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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:
    244. Cardiovascular Genomics: Intro to Cardiovascular Genetics in Electrophysiology with Dr. James Daubert Nov 24, 2022
    Show notes

    The field of Cardiovascular Genomics has advanced tremendously over the past two decades, having a significant clinical impact and changing the perception of the role and scope of genetic testing in several cardiovascular domains. To kickstart the Cardiovascular Genomics series, CardioNerds Dr. Sara Coles (FIT at Duke University), Dr. Colin Blumenthal (CardioNerds Academy faculty and FIT at UPenn), and Dr. Karla Asturias (CardioNerds Academy fellow and medicine resident at Pennsylvania Hospital) have a great discussion with Dr. James Daubert, a clinical electrophysiologist at Duke University, with a particular interest in inherited arrhythmia syndromes and sports cardiology. In this episode, we review basic concepts of cardiovascular genomics and genetics in electrophysiology while discussing when to (and when not to!) test our patients and their families and how to approach those results. Audio editing by CardioNerds academy intern, Pace Wetstein. This episode was developed in collaboration with the American Society of Preventive Cardiology and is supported with unrestricted educational funds from Illumina, Inc. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. This CardioNerds Cardiovascular Genomics series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs. Pearls • Notes • References CardioNerds Cardiovascular Genomics 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 - Genetics in Electrophysiology The first step is identifying the right phenotype! Getting the right phenotype is crucial, as genetic testing done in a patient without a clear phenotype (or an incorrect one) would lead to significant anxiety, unnecessary tests and interventions, and potentially misleading and dangerous conclusions for patients and their families. Genetic testing typically should be reserved for patients with a confirmed or suspected diagnosis of an inherited disease or for individuals with a previously diagnosed pathogenic variant in a first-degree relative.1 Discuss with your patient! Genetic counseling is essential and recommended for all patients before and after genetic testing. It should include a thorough discussion of risks, benefits, and possible outcomes, including variants of uncertain significance.2 Cardiovascular genetics is a dynamic and rapidly evolving field. New information can cause a variant of uncertain significance to be reclassified as a pathogenic or likely pathogenic variant or to be downgraded to benign or likely benign as variant databases expand. Another possibility is that new research might identify novel genes for a particular disease, which could warrant retesting, particularly for phenotype-positive and genotype-negative patients.1 Brugada syndrome is an inherited arrhythmogenic disorder characterized by ST-segment elevation in the right precordial leads and malignant ventricular arrhythmias, with occasional conduction disease and atrial arrhythmias. It is diagnosed in patients with ST-segment elevation ≥ 2 mm in ≥ 1 lead among the right precordial leads, with a type I morphology (J-point elevation with slowly descending or concave ST segment elevation merging into a negative T wave), shown in the image below. This pattern can be observed spontaneously or after provocative drug testing (e.g., procainamide). Pathogenic genetic variants in SCN5A that result in loss of function of the cardiac sodium channel are identified in approximately 20% of cases.3,4 Image adapted from Batchvarov VN. The Brugada Syndrome – Diagnosis, Clinical Implications and Risk Stratification. Eur Cardiol Rev. 2014;9(2):82. doi:10.15420/ECR.2014.9.2.82 Measure the QT interval yourself! A correct determination of the QT interval is essential. Although automatic measurements are widely available, the interval can be underestimated or overestimated, particularly in atrial arrhythmias or complex T-wave morphologies. Determining the end of the T-wave can be challenging in this setting, and can be assessed through the tangent method, which determines the end of the T-wave by the intersection between the baseline (U-P segment) and the “tangent” drawn to the steepest last limb of the presumed T-wave.5,6 Image adapted from Postema PG, De Jong JSSG, Van der Bilt IAC, Wilde AAM. Accurate electrocardiographic assessment of the QT interval: teach the tangent. Hear Rhythm. 2008;5(7):1015-1018. doi:10.1016/J.HRTHM.2008.03.037 When encountering a patient with prolonged QT, it is essential to exclude secondary causes like QT-prolonging drugs and electrolyte imbalances. As the acute cause is removed and the acute illness resolves, “see what happens while the dust is settling” and reassess the QT. Show notes - Genetics in Electrophysiology Notes were developed by Dr. Karla Asturias: What are some key basic concepts in clinical genetics? A mutation is defined as a permanent change in the nucleotide sequence, while a polymorphism is a mutation that occurs in more than 1% of a particular population. While both terms are often used, it can lead to confusion due to incorrect assumptions of pathogenicity. Therefore, both terms have been replaced by the term genetic variant, which we now encounter in the literature and guidelines.Proband is the first presenting person in a family that serves as a starting point for a genetic study.The phenotype refers to the clinical syndrome observed in our patients, while the genotype relates to the genetic composition, including the presence or absence of any genetic variants.In the case of Brugada syndrome, the phenotype includes the type I Brugada pattern on ECG and the presence of ventricular arrhythmias. In many cases, the genotype consists of genetic variants in SCN5A that result in the loss of function of the cardiac sodium channel.While particular genotypes can cause disease, the expression of the clinical phenotype can vary, leading to incomplete penetrance, where only a proportion of individuals carrying a specific genetic variant manifest the phenotype.In patients with Brugada syndrome, there is variability in the frequency of ECG abnormalities, even with the same pathogenic variants. Among individuals with an SCN5A pathogenic variant, only 20-30% have an ECG diagnostic of Brugada syndrome, and approximately 80% manifest the characteristic ECG changes when challenged with a sodium channel blocker.4Additionally, the Brugada phenotype has been reported to be 8 to 10 times more common in men than in women.7 Most cardiovascular diseases exhibit genetic heterogeneity, with mutations in multiple genes causing the same condition, meaning multiple genotypes can cause a similar phenotype. In the cases of congenital long QT syndrome and hypertrophic cardiomyopathy, multiple genes have been implicated in these conditions. How do we classify genetic testing results according to the American College of Medical Genetics and Genomics (ACMG) guidelines? The American College of Medical Genetics and Genomics (ACMG) guidelines are internationally accepted and describe standard terminology and methods in clinical genetic testing.8 They classify genetic variants into five different tiers:PathogenicLikely pathogenicVariant of uncertain significance (VUS)Likely benignBenignIt should be noted that, at present, we have no data to support a quantitative assignment of variant certainty to any of the five categories given the heterogenous nature of most diseases.A variant of uncertain significance does not provide a definitive genetic etiology of disease and should not be used for clinical decision-making nor to determine risk for disease in unaffected relatives. 9 Variant interpretation is a dynamic process, and classification may change over time as additional evidence about the variants becomes available. A negative result does not exclude the possibility of genetic disease but indicates that a causative variant could not be identified with the currently available technology and knowledge. What types of genetic testing are available, and when do we use them?3 Sanger sequencing Method of DNA sequencing for a single geneHigh accuracy and low cost, compared to broader genetic testingUsed during cascade family evaluationPanel sequencingTests for a pre-specified “set” of genes related to a particular phenotype or clinical conditionFirst-line diagnostic test for the probandUsually, tests for exons onlyLarger panels may be warranted for overlap or ambiguous phenotypes, with the recognition that larger panels may lead to the identification of more variants of uncertain significanceFor unequivocal phenotypes, targeted panels are preferred, as larger panels are unlikely to increase clinical yield and may introduce ambiguous resultsWhole-exome and whole-genome sequencingComprehensive genetic characterization of coding regions only (exome) or entire genomeTypically reserved for research settings, but can be considered in the evaluation in proband in very heterogenous conditions Non-sequencing testing is also available through PCR for pre-specified variants What is the role of genetic testing in the management of inherited cardiovascular diseases? 9 Genetic testing is used to identify the underlying genetic etiology in a patient with a known or suspected inherited cardiovascular disease. Genetic testing is beneficial when the result alters the treatment, informs about the prognosis, and leads to testing in immediate family members. Common inherited cardiovascular diseases include Brugada syndrome, long QT syndrome, arrhythmogenic cardiomyopathy, dilated cardiomyopathy, hypertrophic cardiomyopathy, catecholaminergic polymorphic ventricular tachycard


    243. Case Report: A Rare Case of Isolated Non-Compaction Cardiomyopathy – Mount Sinai Medical Center in Miami Nov 20, 2022
    Show notes

    CardioNerds Cofounder Dr. Amit Goyal is joined by Dr. Douglas Salguero (Internal medicine resident), Dr. Francisco Ujueta (Cardiology fellow), and Dr. Priscilla Wessly (Chief cardiology fellow) from the Columbia University Division of Cardiology at Mount Sinai Medical Center in Miami to discuss a rare case of isolated non-compaction cardiomyopathy. Expert commentary is provided by Dr. Christos Mihos (Director, Echocardiography Laboratory, Columbia University Division of Cardiology, Mount Sinai Medical Center). Audio editing by CardioNerds Academy Intern, Shivani Reddy. 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 - Non-Compaction Cardiomyopathy Episode Schematics & Teaching The etiology has been a constant debate since 1980. It has been debated among researchers and clinicians whether LVNC is a physiologic or a pathologic manifestation. Waning et al., classified 327 unrelated patients into 3 categories: 1) genetic, 2) probably genetic, or 3) sporadic, identifying the most common mutations: MYH7, MYBPC3 and TTN in the genetic LVNC patients, which mostly encode for sarcomere, Z-disc and nuclear-envelope proteins. This supports the hypothesis that the inherited phenotype can arise from a gene mutation possibly during embryogenesis, disrupting the physiologic compaction of normally developing myocardium, which progresses from the base to the apex of the cardiac tissue. It is estimated that genetic LVNC accounts approximately 18-44% of cases, with autosomal dominant transmission being the most common form of inheritance. Physiologic remodeling with prominent trabeculations may be noted in athletes and pregnant women, in comparison to pathologic remodeling which may be encountered in patients with cardiomyopathy (e.g. pressure or volume load). (1) There is no pathognomonic signs or symptoms in LVNC. LVNC patients may encounter various potential clinical characteristics. Presentations are myriad and include heart failure symptoms (HFrEF or HFpEF), ventricular tachycardia (VT/VF), atrial fibrillation, thromboembolism including cerebrovascular accident (CVA), and syncope. In a cohort of 95 probands with LVNC investigated in Europe, as many as 32.3% had an ICD/CRT-D implantation, with 11.8% experiencing a cardiovascular death and 18.2% having an appropriate ICD shock. (2) Imaging plays a key role in diagnosis for LVNC. The identification and diagnosis of LVNC is evaluated using 2D echocardiography. The initial proposed method by Chin et al., evaluated the size of the trabeculation in the center. (3) The most commonly used criteria, Jenni et al. (4), entail the following four finding: Two-layer structure, with a thin compacted layer and a thick non-compacted layer measure at end-systole at the parasternal short-axis view. LVNC is defined by a ratio of N/C > 2 Absence of co-existing cardiac structural abnormalities Prominent, excessive trabeculations and deep intra-trabecular recesses Recesses supplied by intraventricular blood on color doppler Cardiac MRI has increased the diagnostic accuracy in the diagnosis of LVNC. It has been suggested that a NC/C ratio of > 2.3 in diastole distinguished pathological non-compaction, with sensitivity of 86% and a specificity of 99%, respectively. Although studies have shown an increase specificity with cardiac MRI, caution is needed as it may overestimate the presence of LVNC. Late gadolinium enhancement which suggests myocardial fibrosis or scar has been shown to have some prognostic value in LVNC patients. (5) Management for LVNC is multifaceted. As above,LVNC has a variety of presentations and prevailing manifestations will differ among patients. Therefore, the diagnostic and management approach much be personalized for a given patient. Heart failure with reduced ejection fraction is the most common presentation, thus treatment follows guided directed medical therapy, including ACEi/ARB/ARNi, beta-blockers, MRA, SGLT2i, etc. The risk for thromboembolism in patients with LVNC has not been well-established although case-series have noted an increase in clot formation due to the increase in intertrabecular recesses. Although no definitive criteria for anticoagulation have been suggestive in patients with LVNC and atrial fibrillation who meet current recommendations. There is a weak recommendation for anticoagulation in patients with LVNC and LVEF


    242. ACHD: Atrial Septal Defects with Dr. Richard Krasuski Nov 15, 2022
    Show notes

    CardioNerds (Dan Ambinder), episode lead Dr. Sarah Fahnhorst (ACHD Cardiologist at Spectrum Health in Grand Rapids, Michigan), and series co-chair Dr. Agnes Koczo (fellow at UPMC) learn about ASD from Dr. Richard Krasuski (ACHD Cardiologist and Director of ACHD at Duke University). Audio editing by CardioNerds Academy Intern, student doctor Adriana Mares An atrial septal defect (ASD) is a common congenital heart disease most often diagnosed in childhood, but initial presentation can be in adulthood. ASDs are abnormal communications between the left and the right atrium. There are four types of ASDs with different embryologic origins. If the defects are large, they will require percutaneous or surgical closure. Unrepaired defects can lead to symptoms of shortness of breath, exercise intolerance, recurrent chest infections, or pulmonary hypertension. This episode of CardioNerds will review the natural history, embryologic origin, diagnostic modalities/findings, indication for closure and long term complications of repaired and unrepaired atrial septal defects. The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Atrial Septal Defects It’s a CLASSIC! – On physical exam a wide fixed split S2 along with a systolic ejection murmur due to increased blood flow across the pulmonary valve and potentially a diastolic rumble across the tricuspid valve are CLASSIC findings with atrial septal defects. Atrial septal defects are not all the same. There are four types of atrial septal defects: secundum ASD, primum ASD, sinus venosus and coronary sinus defects (NOTE – the latter are atrial level defects which actually do not involve the interatrial septum). The different types warrant a different approach to closure. Use your tools and if your suspicion is high for an atrial septal defect, keep looking. Sinus venosus defects can easily be missed since the superior vena cava is difficult to image in adults. Diagnostic tools include: history and physical exam (USE the stethoscope), ECG, echocardiogram, cardiac MRI, cardiac CT, and cardiac catheterization.Not all defects NEED to be closed immediately. Moderate-large defects with a shunt greater than 1.5:1 should be closed due to increased risk of pulmonary hypertension and arrhythmias, barring contraindications. Surgery was previously the gold standard for closure of ASDs, but many defects especially secundum atrial septal defects are closed in the cath lab. Show notes - Atrial Septal Defects Notes (developed by Dr. Sarah Fahnhorst What are the four different types of atrial level defects?Secundum atrial septal defectMost common type of atrial septal defect (75%)Located in the center of the atrial septum (fossa ovalis)Hole in the primum septum due to deficiency of the septum secundumPrimum atrial septal defectAccounts for 15-20% of ASDLocated at the inferior portion of the atrial septumIn the spectrum of atrioventricular septal defects/endocardial cushion defectsDefect in the development of the septum primumAssociated with cleft left AV valve, ventricular septal defects, and subaortic stenosisSinus venosus defectAccounts for 5-10% of atrial level defectNot a “septal” defect!Located near the superior vena cava-right atrial junction or very rarely at the mouth of the inferior vena cava80-90% of sinus venosus defects are associated with partial anomalous pulmonary venous returnCoronary sinus defectLeast common 1.5:1) and no signs of pulmonary hypertensionSymptomatic with a large shunt or signs of right heart enlargement or decreased systolic functionPrimum, sinus venosus, and coronary sinus defects will not close spontaneously What are treatment options available for each type of atrial septal defect?Surgical: Primum, sinus venosus, and coronary sinus defects are typically closed surgically. Some centers are closing sinus venosus defects percutaneously if anatomy is suitable particularly when surgery is deemed high risk.If there are additional structural heart defect such as a VSD or cleft mitral valve, then surgical closure is preferred. Transcatheter device closure: Secundum defects can be closed in the cath lab if they have sufficient rims, otherwise they will require surgical closure What are complications of repaired and unrepaired atrial septal defects?Repaired:TranscatheterResidual defectSmall increased risk for atrial arrhythmiasDevice embolizationSurgicalResidual defectSmall increased risk for atrial arrhythmiasUnrepairedPulmonary hypertensionEisenmenger syndromeAtrial arrhythmias (atrial fibrillation or atrial flutter)Right heart failureDecreased exercise and functional capacityIncreased risk of paradoxical embolism leading to risk of thromboembolic stroke References - Atrial Septal Defects Perloff JK. Surgical Closure of Atrial Septal Defect in Adults. New England Journal of Medicine. 1995;333(8):513-514. doi:10.1056/nejm199508243330809Stout KK, Daniels CJ, Aboulhosn JA, et al. 2018 AHA/ACC Guideline for the Management of Adults With Congenital Heart Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019;139(14):e698-e800. doi:doi:10.1161/CIR.0000000000000603Baumgartner H, De Backer J, Babu-Narayan SV, et al. 2020 ESC Guidelines for the management of adult congenital heart disease: The Task Force for the management of adult congenital heart disease of the European Society of Cardiology (ESC). Endorsed by: Association for European Paediatric and Congenital Cardiology (AEPC), International Society for Adult Congenital Heart Disease (ISACHD). Eur Heart J. 2020;42(6):563-645. doi:10.1093/eurheartj/ehaa554Gatzoulis MA, Webb GD, Daubeney PEF. Diagnosis and management of adult congenital heart disease. 3 ed. Elsevier Health Sciences; 2017.Saremi F. Cardiac CT and MR for Adult Congenital Heart Disease. Springer New York; 2013.Allen HD. Moss & Adams' heart disease in infants, children, and adolescents, including the fetus and young adult. 9 ed. Lippincott Williams and Wilkins; 2016. Meet Our Collaborators! Adult Congenital Heart AssociationFounded in 1998, the Adult Congenital Heart Association is an organization begun by and dedicated to supporting individuals and families living with congenital heart disease and advancing the care and treatment available to our community. Our mission is to empower the congenital heart disease community by advancing access to resources and specialized care that improve patient-centered outcomes. Visit their website (https://www.achaheart.org/) for information on their patient advocacy efforts, educational material, and membership for patients and providers CHiP Network The CHiP network is a non-profit organization aiming to connect congenital heart professionals around the world. Visit their website (thechipnetwork.org) and become a member to access free high-quality educational material, upcoming news and events, and the fantastic monthly Journal Watch, keeping you up to date with congenital scientific releases. Visit their website (https://thechipnetwork.org/) for more information. Heart UniversityHeart University aims to be “the go-to online resource” for e-learning in CHD and paediatric-acquired heart disease....


    241. Case Report: A Massive Surprise – UCLA Nov 11, 2022
    Show notes

    CardioNerds Cofounder Dr. Amit Goyal is joined by an esteemed group of UCLA cardiology fellows – Dr. Patrick Zakka (CardioNerds Academy Chief), Dr. Negeen Shehandeh (Chief Fellow), and Dr. Adrian Castillo – to discuss a case of primary cardiac angiosarcoma. An expert commentary is provided by Dr. Eric Yang, beloved educator, associate clinical professor of medicine, assistant fellowship program director, and founder of the Cardio-Oncology program at UCLA. Case synopsis: A female in her 40s presents to the ED for fatigue that had been ongoing for approximately 1 month. She also developed night sweats and diffuse joint pains, for which she has been taking NSAIDs. She was seen by her PCP and after bloodwork was done, was told she had iron deficiency so was on iron replacement therapy. Vital signs were within normal limits. She was in no acute distress. Her pulmonary and cardiac exams were unremarkable. Her lab studies showed a Hb of 6.6 (MCV 59) and platelet count of 686k. CXR was without significant abnormality, and EKG showed normal sinus rhythm. She was admitted to medicine and received IV iron (had not consented to receiving RBC transfusion). GI was consulted for anemia work-up. Meanwhile, she developed a new-onset atrial fibrillation with rapid ventricular response seen on telemetry, for which Cardiology was consulted. A TTE was ordered in part of her evaluation, and surprisingly noted a moderate pericardial effusion circumferential to the heart. Within the pericardial space, posterior to the heart and abutting the RA/RV was a large mass measuring approximately 5.5x5.9 cm. After further imaging work-up with CMR and PET-CT, the mass was surgically resected, and patient established care with outpatient oncology for chemotherapy. 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 - primary cardiac angiosarcoma Episode Schematics & Teaching Pearls – primary cardiac angiosarcoma The pericardium is composed of an outer fibrous sac, and an inner serous sac with visceral and parietal layers. Pericardial masses can be primary (benign or malignant) or metastatic. There are other miscellaneous pericardial masses. Imaging modalities for the pericardium include echocardiography, cardiac CT and cardiac MRI. There is also role for PET-CT in pericardial imaging for further characterization of pericardial masses. Cardiac angiosarcomas are extremely rare but are the most common cardiac primary malignant tumors. Evidence-based management if lacking because of paucity of clinical data given the rarity of cardiac angiosarcomas. Surgery is the mainstay of therapy. Radiotherapy and chemotherapy are often used as well. Notes – primary cardiac angiosarcoma Pericardial Anatomy The pericardium is a fibroelastic sac composed of two layers. Outer layer: fibrous pericardium (


    240. CardioNerds Rounds: Challenging Cases – Antithrombotic Management with Dr. Deepak Bhatt Nov 03, 2022
    Show notes

    It’s another session of CardioNerds Rounds! In these rounds, Dr. Priya Kothapalli (Interventional FIT at University of Texas at Auston, Dell Medical School) joins Dr. Deepak Bhatt (Dr. Valentin Fuster Professor of Medicine and Director of Mount Sinai Heart) to discuss the nuances of antithrombotic therapy. As one of the most prolific cardiovascular researchers, clinicians, and educators, CardioNerds is honored to have Dr. Bhatt on Rounds, especially given that Dr. Bhatt has led numerous breakthroughs in antithrombotic therapy. Come round with us today by listening to the episodes of #CardsRounds! Audio editing by CardioNerds Academy Intern, Dr. Christian Faaborg-Andersen. 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 Challenging Cases - Atrial Fibrillation with Dr. Hugh Calkins 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 - Antithrombotic Management with Dr. Deepak Bhatt Case #1 Synopsis: A woman in her early 70s with a history of hypertension, hyperlipidemia, and paroxysmal atrial fibrillation presented with sudden-onset chest pressure and diaphoresis while at rest and was found to have an acute thrombotic 99% mid-LAD occlusion. The patient received OCT-guided PCI with a single drug-eluting stent. We discussed what the appropriate antithrombotic strategy would be for a patient with recent acute coronary syndrome and atrial fibrillation. Case #1Takeaways According to the recent 2021 revascularization guidelines, in patients with atrial fibrillation undergoing PCI and taking oral anticoagulant therapy, it is recommended to discontinue aspirin after 1 to 4 weeks while maintaining P2Y12 inhibitors in addition to a non-vitamin K oral anticoagulant or warfarin.There are two recent trials – AUGUSTUS and the ENTRUST-AF PCI trial – that evaluated regimens of apixaban and edoxaban, respectively, that support earlier findings reporting lower bleeding rates in patients maintained on oral anticoagulant plus a P2Y12 inhibitor compared to triple therapy.Of note, none of these trials were specifically powered for ischemic endpoints, but when pooling data from these trials, rates of death, MI and stent thrombosis with dual therapy were similar to those seen in patients on triple therapy.Additionally, all of these patients enrolled in these trials were briefly treated with triple therapy after PCI before the aspirin was discontinued. In the 2021 guidelines, it is noted that analyses of stent thrombosis suggest that 80% of events occur within 30 days of PCI. Thus, it is reasonable to consider extending triply therapy to 1 month after PCI in high risk patients to reduce risk of stent thromboses.In AUGUSTUS, 90% of patients received clopidogrel as their P2Y12 inhibitor Case #2 Synopsis: A man in his mid-50s with a history of peripheral vascular disease with prior SFA stent for chronic limb ischemia, hyperlipidemia, tobacco use, diabetes, and chronic kidney disease presented with a two day history of “reflux” that was worse with exertion and that improved with rest and associated with diaphoresis. He was diagnosed with an NSTEMI. His LHC revealed 99% mid-RCA thrombotic occlusion with moderate disease in the LAD. He underwent thrombectomy and PCI with a single drug-eluting stent to the RCA. We discussed his short-term and long-term antithrombotic therapy Case #2 Takeaways There were several things discussed regarding the management of this patient’s “poly-vascular disease.” One of the aspects was what to do with his antithrombotic therapy after one year and specifically how the COMPASS trial may apply to this patient.In the COMPASS trial, more than 27,000 patients with stable CAD or peripheral arterial disease (PAD) were randomly assigned to rivaroxaban plus aspirin, rivaroxaban alone, or aspirin alone with a mean follow-up of about 23 months. Of note, the dose of rivaroxaban in the combination arm was 2.5 mg orally twice per day. The patients on combination therapy compared to aspirin alone had a 23% relative risk reduction in CV mortality (1.7 vs. 2.2%; HR 0.78 [95% CI 0.64-0.96]) and nearly 50% reduction in ischemic stroke. As expected, there was high rates of major bleeding in the combination arm (3.1 vs. 1.9%; HR 1.7 [95% CI 1.4-2.05]).As with most decisions in medicine, each clinician would need to balance reducing ischemic events with bleeding risk for each individual patient. However, the COMPASS trial provides further evidence that low-dose oral anticoagulant with rivaroxaban in addition to aspirin can be effective in reducing ischemic events and CV mortality in patients with established atherosclerotic disease. Case #3 Synopsis A man in his early 60s with a history of hypertension and active tobacco use presented to a local hospital with anteroseptal STEMI c/b cardiac arrest with ventricular tachycardia. After multiple defibrillation attempts and CPR, the patient was able to achieve return of spontaneous circulation with intact mental status. The patient was pre-loaded with aspirin, ticagrelor, cangrelor and heparin and brought to the catheterization lab. There was diffuse moderate to severe stenoses in the RCA and a hazy distal LM lesion, but the culprit was a complete occlusion of the proximal LAD to which the patient received a single DES and another to the mid LAD. The patient was then brought to a tertiary care center where consideration was given for elective CABG given the residual disease. We discussed timing of CABG and when/if to pursue it, as well as antithrombotic management in this circumstance Case #3 Takeaways Amongst the things we discussed was the role of cangrelor pre-left heart catheterization. Cangrelor is a potent, short-acting, and reversible intravenous P2Y12 inhibitor with rapid onset of platelet inhibition. And within 1 hour of discontinuation, platelet function can be restored.In the small CANTIC trial, patients undergoing primary PCI pre-treated with crushed 180-mg loading dose of ticagrelor were randomized to cangrelor versus placebo. Within five minutes, cangrelor led to significant P2y12 inhibition which persisted throughout the drug infusion. Of note, there were no drug interactions with ticagrelor given concomitantly with cangrelor at the start of PCI. Thus, in this trial, cangrelor proved to be an effective strategy in bridging latent platelet inhibition that can be seen with oral drugs.This trial was not powered for clinical outcomes, but serves as evidence that cangrelor can be considered for pre-treatment to bridge the gap in platelet inhibitor effects in select patients in whom oral absorption may be compromised or slowed. References Eikelboom JW, Connolly SJ, Bosch J et al. Rivaroxaban with or without Aspirin in Stable Cardiovascular Disease. N Engl J Med. 2017 Oct 5;377(14):1319-1330.Franchi F, Rollini F, Rivas A et al. Platelet Inhibition With Cangrelor and Crushed Ticagrelor in Patients With ST-Segment-Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention. Circulation. 2019 Apr 2;139(14):1661-1670.Lopes RD, Heizer G, Aronson R, et al. Antithrombotic therapy after acute coronary syndrome or PCI in atrial fibrillation. N Engl J Med. 2019; 380:1509–1524.Writing Committee Members, Lawton JS, Tamis-Holland JE et al. 2021 ACC/AHA/SCAI Guideline for Coronary Artery Revascularization: Executive Summary: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol. 2022 Jan 18;79(2):197-215 Production Team Karan Desai, MD Natalie Stokes, MD Amit Goyal, MD Daniel Ambinder, MD


    239. CCC: Approach to RV Predominant Cardiogenic Shock with Dr. Ryan Tedford Oct 23, 2022
    Show notes

    CardioNerd (Daniel Ambinder) and series co-chairs Mark Belkin (AHFT Fellow, University of Chicago) and Karan Desai (Cardiologist, Johns Hopkins), join fellow lead, Dr. Pablo Sanchez (FIT, Stanford) for a discussion with Dr. Ryan Tedford (Professor of Medicine at the Medical University of South Carolina) about Right Ventricular (RV) predominant cardiogenic shock. In this episode we explore risk factors, pathophysiology, hemodynamics, and treatment strategies in this common and complex problem. We dissect three cases that epitomize the range of diagnostic dilemmas and management decisions in RV predominant shock, as Dr. Tedford expertly weaves us through the pathophysiology and decision-making involved in managing the “people’s ventricle.” Audio editing by Dr. Gurleen Kaur (Director of the CardioNerds internship program, CardioNerds academy fellow, and IM resident at Brigham and Women’s Hospital). 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 • 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 - RV Predominant Cardiogenic Shock The degree of RV dysfunction and failure are modulated by stretching its capacity to tolerate insults from deranged afterload, preload, and contractility.Afterload insults are MUCH LESS tolerated than other insults and broadly comprise the most common pathophysiologic cause of both acute and chronic RV failure.RV and left ventricular (LV) function are anatomically and physiologically connected. Progressive derangements in RV function can lead to the deadly “RV spiral,” in which poor RV function causes lower LV preload, leading to hypotension, and thus worsening RV perfusion and function.In RV failure/shock, some basic tenets including treating reversible causes, optimizing preload and afterload, and using inotropes and/or temporary MCS for as limited time as possible.Many acute RV failure patients can recover, but multiorgan injury plays an important role. Therefore, thoughtful and expeditious use of mechanical circulatory support is important. Show notes - RV Predominant Cardiogenic Shock Notes drafted by Dr. Pablo Sanchez. What is the basic difference between RV dysfunction and failure?Dysfunction: Abnormalities in systolic/diastolic function of the RV, but not necessarily to the point of leading to end-organ perfusion defects. RV dysfunction leads to poor outcomes regardless of mechanism.1Failure: Clinical syndrome of inability of RV to maintain adequate output despite adequate preload. 1 How is the RV different from the LV and what impact does it have on pathophysiology and hemodynamics?The LV and RV originate from different embryologic “heart fields.”1,2The RV wall is thinner and more compliant and has only two layers (instead of 3 like the LV).3 Furthermore, unlike the LV which has a significant proportion of endocardial and epicardial transverse myocardial fibers, the RV myocardial fibers are aligned in a longitudinal plane for the most part. Thus, a more significant proportion of RV systolic contraction is longitudinal – base of the ventricle moving towards the apex.The RV is crescent-shaped and has a large surface-to-volume ratio meaning smaller inward motion ejects the same stroke volume. 1Hemodynamically, the RV takes blood from a low-pressure venous system and gives it to a distensible system with low impedance (the normal pulmonary circuit at baseline typically has a resistance one-tenth of the systemic resistance). Therefore, volume loads (preload) are much better handled than pressure (afterload).1 What is RV-PA coupling?As Dr. Tedford noted, RV-PA coupling describes “the interaction of RV contractility and afterload (resistive and pulsatile components). It is the most comprehensive description of RV function and therefore the Gold Standard.” Whether we are referring to the LV or RV, the basic concept of coupling describes the energy transfer between ventricular contractility and arterial afterload.RV-PA coupling has typically been assessed by pressure-volume loops, with ventricular contractility assessed by end-systolic elastance (a load-independent measure of systolic function) and arterial afterload by effective arterial elastance.MODUS OPERANDI: RV dysfunction and eventual failure is modulated by stretching its capacity to tolerate insults from afterload, preload, and contractility. What leads to ACUTE right heart failure?Most commonly results from:1Abrupt increases in afterload (e.g., think PE, hypoxia, and acidemia).Decreased contractility (e.g., think ischemia such as RV infarction, myocarditis, and post-cardiotomy).Volume overload can sometimes lead to acute right heart failure, particularly in the setting of another categorical insult such as septic cardiomyopathy or LVAD support. What leads to CHRONIC right heart failure?This is different than acute right heart failure. Most commonly chronic right heart failure results from:1Gradual increases in afterload (e.g., think pulmonary arterial hypertension).Chronic volume overload (e.g., longstanding tricuspid regurgitation, atrial septal defect, and other congenital lesions like double outlet RV).Contractility (e.g., including the isolated RV cardiomyopathies like arrhythmogenic right ventricular cardiomyopathy or ischemic cardiomyopathy).Other pathologies certainly affect multiple categories (e.g., Ebstein’s anomaly which is a function of contractility and volume overload or single ventricle physiology like post-Fontan patients – for more on these and other ACHD lesions, enjoy the CardioNerds ACHD Series!)MODUS OPERANDI: The cardiovascular system is wholly connected, and acute decompensation leads to progressive derangements in the above levers (including LV function). This phenomenon is called the RV spiral. How do we manage RV failure?The most important and first step is the treatment of reversible causes. For instance, acute coronary syndrome involving the RV requires percutaneous intervention (PCI) or pulmonary embolism requires anticoagulation and/or thrombolytic/device/surgical therapy.PRELOAD OPTIMIZATIONEnsuring that there is adequate preload is a key tenet of diagnosing and treating RV failure. This may require diuresis or judicious volume resuscitation to maintain cardiac output.While guiding fluid management in the setting of RV failure, one should STRONGLY consider invasive hemodynamic monitoring (e.g., over-resuscitation can lead to decreased LV output through septal shift and ventricular interdependence from pericardial constraint).1General target: We could consider a CVP 10-15 mmHg; however, this will be individualized. Another general rule would also be if that a bolus of 500 cc of crystalloid does not result in hemodynamic improvement, further loading should not be continued, especially without invasive hemodynamic guidance.AFTERLOAD OPTIMIZATION The goal should be to correct reversible causes of elevated pulmonary vascular resistance (e.g., acidosis, hypercapnia, hypoxia, and generally in ventilated patients avoid elevated inspiratory pressures > 30mmHg).1With specialized expert guidance, we can consider selective pulmonary vasodilators (acutely and short-term):One example includes inhaled NO, and in observational studies, short-term use lowered PVR and increased RV ejection.4We also have to remember the consequences of reducing RV afterload. Acutely increasing LV preload in a baseline abnormal LV may lead to distention, lowered cardiac output, and pulmonary edema.1Pulmonary vasodilators can act on specific pathways (e.g., nitric oxide, prostacyclin, endothelin-1, and soluble guanylate cyclase stimulators) and come in various forms (oral, inhaled, and intravenous).CONTRACTILITY AUGMENTATION (INOTROPES)We typically utilize inotropes in concert with the prior two but optimize loading so the time we need inotropes is minimal.1Short-term use can improve hemodynamics. Longer-term use will typically increase myocardial O2 consumption and is associated with increased mortality. The RV has coronary perfusion in systole and diastole, so peripheral vasopressors are helpful to maintain perfusion, especially if systolic blood pressure is less than RV systolic pressure.1GOAL: Increase contractility without increasing RV afterload.For those failing to respond to these above measures to optimize preload, afterload, and contractility, there may be a role for temporary mechanical circulatory support (see #10 below). How do we decide between dobutamine and milrinone?BOTH inotropes can lead to hypotension, have similar clinical outcomes, hemodynamic efficacy and arrhythmogenic potential1 (despite the adage that attributes more arrhythmias to dobutamine, studies show the risk is typically the same in both5).Milrinone is a more potent vasodilator (systemic and pulmonary) typically leading to greater decreases in end-diastolic pressures in the ventricles.1 It is renally cleared, has a longer half-life, and acts through a separate mechanism pathway compared to beta-blockade, thus patients can be on milrinone and beta blockers at the same time on a case-by-case basis.1Dobutamine has a shorter half-life, with rapid onset/offset and so may be more ideal in unstable/hypotensive patients.1 What if the patient is hypotensive?In this circumstance, we would need an ino-constrictor or peripheral vasoconstrictor.Vasopressin has almost no impact on PVR, so unlike catecholamines, it does not directly worsen RV afterload.1 What are some important invasive hemodynamic parameters to be aware of?...


    238. Cardio-Oncology: Radiation-Associated Cardiovascular Disease with Dr. Eric Yang Oct 13, 2022
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    CardioNerds (Dr. Patrick Azcarate, Dr. Teodora Donisan, and Amit Goyal) discuss Radiation-Associated Cardiovascular Disease (RACD) with Dr. Eric Yang, cardio-oncologist, assistant professor of medicine, and associate fellowship program director at UCLA. RACD is a consequence of radiation treatment for various mediastinal tumors (breast, lung, lymphoma). It is the second most common cause of morbidity and mortality in patients treated with mediastinal radiation for cancer. While novel techniques decrease radiation exposure during cancer treatment, the incidence is expected to increase because of historical practices and delayed onset of symptoms. The prevalence of RACD is difficult to estimate given under-recognition. Additionally, most of the data comes from patients treated with radiation techniques from decades ago. In this discussion we review every nook and cranny of RACD to help guide you the next time you see a patient with a history of chest radiation. Review this CardioNerds Case Report of radiation associated cardiovascular disease for more: Episode #169. Chest pain in a Young Man – “A Gray (Gy) Area” – UC San Diego. Audio editing by CardioNerds Academy Intern, student doctor Yousif Arif. This episode is supported by a grant from Pfizer Inc. This CardioNerds Cardio-Oncology series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Giselle Suero Abreu, Dr. Dinu Balanescu, and Dr. Teodora Donisan. Pearls • Notes • References • Production Team 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 - Radiation-Associated cardiovascular disease Due to the legacy effect, the incidence of RACD will continue to increase in the next few years. When treating patients with a history of mediastinal radiation, we should remember to ask: How much radiation was given? Could the heart have been exposed? Radiation can affect every part of the heart by causing coronary artery disease (CAD), valvulopathy, myocardial disease, conduction disease, and pericardial disease. Exposure to ~25-30 Gy or more significantly increases the risk but RACD can occur at lower doses. Try to delay surgery as much as possible and do all you can in one operation to avoid re-operation in the future. For revascularization, percutaneous coronary intervention (PCI) is typically preferred over coronary artery bypass grafting (CABG) but the choice should be individualized in consultation with a multidisciplinary heart team experienced in the management of RACD. In general, for aortic valve disease, transcatheter replacement is recommended over surgical aortic valve replacement. For mitral valve disease, surgical replacement is recommended over repair. Every decision should be made with a heart team approach and made unique to that specific patient. Show notes - Radiation-Associated cardiovascular disease Notes were drafted by Dr. Patrick Azkarate. 1. Understand the pathophysiology of RACD Ionizing radiation has the potential to damage DNA. Both normal cells and cancer cells get damaged, but cancer has less effective DNA repair mechanisms and therefore malignant cells are more vulnerable to radiation therapy. After radiation causes acute damage, this sets off an inflammatory cascade leading to myofibroblast activation, fibrosis and collagen deposition, and subsequent stiffening of the myocardium and vessels. 2. What may increase one’s risk of developing RACD? Young age (30 Gy) or high dose of radiation fractions (>2 Gy/day) Anterior or left chest radiation (breast cancer, lung cancer, lymphoma) Pre-existing cardiovascular disease Tumor in or next to the heart Concomitant chemotherapy (e.g. anthracyclines) 3. What are some techniques being used to reduce radiation exposure? Shielding Respiratory gating techniques (e.g. deep inspiratory breath-hold, activated breathing control) Smaller repeated fractions Narrow tangential beams Proton therapy 4. What are prevention and screening strategies for RACD? Annual history and physical examinationTreat pre-existing conditionsScreen for RACD (myocardial, valvular, pericardial, CAD, or conduction system disease)5 years post-exposure, screen for CAD and consider stress test every 2 years10 years post-exposure, screen for valvular heart disease with an echocardiogram every 2 years1 5. Discuss diagnosis and management of specific complications of RACD CAD The risk of radiation induced CAD (RICAD) is 7.5% per Grey Unit (Gy). The risk is roughly constant, begins several years after exposure, and persists for at least 2-3 decades (>50% of excess ischemic events occurring >10 years after RT).2 Radiation causes inflammatory plaque with high collagen and fibrin content, similar to accelerated atherosclerosis. Angiographic characteristics: Ostial or proximal Anterior and central (predominantly affecting the left anterior descending and the right coronary arteries) Severe, diffuse Long, smooth, concentric, and tubular Treatment: CABG vs PCI While there are no head-to-head trials comparing CABG vs PCI in patients with RICAD, it is known that compared to the general population, following CABG they have worse outcomes (increased risk of wound dehiscence, infection, graft failure, and death).3 The data for PCI is mixed but most recently have shown that patients with RICAD undergoing PCI have similar outcomes compared to patients without radiation exposure.4 Unless there is an additional indication for surgery, PCI for chronic CAD usually preferred. If multi-vessel CAD or higher Syntax score (≥ 22) consider CABG. Other considerations might guide percutaneous vs surgical revascularization Porcelain aorta Fibrotic bypass grafts (internal mammary artery) in the radiation field Multi-valvular disease Valvular disease Radiation causes progressive valve thickening and calcification leading to valve leaflet retraction, followed by regurgitation and then stenosis. Patients usually become symptomatic 1-2 decades after radiation exposure (later than CAD). Prevalence of aortic regurgitation (AR) at 10 years is 4% and at 20 years is 60%. The prevalence of aortic stenosis (AS) at 10 years 0% but at 20 years: 16% Mitral regurgitation (MR) and AR are the most common and occur due to leaflet retraction. These ultimately progress to stenosis. MR is the most common reason for surgery. Echocardiogram is done to evaluate the valves. Surrounding structures may show calcification, such as the annulus, subvalvular apparatus, or aorta-mitral curtain (a hallmark of previous heart irradiation which is associated with mortality in patients undergoing cardiac surgery). Management decisions are complex, depends on the valvular lesion(s) involved, and should be guided by a heart team approach. For aortic valve disease, TAVR is preferred over SAVR (unless there is another indication for surgery or there is excess risk for coronary obstruction or annular rupture). If SAVR is pursued, usually try to replace all valves (even if one is just mild to moderate) to avoid re-operation. For the mitral valve, data is mixed between surgical vs transcatheter approaches. In general, if surgery is indicated then the valve is replaced and not repaired (irradiated valve tissue is fibrotic and calcified) Given increased risk of reoperation, mechanical prostheses may be appealing, especially for younger patients. If there are contraindications to anticoagulation, then a bioprosthesis should be used. General cardiothoracic surgery principles in patients with RACD Worse long-term outcomes compared to age and sex-matched controls undergoing similar procedures Reoperation portends significantly higher risk compared to non-RACD patients Delay surgical intervention as long as possible Address all issues with a complete operation the first time Surgical planning may involve cardiac magnetic resonance imaging (CMR) to look for fibrosis, computer tomography (CT) to identify calcified structures (intra- and extra-cardiac), transthoracic echocardiogram (TTE), right and left heart catheterization to evaluate for restriction vs constriction, coronary angiogram. Myocardial disease In terms of pathophysiology, radiation causes an acute inflammatory cascade, then a pro-fibrotic milieu which leads to myocardial fibrosis and reduced microvascular proliferation and density. RACD-related myocardial dysfunction is defined as >10% decrease in LVEF to a value


    237. CCC: Approach to LV Predominant Cardiogenic Shock with Dr. Shashank Sinha Oct 08, 2022
    Show notes

    Cardiogenic shock (CS) remains a complex, multifactorial syndrome associated with significant morbidity and mortality. The CardioNerds Critical Care Cardiology Series tackles this important syndrome in a series of several episodes including: LV-predominant Shock, RV-predominant Shock, and Bi-ventricular Shock. In this episode, we review the definitions, pathophysiology, evaluation, and contemporary management, including use of inotropes and mechanical circulatory support, of left ventricular (LV) predominant CS. Series co-chairs Dr. Eunice Dugan and Dr. Karan Desai along with CardioNerds Co-founders Dr. Amit Goyal and Dr. Daniel Ambinder were joined by FIT lead, Dr. Vanessa Blumer, the recipient of the AHA 2021 Laennec Fellow in Training Clinician Award and currently pursuing Advanced Heart Failure and Transplant fellowship at the Cleveland Clinic. Our episode expert is Dr. Shashank Sinha, an Advanced Heart Failure, Mechanical Circulatory Support, and Cardiac Transplant cardiologist, Medical Director of the Cardiac Intensive Care Unit, and Director of the Cardiovascular Critical Care Research Program at INOVA Fairfax Hospital. His illustrious career accomplishments include being a Steering Committee member and site Principal Investigator for the multicenter Cardiogenic Shock Working Group and Critical Care Cardiology Trials Network. Audio editing by CardioNerds academy intern, Anusha Gandhi. 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 • 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 - LV Predominant Cardiogenic Shock LV-CS is complex! It is important to recognize that the pathophysiology of heart failure-related cardiogenic shock (HF-CS) is distinct from that of acute myocardial infarction (AMI-CS), and also crucial to differentiate between LV-dominant, right ventricular (RV)-dominant and biventricular (BiV)-shock.The SCAI SHOCK Stage Classification provides a unified and standardized vocabulary when assessing severity of CS, and facilitates communication about the diagnosis, presentation, and evolving nature of CS.Norepinephrine is considered the initial vasopressor of choice in most CS patients; the initial inotrope choice is a bit more nuanced!When considering mechanical circulatory support (MCS) for LV shock, high-quality data to guide therapy is lacking but one must always consider “the right patient, for the right device, at the right time” and remember that “pumps pump blood, decisions save lives”.Multidisciplinary, team-based care is paramount to improving survival of the critically ill patient with CS. Show notes - LV Predominant Cardiogenic Shock Notes drafted by Dr. Vanessa Blumer. 1. What tools do you use to define LV CS? CS is a hemodynamically complex and multifactorial syndrome, one of the most common indications for admission to a cardiac intensive care unit, with short-term mortality ranging from 35-50%.It is defined by systemic hypoperfusion and tissue hypoxia due to a primary cardiac insult or dysfunction.Clinical criteria used to define CS typically include evidence of hypotension (classically defined as SBP 90 mmHg) AND evidence of end-organ hypoperfusion (for example, serum lactic acid > 2 mmol/L, acute kidney injury, acute liver injury, altered mental status) in the setting of acute coronary syndrome or acute decompensated heart failure.Laboratory markers, including serum lactic acid, liver function tests, kidney function, and biomarkers including troponin and natriuretic peptides may be helpful. An echocardiogram is an excellent point of care tool to help demonstrate and confirm evidence of LV systolic dysfunction and/or valvular abnormalities. Finally, a right heart catheterization (demonstrating an abnormally low cardiac output and index with elevated filling pressures) may be useful in facilitating the diagnosis and subsequent management. 2. How do HF-CS and AMI-CS lead to different phenotypes? It is important to recognize that HF-CS is now the predominant cause of CS, accounting for more than half of all CS.AMI-CS is characterized by an abrupt presentation due to a primary myocardial ischemic insult leading to necrosis (occurring in 5-10% of AMI patients) and can occur after STEMI or NSTEMI. The canonical clinical course is hypotension due to primary myocardial dysfunction leading to hypoperfusion with congestion as a later clinical or hemodynamic finding.Conversely, a patient with heart failure related shock commonly presents with acutely decompensated heart failure and congestion, leading to hypoperfusion, and culminating in hypotension. 3. How do you distinguish LV-dominant, RV-dominant and BiV shock? LV predominant CS is characterized by high pulmonary capillary wedge pressure (PCWP) and normal or reduced central venous pressure (CVP) in the setting of reduced cardiac output (CO).RV dominant CS is characterized by elevated CVP, normal to low PCWP, and normal to reduced CO.BiV shock is characterized by hypotension, elevated CVP, normal or elevated PCWP, and reduced CO. 4. What is the current role for inotropes, vasodilators, and vasopressors in the management of LV CS? The Acute Cardiovascular Care Association of the European Society of Cardiology published a position statement for the diagnosis and treatment of patients with AMI complicated by CS in 2020. According to this, vasopressors (norepinephrine preferable over dopamine) in the presence of persistent hypotension received a Level of IIb/B recommendation. Intravenous inotropes to increase cardiac output received a IIb/C recommendation.Based on the available evidence and its accompanying limitations, norepinephrine is considered the initial vasopressor of choice in most CS patients. 5. When should we consider management with temporary mechanical circulatory support (t-MCS) devices and how should one strategize device selection? Initiation or escalation of t-MCS largely depends on matching the right device to the right patient at the right time. Because the risk and number of complications increases with duration and type of MCS, these decisions are complex, nuanced, and must consider operator and institutional expertise.When considering type of device (IABP, Impella, ECMO), SCAI Staging and phenotyping (AMI vs HF CS) are absolutely critical. 6. What are treatment goals when following patients with LV CS? Optimize preload, afterload, and contractilityPerform serial reassessment (≤ q 6hr) of hemodynamics & end-organ perfusionAim for timely and tailored treatment escalation/de-escalation Assess for LV and RV recovery (wean t-MCS, vasopressors and inotropes as ableEarly identification of worsening shock: Rising Lactate Increasing pressor requirement Worsening end-organ function CPO 15 and/or PCWP > 15 References - LV Predominant Cardiogenic Shock Abraham J, Blumer V, Burkhoff D, Pahuja M, Sinha SS, Rosner C, Vorovich E, Grafton G, Bagnola A, Hernandez-Montfort JA, Kapur NK. Heart Failure-Related Cardiogenic Shock: Pathophysiology, Evaluation and Management Considerations: Review of Heart Failure-Related Cardiogenic Shock. J Card Fail. 2021 Oct;27(10):1126-1140. doi: 10.1016/j.cardfail.2021.08.010. PMID: 34625131. Kapur NK, Kanwar M, Sinha SS, Thayer KL, Garan AR, Hernandez-Montfort J, Zhang Y, Li B, Baca P, Dieng F, Harwani NM, Abraham J, Hickey G, Nathan S, Wencker D, Hall S, Schwartzman A, Khalife W, Li S, Mahr C, Kim JH, Vorovich E, Whitehead EH, Blumer V, Burkhoff D. Criteria for Defining Stages of Cardiogenic Shock Severity. J Am Coll Cardiol. 2022 Jul 19;80(3):185-198. doi: 10.1016/j.jacc.2022.04.049. PMID: 35835491. CardioNerds Cardiac Critical Care Production Team Karan Desai, MD Dr. Mark Belkin Dr. Yoav Karpenshif Amit Goyal, MD Daniel Ambinder, MD


    236. CardioNerds Rounds: Challenging Cases – Mitral Regurgitation with Dr. Rick Nishimura Oct 06, 2022
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    It’s another session of CardioNerds Rounds! In these rounds, Dr. Natalie Stokes (Formerly FIT at University of Pittsburgh and now General Cardiology Faculty at University of Pittsburgh) and Dr. Karan Desai (formerly FIT at University of Maryland and now General Cardiology faculty at Johns Hopkins) join Dr. Rick Nishimura (Professor of Medicine at Mayo Clinic) to discuss the nuances of managing mitral regurgitation through real cases. Dr. Nishimura has been an author or Chair of the ACC/AHA valve guidelines going back 20 years and has been recognized internationally as one of the world’s best educators, so you don’t want to miss the #NishFactor on these #CardsRounds! Audio editing by CardioNerds academy intern, Pace Wetstein. 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 Challenging Cases - Atrial Fibrillation with Dr. Hugh Calkins 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 - Mitral Regurgitation with Dr. Rick Nishimura Case #1 Synopsis: A man in his 70s with a history of non-ischemic cardiomyopathy (last known LVEF 15-20%) and atrial fibrillation, presented with decompensated heart failure in the setting of moderate to severe mitral regurgitation. He was diuresed, transitioned to GDMT, and referred to cardiac rehabilitation. Over the next 6 months, he continued to have debilitating dyspnea (NHYA Class IIIa) and his outpatient physicians were limited on titrating GDMT further due to hypotension. A TEE was done which demonstrated EF 15%, severe MR by color and quantitation (EROA of 0.5 cm2; Regurgitant Volume of 65 mL), systolic flow reversal in the pulmonary vein and severe tricuspid regurgitation. We were asked how we would approach this case Case #1Takeaways In attempting to keep the evaluation of chronic mitral regurgitation relatively simple, we should ask ourselves three primary questions: (1) What is causing the MR; (2) How much MR is there; and (3) What is the hemodynamic consequence of the MR.To the first question of what is the etiology of the MR – a simple framework is to think of the etiology as an issue of the valve (primary) or an issue of the ventricle/atria (secondary). There is further classification that can be made based on the Carpentier Classification which speaks to the valve leaflet movement and position (normal leaflet motion, excessive leaflet motion [e.g., prolapse], or restricted in systole and/or diastole [e.g., rheumatic heart disease]).During rounds, Dr. Nishimura provided some historical context in that the original valve guidelines had recommendations for intervention on primary mitral regurgitation and not secondary – given that it is considered a disease of the ventricle. Trials like the COAPT trial have greatly shifted our practice in treating secondary mitral regurgitation. Though, we have to be familiar with which patients with secondary MR would truly derive benefit from mitral valve interventionIn regards to the COAPT trial, patients with moderate to severe (3+) or severe (4+) mitral regurgitation who remained symptomatic despite maximally tolerated guideline-directed medical therapy (GDMT) were included. Dr. Nishimura makes the point that about one-third of patients intended to be enrolled in the trial were not included because they improved so much on GDMT. And thus, when evaluating patients for consideration of mitral valve intervention in secondary MR – and specifically transcatheter edge to edge repair (TEER) – every effort to optimize GDMT should be made first before intervening. Other important inclusion and exclusion criteria included that patients had LVEF between 20-50%, LV end-systolic diameter less than or equal to 70 mm, and absence of severe pulmonary hypertension (defined as pulmonary artery systolic pressure > 70 mmHg despite vasodilator therapy) or moderate to severe right ventricular failure.Dr. Nishimura asks our audience if the patient is truly on optimal GDMT and/or optimized? There are basic tools that clue us into optimization including chest x-ray (e.g., is there still pulmonary vascular congestion) and physical examination (e.g., what is the venous pressure).Dr. Nishimura makes an interesting point in correlating our examination with the echocardiographic findings. In patients with largely secondary MR, where the leaflets have poor coaptation and we have a weak ventricle we may not expect to hear a very loud murmur on examination (e.g., there isn’t enough pump to generate the murmur). However, if we hear a significant murmur (e.g., like our patient described in the case with a loud, 3/6, blowing murmur) with presumed secondary MR, our antennae should be up for a possible primary component. Case #2 Synopsis: A man in his early 60s with a history of prior LAD PCI in the setting of an NSTEMI and diabetes presented to your hospital in SCAI Stage C to D Cardiogenic Shock with the background of worsening orthopnea and edema several weeks prior. You are told the patient had a recent echo with LVEF 15%, mild LV dilation, reduced RV function and moderate to severe functional MR. When you meet the patient, he is confused, nauseous and with poor perfusion (e.g., cool extremities and Lactate of 7 mmol/L). The patient is taken for left and right heart catheterization with RHC showing significant elevated filling pressures, large V-waves, and low cardiac index. An IABP is placed and LHC is performed where an acute appearing lesion in the proximal LAD and Mid-RCA are treated with PCI. Over the next week the IABP is weaned and removed and low doses of GDMT started. But once the IABP is removed, nausea returns and lactate starts rising again. Hemodynamics and TEE images are obtained with the IABP at 1:1 and on standby and show significant worsening of the hemodynamics and MR with IABP on standby, with the MR in the severe category, and we are asked to comment on what to do next. Case #2 Takeaways Dr. Nishimura suggests we approach this complex case with a simple question: how much of his shock/congestion is a result of his pump (the LV) versus how much is a result of his valve? Dr. Nishimura notes there is a subset of patients who have dynamic mitral regurgitation, which is primarily related to changes in the structure of the annulus/apparatus that happen with changes in preload/afterload/contractility. These patients can go from mild to severe depending on the loading conditions, as they are exquisitely sensitive to these conditionsDr. Nishimura notes the continuous wave doppler of the mitral regurgitation can give us a rich amount of detail. The MR continuous wave doppler signal reflects the instantaneous doppler between the left ventricle and left atrium. If we pay attention to the signal during isovolumic contraction – if there is a rapid rise in the signal, that suggests that we are generating LV systolic pressure rather quickly and contractility may be preserved (e.g., this refers to dP/dT which has several caveats but qualitatively can be informative us).These patients with dynamic MR who we cannot control the loading conditions, it may be better to treat the MR itself. References Stone GW, Lindenfeld J, Abraham WT, Kar S, Lim DS, Mishell JM, Whisenant B, Grayburn PA, Rinaldi M, Kapadia SR, Rajagopal V, Sarembock IJ, Brieke A, Marx SO, Cohen DJ, Weissman NJ, Mack MJ; COAPT Investigators. Transcatheter Mitral-Valve Repair in Patients with Heart Failure. N Engl J Med. 2018 Dec 13;379(24):2307-2318.Writing Committee Members, Otto CM, Nishimura RA, Bonow RO, Carabello BA, Erwin JP 3rd, Gentile F, Jneid H, Krieger EV, Mack M, McLeod C, O'Gara PT, Rigolin VH, Sundt TM 3rd, Thompson A, Toly C. 2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol. 2021 Feb 2;77(4):e25-e197. Production Team Karan Desai, MD Natalie Stokes, MD Amit Goyal, MD Daniel Ambinder, MD


    235. CCC: Post-cardiotomy Shock with Dr. Gavin Hickey and Dr. David Kaczorowski Sep 30, 2022
    Show notes

    In this episode, Dr. Carly Fabrizio (Advanced Heart Failure and Transplant Cardiology Physician at Christiana Care Hospital), CardioNerds Critical Care Series Co-Chair Dr. Mark Belkin (Advanced Heart Failure and Transplant Fellow at University of Chicago) and CardioNerds Co-Founder Dr. Amit Goyal (Cleveland Clinic) join Dr. Gavin Hickey (Director of the AHFTC Fellowship and medical director of the left ventricular assist device program at UPMC) and Dr. David Kaczorowski (Surgical Director for the Advanced Heart Failure center, Department of Cardiothoracic Surgery at UPMC) for a discussion on post-cardiotomy shock. Audio editing by CardioNerds Academy Intern, student doctor, Shivani Reddy. Post-cardiotomy shock is characterized by heart failure that results in the inability to wean from cardiopulmonary bypass or develops post cardiac surgery. Patients who develop post-cardiotomy shock typically require inotropic support and may ultimately require temporary mechanical circulatory support. Post-cardiotomy shock carries a high mortality rate. However, early recognition and prevention strategies can help mitigate the risk for developing post-cardiotomy shock. 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 • 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 - Post-cardiotomy Shock Weaning from cardiopulmonary bypass is an intricate process that includes: rewarming the patient, de-airing the cardiac chambers, ensuring a perfusing heart rhythm, confirming adequate ventilation and oxygenation, removing the intracardiac catheters and cannulas and slowly reducing the blood diverted to the cardiopulmonary circuit and returning it small aliquots to the patient. Much to monitor during the process! Assessing the risk for post-cardiotomy shock prior to going to the OR is important. Consider left ventricular, right ventricular, and valvular function, and don’t forget about the value of hemodynamic assessments (pulmonary artery catheter evaluations) to ensure patients are adequately compensated. Close peri-operative monitoring of hemodynamics, hemo-metabolic derangements, and acid/base status can help identify patients who are failing therapy and may require upgrade to temporary MCS. RV assessment is challenging. Utilizing both imaging and hemodynamic evaluations can help understand which RV’s will require more support. Multi-disciplinary discussions with a heart team approach prior to cardiac surgery are valuable in identifying high risk patients for post cardiotomy shock and discussing contingency plans if issues arise. Show notes - Post-cardiotomy Shock (drafted by Dr. Carly Fabrizio) How can we diagnose post cardiotomy shock?We can diagnose post cardiotomy shock as patients who are undergoing cardiac surgery that develop hypotension and or tachycardia with hypoperfusion and end organ dysfunction. How can assess the risk of developing postcardiotomy shock prior to going to the OR?LV systolic function is not the only evaluation of cardiac functionDon’t ignore the RV!Valvular function must be evaluated in conjunction with LV/RV functionHemodynamics can be helpful prior to going to the ORFilling pressures and CO/CI evaluation --> the more normal range - the less risk of post cardiotomy shockIf going in more deranged --> more complications are likely to occurThink about what options are available post operatively if issues ariseInclude a multi-disciplinary discussions and planning prior to going to the OR Are there any specific pre-operative or intra-operative risk factors that may predispose someone to developing post cardiotomy shock?Many factors can lead to postcardiotomy shock. Some pre-op factors include:Poor pre-operative cardiac function (RV and /or LV function)Entering the OR in cardiogenic shock (inotropes, temporary MCS)Well compensated patients with chronic ventricular dysfunctionIntra-operative factors:Prolonged cross-clamp timeProlonged cardiopulmonary bypass (CPB) times (often seen in complex operations)Inadequate myocardial protectionVentricular distentionTechnical factors What is actually occurring in the OR when weaning from CPB?After the aorta cross clamp is removed- the heart is allowed to re-perfuseRemember that the heart has been ischemic for a considerable amount of timeLungs are re-inflatedTemporary atrial and ventricular pacing wires are placedStable rhythm is achieved and the heart is paced if necessaryAcid / base status and electrolytes (potassium) are optimizedOnce the heart is de-aired, CPB is gradually weanedThe flow of the CPB circuit is gradually reduced and more of the patient’s blood volume is gradually allowed to pass through the heart and lungsTEE is performed while weaning bypassOnce bypass is completely weaned, the cannulas used to establish CPB are removedAnticoagulation is reversedAssess for hemostasisChest tubes are placed, and closure occurs What are the clinical and laboratory parameters which help determine whether vasoactive support alone will be enough vs. when temporary MCS may be needed?Assess perfusion firstBPUrine outputLactic acidPA catheter data / hemodynamic dataCardiac output/index (CO/CI)Pulmonary artery pressures (PAP)Central venous pressures (CVP)Mixed venous oxygen saturationCardiac power output (CPO) and cardiac power index (CPI)CPO consider escalation to temporary MCS Left ventricular assist devices (LVAD) do not support the right ventricle. How can we identify RV failure in these patients and when should you upgrade to RV mechanical circulatory support?Most patient that require left-sided support by nature often have underlying right-sided dysfunction as wellPre-operative - assessment of the RV is important:CVPPAPi (PA systolic pressure- PA diastolic pressure / CVP)CVP: PCWP ratioRV failure can occur in any patientNo great, reliable, and reproducible data on when or how to support the RV following LVAD implantation, or cardiogenic shock in general. More studies are needed. What’s different about how you assess the RV dysfunction in the OR compared to someone who is in the ICU? When do you consider using RV mechanical support upfront in the OR?Intra-operative TEE and direct visualization are both used in the OR to assess RV functionTry to avoid upfront RV mechanical support in the OROptimize with invasive hemodynamic monitoring prior to ORTemporary MCS can be used to optimize patient and help with diuresis pre-operativelyContinue to optimize the RV while in the ORRemove volume through hemoconcentration while on CPB circuit to optimize volume statusConsider temporary MCS for the RV when medical therapy is maximized, and the patient still remains marginal as measured by:LVAD flows, cardiac output/index, mixed venous gases and metabolic parameters Are there any surgical consideration to influence the type of temporary MCS for postcardiotomy shock?Strategize first by asking:What is failing? LV, RV, lungs, or a combinationWhat access is available?Ex: Bi-ventricular failure with hypoxemia and peripheral arterial disease: consider central VA ECMOEx: Pure LV failure but RV and lungs OK --> temporary LV assist device How can we prevent, or decrease the risk, of post-cardiotomy shock ?Optimized hemodynamics going into the OR using a PA catheterMulti-disciplinary discussion with cardiac anesthesia, critical care team, etc. for high-risk casesEnsure adequate end-organ perfusionAvoid pre-operative medications that worsen peri-operative vasoplegiaACE-i/ARB/ARNI, milrinone etc. What is role of advanced therapy evaluations when assessing high risk patients going to the OR?Important to think about options pre-operativelySelection committee discussions to weigh-in on candidacy for LVAD or cardiac transplant and if that may be more beneficial than other cardiac surgical interventions How does team-based care help with decision making?Optimize patients pre procedure and support them peri-procedureInvolving palliative care team and establishing patient goals prior to surgery References - Post-cardiotomy Shock Lorusso, Raffa, Alenizy, et al. “Structured review of post-cardiotomy extracorporeal membrane oxygenation: part 1—Adult patients.” JHLT. 38(11): 1125-1143. 2019.https://www.sciencedirect.com/science/article/pii/S1053249819316328Fukuhara, Takea, Garan, et al. “Contemporary mechanical circulatory support therapy for postcardiotomy shock.” Curr Topics Review Article. 64:183-191. 2016. https://link.springer.com/content/pdf/10.1007/s11748-016-0625-4.pdf CardioNerds Cardiac Critical Care Production Team Karan Desai, MD Dr. Mark Belkin Dr. Yoav Karpenshif Amit Goyal, MD Daniel Ambinder, MD


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