Cardionerds: A Cardiology Podcast

The following question refers to Section 4.3 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Texas Tech University medical student and CardioNerds Academy Intern Dr. Adriana Mares, answered first by Rochester General Hospital cardiology fellow and Director of CardioNerds Journal Club Dr. Devesh Rai, and then by expert faculty Dr. Eldrin Lewis. Dr. Lewis is an Advanced Heart Failure and Transplant Cardiologist, Professor of Medicine and Chief of the Division of Cardiovascular Medicine at Stanford University.  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 #26 A 45-year-old man presents to cardiology clinic to establish care. He has had several months of progressive dyspnea on exertion while playing basketball. He also reports intermittent palpitations for the last month. Two weeks ago, he passed out while playing and attributed this to exertion and dehydration. He denies smoking and alcohol intake.   Family history is significant for sudden cardiac death in his father at the age of 50 years. Autopsy has shown a thick heart, but he is unaware of the exact diagnosis. He has two children, ages 12 and 15 years old, who are healthy.   Vitals signs are blood pressure of 124/84 mmHg, heart rate of 70 bpm, and normal respiratory rate. On auscultation, a systolic murmur is present at the left lower sternal border. A 12-lead ECG showed normal sinus rhythm with signs of LVH and associated repolarization abnormalities. Echocardiography reveals normal LV chamber volume, preserved LVEF, asymmetric septal hypertrophy with wall thickness up to 16mm, systolic anterior motion of the anterior mitral valve leaflet with 2+ eccentric posteriorly directed MR, and resting LVOT gradient of 30mmHg which increases to 60mmHg on Valsalva.   You discuss your concern for an inherited cardiomyopathy, namely hypertrophic cardiomyopathy. In addition to medical management of his symptoms and referral to electrophysiology for ICD evaluation, which of the following is appropriate at this time? A  Order blood work for genetic testing B  Referral for genetic counseling C  Cardiac MRI D  Coronary angiogram E  All of the above Answer #26 Explanation   The correct answer is B – referral for genetic counseling.  Several factors on clinical evaluation may indicate a possible underlying genetic cardiomyopathy. Clues may be found in: ·       Cardiac morphology – marked LV hypertrophy, LV noncompaction, RV thinning or fatty replacement on imaging or biopsy ·       12-lead ECG – abnormal high or low voltage or conduction, and repolarization, altered RV forces ·       Presence of arrhythmias – frequent NSVT or very frequent PVCs, sustained VT or VF, early onset AF, early onset conduction disease ·       Extracardiac features – skeletal myopathy, neuropathy, cutaneous stigmata, and other possible manifestations of specific syndromes In select patients with nonischemic cardiomyopathy, referral for genetic counseling and testing is reasonable to identify conditions that could guide treatment for patients and family members (Class 2a, LOE B-NR). In first-degree relatives of selected patients with genetic or inherited cardiomyopathies, genetic screening and counseling are recommended to detect cardiac disease and prompt consideration of treatments to decrease HF progression and sudden death (Class 1, LOE B-NR). No controlled studies have shown clinical benefits of genetic testing for cardiomyopathy, but genetic testing contributes to risk stratification and has implications for treatment, currently most often for decisions regarding defibrillators for primary prevention of sudden death and regarding exercise limitation for hypertrophic cardiomyopathy and the desmosomal variants. Consultation with a trained counselor before and after genetic testing helps patients to understand and weigh the implications of possible results for their own lives and those of family members, including possible discrimination on the basis of genetic information. Unless shown to be free of the genetic variant(s) implicated in the proband, first-degree relatives of affected probands should undergo periodic screening with echocardiography and electrocardiography. In this patient with likely hypertrophic cardiomyopathy, a family history of sudden cardiac death, recent unexplained syncope, and two children, a referral for genetic counseling is appropriate at this time. However, option A is incorrect because ordering genetic testing without meeting a trained counselor is not advised.  Main Takeaway  Patients with the possibility of genetic cardiomyopathies should be referred to trained genetic counselors before and after genetic testing to understand the implications of the testing and results. Guideline Loc.  Section 4.3, Table 7 Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

CardioNerds co-founder Dr. Dan Ambinder joins Dr. Abdelrhman Abumoawad, Dr. Leili Behrooz from the Boston University Vascular Medicine over hot chocolate in Boston. They discuss two interesting cases of lower extremity edema caused by May-Thurner syndrome. Dr. Naomi Hamburg (Professor of Vascular Medicine and Cards at BU/BMC) provides the ECPR for this episode. Audio editing by CardioNerds Academy Intern, Dr. Akiva Rosenzveig. “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 PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Synopses – May-Thurner syndrome Case 1: A 34-year-old woman with HIV on HAART presenting with left leg swelling and non-healing new foot ulcer for 3 months. She works as a cashier. On exam, her BMI is 35 kg/m2 and there are intact pulses bilaterally. Her left leg has varicose veins in the territory of the great saphenous vein, hyperpigmentation, edema, and a foot ulcer. Her right leg appears normal. Venous Duplex ultrasonography showed chronic partially occlusive thrombus in the left common femoral and profunda femoral veins and decreased doppler respiratory variation on the left side. She was treated with debridement and compression therapy for ulcer healing. She was referred to vascular surgery and underwent contrast venography that demonstrated collateral circulation from the left lower extremity (LE) to the right lower extremity, and stenotic lesion at the left common iliac vein (LCIV). She was diagnosed with May-Thurner syndrome, and a venous stent was placed, and the patient was started on aspirin 81 mg daily for 6 months. Case 2: A 71-year-old man presented with left lower extremity pain and edema. He underwent a left lower extremity venous Duplex ultrasound that showed chronic thrombus in the left proximal to distal femoral vein and acute thrombus in the left popliteal vein and was started on anticoagulation (AC). The patient was also having palpitations and was found to have paroxysmal atrial fibrillation. He underwent pulmonary vein isolation during which it was noted that his LCIV was subtotally occluded. He underwent CT venogram which showed lumbosacral osteophytic compression of the LCIV known as bony May-Thurner syndrome. Given minimal symptoms, the decision was made not to pursue interventional options and to manage conservatively with AC which the patient needs regardless. Case Media – May-Thurner syndrome Pearls – May-Thurner syndrome An often under-recognized, but treatable cause of DVT is left common iliac vein compression known as May-Thurner syndrome. Most patients who have May-Thurner anatomy are asymptomatic. Only a minority of patients with the May-Thurner anatomy present with symptoms such as left leg edema/pain and DVT. Young women are at a higher risk of developing May-Thurner syndrome compared to men.  A high degree of suspicion is needed to investigate patients with unilateral left-sided leg symptoms and venous duplex features of May-Thurner syndrome. The diagnosis is made with non-invasive imaging including venous duplex, CT/MR venography, intravascular Ultrasound (IVUS), and catheter-based venography. Although IVUS is the gold standard for diagnosis, due to its invasive nature, it has been replaced by CT/MR imaging. Treatment includes anticoagulation if a thrombus is present. Most patients receive venous stenting at the obstructed site to prevent compression of the left common iliac vein. Some patients need catheter-directed thrombolysis prior to stent placement. Show Notes -May-Thurner syndrome What is May-Thurner syndrome? Classic May-Thurner syndrome is venous outflow obstruction due to external compression of the left common iliac vein by the right common iliac artery causing venous stasis which can lead to DVT. It is more common in women of reproductive age. Osteophytic/bony variant of May-Thurner Syndrome is when a prominent vertebral osteophyte compresses the iliac vein which is more common in older patients. For another fascinating case of May-Thurner Syndrome, presenting with CTEPH, enjoy CardioNerds episode 53. Case Report: CTEPH & May Thurner Syndrome – Temple University. What is the presentation of May-Thurner Syndrome and what are the risk factors? May-Thurner syndrome is often asymptomatic but may present with pain and swelling of the left leg with or without the presence of DVT. Some patients will develop signs of venous insufficiency such as varicose veins, pigmentations, and venous ulcers. Risk factors include scoliosis, female sex, use of oral contraceptives, and pregnancy. As demonstrated in CardioNerds episode #53, chronic thrombo-embolic pulmonary hypertension may be a long-term sequela. How do we diagnose May-Thurner Syndrome? Features suggestive of proximal obstruction in the venous Duplex for the initial assessment of DVT or venous insufficiency raise suspicion for May-Thurner syndrome. These features include loss of respiratory variation of the venous blood flow. IVUS is the gold standard to diagnose May-Thurner Syndrome and can also provide information regarding the chronicity of the thrombus, which could help decide management (for example, whether to perform thrombolysis of acute clot burden). CT/MR venography may have high sensitivity and specificity to detect iliac vein compression nearing 95%. It is also useful in ruling out other causes of iliac vein compression such as osteophyte compression of the iliac vein. How do you treat May-Thurner Syndrome? Management mainly focuses on addressing the patient’s symptoms. For patients with moderate to severe symptoms and significant venous stenosis, endovenous stenting is used rather than conservative management. There are a paucity of data to clarify the optimal antithrombotic regimen following venous stent placement. Practrice patterns varry significantly in terms of antiplatelet/anticoagulant choice and the duration of treatment. The presenct of complications such as DVT, venous stasis ulcer, etc should be managed as usual. References Mangla A, Hamad H. May-Thurner Syndrome. In: StatPearls. Treasure Island (FL): StatPearls Publishing; November 30, 2022. https://www.ncbi.nlm.nih.gov/books/NBK554377/ Kaltenmeier CT, Erben Y, Indes J, et al. Systematic review of May-Thurner syndrome with emphasis on gender differences. J Vasc Surg Venous Lymphat Disord. 2018;6(3):399-407.e4. doi:10.1016/j.jvsv.2017.11.006    https://pubmed.ncbi.nlm.nih.gov/29290600/ Poyyamoli S, Mehta P, Cherian M, et al. May-Thurner syndrome. Cardiovasc Diagn Ther. 2021;11(5):1104-1111. doi:10.21037/cdt.2020.03.07 https://pubmed.ncbi.nlm.nih.gov/34815961/ Knuttinen MG, Naidu S, Oklu R, et al. May-Thurner: diagnosis and endovascular management. Cardiovasc Diagn Ther. 2017;7(Suppl 3):S159-S164. doi:10.21037/CDT.2017.10.14 https://cdt.amegroups.com/article/view/17529/18075

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. 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 SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! 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 exam Sinus tachycardia is considered a “harbinger of doom”, when the body compensates for low cardiac output by ramping up the heart rate The presence of sinus tachycardia and low pulse and/or blood pressure in a patient with a large anterior MI should raise suspicion for cardiogenic shock Be 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 support Intra-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 exam RV infarct triad: hypotension, elevated JVP, clear lungs Hypotension precipitated by nitroglycerin administration highlights the preload dependent state of an infarcted RV GI 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 Rhythm AV synchrony plays an important role in RV infarct given the dependence on preload If 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 output However, 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 reperfusion Maintain RV preload Inotropes Avoid 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! Management Prompt reperfusion IV 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 rupture Posteromedial papillary more likely to be affected due to single coronary blood supply Papillary muscles are subendocardial so rupture can occur with non-transmural infarcts Presents with acute dyspnea from flash pulmonary edema and hypotension from drop in cardiac output Exam 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 rupture Risk factors: advanced age, female sex, first MI with lack of coronary collaterals Presents with hypotension, chest discomfort, dyspnea Exam with harsh systolic murmur with palpable thrill; pulmonary congestion is unusual unusual V 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 catheterization Inferobasal 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 rupture Risk factors: advanced age, female sex, first MI with lack of coronary collaterals Partial rupture may present as a vagal event that heralds the initial tear; TTE with new pericardial effusion should raise suspicion of an incomplete rupture Full 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 characteristics Intervention 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. 2012;367(14):1287-1296. doi:10.1056/nejmoa1208410. https://www.nejm.org/doi/full/10.1056/nejmoa1208410 Ouweneel DM, Eriksen E, Sjauw KD, et al. Percutaneous mechanical circulatory support versus intra-aortic balloon pump in cardiogenic shock after acute myocardial infarction. Journal of the American College of Cardiology. 2017;69(3):278-287. doi:10.1016/j.jacc.2016.10.022. https://www.jacc.org/doi/epdf/10.1016/j.jacc.2016.10.022 O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2013;127:e362-425. https://www.ahajournals.org/doi/10.1161/CIR.0b013e3182742cf6 Authors/Task Force members, Windecker S, Kolh P, et al. 2014 ESC/EACTS Guidelines on myocardial revascularization: The Task Force on Myocardial Revascularization of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS)Developed with the special contribution of the European Association of Percutaneous Cardiovascular Interventions (EAPCI). Eur Heart J 2014;35:2541-619. https://pubmed.ncbi.nlm.nih.gov/25173339/ Damluji AA, van Diepen S, Katz JN, et al. Mechanical complications of acute myocardial infarction: A scientific statement from the American Heart Association. Circulation. 2021;144(2). doi:10.1161/cir.0000000000000985. https://www.ahajournals.org/doi/full/10.1161/CIR.0000000000000985

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? A Initiate statin for goal LDL <100 mg/dl B Assess family history of premature CVD C Counsel on ketogenic diet D Stop smoking and lifestyle recommendations Answer #31 Explanation The 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 Takeaway A 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 CardioNerds Decipher the Guidelines – 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

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   Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

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. 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 Aortic Stenosis SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! 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. “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 PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! 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. Although major bleeding occurred in 10% of patients, there was no intracranial hemorrhage (12). The OPTALYSE trial aimed to determine the optimal dose of tissue plasminogen activator (TPA) and found that a lower dose delivered over a shorter duration resulted in improved right ventricular function and reduced clot burden compared to baseline (13). In contrast, the SUNSET trial failed to demonstrate better outcomes or safety profile between CDT and systemic anticoagulation (14). Pure mechanical catheter thrombectomy, such as the FlowTriever system, can be used in patients with contraindications to fibrinolysis and has been shown to result in a 25% reduction in RV/LV ratio in submassive PE in a multicenter study. However, there is still a lack of significant mortality data or large randomized controlled trials for catheter-based therapy (15). What are common complications after submassive pulmonary emboli? There is a spectrum of long-term complications after an acute PE (including intermediate risk PE), called Post-PE syndrome. These include limitations in functional capacity, cardiopulmonary dysfunction, and an overall decreased quality of life. In addition, chronic thromboembolic pulmonary disease (CTEPH) can occur which is characterized by persistent pulmonary vasoconstriction and arterial obstruction (16). The pathophysiology behind these complications are likely due to maladaptive vascular remodeling from residual thrombus or arteriopathy which results in increased pulmonary vascular resistance and possibly further RV dysfunction (17). In the ELOPE study, a prospective cohort study, almost half of acute PE patients had exercise limitations at 1 year on cardiopulmonary exercise testing, based on a VO2-max <80% predicted (18). Further, another study found that approximately 45% to 52% of surviving PE patients exhibit a New York Heart Association Score of ≥2 even up to 3 years after the acute incident (19). The evidence for thrombolytics is still controversial with regards to impact on long term outcomes. Though the PEITHO study has the largest long term follow up of advanced therapies and thrombolysis, there was no significant reduction in chronic PE complications, RV dysfunction, or persistent symptoms with thrombolysis (1,2). However, several smaller studies have now reported long term benefits of thrombolysis (TOPCOAT and MOPPET trial) with improved functional outcomes and quality of life (2). What is a PERT team and what is their role in the management of pulmonary emboli? A PERT or pulmonary embolism response team brings together a multidisciplinary group of clinicians who can rapidly assess and provide treatments for acute PE, who can exercise a full range of medical, endovascular, and surgical therapies, and who can provide appropriate follow up for patients (2, 17). PERT teams’ structures are variable based on the institution and the optimal PERT structure is not fully known. Often, however, a team will include emergency medicine, critical care, non-invasive and interventional cardiology, vascular medicine, vascular surgery, hematology, cardiac surgery, and clinical pharmacy.  To date, there are officially 89 institutions who are a part of the PERT consortium (17). PERT are useful in the decision making of not only submassive or massive PE, but also low risk PE with complex comorbidities. Though there has not been a formal randomized controlled trial to evaluate the PERT approach for survival, complications, and cost effectiveness, there have been several retrospective and prospective studies that have addressed these questions. Overall, PERT allows earlier access to advanced therapies, a streamlined approach to facilitate multidisciplinary communication, and an ability to quickly mobilize resources. There has been a proportional increase in the utilization of advanced therapies based on descriptive studies (from 9-19% in one study) without a significant increase in bleeding complications or mortality (20). One interesting development is the incorporation of AI. AI is at the forefront of cardiovascular care now, and this includes PE management. There are AI powered PE care coordination software (Viz AI for example), which have been useful in resource limited settings. Alerts are provided to the team with relevant clinical information and even automated imaging analysis (21). Though bringing together multiple perspectives can be helpful, it is also resource intensive that requires infrastructure. Future research is needed also in the costs associated with developing and maintaining a team. Outpatient follow up is additionally an important area for growth, specifically with post procedural care, medication adherence, and age appropriate cancer screening (2). References Nguyen, P. C., Stevens, H., Peter, K., & McFadyen, J. D. (2021). Submassive pulmonary embolism: current perspectives and future directions. Journal of Clinical Medicine, 10(15), 3383.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8347177/#:~:text=What%20Is%20the%20Definition%20of,%2C%20and%20standard%2Drisk%20PE. Jaff, M. R., McMurtry, M. S., Archer, S. L., Cushman, M., Goldenberg, N., Goldhaber, S. Z., … & Zierler, B. K. (2011). Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. Circulation, 123(16), 1788-1830. https://www.ahajournals.org/doi/10.1161/cir.0b013e318214914f#d1e2825 Konstantinides, S. V., Meyer, G., Becattini, C., Bueno, H., Geersing, G. J., Harjola, V. P., … & Zamorano, J. L. (2020). 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS) The Task Force for the diagnosis and management of acute pulmonary embolism of the European Society of Cardiology (ESC). European heart journal, 41(4), 543-603. https://academic.oup.com/eurheartj/article/41/4/543/5556136 Chodakowski, J. D., & Courtney, D. M. (2018). Pulmonary embolism critical care update: prognosis, treatment, and research gaps. Current opinion in critical care, 24(6), 540-546. https://journals.lww.com/co-criticalcare/Abstract/2018/12000/Pulmonary_embolism_critical_care_update_.18.aspx Ronny, C., Pablo, L., Victor, N., & Brooks, M. (2012). Echocardiographic findings in pulmonary embolism: An important guide for the management of the patient. World Journal of Cardiovascular Diseases, 2012. DOI:10.4236/wjcd.2012.23027 Mattia Arrigo, Lars Christian Huber, Pulmonary Embolism and Heart Failure: A Reappraisal, Cardiac Failure Review 2021;7:e03. https://doi.org/10.15420/cfr.2020.26 Piazza, G. (2020). Advanced management of intermediate-and high-risk pulmonary embolism: JACC focus seminar. Journal of the American College of Cardiology, 76(18), 2117-2127. https://www.jacc.org/doi/abs/10.1016/j.jacc.2020.05.028 Meyer G, et al. “Fibrinolysis for patients with intermediate-risk pulmonary embolism”. The New England Journal of Medicine. 2014. 370(15):1402-1411. https://www.nejm.org/doi/full/10.1056/NEJMoa1302097 Sharifi M, et al. “Moderate pulmonary embolism treated with thrombolysis”. The American Journal of Cardiology. 2013. 111(2):273-277. https://www.sciencedirect.com/science/article/abs/pii/S0002914912022059 Pei, D. T., Liu, J., Yaqoob, M., Ahmad, W., Bandeali, S. S., Hamzeh, I. R., … & Alam, M. (2019). Meta-analysis of catheter directed ultrasound-assisted thrombolysis in pulmonary embolism. The American journal of cardiology, 124(9), 1470-1477. https://www.sciencedirect.com/science/article/abs/pii/S0002914919308707 Kucher, N., Boekstegers, P., Müller, O. J., Kupatt, C., Beyer-Westendorf, J., Heitzer, T., … & Baumgartner, I. (2014). Randomized, controlled trial of ultrasound-assisted catheter-directed thrombolysis for acute intermediate-risk pulmonary embolism. Circulation, 129(4), 479-486. https://www.ahajournals.org/doi/full/10.1161/CIRCULATIONAHA.113.005544 Piazza, G., Hohlfelder, B., Jaff, M. R., Ouriel, K., Engelhardt, T. C., Sterling, K. M., … & SEATTLE II Investigators. (2015). A prospective, single-arm, multicenter trial of ultrasound-facilitated, catheter-directed, low-dose fibrinolysis for acute massive and submassive pulmonary embolism: the SEATTLE II study. Cardiovascular Interventions, 8(10), 1382-1392. https://www.jacc.org/doi/abs/10.1016/j.jcin.2015.04.020 Tapson, V. F., Sterling, K., Jones, N., Elder, M., Tripathy, U., Brower, J., … & Goldhaber, S. Z. (2018). A randomized trial of the optimum duration of acoustic pulse thrombolysis procedure in acute intermediate-risk pulmonary embolism: the OPTALYSE PE trial. JACC: Cardiovascular Interventions, 11(14), 1401-1410. https://www.jacc.org/doi/abs/10.1016/j.jcin.2018.04.008 Avgerinos, E. D., Jaber, W., Lacomis, J., Markel, K., McDaniel, M., Rivera-Lebron, B. N., … & Chaer, R. (2021). Randomized trial comparing standard versus ultrasound-assisted thrombolysis for submassive pulmonary embolism: the SUNSET sPE trial. Cardiovascular Interventions, 14(12), 1364-1373. https://www.jacc.org/doi/abs/10.1016/j.jcin.2021.04.049 Bishay, V. L., Adenikinju, O., & Todd, R. (2021). FlowTriever Retrieval System for the treatment of pulmonary embolism: overview of its safety and efficacy. Expert Review of Medical Devices, 18(11), 1039-1048. https://www.tandfonline.com/doi/abs/10.1080/17434440.2021.1982379 Piazza, G. (2020). Advanced management of intermediate-and high-risk pulmonary embolism: JACC focus seminar. Journal of the American College of Cardiology, 76(18), 2117-2127. https://www.jacc.org/doi/abs/10.1016/j.jacc.2020.05.028 Rosovsky R, Zhao K, Sista A, Rivera-Lebron B, Kabrhel C. Pulmonary embolism response teams: Purpose, evidence for efficacy, and future research directions. Res Pract Thromb Haemost. 2019;3(3):315-330. Published 2019 Jun 9. doi:10.1002/rth2.12216. https://www.sciencedirect.com/science/article/pii/S2475037922016181 Kahn SR, Akaberi A, Granton JT, Anderson DR, Wells PS, Rodger MA, et al. Quality of life, dyspnea, and functional exercise capacity following a first episode of pulmonary embolism: results of the ELOPE cohort study. Am J Med. 2017;130:990 e9–e21. [PubMed] Stevinson BG, Hernandez‐Nino J, Rose G, Kline JA. Echocardiographic and functional cardiopulmonary problems 6 months after first‐time pulmonary embolism in previously healthy patients. Eur Heart J. 2007;28:2517–24. https://academic.oup.com/eurheartj/article/28/20/2517/415870  Rosovsky R, Chang Y, Rosenfield K, Channick R, Jaff MR, Weinberg I, et al. Changes in treatment and outcomes after creation of a pulmonary embolism response team (PERT), a 10‐year analysis. J Thromb Thrombolysis. 2018;47:31-40. [PubMed] ) 

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.  Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Pearls • Notes • References • Production Team CardioNerds Cardio-Oncology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! 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 webinars The American Society of Echocardiography (ASE) webinars on global longitudinal strain The 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 disease Immune checkpoint inhibitor myocarditis Chemotherapy-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. 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/.

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? A Increase atorvastatin for goal LDL-C < 55 mg/dL B No change in management C Add isosorbide mononitrate 30 mg daily D Stop aspirin E Start 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 Takeaway For 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 CardioNerds Decipher the Guidelines – 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

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 Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!