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    Health & Fitness

    Cardionerds: A Cardiology Podcast

    Welcome to CardioNerds, where we bring you in-depth discussions with leading experts, case reports, and updates on the latest advancements in the world of cardiology. Tune in to expand your knowledge, sharpen your skills, and become a true CardioNerd!

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    Latest Episodes:
    224. Atrial Fibrillation: Assessment of Stroke & Bleeding Risk with Dr. Elaine Hylek Jul 26, 2022
    Show notes

    CardioNerds (Amit Goyal), Dr. Colin Blumenthal (CardioNerds Academy House Faculty Leader and FIT at the University of Pennsylvania), and Dr. Anjali Wagle (CardioNerds Ambassador and FIT at Johns Hopkins University), discuss the baseline assessment of stroke and bleeding risk in patients with atrial fibrillation (AF) with Dr. Elaine Hylek. Dr. Hylek is a professor of medicine at the Boston University School of Medicine and is the Director of the Thrombosis and Anticoagulation Service at Boston Medical Center. Stroke is a potentially devastating and preventable complication of AF. Understanding the balance between stroke and bleeding risk is crucial in determining who should be on anticoagulation. Join us to discuss this topic! In the next episode of the series, we will discuss situational risk assessment in the context of peri-cardioversion, peri-procedural status, triggered atrial fibrillation, and more. Audio editing by CardioNerds Academy Intern, Pace Wetstein. This CardioNerds Atrial Fibrillation 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. Kelly Arps and Dr. Colin Blumenthal. This series is supported by an educational grant from the Bristol Myers Squibb and Pfizer Alliance. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. We have collaborated with VCU Health to provide CME. Claim free CME here! Disclosures: Dr. Hylek discloses grant and research support from Medtronic and Janssen, and honoraria and/or consulting fees from Boehringer Ingelheim, and Bayer. CardioNerds Atrial Fibrillation 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 - Atrial Fibrillation: Assessment of Stroke & Bleeding Risk The CHA2DS2-VASc should be used to determine stroke risk in all patients. It was updated from the CHADS2 score to better separate patients into high and low risk and a score of 0 has a very low risk of a stroke. Understanding a given model’s derivation is key to application for any risk model. Understanding who was and was not included when a risk score was derived helps determine how to clinically use it. For example, mechanical valves, hypertrophic cardiomyopathy, cardiac amyloidosis, and moderate to severe MS were all excluded or poorly represented and should receive AC in AF regardless of CV. The HAS-BLED score should be used to identify modifiable risk factors for bleeding and address them. It is less useful to determine when we should stop AC. Factors that go into the score are dynamic and the intention was to alert the provider of potentially modifiable factors that could be addressed to lower bleeding risk (such as better BP control). Fear the clot. Patients should be on AC unless there is a serious contraindication as embolic strokes can be devastating with a high mortality (~24% mortality at 30 days) “What am I saying by not writing the prescription... I am saying that it’s OK to have an ischemic stroke.” Survey data shows that patients are willing to experience 3.5 GI bleeds on average before 1 stroke, so favoring AC is often a patient centered approach Notes - Atrial Fibrillation: Assessment of Stroke & Bleeding Risk Notes drafted by Dr. Anjali Wagle 1. Why do strokes happen in atrial fibrillation? Why is reducing stroke risk so important? Atrial fibrillation is associated with a significantly increased risk of stroke. The mortality of strokes related to AF have been estimated to be around 25% at 30 days in early studies which included either persistent or permanent AF, though of note, these studied were biased towards larger strokes since the diagnosis was based on physical exam and not high resolution imaging. AF promotes thrombogenesis through Virchow’s triad which includes: Abnormal blood flow Endothelial damage Hypercoagulability In atrial fibrillation, patients usually have a dilated left atrium and decreased blood flow through the atrial appendage which contribute to thrombogenesis. Multiple risk scores have been derived (i.e., CHA2DS2VASc) for estimation of stroke risk in patient with AF to identify whom to treat with anticoagulation to reduce the stroke risk. 2. How were CHADS2 and CHA2DS2VASc (CV) created and validated? The CHADS2 score was derived in 2001 by Gage et al from data including hospitalized patients with nonrheumatic AF who were not prescribed warfarin at hospitalized discharge. The CHADS2 score assigns one point to congestive heart failure, hypertension, age ≥ 75 years, and diabetes mellitus and two points to a previous history of stroke or transient ischemic attack (TIA) for a total of 6 points. Stroke rate per 100 patient-years rose by a factor of 1.5 for each 1-point increase in the CHADS2 score. However, it was found that there were several limitations associated with the CHADS2 score including that more than half of the patients were classified as moderate risk, making it unclear if antiplatelet or anticoagulation should be used in this population. Additionally, there were other “minor” risk factors (female sex, CAD, age 65-74) that were not included in the score. In 2010, Lip et al proposed the CHA2DS2VASc score that included these three additional factors: female gender, vascular events, and age 65-74. These additions to the original CHADS2 score allowed the CHA2DS2VASc score to reclassify patients in the moderate risk group into either the high or low risk groups (CV 2), making the decision of when to start anticoagulation easier. Some weaknesses of the CV score include that the individual factors are binary. For example, one point for diabetes does not discriminate risk based on if the patient’s A1c is 14 vs. 7. Similarly, the score is static and assumes the risk from each risk factor doesn’t change over time even though the endothelial dysfunction caused by a specific disease state isn’t fixed. Additionally, the C-statistic for the CV score is only 0.6 with newer scores that are more accurate including such as GARFIELD-AF (but these newer scores are less user friendly). That being said, the score still does a very good job of differentiating between high and low risk patients, which is the most important clinical question when deciding if someone needs anticoagulation. 3. Which populations were not studied in the validation of the CV score? Many of these studies have woefully low enrollment of racially diverse populations. Additionally, patients with amyloidosis, moderate-severe MS, and HOCM have a baseline higher risk of stroke were excluded from these studies. Patients with bioprosthetic valves were also excluded from the original derivation though there is now limited data showing use of the CV is reasonable. 4. How does AF burden affect stroke risk? Is there a temporal association between AF and stroke? Early trials did not find a temporal association between AF and stroke, though these trials often used physical exam definitions for stroke and current technology like implantable loop recorders (ILRs) didn’t exist to monitor 24/7. More modern studies like the TREND and KP-RHYTHM trials showed that stroke risk is related to AF burden. Longer episodes of AF seem to clearly be associated with stroke, but shorter episodes of AF aren’t as temporally related to stroke. In the LOOP trial use of ILRs to detect episodes of AF longer than 6 minutes led to a 3-fold increase in AF detection and initiation of AF, but did not reduce the number of strokes. This could indicate that there is some amount of AF that doesn’t require AC or that short runs of AF are associated with atrial myopathy that could be causing the strokes. It remains unclear what is the “chicken and egg” in this scenario. 5. How can we assess bleeding risk for patients with atrial fibrillation? How can we use these scores in our clinical practice? Developed and published in 2010 by Pisters et al., the HAS-BLED (hypertension, abnormal renal/liver function, stroke, bleeding history or predisposition, labile INR, elderly [age >65], medication predisposing to bleeding, excessive alcohol use) score aimed to create an easy to calculate and clinically meaningful score to estimate bleeding risk. It was validated using 3,978 patients from the Euro Heart Survey on AF and had good predictive accuracy (C-statistic 0.72). Of note, the score uses the less severe ISTH definition for a major hemorrhage, which doesn’t require as severe bleeding as the TIMI major bleeding definition. Many of the factors that go into the score are dynamic (for example HTN is SBP > 160 and not a history of HTN). The intention was to alert the provider of potentially modifiable factors that could be addressed to lower bleeding risk (such as better BP control). This would reduce the patients HAS-BLED score and therefore their bleeding risk. There is no absolute cutoff where anticoagulation in AF would be considered prohibitive. 6. What is the approach for patients with borderline stroke risk with a CV of 1 in men or 2 in women? Patients with a CV of 1 have between a 0.6% and a 0.9% risk of stroke/TIA/systemic embolism in a given year. That means even with a CV of 1 they have close to a 1/100 risk of an event in a given year. Given the high mortality and morbidity with embolic strokes and the lower incidence of major bleeding with modern DOACs, should have shared decision-making conversation with patients about starting AC at this risk level. One can consider other risk factors not in CV like LA function, appendage morphology, AF burden etc to help as tie breakers. References - Atrial Fibrillation: Assessment of Stroke & Bleeding Risk Pisters R, Lane DA, Nieuwlaat R, de Vos CB, Crijns HJ,...


    223. CCC: Approach to Acute Myocardial Infarction Cardiogenic Shock with Dr. Venu Menon Jul 17, 2022
    Show notes

    With the advent and rapid evolution of contemporary percutaneous coronary intervention (PCI), the early invasive management of acute myocardial infarction (AMI) has become a mainstay in therapy with significant impact on patient outcomes. However, despite modern advances in technology and system-based practices, AMI presenting with cardiogenic shock (CS) continues to portend a high risk of morbidity and mortality. Few randomized controlled clinical trials are available to guide decision-making in this uniquely challenging patient population. Understanding the pathophysiologic mechanism by which injury occurs and propagates the shock cycle can be instrumental in selecting an appropriate strategy for revascularization and left ventricular unloading. In this episode we are joined by Dr. Venu Menon, The Mehdi Razavi Endowed Chair and Professor of Medicine at the Cleveland Clinic Lerner College of Medicine, section head of clinical cardiology, fellowship program director, and director of the Cardiac intensive care unit at the Cleveland Clinic. Dr. Menon shares his wealth of knowledge and experience to help us review the contemporary data available for AMI CS management in a case-based discussion. We are also joined by Dr. Priya Kothapalli, star chief fellow and future interventionalist from University of Texas at Austin, series co-chair Dr. Yoav Karpenshif, and CardioNerds Co-founders Amit Goyal and Daniel Ambinder. Audio editing by CardioNerds Academy Intern, Dr. Christian Faaborg-Andersen. The CardioNerds Cardiac Critical Care 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. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif. Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardiac Critical Care 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 - Approach to Acute Myocardial Infarction Cardiogenic Shock with Dr. Venu Menon The H&P does matter! Age, location of infarction, heart rate, systolic blood pressure, and heart failure symptoms all carry weight in determining prognosis and risk of mortality.Define functional status, comorbid conditions, and life expectancy to help guide clinical decision-making. Do a quick bedside echocardiogram if possible to elucidate the predominant mechanism driving CS and rule out mechanical complications.Act with urgency! Get to the catheterization lab to characterize coronary anatomy and revascularize the culprit vessel as soon as possible.Minimize/avoid the use of vasopressors; if needed, wean as quickly as possible to avoid worsening myocardial ischemia. Consider mechanical circulatory support early!Despite dramatic advances in AMI management, data is limited in AMI CS management. Ask the important questions, get involved in the scientific inquiry as a trainee! Show notes - Approach to Acute Myocardial Infarction Cardiogenic Shock with Dr. Venu Menon 1. Why is it important to recognize AMI complicated by CS? AMI CS occurs in 7-10% of patients presenting with AMI and has a higher prevalence among elderly patients.The SHOCK trial (1999) showed significant survival benefit at 6 months with early revascularization with balloon angioplasty compared to medical therapy alone in AMI CS.Registry data suggests that early revascularization is beneficial in AMI CS even in elderly patients. Decision-making should be guided using a holistic view of the patient’s overall biology.Despite advances in revascularization techniques and availability of mechanical support, AMI CS portends a 40-45% risk of 30-day mortality in the modern era.Significant variation in management strategy exists between centers and data to guide decision-making is limited.The Society for Cardiovascular Angiography and Intervention (SCAI) classification system of shock stage may be helpful in characterizing patient risk and guiding clinical decision-making. 2. Which patients with AMI CS should undergo invasive monitoring and revascularization? What should be the timing of any intervention? In viable patients presenting with AMI CS, the primary goal should be to get to the catheterization laboratory to characterize the anatomy and revascularize the culprit vessel as soon as possible.Patient history, physical exam, laboratory exam, and echocardiography, if available, are critical pieces of information that should be obtained without delaying catheterization laboratory transfer.Patients presenting in SCAI shock stages C-E may require stabilization pre-procedure while minimizing delays to revascularization.Anticipating potential sequelae (such as acute pulmonary edema with respiratory failure requiring intubation) is crucial to minimizing delays.Maintain adequate perfusion pre-procedure (goal mean arterial blood pressure of >65mmHg). Minimize use and avoid escalation of vasopressor or inotropic therapy, as these agents worsen myocardial ischemia.The prevalence of multivessel disease, left main or proximal left anterior descending artery disease in AMI CS is high. Revascularization with restoration of TIMI 3 flow as soon as possible should be the primary goal, regardless of strategy. 3. When should mechanical circulatory support (MCS) be used in AMI CS? Immediate MCS may be beneficial in patients with persistent hemodynamic or electrical instability or patients at high risk for developing instability. MCS should be placed early and maintained until the shock cycle is reversed.If the primary mechanism for CS is left ventricular failure, an intra-aortic balloon pump (IABP) or transvalvular axial flow pump (Impella) may be considered. Additional strategies include venoarterial extracorporeal membrane oxygenation with left ventricular venting strategy or TandemHeart percutaneous assist device.There is limited data regarding the role of MCS in AMI; this is an area of active clinical investigation. Mechanistically, MCS provides the obvious benefits of supporting systemic perfusion while reducing cardiac workload; risks include bleeding, thrombosis, hemolysis, limb ischemia, and other vascular complications.MCS should be weaned slowly using multiple clinical and hemodynamic parameters, including Swan Ganz catheter data.If unable to wean MCS due to insufficient myocardial recovery despite support over a prolonged period in the setting of adequate revascularization, additional options such as durable MCS, heart transplantation, or palliative care should be considered. 4. What is the current evidence base for culprit-only vs. complete revascularization in AMI CS? The CULPRIT-SHOCK trial showed an increased 30-day and 1-year risk of a composite of all-cause mortality and need for renal replacement therapy in patients that underwent culprit and immediate non-culprit vessel revascularization in AMI CS.While there is no definitive data to support complete revascularization in AMI CS, this strategy may be considered in patients with multiple possible culprit lesions or subtotal non-culprit lesions with reduced TIMI grade flow corresponding with wall motion abnormality and normal wall thickness suggestive of viable myocardium. References - Approach to Acute Myocardial Infarction Cardiogenic Shock with Dr. Venu Menon Tehrani BN, Truesdell AG, Psotka MA, et al. A Standardized and Comprehensive Approach to the Management of Cardiogenic Shock. JACC Hear Fail. 2020;8(11):879-891. doi:10.1016/j.jchf.2020.09.005Kapur NK, Davila CD. Timing, timing, timing: the emerging concept of the ‘door to support’ time for cardiogenic shock. Eur Heart J. 2017;38(47):3532-3534. doi:10.1093/eurheartj/ehx406Hochman JS, Sleeper LA, Webb JG, et al. Early Revascularization in Acute Myocardial Infarction Complicated by Cardiogenic Shock. N Engl J Med. 1999;341(9):625-634. doi:10.1056/NEJM199908263410901Ibanez B, Halvorsen S, Roffi M, et al. Integrating the results of the CULPRIT-SHOCK trial in the 2017 ESC ST-elevation myocardial infarction guidelines: viewpoint of the task force. Eur Heart J. 2018;39(48):4239-4242. doi:10.1093/eurheartj/ehy294Shah AH, Puri R, Kalra A. Management of cardiogenic shock complicating acute myocardial infarction: A review. Clin Cardiol. 2019;42(4):484-493. doi:10.1002/clc.23168Basir MB, Kapur NK, Patel K, et al. Improved Outcomes Associated with the use of Shock Protocols: Updates from the National Cardiogenic Shock Initiative. Catheter Cardiovasc Interv. 2019;93(7):ccd.28307. doi:10.1002/ccd.28307Doll JA, Ohman EM, Patel MR, et al. A team-based approach to patients in cardiogenic shock. Catheter Cardiovasc Interv. 2016;88(3):424-433. doi:10.1002/ccd.26297Thiele H, Ohman EM, de Waha-Thiele S, Zeymer U, Desch S. Management of cardiogenic shock complicating myocardial infarction: an update 2019. Eur Heart J. 2019;40(32):2671-2683. doi:10.1093/eurheartj/ehz363Thiele H, Akin I, Sandri M, et al. PCI Strategies in Patients with Acute Myocardial Infarction and Cardiogenic Shock. N Engl J Med. 2017;377(25):2419-2432. http://www.nejm.org/doi/10.1056/NEJMoa1710261. Accessed April 10, 2021.Van Diepen S, Katz JN, Albert NM, et al. Contemporary Management of Cardiogenic Shock: A Scientific Statement from the American Heart Association. Circulation. 2017;136(16):e232-e268. doi:10.1161/CIR.0000000000000525Henry, Timothy D., et al. “Invasive Management of Acute Myocardial Infarction Complicated by Cardiogenic Shock: A Scientific Statement from the American Heart Association.” Circulation, vol. 143, no. 15, 2021, doi: 10.1161/cir.0000000000000959. Guest Profiles Dr. Venu Menon Dr. Venu Menon earned his medical degree from Jawaharlal Institute of Postgraduate Medical Education and Research in Pondicherry, India....


    222. CardioNerds Rounds: Challenging Cases – Nuances in Pulmonary Hypertension Management with Dr. Ryan Tedford Jul 14, 2022
    Show notes

    It’s another session of CardioNerds Rounds! In these rounds, Co-Chair, Dr. Karan Desai (previous FIT at the University of Maryland Medical Center, and now faculty at Johns Hopkins) joins Dr. Ryan Tedford (Professor of Medicine and Chief of Heart Failure and Medical Directory of Cardiac Transplantation at the Medical University of South Carolina in Charleston, SC) to discuss the nuances of managing pulmonary hypertension in the setting of left-sided heart disease. Dr. Tedford is an internationally-recognized clinical researcher, educator, clinician and mentor, with research focuses that include the hemodynamic assessment of the right ventricle and its interaction with the pulmonary circulation and left heart. This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes. Speaker disclosures: None Cases discussed and Show Notes • References • Production Team CardioNerds Rounds PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes - Challenging Cases - Nuances in Pulmonary Hypertension Management with Dr. Ryan Tedford Case #1 Synopsis: A woman in her late 30s presented to the hospital with 4 weeks of worsening dyspnea. Her history includes dilated non-ischemic cardiomyopathy diagnosed in the setting of a VT arrest around 10 years prior. Over the past 10 years she has been on guideline-directed medical therapy with symptoms that had been relatively controlled (characterized as NYHA Class II), but without objective improvement in her LV dimensions or ejection fraction (LVEF 15-20% by TTE and CMR and LVIDd at 6.8 cm). Over the past few months she had been noting decreased exercise tolerance, worsening orthopnea, and episodes of symptomatic hypotension at home. When she arrived to the hospital, she presented with BP 95/70 mmHg, increased respiratory effort, congestion and an overall profile consistent with SCAI Stage C-HF shock. In the case, we go through the hemodynamics at various points during her hospitalization and discuss options for management including medical therapy and mechanical support. The patient was eventually bridged to transplant with an Impella 5.5. Initial Hemodynamics Right Atrium (RA) Pressure Tracing: Right Ventricle (RV) Pressure Tracing: Pulmonary Artery (PA) Pressure Tracing: Pulmonary Capillary Wedge Pressure (PCWP) Tracing: Case 1 Rounding Pearls One of the first points that Dr. Tedford made was thinking about our classic frameworks of characterizing acute decompensated heart failure, specifically the “Stevenson” classification developed by Dr. Lynne Stevenson that phenotypes patients along two axes: congestion (wet or dry) and perfusion (warm or cold). Dr. Tedford cautioned that young patients may not fit into these classic boxes well, and that a normal lactate should not re-assure the clinician that perfusion is normal.In reviewing the waveforms, Dr. Tedford took a moment to note that besides just recording the absolute values of the pressures transduced in each chamber or vessel, it is critical to understand the morphology of the tracings themselves. For instance, with the RA pressure tracing above, there is no respiratory variation in the mean pressure. This is essentially a “resting Kussmaul’s sign,” which is typically indicative of significant RV dysfunction. Thus, even though our echocardiogram in this case did not necessarily show a significantly dilated RV with mildly reduced longitudinal function (TAPSE), hemodynamically the patient is demonstrating significant RV compromise.If we compare the RA pressure tracing to the PCWP, we see that there is respiratory variation in the PCWP tracing. We typically think of pronounced respiratory variation in the RA or PCWP tracing in the setting of obesity or lung disease, but loading conditions can also lead to significant respiratory variation.As was noted during the case discussion, irreversible pulmonary hypertension is considered an absolute contraindication to heart transplantation though there is variation on the absolute threshold above which transplantation is contraindicated. Generally, a pulmonary vascular resistance (PVR) of 3 Woods Units is considered a contraindication to isolated cardiac transplantation. Testing for reversibility of an elevated PVR with a vasodilator like nitroprusside is common in this patient population.In a study by Dr. Steven Hsu and colleagues, Pulmonary Artery Pulsatility Index (PAPi) was shown to be the hemodynamic factor that best correlated with intrinsic RV myocyte dysfunction in patients with advanced heart failure (using a cutoff of PAPi of 1.85). Dr. Tedford made note to remember that PAPi is highly influenced by RA pressure (the denominator in the ratio). Case #2 Synopsis: A woman in her late 40s presented to clinic for another opinion regarding her PH management. In regards to her history, in the 1990s she underwent a mechanical mitral valve replacement (MVR) for mixed mitral valve disease in the setting of rheumatic fever as well as a single vessel CABG (SVG to the RCA). In the early 2000s, she had developed severe and symptomatic tricuspid regurgitation (TR) and underwent redo sternotomy for TV repair (TVr). She had generally done well until the past year when she started developing dyspnea on light exertion, abdominal fullness, lower extremity edema and over the course of a year she had four hospitalizations for heart failure. Over her hospitalizations, she was also diagnosed with hemolytic anemia. Diagnostic work-up revealed pre and post-capillary PH. Dr. Tedford reviews the subsequent hemodynamic evaluation and provides insight on managing PH post valvular intervention. She was ultimately diagnosed with mitral paravalvular regurgitation treated with transcatheter PVL closure. Initial Hemodynamics RA Pressure Tracing RV Pressure Tracing PA Pressure Tracing PCW Pressure Tracing Left Ventricular (LV) Pressure Tracing PCW and LV Simultaneous Pressure Tracing Case 2 Rounding Pearls: The patient had been placed on sildenafil for persistent PH post-valve intervention. Dr. Tedford briefly mentioned the SIOVAC trial which was designed to evaluate treatment with sildenafil (40 mg TID) compared with placebo amongst patients with persistent PH (mean PA pressure ≥ 30 mmHg) 1 year after valvular replacement or repair (majority of whom were patients that had mitral valve intervention). In this study, sildenafil was associated with worse functional status, specifically heart failure or dyspnea compared to placebo (34% vs. 20%, p = 0.04).Dr. Tedford briefly touched upon the prognostic value of the diastolic pulmonary gradient (DPG, calculated as diastolic PA pressure subtracted by PCWP) in patients being considered for cardiac transplantation. We commonly use PVR and transpulmonary gradient (TPG) to characterize the degree of pre-capillary PH and suitability for transplantation. However, these markers are not ideal surrogates for pulmonary vascular remodeling and differentiating between fixed remodeling versus reversible changes. For instance, the TPG can be elevated not only as a result of pulmonary vascular remodeling but elevated LA pressures passively transmitted back to the pulmonary vasculature leading to elevations in the diastolic PA pressure.The DPG was thought to potentially define higher risk left heart failure patients with clinically significant pre-capillary PH. However, in Dr. Tedford’s 2014 analysis, the DPG did not delineate higher risk among patients with elevated TPG and PVR undergoing cardiac transplantation. There could be several explanations including that the cutoff for abnormal DPG is low (≥7) and thus small errors in measurement could have significant influence on what is characterized as abnormal. Furthermore, the diastolic PA pressure measurement is particularly prone to ringing artifact. References - Challenging Cases - Nuances in Pulmonary Hypertension Management with Dr. Ryan Tedford Aslam MI, Jani V, Lin BL, et al. Pulmonary artery pulsatility index predicts right ventricular myofilament dysfunction in advanced human heart failure. Eur J Heart Fail. 2021 Feb;23(2):339-341. doi: 10.1002/ejhf.2084. Epub 2021 Jan 5. PMID: 33347674; PMCID: PMC8574988.Bermejo J, Yotti R, García-Orta R, et al., on behalf of the Sildenafil for Improving Outcomes after VAlvular Correction (SIOVAC) investigators. Sildenafil for improving outcomes in patients with corrected valvular heart disease and persistent pulmonary hypertension: a multicenter, double-blind, randomized clinical trial.Mehra MR, Canter CE, Hannan MM, et al; International Society for Heart Lung Transplantation (ISHLT) Infectious Diseases, Pediatric and Heart Failure and Transplantation Councils. The 2016 International Society for Heart Lung Transplantation listing criteria for heart transplantation: A 10-year update. J Heart Lung Transplant. 2016 Jan;35(1):1-23. doi: 10.1016/j.healun.2015.10.023. PMID: 26776864.Tedford RJ, Beaty CA, Mathai SC et al. Prognostic value of the pre-transplant diastolic pulmonary artery pressure-to-pulmonary capillary wedge pressure gradient in cardiac transplant recipients with pulmonary hypertension. J Heart Lung Transplant. 2014 Mar;33(3):289-97. doi: 10.1016/j.healun.2013.11.008. Epub 2013 Nov 28. Erratum in: J Heart Lung Transplant. 2019 Feb;38(2):233. PMID: 24462554; PMCID: PMC3955214.Thibodeau JT, Drazner MH....


    221. Guidelines: 2021 ESC Cardiovascular Prevention – Question #18 with Dr. Jaideep Patel Jul 12, 2022
    Show notes

    The following question refers to Section 6.2 of the 2021 ESC CV Prevention Guidelines. The question is asked by Dr. Christian Faaborg-Andersen, answered first by Houston Methodist medicine resident Dr. Najah Khan, and then by expert faculty Dr. Jaideep Patel. Dr. Patel recently graduated from Virginia Commonwealth University cardiology fellowship and is now a preventive cardiologist at the Johns Hopkins Hospital. 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. Question #18 A 60-year-old Black woman with a history of hypertension and heart failure with reduced ejection fraction (EF 40%) presents to clinic for follow-up. She is currently doing well with NYHA class II symptoms. She is taking carvedilol 25 mg BID, sacubitril/valsartan 97/103 mg BID, and spironolactone 25 mg daily, all of which have been well tolerated. In clinic, her BP is 125/80 mmHg, and her HR is 55 bpm. Routine labs are within normal limits including Cr of 1.0, K of 4.0, and HbA1c of 6.0. What is the most appropriate next step in her management? A. No change in management B. Reduce beta blocker C. Add an SGLT2 inhibitor (dapagliflozin or empagliflozin) D. Add vericiguat E. Add hydralazine/isosorbide dinitrate Answer #18 The correct answer is C – Add an SGLT2 inhibitor (dapagliflozin or empagliflozin) For patients with symptomatic HFrEF, neurohormonal antagonists (ACEi, ARB, ARNI; BB; MRA) improve survival and reduce the risk of HF hospitalization. This patient is already on these agents. The addition of an SGLT2 inhibitor on top of neurohormonal blockade reduces the risk of CV death and worsening HF in patients with symptomatic HFrEF and is the next best step for this patient (Class I, LOE A). Vericiguat may be considered in patients with symptomatic HFrEF with HF worsening despite already being on maximally tolerated neurohormonal blockade (Class IIb, LOE B), but first-line therapies should be started first. Hydralazine/Isosorbide dinitrate should be considered in self-identified Black patients or people who have EF ≤ 35% or


    220. Guidelines: 2021 ESC Cardiovascular Prevention – Question #17 with Dr. Melissa Tracy Jul 07, 2022
    Show notes

    The following question refers to Section 4.9 of the 2021 ESC CV Prevention Guidelines. The question is asked by Dr. Christian Faaborg-Andersen, answered first by UCSD fellow Dr. Patrick Azcarate, and then by expert faculty Dr. Melissa Tracy. Dr. Tracy is a preventive cardiologist, former Director of the Echocardiography Lab, Director of Cardiac Rehabilitation, and solid organ transplant cardiologist at Rush University. 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. Question #17 A 74-year-old man with a history of hypertension, chronic kidney disease, and gastroesophageal reflux presents with chest pain and is found to have an NSTEMI due to an obstructive lesion in the proximal LAD. One drug-eluting stent is placed, and he is started on dual antiplatelet therapy with aspirin and clopidogrel. He is concerned about the risk of bleeding from his gastrointestinal tract. What would you recommend to reduce his risk of bleeding? A. Lansoprazole, a proton pump inhibitor B. Famotidine, a histamine-2 blocker C. Calcium carbonate, an antacid D. None, proton pump inhibitors are contraindicated. Answer #17 The correct answer is A. The ESC recommends that patients at high risk for GI bleeding who are receiving antiplatelet therapy take proton pump inhibitors (Class I, LOE A). High risk for bleeding includes patients who are age ≥65, history of peptic ulcer disease, Helicobacter pylori infection, dyspepsia or GERD symptoms, chronic renal failure, diabetes mellitus, and concomitant use of other antiplatelet agents, anticoagulants, nonsteroidal anti-inflammatory drugs, or steroids. Coadministration of proton pump inhibitors that specifically inhibit CYP2C19 (omeprazole or esomeprazole) may reduce the pharmacodynamic response to clopidogrel. Although this interaction has not been shown to affect the risk of ischemic events, coadministration of omeprazole or esomeprazole with clopidogrel is not recommended. Main Takeaway In patients with high gastrointestinal bleeding risk who are receiving antiplatelet therapy, proton pump inhibitors are recommended. Omeprazole and esomeprazole may reduce the efficacy of clopidogrel and should not be used concomitantly with clopidogrel. Guideline Location Section 4.9.3, Page 3291 Figure 13 page 3278; recommendation table page 3279. CardioNerds Decipher the Guidelines - 2021 ESC Prevention Series CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!


    219. Guidelines: 2021 ESC Cardiovascular Prevention – Question #16 with Dr. Roger Blumenthal Jul 05, 2022
    Show notes

    The following question refers to Section 4.6 and Figure 13 of the 2021 ESC CV Prevention Guidelines. The question is asked by student doctor Shivani Reddy, answered first by NP Carol Patrick, and then by expert faculty Dr. Roger Blumenthal. Dr. Roger Blumenthal is professor of medicine at Johns Hopkins where he is Director of the Ciccarone Center for the Prevention of Cardiovascular Disease. He was instrumental in developing the 2018 ACC/AHA CV Prevention Guidelines. 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. Question #16 True or False: For patients with established ASCVD, secondary prevention entails adding a PCSK9 inhibitor if goal LDL is not met on maximum tolerated doses of a statin and ezetimibe. Answer #16 The correct answer is True. The ultimate on-treatment LDL-C goal of


    218. Guidelines: 2021 ESC Cardiovascular Prevention – Question #15 with Dr. Kim Williams Jul 05, 2022
    Show notes

    The following question refers to Section 4.3 of the 2021 ESC CV Prevention Guidelines. The question is asked by CardioNerds Academy Intern Dr. Maryam Barkhordarian, answered first by pharmacy resident Dr. Anushka Tandon and then by expert faculty Dr. Kim Williams. Dr. Williams is Chief of the Division of Cardiology and is Professor of Medicine and Cardiology at Rush University Medical Center. He has served as President of ASNC, Chairman of the Board of the Association of Black Cardiologists (ABC, 2008-2010), and President of the American College of Cardiology (ACC, 2015-2016). 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. Question #15 Your patient mentions that she drinks “several” cups of coffee during the day. She also describes having a soda daily with lunch and occasionally a glass of wine with dinner. Which of the following recommendations is appropriate? A. Coffee consumption is not harmful and may even be beneficial, regardless of the number of drinks per day. B. Drinking two glasses of wine/day is safe from a cardiovascular prevention standpoint. C. Soft drinks (and other sugar-sweetened beverages) must be discouraged. D. None of the above Listen to this podcast episode! Answer #15 The correct answer is C. Soft drinks (and other sugar-sweetened beverages) must be discouraged. Sugar-sweetened beverages have been associated with a higher risk of CAD and all-cause mortality. The ESC guidelines give a class I recommendation for restriction of free sugar consumption (in particular sugar-sweetened beverages) to a maximum of 10% of energy intake. This is a class IIa recommendation in the ACC/AHA guidelines. Choice A is incorrect because: the consumption of nine or more drinks a day of non-filtered coffee (such as boiled, Greek, and Turkish coffee and some espresso coffees) may be associated with an up to 25% increased risk of ASCVD mortality. Moderate coffee consumption (3-4 cups per day) is probably not harmful, and perhaps even moderately beneficial. Choice B is incorrect: It is a class I recommendation to restrict alcohol consumption to a maximum of 100 g per week. The standard drink in the US contains 14 g of alcohol, so 100 mg of alcohol translate to: o 84 ounces of beer (5% alcohol) o Or 56 – 63 ounces of malt liquor (75% alcohol) or o Or 35 ounces of wine (12% alcohol) or ONE 5 fl oz glass of wine/day. o Or 31.5 ounces of distilled spirits (40% alcohol). The ACC/AHA guidelines recommended limiting alcohol consumption only for the management of hypertension to: ≤2 drinks daily for men and: ≤1 drink daily for women. Main Takeaway The main takeaway: ASCVD risk reduction can be achieved by restricting sugar-sweetened beverages to a maximum of 10% of energy intake. Guideline Location Section 4.3.2, Page 3271 CardioNerds Decipher the Guidelines - 2021 ESC Prevention Series CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!


    217. Guidelines: 2021 ESC Cardiovascular Prevention – Question #14 with Dr. Allison Bailey Jul 01, 2022
    Show notes

    The following question refers to Sections 3.3-3.4 of the 2021 ESC CV Prevention Guidelines. The question is asked by student Dr. Adriana Mares, answered first by early career preventive cardiologist Dr. Dipika Gopal, and then by expert faculty Dr. Allison Bailey. Dr. Bailey is a cardiologist at Centennial Heart. She is the editor-in-chief of the American College of Cardiology's Extended Learning (ACCEL) editorial board and was a member of the writing group for the 2018 American Lipid Guidelines. 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. Question #14 Ms. Soya M. Alone is a 70-year-old woman of Bangladeshi ethnicity with a history of anxiety and depression. She currently lives at home by herself, does not have many friends and family that live nearby, and has had a tough year emotionally after the passing of her husband. She spends most of her time in bed with low daily physical activity and has experienced more weakness and exhaustion over the past year along with loss of muscle mass. Which of the following are potential risk modifiers in this patient when considering her risk for CVD?A. Bangladeshi ethnicity B. Psychosocial factorsC. Frailty D. History of anxiety and depressionE. All of the above Answer #14 The correct answer is E – All of the above.Traditional 10-year CVD risk scores do not perform adequately in all ethnicities. Therefore, multiplication of calculated risk by relative risk for specific ethnic subgroups should be considered (Class IIa, LOE B). Individuals from South Asia have higher CVD rates. The ESC guidelines recommend using a correction factor by multiplying the predicted risk by 1.3 for Indians and Bangladeshis, and 1.7 for Pakistanis. These correction factors are derived from data from QRISK3. In the UK, the QRISK calculator algorithm has been derived and validated in 2.3 million people to estimate CVD risk in different ethnic groups and unlike other calculators, it counts South Asian origins as an additional risk factor. The reasons for such differences remain inadequately studied, as do the risks associated with other ethnic backgrounds. Barriers to developing accurate risk prediction tools include the wide heterogeneity amongst the population.The 2019 ACC/AHA guidelines also list high-risk race/ethnicities such as South Asian ancestry as a risk-enhancing factor. However, there is no separate pooled cohort equation for different ethnicities, and consideration should be given that the pooled cohort equations will underestimate ASCVD risk in South Asians.Psychosocial stress including loneliness and critical life events are associated, in a dose-response pattern, with the development and progression of ASCVD, with relative risks between 1.2 and 2.0. Conversely, indicators of mental health, such as optimism and a strong sense of purpose, are associated with lower risk. While there is not a specific way proposed by the guidelines for psychosocial factors to improve risk classification, it is important to screen patients with ASCVD for psychological stress, and clinicians should attend to somatic and emotional causes of symptoms as well. The ESC guidelines give a Class IIa (LOE B) recommendation for assessment of stress symptoms and psychosocial stressors.This patient should also be formally screened for frailty, which is not the same as aging but includes factors such as slowness, weakness, low physical activity, exhaustion and shrinking, and makes her more vulnerable to the effect of stressors and is a risk factor for both high CV and non-CV morbidity and mortality. However, the ability of frailty measures to improve CVD risk prediction has not been formally assessed, so the guidelines do not recommend integrating it into formal CVD risk assessment. Frailty may however, influence treatment as it can help build an individualized care plan.Mental disorders such as anxiety and depression are associated with the development of CVD as well. Detrimental effects may be potentially caused by unhealthy lifestyle, increased exposure to socioeconomic stressors, and cardiometabolic side-effects of medications. The ESC guidelines give a Class 1 (LOE C) recommendation that mental disorders with either significant functional impairment or decreased use of healthcare systems be considered as influencing total CVD risk.Main TakeawayPsychosocial stress and frailty are associated with risk of ASCVD and should be assessed in patients when considering CVD risk. In addition, current risk scores may under-or over-estimate CVD risk in different ethnic minority groups.Guideline LocationSection 3.3.1, 3.3.2, 3.3.4, 3.4.10, page 3258 – 3259, 3265 – 3266 CardioNerds Decipher the Guidelines - 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor RollCardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!


    216. Guidelines: 2021 ESC Cardiovascular Prevention – Question #13 with Dr. Eugene Yang Jun 30, 2022
    Show notes

    The following question refers to Section 3.2 of the 2021 ESC CV Prevention Guidelines. The question is asked by student Dr. Hirsh Elhence, answered first by Mayo Clinic Fellow Dr. Teodora Donisan, and then by expert faculty Dr. Eugene Yang. Dr. Yang is professor of medicine of the University of Washington where he is 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 current 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. Question #13 You are seeing a 45-year-old woman with a past medical history of hypertension, overweight status, hyperlipidemia, and active tobacco use disorder. Her BMI is 27 kg/m2, BP is 150/75, HbA1C is 5.8%, total cholesterol is 234 mg/dL, HDL is 59 mg/dL, and LDL is 155 mg/dL. She is from Romania, a country with very high CVD risk. Which of the following statements is CORRECT? A. LDL-C needs to be decreased by at least 50%, as small absolute LDL-C reductions would not provide clinical benefit B. Hypertension is not an important CVD risk factor in our patient, as she is young. C. Prediabetes is not a significant CV risk factor for our patient, as she is not yet diabetic. D. Smoking confers a higher CVD risk for women than for men. E. Her weight does not increase her CVD risk, as she is overweight rather than obese Answer #13 The correct answer is D – Smoking confers a higher CVD risk for women than for men. Prolonged smoking increases the CVD risk more in women than in men. Our patient is 45 years old. CVD risk in smokers


    215. Atrial Fibrillation: Screening, Detection, and Diagnosis of Atrial Fibrillation with Dr. Ben Freedman Jun 27, 2022
    Show notes

    CardioNerds (Dr. Kelly Arps, Dr. Colin Blumenthal, Dr. Dan Ambinder, and Dr. Teodora Donisan) discuss the screening, detection, and diagnosis of atrial fibrillation (AF) with Dr. Ben Freedman. AF is frequently undiagnosed and its first manifestation can be a debilitating stroke. European and American guidelines differ slightly with regards to guidelines for AF screening in asymptomatic individuals. There are multiple methods available to screen for AF; the setting and the clinical scenario can help guide the choice. Consumer-led screening has its own challenges, as it can detect AF in a younger population where we should prioritize aggressive management of risk factors and comorbidities. There is uncertainty regarding the minimum AF burden that increases thromboembolic risk, however a high CHAD2S2-VASc score remains the strongest predictor of stroke risk independent of AF burden. Perioperative AF associated with non-cardiac surgery has increased risk of future stroke and adverse cardiac outcomes and should likely be treated as a new diagnosis of chronic AF. This CardioNerds Atrial Fibrillation 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. Kelly Arps and Dr. Colin Blumenthal. This series is supported by an educational grant from the Bristol Myers Squibb and Pfizer Alliance. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. We have collaborated with VCU Health to provide CME. Claim free CME here! Disclosures: Dr. Ben Freedman disclosed that he has received grant or research support from Pfizer. Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Atrial Fibrillation 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 - Screening, Detection, and Diagnosis of Atrial Fibrillation “Stroke is a poor early sign of AF.” AF remains frequently undiagnosed and there remains uncertainty about the optimal target population and screening methodology. “We have to tailor AF screening to the purpose we’re using it for” If in a primary care setting, check the pulse. If the goal is to exclude high-risk AF – handheld ECG for heart rhythm snapshots are appropriate. If the goal is to identify or exclude AF with a high level of certainty, continuous monitors are necessary for greater sensitivity. Consumer-led screening is performed by (mostly young) individuals using commercial monitors and smart watches, facilitating earlier recognition of paroxysmal AF in this population. In these cases, we should prioritize aggressive management of risk factors and comorbidities to reduce the risk of progression to persistent AF. There is no specific cutoff for AF duration which has been identified to predict elevated stroke risk; AF is likely both a risk factor and a risk marker for stroke, suggesting an underlying atrial myopathy. Non-cardiac surgeries and procedures can be considered “AF stress tests.” If AF occurs in these settings, it is usually more clinically significant and has a higher risk of stroke and death than AF associated with cardiac surgeries. Notes - Screening, Detection, and Diagnosis of Atrial Fibrillation Notes drafted by Dr. Teodora Donisan and reviewed by Dr. Kelly Arps 1. Why is it important to screen for AF and who should be screened? AF is frequently undiagnosed and its first manifestation can be a debilitating stroke or death. Let’s go over a few numbers: 15% of people with AF are currently undiagnosed and 75% of those individuals would be eligible for anticoagulation.1 10-38% of individuals with ischemic strokes are found to have AF as a plausible cause, and the true proportion may be even higher, given difficulties in detecting intermittent AF.2 Current guideline recommendations: European guidelines: opportunistic screening for AF is recommended for individuals ≥65 years old.3 American guidelines: AF screening is recommended in patients with cryptogenic strokes and those with device-recorded atrial high-rate episodes.4 Opportunistic screening for AF can be done by checking the pulse or noticing the irregular heart rate on blood pressure monitors. When AF is found by opportunistic screening at a single time point, it is usually persistent AF. Continuous ambulatory heart rhythm monitoring can identify shorter episodes of paroxysmal AF, perhaps earlier in the AF disease course. In patients with unexplained stroke we have different ways to search for occult AF: In the hospital: all patients should have 72h of ECG monitoring. There is evidence that nurse-led ECG surveillance detects more paroxysmal AF earlier and more frequently than 24-hour Holter recordings.5 After discharge: if clinical suspicion for occult AF is high (e.g., cerebral imaging concerning for cardioembolic source, evidence of left atrial enlargement, elevated BNP), consider more prolonged monitoring via cutaneous patches, multiple Holter recordings, or implantable cardiac monitors. 2. What tools are currently available to screen for AF? There are multiple tools available for AF screening: pulse palpation, oscillometry, and ambulatory heart rhythm ECG monitoring with external or subcutaneous devices. Handheld ECG devices are very convenient options, as they can diagnose AF in 30 seconds directly, whereas other methods such as oscillometry would ultimately require ECG confirmation. If in the office for a quick screen: check the pulse; If you’re looking for high-burden AF: handheld one-time ECG; If you’re looking to identify or rule out AF with a high degree of certainty: continuous monitoring with transcutaneous patch or implantable monitor. 3. How should commercial monitor/smart watch data be incorporated into clinical practice? We need to be aware of the population who have access to and more often use these modern technologies; use is unequally distributed around the world and across the age span.6 These devices are most often used by people who are 35-40 years old, not the typical population for whom AF screening may be more impactful. If we do identify AF in these younger individuals, starting anticoagulation may not be indicated. It is important, however, to emphasize more aggressive management of risk factors and comorbidities (e.g., weight loss, diet, exercise, alcohol reduction, hypertension control, screening for and treating prediabetes and diabetes, screening for obstructive sleep apnea, and assessing thyroid function) to reduce the risk of AF progression. 4. How much atrial fibrillation is clinically relevant? There is uncertainty regarding the minimum AF burden that increases the thromboembolic risk above an individual’s baseline risk, with studies exploring durations of ≥ 5 minutes to ≥ 24 hours.7,8 Several studies show that there isn’t a clear temporal relationship between device-detected high-rate episodes and strokes either, with only a small number of patients experiencing arrhythmia in the month before a stroke.9 The CHA2DS2-VASc score is very important when discussing thromboembolic risk: if it is low, then the risk of stroke is low; if it is high, risk of stroke is higher, even if there is a low burden of AF. AF is likely both a risk factor and a risk marker for stroke, suggesting an underlying atrial myopathy. This would explain why a specific cutoff point for AF duration is not necessarily relevant to predict stroke risk. 5. How should clinicians approach peri-operative AF? Perioperative AF is associated with increased perioperative morbidity, higher stroke rates, more readmissions, and lower survival.10 The significance of AF is different depending on the type of surgery: With AF after cardiac surgery (which involves opening the pericardium and direct irritation of the atria), the incidence of perioperative AF is greater (20-30%). Roughly 25% of patients with AF after CABG experience asymptomatic recurrent AF episodes during the first month after the procedure.11 Many individuals with AF after cardiac surgery do not go on to have chronic AF. With AF after general surgery, the chance of chronic AF and future risk of adverse events are significantly elevated, as AF should not be a direct result of the procedure itself and instead likely represents a previously undiagnosed atrial myopathy. Consider noncardiac procedures as an “AF stress test”. Give this information, we should strongly consider anticoagulation after identifying AF associated with non-cardiac surgeries or procedures, when indicated by the CHA2DS2-VASc score. We should start anticoagulation in individuals with AF associated with cardiac surgeries only if there are other risk factors or clini Opportunistic screening for AF can be done by checking the pulse or noticing the irregular heart rate on blood pressure monitors. When AF is found by opportunistic screening at a single time point, it is usually persistent AF. Continuous ambulatory heart rhythm monitoring can identify shorter episodes of paroxysmal AF, perhaps earlier in the AF disease course. In patients with unexplained stroke we have different ways to search for occult AF: In the hospital: all patients should have 72h of ECG monitoring. There is evidence that nurse-led ECG surveillance detects more paroxysmal AF earlier and more frequently than 24-hour Holter recordings.5 After discharge: if clinical suspicion for occult AF is high (e.g., cerebral imaging concerning for cardioembolic source, evidence of left atrial enlargement, elevated BNP), consider more prolonged monitoring via cutaneous patches, multiple Holter recordings, or implantable cardiac monitors. References - Screening, Detection,...


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