SR, Kodali S, Makkar R, et al. Protection Against Cerebral Embolism During Transcatheter Aortic Valve Replacement. Journal of the American College of Cardiology. 2017;69(4):367-377.

Khan MZ, Zahid S, Khan MU, et al. Use and outcomes of cerebral embolic protection for transcatheter aortic valve replacement: A US nationwide study. Catheter Cardiovasc Interv. 2021;98(5):959-968.

CardioNerds cofounders Dr. Amit Goyal and Dr. Daniel Ambinder join Dr. Isabel Balachandran, Dr. Diego Celli from the Texas Heart Institute. They discuss the nuances of risk stratification management of intermediate risk pulmonary embolism. The ECPR for this episode was provided by Dr. Alam Mahboob (Associate Professor of Medicine at Baylor College of Medicine and the Department of Medicine and Associate Program Director for the Cardiovascular Disease Fellowship Program at Baylor). Audio editing by CardioNerds Academy Intern, Dr. Chelsea Amo Tweneboah.

US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here.

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Case Media - Caring for the Middle Child of Pulmonary Embolism – Texas Heart Institute

Pearls - Caring for the Middle Child of Pulmonary Embolism – Texas Heart Institute

Submassive pulmonary embolism is defined as an intermediate risk group of acute pulmonary embolism, which presents with signs of RV dysfunction and myocardial injury without hemodynamic instability.

The AHA, ACCP, and ESC have variable definitions of submassive PE. Non-invasive tools such as EKG, TTE, and CT are critical to defining RV dysfunction. The Pulmonary Embolism Severity Index (PESI) score is a validated tool to help risk stratify patients with PE.

Advanced therapies for submassive PE include systemic thrombolysis, catheter-based intervention, surgical embolectomy, and mechanical circulatory support. The decision between these therapies is based on individual patient risk profiles, local expertise, and the risk of major bleeding.

There is a spectrum of long-term complications after an acute PE, ranging from post PE syndrome to CTEPH (chronic thromboembolic pulmonary hypertension) caused by a maladaptive vascular remodeling from residual thrombus or arteriopathy. Thrombolytic therapies are still controversial in reducing the risk of post PE complications.

PERT is a multidisciplinary group of clinicians who can rapidly assess and triage patients with acute PE, coordinate access to medical and advanced therapies, and provide the necessary follow up care.

Show Notes - Caring for the Middle Child of Pulmonary Embolism – Texas Heart Institute

How do you define “submassive” pulmonary embolism?

Venous thromboembolism, which includes deep vein thrombosis and acute pulmonary emboli (PE) are the third most common cardiovascular disorder in the United States with approximately 900,000 cases occurring each year (1). The morbidity and mortality associated with pulmonary emboli are also great, with approximately 33% of PE cases being fatal (1).Until recently, PE was previously classified into massive or non-massive. Massive PE was defined as those with cardiogenic shock. A newer group, “submassive PE”, was defined as an “intermediate” risk group. According to the American Heart Association (AHA) Scientific Statement on the management of massive and submassive PE, patients in this group presented with signs of RV dysfunction and myocardial necrosis without hemodynamic instability (2).

Intermediate-risk PE covers a broad range of risk and management decisions remain challenging. Intermediate-risk PE convers increased risk for mortality and complications compared with low-risk PE. 

How do you risk-stratify intermediate-risk pulmonary emboli?

The AHA, American College of Chest Physicians (ACCP), and European Society of Cardiology (ESC) have variable definitions of submassive PE and which biomarkers should be used (1,3). The contents are summarized as below (Table 1)

Each major guideline highlights the importance of the evaluation of RV dysfunction (RVD) and elevated biomarkers. To summarize, the AHA defines submassive PE with either RVD or elevated biomarkers, specifically troponin levels (2). The ACCP similarly defines an intermediate risk PE with either RVD or elevated biomarkers, though with both elevated BNP/NT-proBNP or troponin levels (4). Finally, the ESC subdivides intermediate risk into intermediate-high and intermediate-low risk groups based on the PESI score and if there are elevated troponin levels (3).

As of 2019, the AHA published a consensus statement revising the nomenclature of PE. The terminology is now high risk, intermediate risk, and low risk (4).

 The AHA 2011 guidelines define RVD based on the following non-invasive tools (EKG, CT and transthoracic echocardiography) (2).By EKG, concerning changes include a new or incomplete right bundle branch block, anteroseptal ST elevation or depression, or anteroseptal T wave inversions. Other pertinent findings include sinus tachycardia (the most common abnormality), atrial arrhythmias, low voltages, right axis deviation, S1Q3T3, or Qr pattern in V1 (2).By CT, RV enlargement is defined as an RV to LV diameter ratio > 0.90 (2).By TTE, RV enlargement (RV to LV diameter ratio > 0.9), systolic dysfunction (TAPSE <17 mm or S’ <0.1 m/s) or hypokinesis (sometimes with the preservation of apical contractility- aka McConnell’s sign) (2). There can also be signs of pulmonary hypertension, which include flattening of the interventricular septum during systole or a tricuspid regurgitant velocity > 2.7 m /sec. Finally, there can also be direct visualization of thrombus within the right sided chambers (5).

The PESI or Pulmonary Embolism Severity Index is a validated tool using markers such as age, sex, vital signs, presence of hypoxemia, altered mental status, and comorbidities (such as cancer, heart failure, and chronic lung disease) to risk stratify patients with PE. A high PESI score is suggestive of an elevated 30-day mortality (6).

What is the general approach to therapeutic interventions and treatment for submassive PE?

With confirmed PE and no contraindications to systemic anticoagulation prompt use of low molecular weight heparin (LMWH), unfractionated heparin, or fondaparinux should be used. For those confirmed with heparin induced thrombocytopenia, a non-heparin based anticoagulant (such as argatroban or bivalirudin) should be used (2). In regards to direct oral anticoagulation (DOAC), in large studies (including the EINSTEIN and AMPLIFY trials), patients with submassive PE predominantly received LMWH prior to DOAC initiation. It is uncertain whether direct initiation of DOAC is comparable in outcomes (1).

Treatment with systemic anticoagulation alone in normotensive patients with RV dysfunction, is controversial and the use of more aggressive therapies has been studied extensively. Advanced therapies for submassive PE include systemic thrombolysis, catheter-based interventions, surgical embolectomy, and mechanical circulatory support. The decision between these therapies is based on individual patient risk as well as the risk of major bleeding, best guided by pulmonary embolism response teams (PERT) (7).

Finally, surgical embolectomy is considered in those with submassive and massive PE in whom fibrinolytic therapy has failed or is contraindicated. Other indications include paradoxical emboli, clot in transit, or hemodynamic collapse. In large, high-volume centers, this has been found to be a safe and effective approach (1).

Hemodynamic support is important to consider for management of RV failure. If a limited intravenous fluid trial fails, early vasopressor and inotropic support should be initiated. ECMO is indicated for hemodynamic and ventilatory support in patients with severe RV failure and refractory cardiogenic shock (7).

When do you consider systemic thrombolysis or catheter directed therapies for patients with intermediate-risk PE?

Systemic thrombolysis works by rapidly acting on acute thrombus, thereby reducing pulmonary pressures and RV dysfunction, along with improving hemodynamics. This has been shown to be superior to anticoagulation alone in massive PE with reductions in mortality at the cost of increased major bleeding (1,2). The PEITHO trial was the largest randomized control trial of systemic thrombolysis in PE. Thrombolytic treatment with Tenecteplase reduced a composite outcome of all-cause mortality at 7 days and hemodynamic decompensation versus anticoagulation with heparin alone. This, however, came at the expense of an increased risk of major bleeding (including intracranial hemorrhage) (8). Given this concern, the MOPPET-3 trial in 2013 evaluated the effect of low dose thrombolysis on outcomes in patients with submassive PE. It was found that low dose tPA reduced the incidence of pulmonary hypertension. However, tPA did not reduce the rates of a combined outcome of recurrent PE or all-cause mortality (9).

Catheter-based therapy, including pharmacomechanical therapy, catheter-directed thrombolysis, and mechanical embolectomy, is a widely studied approach for treating pulmonary embolism (PE) (10). In 2013, the ULTIMA trial compared CDT plus anticoagulation versus anticoagulation alone in intermediate-high risk PE and found that CDT resulted in a statistically significant improvement in the right ventricular/left ventricular (RV/LV) ratio at 24 hours. At 90 days, there was no difference in mortality or major bleeding events between the two groups (11). A recent meta-analysis compared CDT to systemic anticoagulation (sAC) alone and showed lower rates of in-hospital, 30-day, and 90-day mortality, with no differences in major or minor bleeding or blood transfusions (10).

The most widely studied technique is ultrasound-facilitated catheter-directed fibrinolysis (EKOS), which combines local fibrinolysis with mechanical thrombectomy. The SEATTLE II trial found a reduction in mean RV/LV ratio and mean pulmonary artery systolic pressure at 48 hours post-thrombolysis....

CardioNerds cofounder Dr. Daniel Ambinder, series co-chair Dr. Dinu Balanescu (FIT, Mayo Clinic), and episode lead Dr. Anjali Rao (FIT, UTSW) discuss training in cardio-oncology with Dr. Stephanie Feldman from Rutgers University. In this episode, the group discusses some of the most burning questions about educating the next wave of cardio-oncologists. As Dr. Feldman mentions, the projected number of cancer survivors is predicted to be around 24 million by 2024, underscoring the growing importance of cardio-oncology in our practice. We highlight some of the challenges facing trainees and training programs alike, including how to integrate cardio-oncology education into general cardiology training, the optimal structure for an advanced cardio-oncology fellowship, and the role of cardio-oncology in the inpatient setting. We also talk about the takeaways from the ACC Cardio-Oncology Leadership Council document. Dr. Feldman reflects on the importance of flexibility in education in the current landscape, drawing on her personal experience as a cardio-oncologist during the COVID-19 era. Notes were drafted by Dr. Anjali Rao. Audio editing was performed by student doctor, Shivani Reddy.

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. 

Pearls • Notes • References • Production Team

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Pearls and Quotes - Cardio-Oncology: Training and Future Directions

It may be possible to achieve “COCATS level 2” cardio-oncology training during general cardiology fellowship. A dedicated cardio-oncology year may appeal to trainees who want to achieve “COCATS level 3”, i.e., dedicate their practice to caring for patients with complex cardio-oncology needs, become involved in clinical trials, and lead cardio-oncology clinical and training programs.

Supplemental learning opportunities for general fellows can include:

Rotating in a cardio-oncology clinic, ideally attached to a National Cancer Institute-designated cancer center

Multi-modality cardiac imaging

Participating in cardio-oncology research

Some currently available educational opportunities include:The International Cardio-Oncology Society (ICOS) weekly webinarsThe American Society of Echocardiography (ASE) webinars on global longitudinal strainThe American Society of Nuclear Cardiology lecture series on cardiac amyloidosis

Cardio-oncology focused conferences, such as the American College of Cardiology’s (ACC) Advancing the Cardiovascular Care of the Oncology Patient and Memorial Sloan Kettering’s Cardio-Oncology Symposium.

Each institution may have different inpatient cardio-oncology needs depending on whether there is a stand-alone cancer hospital or another format. Examples of inpatient consults that may benefit from having a cardio-oncologist involved include:Cardiovascular risk assessment prior to bone marrow transplant or cancer related surgery in a patient with known coronary artery diseaseImmune checkpoint inhibitor myocarditisChemotherapy-related cardiac dysfunction

Management of systemic anticoagulation in a patient with high CHA2DS2-VASc and chemotherapy related thrombocytopenia.

Show notes - Cardio-Oncology: Training and Future Directions

The need for cardio-oncology experience is undeniable given the growing population of patients with cancer and cardiovascular disease, particularly given the number of anti-neoplastic therapies with potential cardiovascular side effects. There are several strategies for incorporating cardio-oncology experiences into general cardiology training. These may include rotating through a cardio-oncology clinic, enhanced exposure to multimodality cardiac imaging including global longitudinal strain and participating in cardio-oncology research.

The need for dedicated formal training in cardio-oncology is more nuanced. If the goals of a formal fellowship align with a trainee’s career goals, an additional year of training can provide advanced exposure to complex medical decision-making, cardio-oncology specific imaging training (i.e., global longitudinal strain, MRI, PET), and even inpatient cardio-oncology experience at several centers. Prospective cardio-oncology trainees should gain clinical exposure during general cardiology fellowship and research exposure where available, and these experiences can factor into their decision to pursue a cardio-oncology fellowship.

Additional resources from national societies (e.g., ICOS, ACC, ASE) for cardio-oncology education can be made available to general cardiology trainees to expand their knowledge base. In some institutions, inpatient cardio-oncology consults may be appropriate. As a general rule, consultations regarding chemo- or immunotherapy-related cardiotoxicities or pre-stem cell transplant risk stratification may benefit from involvement of cardio-oncology in some form.

The future of cardio-oncology is bright, especially with the development of programs to train the next generation of cardio-oncologists!

References - Cardio-Oncology: Training and Future Directions

Tuzovic M, Brown SA, Yang EH, et al. Implementation of Cardio-Oncology Training for Cardiology Fellows. JACC CardioOncol. 2020;2(5):795-799. Published 2020 Dec 15. · CardioOncology Education and Training.

Alvarez-Cardona JA, Ray J, Carver J, et al. Cardio-Oncology Education and Training: JACC Council Perspectives. J Am Coll Cardiol. 2020;76(19):2267-2281.

Cardio-oncology Training in the COVID-19 Era. Feldman S, Liu J, Steingart R, Gupta D. Cardio-oncology Training in the COVID-19 Era. Curr Treat Options Oncol. 2021;22(7):58. Published 2021 Jun 7.

The following question refers to Section 6.1 of the 2021 ESC CV Prevention Guidelines. The question is asked by MGH internal medicine resident Dr. Christian Faaborg-Andersen, answered first by UCSD early career preventive cardiologist Dr. Harpreet Bhatia, and then by expert faculty Dr. Eugenia Gianos.

Dr. Gianos specializes in preventive cardiology, lipidology, cardiovascular imaging, and women’s heart disease; she is the Director of Women’s Heart Health at Lenox Hill Hospital and Director of Cardiovascular Prevention for Northwell Health.

The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #30

A 65-year-old woman with a history of hypertension, type 2 diabetes mellitus, and coronary artery disease with remote PCI to the RCA presents for follow-up. She has stable angina symptoms that are well controlled with metoprolol tartrate 25 mg BID and are not lifestyle limiting. She takes aspirin 81 mg daily and atorvastatin 40 mg daily. Her LDL-C is 70 mg/dL, hemoglobin A1c is 7.0%, and eGFR is >60. In clinic, her BP is 118/80 mmHg. What is the next step in management?AIncrease atorvastatin for goal LDL-C < 55 mg/dLBNo change in managementCAdd isosorbide mononitrate 30 mg dailyDStop aspirinEStart a sulfonylurea

Answer #30

Explanation The correct answer is A – increase atorvastatin for goal LDL-C < 55 mg/dL.In patients with established ASCVD, the ESC guidelines advocate for an LDL goal of < 55 mg/dL with at least a 50% reduction from baseline levels (Class I, LOE A). This patient has stable angina which is not lifestyle limiting; as such, further anti-anginal therapy is not necessary. She has known CAD with prior PCI, so aspirin therapy is appropriate for secondary prevention (Class I, LOE A). There is no indication for a sulfonylurea as her diabetes is well controlled. Notably, in persons with type 2 DM and ASCVD, the use of a GLP-1RA or SGLT2 inhibitor with proven outcome benefits is recommended to reduce CV and/or cardiorenal outcomes (Class I, LOE A).Main TakeawayFor people with established ASCVD, the ESC-recommended LDL-C goal is < 55 mg/dL with a goal reduction of at least 50%.Guideline Loc.Section 6.1

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The following question refers to Sections 10.2 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by Western Michigan University medical student and CardioNerds Intern Shivani Reddy, answered first by Mayo Clinic Cardiology Fellow and CardioNerds Academy House Faculty Leader Dr. Dinu Balanescu, and then by expert faculty Dr. Ileana Pina.

Dr. Pina is Professor of Medicine and Quality Officer for the Cardiovascular Line at Thomas Jefferson University, Clinical Professor at Central Michigan University, and Adjunct Professor of Biostats and Epidemiology at Case Western University. She serves as Senior Fellow and Medical Officer at the Food and Drug Administration’s Center for Devices and Radiological Health.

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.

Question #24

Mr. E. Regular is a 61-year-old man with a history of HFrEF due to non-ischemic cardiomyopathy (latest LVEF 40% after >3 months of optimized GDMT) and persistent atrial fibrillation. He has no other medical history. He has been on metoprolol and apixaban and has also undergone multiple electrical cardioversions and catheter ablations for atrial fibrillation but remains symptomatic with poorly controlled rates. His blood pressure is 105/65 mm Hg. HbA1c is 5.4%. Which of the following is a reasonable next step in the management of his atrial fibrillation?

A

Anti-arrhythmic drug therapy with amiodarone. Stop apixaban.

B

Repeat catheter ablation for atrial fibrillation. Stop apixaban.

C

AV nodal ablation and RV pacing. Shared decision-making regarding anticoagulation.

D

AV nodal ablation and CRT device. Shared decision-making regarding anticoagulation.

Answer #24

Explanation

The correct answer is D – AV nodal ablation and CRT device along with shared decision-making regarding anticoagulation.”

Maintaining sinus rhythm and atrial-ventricular synchrony is helpful in patients with heart failure given the hemodynamic benefits of atrial systole for diastolic filling and having a regularized rhythm.

Recent randomized controlled trials suggest that catheter-based rhythm control strategies are superior to rate control and chemical rhythm control strategies with regards to outcomes in atrial fibrillation. For patients with heart failure and symptoms caused by atrial fibrillation, ablation is reasonable to improve symptoms and quality of life (Class 2a, LOE B-R). However, Mr. Regular has already had multiple failed attempts at ablations (option B).

For patients with AF and LVEF ≤50%, if a rhythm control strategy fails or is not desired,

and ventricular rates remain rapid despite medical therapy, atrioventricular nodal ablation with implantation of a CRT device is reasonable (Class 2a, LOE B-R). The PAVE and BLOCK-HF trials suggested improved outcomes with CRT devices in these patients.

RV pacing following AV nodal ablation has also been shown to improve outcomes in patients with atrial fibrillation refractory to other rhythm control strategies. In patients with EF >50%, there is no evidence to suggest that CRT is more beneficial compared to RV-only pacing. However, RV pacing may produce ventricular dyssynchrony and when compared to CRT in those with reduced EF (≤ 50%), CRT produced more benefit (Option C).

Although adjustments in antiarrhythmic medications and repeat ablation may be considered, these are unlikely to provide long-term benefit to Mr. E. Regular, who already failed antiarrhythmic regimens and multiple attempts at cardioversion and ablation (Options A, B).

In patients with chronic heart failure and atrial fibrillation, the decision to use anticoagulation for the prevention of cerebrovascular events is generally based on the CHA2DS2-VASc score. Mr. Regular’s CHA2DS2-VASc score is 1 (+1 for HF, no points for: hypertension, age 65-74 or ≥75, diabetes, stroke/TIA/TE, vascular disease, female gender). Chronic anticoagulation therapy is recommended for patients with CHA2DS2-VASc scores ≥2 for men and ≥3 for women (Class 1, LOE A). Therefore, based on the CHA2DS2-VASc score alone, Mr. Regular would not necessarily warrant anticoagulation. However, HF is a hypercoagulable state and serves as an independent risk factor for stroke, systemic embolism, and mortality in the setting of AF. In patients

with HF and a CHA2DS2-VASc score of 1, those with AF had a 3-fold higher risk compared with individuals without concomitant AF. Because HF is a risk factor, additional risk factors may not be required to support the use of anticoagulation in patients with HF, and the decision to anticoagulate can be individualized according to risk versus benefit. The guidelines give a Class 2a recommendation for chronic anticoagulation in men and women with chronic HF and permanent-persistent-paroxysmal AF who have no additional risk factors (LOE B-NR). Therefore, decisions regarding anticoagulation in this context should incorporate patient values, comorbidities, and informed shared decision making.  

Main Takeaway

In summary, the “ablate and pace” strategy of AV nodal ablation and CRT device implantation improve outcomes in patients with heart failure with reduced LVEF and atrial fibrillation refractory to chemical and catheter-based rhythm control strategies and failure of rate control options.

Guideline Loc.

Section 10.2

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In this episode, CardioNerds co-founder Amit Goyal joins Dr. Iva Minga, Dr. Kevin Lee, and Dr. Juan Pablo Salazar Adum from the University of Chicago - Northshore in Evanston, IL to discuss a case of primary cardiac diffuse large B-cell lymphoma. The ECPR for this episode is provided by Dr. Amit Pursnani (Advanced Cardiac Imaging, Fellowship program director, NorthShore University HealthSystem). Audio editing by CardioNerds Academy Intern, Dr. Akiva Rosenzveig.

Case synopsis: A 77-year-old man with no significant medical history presents to the emergency department with progressive shortness of breath for 1 week. He reports an unintentional 15-pound weight loss in the prior month as well as constipation and abdominal/flank pain. On examination he was found to be tachycardic with a regular rhythm and further evaluation with a chest X-ray and chest CT scan demonstrated a large pericardial effusion. This was further investigated with an urgent echocardiogram that revealed a large pericardial effusion with a large mass attached to the pericardial side of the RV free wall, as well as signs of early cardiac tamponade. A pericardiocentesis was performed and 550mL of bloody fluid was withdrawn. The fluid was sent for laboratory analysis and cytology. A cardiac MRI demonstrated a large invasive mass in the pericardium and RV wall consistent with cardiac lymphoma. Cytology confirmed diffuse large B-cell lymphoma. Subsequent CT and PET scans did not find any other site of malignancy, giving the patient a diagnosis of primary cardiac diffuse large B-cell lymphoma. The patient underwent R-CHOP chemotherapy and was followed closely with repeat cardiac MRI and PET scans which demonstrated resolution of the cardiac mass at his one-year surveillance follow-up.

This case was published in US Cardiology Review, the official journal of CardioNerds. To learn more, access the case report article here.

CardioNerds is collaborating with Radcliffe Cardiology and US Cardiology Review journal (USC) for a ‘call for cases’, with the intention to co-publish high impact cardiovascular case reports, subject to double-blind peer review. Case Reports that are accepted in USC journal and published as the version of record (VOR), will also be indexed in Scopus and the Directory of Open Access Journals (DOAJ).

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Pearls - A Mystery Mass in the Heart - Cardiac Lymphoma

The most common cause of malignant cardiac masses is metastasis.

Primary cardiac tumors are rare.

Cardiac tumors are separated into 2 categories: benign and malignant. They are often differentiated based on their location and their degree of tissue invasion.

Multimodality imaging is essential in the diagnosis, management, and surveillance of cardiac masses.

A multidisciplinary team approach is invaluable for management of patients with cardiac tumors.

Show Notes - A Mystery Mass in the Heart - Cardiac Lymphoma

1. What is the clinical presentation of cardiac masses?

Cardiac masses can have a variable presentation. They can present with arrhythmias, angina, heart failure symptoms, or pericardial effusion. Patients can also be asymptomatic; the masses can be found incidentally on cardiac or chest imagining.

2. What is the differential diagnosis for cardiac masses?

Cardiac masses are separated into benign and malignant. The most common malignant cardiac masses are metastases from a distant source. The location of the mass is important in narrowing the differential.

3. What imaging modalities are used to diagnose cardiac masses?

Multimodality imaging is needed to describe the mass in detail and guide diagnosis. An echocardiogram is usually the first imaging modality. Cardiac MRI is a great modality that allows for the detailed visualization as well as tissue characterization of the mass. Cardiac CT, chest CT, and PET scans are also imagining modalities that can be used in the management of the mass.

4. How do you manage cardiac masses?

Management of cardiac masses depends on etiology (benign or malignant) and the associated hemodynamic changes associated with it. For example, if a benign cardiac mass is associated with significant valvular regurgitation, cardiac surgery needs to be considered for management. A multidisciplinary team including cardiology, heart failure, critical care cardiology, cardio-oncology, oncology, cardiac surgery, and other specialties may be involved in the management of cardiac masses and their manifestations.

References - A Mystery Mass in the Heart - Cardiac Lymphoma

1. Alerhand, S., & Carter, J. (2019). What echocardiographic findings suggest a pericardial effusion is causing tamponade? American Journal of Emergency Medicine, 37(2), 321-326.

2. McAllister, H. A., & Fenoglio, J. J. (1978). Tumors of the Cardiovascular System. Atlas of Tumor Pathology, Series 2. Armed Forces Institute of Pathology, Washington DC, 2, 20.

3. Tyebally, S., Chen, D., Bhattacharyya, S., Mughrabi, A., Hussain, Z., Manisty, C., Westwood, M., Ghosh, A. K., & Guha, A. (2020). Cardiac Tumors: JACC CardioOncology State-of-the-Art Review. JACC. CardioOncology, 2(2), 293-311.

4. Motwani, M., Kidambi, A., Herzog, B. A., Uddin, A., Greenwood, J. P., & Plein, S. (2013). MR imaging of cardiac tumors and masses: a review of methods and clinical applications. Radiology, 268(1), 26-43.

5. Spodick, D. H. (2003). Acute cardiac tamponade. New England Journal of Medicine, 349(7), 684-690.

In this episode, Dr. Gurleen Kaur (medicine resident at Brigham and Women’s Hospital and Director of CardioNerds Internship) and CardioNerds Academy interns Dr. Akiva Rosenzveig (medicine intern at Cleveland Clinic), Dr. Chelsea Tweneboah (medicine intern at Stonybrook University), student doctor Shivani Reddy (medical student at Western Michigan University), student doctor Diane Masket (medical student at Rowan School of Osteopathic Medicine), and student doctor Tina Reddy (medical student at Tulane University School of Medicine) discuss with Dr. Michelle Kittleson (Director of Education in Heart Failure and Transplantation, Director of HF Research, and Professor of Medicine at Cedars Sinai) about Mastering the Art of Patient Care. Dr. Kittleson shares pearls of wisdom from her book on topics including career transitions, mentorship, dealing with uncertainty, learning from mistakes, delivering difficult news, and being a woman and parent in medicine.  

This episode was planned by Dr. Gurleen Kaur and episode audio was edited by student doctor Tina Reddy.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

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