PRIMARY CARDIAC BURKITT LYMPHOMA PRESENTING WITH ABDOMINAL PAIN

Background: Primary cardiac lymphomas are rare, carry high mortality rates and are often due to aggressive B cell lymphomas, including Burkitt Lymphoma (BL). BL is rare in the immunocompetent though more prevalent among AIDS patients. Case: A 41yo man with a history of alcohol abuse presented with 1 month of B-symptoms and abdominal pain. Initial labs found a positive HIV-1 antibody, elevated viral load and low CD4 count. CT chest and abdomen on arrival revealed a large infiltrating lobulated right atrial mass (RAM) (Figure 1A). Decision-making: Cardiac masses are often due to metastatic disease and warrant evaluation for extra-cardiac origin. TTE, TEE (Figures 1B & 1C) and cardiac magnetic resonance imaging identified a 2.8cm subcarinal lymph node and found the RAM to be infiltrating the inter-atrial septum, partially surrounding the pulmonary veins, obstructing the superior vena cava and extending to the aortic root (Figure 1D). Cytology of the subcarinal lymph node biopsy was consistent with BL. Highly active anti-retroviral therapy and chemotherapy were initiated. CT chest after 1 treatment cycle showed a marked reduction in RAM size (Figure 1E). Conclusion: Our case underscores the central role of advanced imaging in the evaluation of cardiac masses by identifying a malignant etiology, staging, identifying a target for pathologic diagnosis and monitoring treatment response. Early use of multimodality imaging for cardiac masses in the HIV population allows for timely use of lifesaving therapies

Can the Use of Art and Active Learning Improve Retention and Observational Skill Confidence Among Audiology Graduate Students

Human anatomy and physiology is considered one of the most difficult courses a student can take in a pre-health professional major in the US (Slominski, et. al., 2017). Research has revealed benefits of the use of art and anatomy within medical education, including improved clinical observational skills, greater understanding of disease and patient perspectives, and greater ability to empathize (Bell & Evans, 2014). Bell and Evans (2014) argue that observational skills are often overlooked in medical education. Use of art assignments in a graduate anatomy and physiology course will be discussed with reference to design and learning outcomes. The purpose of this study was to evaluate the relationship between art and medical education for audiology students. This study aimed to incorporate STEAM education (art assignments, the teaching effect, and community outreach) into audiology curriculum. Auburn University’s Au.D. class of 2022 participated in this study, consisting of 10 students. The Student Assessment of Learning Gains (SALG) questionnaire was conducted and provided qualitative and quantitative evidence supporting the integration of art in the Doctor of Audiology curriculum. BASE (pre) and SALG (post) outcomes assessed that the use of STEAM assignments can help improve the retention of the anatomy and physiology within of the auditory system. Cross-tabulations of pre and post course responses show a positive increase in student understanding of course material. A positive perception that art assignments enhanced student confidence and clinical observation skills related to the course was observed.  Many students felt they had a great gain in understanding covered topics. The effects of utilizing the teaching effect and community outreach were also positively seen by student participants. Students’ opinions following coursework and cross-tabulations support a place for art in health education and healthcare

Hemodynamic and Echocardiographic Assessment of Left Ventricle Recovery with Left Ventricular Assist Devices: Do We Explant?

Introduction: Explantation of left ventricular assist devices (LVAD) after left ventricular (LV) recovery is estimated to occur in 1-2% of cases. Herein, we present a case of hemodynamic and echocardiographic assessment of LV recovery during outflow graft balloon occlusion leading to LVAD explantation. Case Report: A 56-year-old female with medical history of systolic heart failure due to non-ischemic cardiomyopathy with LVEF 25%. She underwent an urgent HeartMate 3 LVAD implant after an admission for cardiogenic shock. Post LVAD course was complicated by driveline infection. History was notable for admissions due to low-flow alarms in the setting of dehydration. On echocardiogram, progressive LVEF improvement was noted although with suboptimal images. CT angiography did not demonstrate any occlusion of the cannulas. Right heart catheterization showed stable cardiac index despite minimal flow on LVAD. Cardiopulmonary testing was favorable. After multi-disciplinary discussion, patient underwent LVAD wean study in the cath lab under hemodynamic and transesophageal echo (TEE) guidance with therapeutic anticoagulation. LVAD was turned off for 10 minutes with outflow graft occluded by Armada 14 mm x 20 cm peripheral balloon. Wiring of the outflow graft from aorta and balloon occlusion were visualized by TEE (Figure). The left and right ventricular function were similar to baseline with no change in mitral regurgitation. Cardiac index was normal (Figure). Patient subsequently underwent successful LVAD explant. She is doing well with NYHA class I symptoms and LVEF 45-50% noted upon 3-months follow-up LVAD explantation is a feasible option in LV recovery after appropriate hemodynamic and echocardiographic assessment. TEE is an essential tool, especially in patients with suboptimal windows. Outflow graft balloon occlusion can be used if there is concern about falsely poor results related to backflow or ongoing LVAD support at low speed leading to falsely improved results

Cardiac Tamponade Secondary to COVID-19

A 67-year-old female presented with upper respiratory symptoms and was diagnosed with COVID-19. She was found to have a large hemorrhagic pericardial effusion with echocardiographic signs of tamponade and mild left ventricular impairment. Clinical course was complicated by development of Takotsubo cardiomyopathy. She was treated with pericardiocentesis, colchicine, corticosteroids and hydroxychloroquine with improvement in symptoms

Prognostic Utility of a Modified HEART Score When Different Troponin Cut-points Are Used

BACKGROUND: Although the recommended cut-point for cardiac troponin (cTn) is the 99th percentile, many institutions use cut-points that are multiples higher than the 99th percentile for diagnosing acute myocardial infarction (AMI). Prior studies have shown that patients with a HEART score (HS) ≤ 3 and normal serial cTn values (modified HS) are at low risk for adverse events. This study aimed to evaluate the prognostic utility of the HS when various cTn cut-points are used. METHODS: This was a sub-study of TRAPID-AMI, a multicenter, international trial evaluating a rapid rule-out AMI study using high sensitivity cTnT (hs-cTnT). 1,282 patients were evaluated for AMI from 12 centers in Europe, United States of America, and Australia from 2011-2013. Blood samples of hs-cTnT were collected at presentation and 2 hours, and each patient had a HS calculated. The US Food and Drug Administration approved 99th percentile for hs-cTnT (19 ng/L) was used. RESULTS: There were 213 (17%) AMIs. Within 30 days, there were an additional 2 AMIs and 8 deaths. The adverse event rates at 30 days (death/AMI) for a HS ≤ 3 and non-elevated hs-cTnT over 2 hours using increasing hs-cTnT cut-points ranged from 0.6% to 5.1%. CONCLUSIONS: Using the recommended 99th percentile cut-point for hs-cTnT, the combination of a HS ≤ 3 with non-elevated hs-cTnT values over 2 hours identifies a low-risk cohort who can be considered for discharge from the emergency department without further testing. The prognostic utility of this strategy is greatly lessened as higher hs-cTnT cut-points are used

Autoantibodies neutralizing type I IFNs are present in ~4% of uninfected individuals over 70 years old and account for ~20% of COVID-19 deaths

Publisher Copyright: © 2021 The Authors, some rights reserved.Circulating autoantibodies (auto-Abs) neutralizing high concentrations (10 ng/ml; in plasma diluted 1:10) of IFN-alpha and/or IFN-omega are found in about 10% of patients with critical COVID-19 (coronavirus disease 2019) pneumonia but not in individuals with asymptomatic infections. We detect auto-Abs neutralizing 100-fold lower, more physiological, concentrations of IFN-alpha and/or IFN-omega (100 pg/ml; in 1:10 dilutions of plasma) in 13.6% of 3595 patients with critical COVID-19, including 21% of 374 patients >80 years, and 6.5% of 522 patients with severe COVID-19. These antibodies are also detected in 18% of the 1124 deceased patients (aged 20 days to 99 years; mean: 70 years). Moreover, another 1.3% of patients with critical COVID-19 and 0.9% of the deceased patients have auto-Abs neutralizing high concentrations of IFN-beta. We also show, in a sample of 34,159 uninfected individuals from the general population, that auto-Abs neutralizing high concentrations of IFN-alpha and/or IFN-omega are present in 0.18% of individuals between 18 and 69 years, 1.1% between 70 and 79 years, and 3.4% >80 years. Moreover, the proportion of individuals carrying auto-Abs neutralizing lower concentrations is greater in a subsample of 10,778 uninfected individuals: 1% of individuals 80 years. By contrast, auto-Abs neutralizing IFN-beta do not become more frequent with age. Auto-Abs neutralizing type I IFNs predate SARS-CoV-2 infection and sharply increase in prevalence after the age of 70 years. They account for about 20% of both critical COVID-19 cases in the over 80s and total fatal COVID-19 cases.Peer reviewe

The risk of COVID-19 death is much greater and age dependent with type I IFN autoantibodies

SignificanceThere is growing evidence that preexisting autoantibodies neutralizing type I interferons (IFNs) are strong determinants of life-threatening COVID-19 pneumonia. It is important to estimate their quantitative impact on COVID-19 mortality upon SARS-CoV-2 infection, by age and sex, as both the prevalence of these autoantibodies and the risk of COVID-19 death increase with age and are higher in men. Using an unvaccinated sample of 1,261 deceased patients and 34,159 individuals from the general population, we found that autoantibodies against type I IFNs strongly increased the SARS-CoV-2 infection fatality rate at all ages, in both men and women. Autoantibodies against type I IFNs are strong and common predictors of life-threatening COVID-19. Testing for these autoantibodies should be considered in the general population

The risk of COVID-19 death is much greater and age dependent with type I IFN autoantibodies

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection fatality rate (IFR) doubles with every 5 y of age from childhood onward. Circulating autoantibodies neutralizing IFN-α, IFN-ω, and/or IFN-β are found in ∼20% of deceased patients across age groups, and in ∼1% of individuals aged 4% of those >70 y old in the general population. With a sample of 1,261 unvaccinated deceased patients and 34,159 individuals of the general population sampled before the pandemic, we estimated both IFR and relative risk of death (RRD) across age groups for individuals carrying autoantibodies neutralizing type I IFNs, relative to noncarriers. The RRD associated with any combination of autoantibodies was higher in subjects under 70 y old. For autoantibodies neutralizing IFN-α2 or IFN-ω, the RRDs were 17.0 (95% CI: 11.7 to 24.7) and 5.8 (4.5 to 7.4) for individuals <70 y and ≥70 y old, respectively, whereas, for autoantibodies neutralizing both molecules, the RRDs were 188.3 (44.8 to 774.4) and 7.2 (5.0 to 10.3), respectively. In contrast, IFRs increased with age, ranging from 0.17% (0.12 to 0.31) for individuals <40 y old to 26.7% (20.3 to 35.2) for those ≥80 y old for autoantibodies neutralizing IFN-α2 or IFN-ω, and from 0.84% (0.31 to 8.28) to 40.5% (27.82 to 61.20) for autoantibodies neutralizing both. Autoantibodies against type I IFNs increase IFRs, and are associated with high RRDs, especially when neutralizing both IFN-α2 and IFN-ω. Remarkably, IFRs increase with age, whereas RRDs decrease with age. Autoimmunity to type I IFNs is a strong and common predictor of COVID-19 death.The Laboratory of Human Genetics of Infectious Diseases is supported by the Howard Hughes Medical Institute; The Rockefeller University; the St. Giles Foundation; the NIH (Grants R01AI088364 and R01AI163029); the National Center for Advancing Translational Sciences; NIH Clinical and Translational Science Awards program (Grant UL1 TR001866); a Fast Grant from Emergent Ventures; Mercatus Center at George Mason University; the Yale Center for Mendelian Genomics and the Genome Sequencing Program Coordinating Center funded by the National Human Genome Research Institute (Grants UM1HG006504 and U24HG008956); the Yale High Performance Computing Center (Grant S10OD018521); the Fisher Center for Alzheimer’s Research Foundation; the Meyer Foundation; the JPB Foundation; the French National Research Agency (ANR) under the “Investments for the Future” program (Grant ANR-10-IAHU-01); the Integrative Biology of Emerging Infectious Diseases Laboratory of Excellence (Grant ANR-10-LABX-62-IBEID); the French Foundation for Medical Research (FRM) (Grant EQU201903007798); the French Agency for Research on AIDS and Viral hepatitis (ANRS) Nord-Sud (Grant ANRS-COV05); the ANR GENVIR (Grant ANR-20-CE93-003), AABIFNCOV (Grant ANR-20-CO11-0001), CNSVIRGEN (Grant ANR-19-CE15-0009-01), and GenMIS-C (Grant ANR-21-COVR-0039) projects; the Square Foundation; Grandir–Fonds de solidarité pour l’Enfance; the Fondation du Souffle; the SCOR Corporate Foundation for Science; The French Ministry of Higher Education, Research, and Innovation (Grant MESRI-COVID-19); Institut National de la Santé et de la Recherche Médicale (INSERM), REACTing-INSERM; and the University Paris Cité. P. Bastard was supported by the FRM (Award EA20170638020). P. Bastard., J.R., and T.L.V. were supported by the MD-PhD program of the Imagine Institute (with the support of Fondation Bettencourt Schueller). Work at the Neurometabolic Disease lab received funding from Centre for Biomedical Research on Rare Diseases (CIBERER) (Grant ACCI20-767) and the European Union's Horizon 2020 research and innovation program under grant agreement 824110 (EASI Genomics). Work in the Laboratory of Virology and Infectious Disease was supported by the NIH (Grants P01AI138398-S1, 2U19AI111825, and R01AI091707-10S1), a George Mason University Fast Grant, and the G. Harold and Leila Y. Mathers Charitable Foundation. The Infanta Leonor University Hospital supported the research of the Department of Internal Medicine and Allergology. The French COVID Cohort study group was sponsored by INSERM and supported by the REACTing consortium and by a grant from the French Ministry of Health (Grant PHRC 20-0424). The Cov-Contact Cohort was supported by the REACTing consortium, the French Ministry of Health, and the European Commission (Grant RECOVER WP 6). This work was also partly supported by the Intramural Research Program of the National Institute of Allergy and Infectious Diseases and the National Institute of Dental and Craniofacial Research, NIH (Grants ZIA AI001270 to L.D.N. and 1ZIAAI001265 to H.C.S.). This program is supported by the Agence Nationale de la Recherche (Grant ANR-10-LABX-69-01). K.K.’s group was supported by the Estonian Research Council, through Grants PRG117 and PRG377. R.H. was supported by an Al Jalila Foundation Seed Grant (Grant AJF202019), Dubai, United Arab Emirates, and a COVID-19 research grant (Grant CoV19-0307) from the University of Sharjah, United Arab Emirates. S.G.T. is supported by Investigator and Program Grants awarded by the National Health and Medical Research Council of Australia and a University of New South Wales COVID Rapid Response Initiative Grant. L.I. reports funding from Regione Lombardia, Italy (project “Risposta immune in pazienti con COVID-19 e co-morbidità”). This research was partially supported by the Instituto de Salud Carlos III (Grant COV20/0968). J.R.H. reports funding from Biomedical Advanced Research and Development Authority (Grant HHSO10201600031C). S.O. reports funding from Research Program on Emerging and Re-emerging Infectious Diseases from Japan Agency for Medical Research and Development (Grant JP20fk0108531). G.G. was supported by the ANR Flash COVID-19 program and SARS-CoV-2 Program of the Faculty of Medicine from Sorbonne University iCOVID programs. The 3C Study was conducted under a partnership agreement between INSERM, Victor Segalen Bordeaux 2 University, and Sanofi-Aventis. The Fondation pour la Recherche Médicale funded the preparation and initiation of the study. The 3C Study was also supported by the Caisse Nationale d’Assurance Maladie des Travailleurs Salariés, Direction générale de la Santé, Mutuelle Générale de l’Education Nationale, Institut de la Longévité, Conseils Régionaux of Aquitaine and Bourgogne, Fondation de France, and Ministry of Research–INSERM Program “Cohortes et collections de données biologiques.” S. Debette was supported by the University of Bordeaux Initiative of Excellence. P.K.G. reports funding from the National Cancer Institute, NIH, under Contract 75N91019D00024, Task Order 75N91021F00001. J.W. is supported by a Research Foundation - Flanders (FWO) Fundamental Clinical Mandate (Grant 1833317N). Sample processing at IrsiCaixa was possible thanks to the crowdfunding initiative YoMeCorono. Work at Vall d’Hebron was also partly supported by research funding from Instituto de Salud Carlos III Grant PI17/00660 cofinanced by the European Regional Development Fund (ERDF/FEDER). C.R.-G. and colleagues from the Canarian Health System Sequencing Hub were supported by the Instituto de Salud Carlos III (Grants COV20_01333 and COV20_01334), the Spanish Ministry for Science and Innovation (RTC-2017-6471-1; AEI/FEDER, European Union), Fundación DISA (Grants OA18/017 and OA20/024), and Cabildo Insular de Tenerife (Grants CGIEU0000219140 and “Apuestas científicas del ITER para colaborar en la lucha contra la COVID-19”). T.H.M. was supported by grants from the Novo Nordisk Foundation (Grants NNF20OC0064890 and NNF21OC0067157). C.M.B. is supported by a Michael Smith Foundation for Health Research Health Professional-Investigator Award. P.Q.H. and L. Hammarström were funded by the European Union’s Horizon 2020 research and innovation program (Antibody Therapy Against Coronavirus consortium, Grant 101003650). Work at Y.-L.L.’s laboratory in the University of Hong Kong (HKU) was supported by the Society for the Relief of Disabled Children. MBBS/PhD study of D.L. in HKU was supported by the Croucher Foundation. J.L.F. was supported in part by the Evaluation-Orientation de la Coopération Scientifique (ECOS) Nord - Coopération Scientifique France-Colombie (ECOS-Nord/Columbian Administrative department of Science, Technology and Innovation [COLCIENCIAS]/Colombian Ministry of National Education [MEN]/Colombian Institute of Educational Credit and Technical Studies Abroad [ICETEX, Grant 806-2018] and Colciencias Contract 713-2016 [Code 111574455633]). A. Klocperk was, in part, supported by Grants NU20-05-00282 and NV18-05-00162 issued by the Czech Health Research Council and Ministry of Health, Czech Republic. L.P. was funded by Program Project COVID-19 OSR-UniSR and Ministero della Salute (Grant COVID-2020-12371617). I.M. is a Senior Clinical Investigator at the Research Foundation–Flanders and is supported by the CSL Behring Chair of Primary Immunodeficiencies (PID); by the Katholieke Universiteit Leuven C1 Grant C16/18/007; by a Flanders Institute for Biotechnology-Grand Challenges - PID grant; by the FWO Grants G0C8517N, G0B5120N, and G0E8420N; and by the Jeffrey Modell Foundation. I.M. has received funding under the European Union’s Horizon 2020 research and innovation program (Grant Agreement 948959). E.A. received funding from the Hellenic Foundation for Research and Innovation (Grant INTERFLU 1574). M. Vidigal received funding from the São Paulo Research Foundation (Grant 2020/09702-1) and JBS SA (Grant 69004). The NH-COVAIR study group consortium was supported by a grant from the Meath Foundation.Peer reviewe

Drugs to Avoid in Acute Decompensated Heart Failure (ADHF): Contraindicated Medications and Interactions

Following diuretics, vasodilators are the most commonly used intravenous (IV) therapy for acute decompensated heart failure (ADHF), but strong evidence is lacking for the use of nitrates, nitroprusside, and nesiritide on clinical outcomes and therefore these drugs are most commonly used for symptomatic improvement. The long-term use of angiotensin converting enzyme (ACE) inhibitors is associated with improved symptoms and lower mortality in patients with systolic heart failure. However, the benefits of early IV ACE inhibitors in ADHF have not been established and may actually be harmful. In the CONSENSUS 2 trial, early IV enalapril was studied in patients with acute myocardial infarction (AMI). In patients with AMI and ADHF, IV enalapril was associated with decreased survival 180 days after AMI. The American College of Emergency Physicians supports the early use of IV ACE inhibitors, while the European Society of Cardiology does not. Until studied further, IV ACE inhibitors should be avoided in the setting of ADHF

A Case of Sarcoidosis Presenting as Refractory Arrhythmias: Quieting the Storm

Introduction: Sarcoidosis is a multisystem granulomatous disorder of unknown etiology. Cardiac sarcoidosis can manifest as conduction abnormality, ventricular tachycardia (VT), heart failure or sudden cardiac death. Although well studied in the literature, we present an uncommon case of arrhythmia as a presenting manifestation of this disease. Case: 45-year-old female with no significant past medical history presented with acute onset shortness of breath and palpitations. Initial transthoracic echocardiogram revealed an ejection fraction of 50%. Electrophysiology (EP) study showed a chemically inducible accelerated idioventricular rhythm with right bundle morphology. Left heart catheterization showed angiographically normal vessels and cardiac MRI showed no regional wall motion abnormalities or abnormal delayed enhancement. Patient presented to the hospital again due to recurrence of arrhythmia, found to be VT. Nuclear medicine whole body PET scan showed perfusion defects consistent with cardiac sarcoidosis. A mediastinal lymph node biopsy demonstrated focal non-granulomatous inflammation. Patient was initiated on anti-arrhythmics and underwent a single-chamber ICD placement. She continued to have episodes of wide QRS tachycardia, and was evaluated by Advanced Heart Failure for refractory arrhythmias. Decision-making: Patient was initially managed with Amiodarone and a beta-blocker. Due to unstable VT, she was taken to EP lab where a focal origin of the VT was successfully found in the basal anterolateral endocardial left ventricle and at the base of one of the papillary muscles. Ablations were performed in these areas with reduction in VT rate. Patient was also discovered to have complete atrioventricular block. Subsequently, she developed recurrence of arrhythmia and was admitted again for VT management. Patient was taken back to the EP lab for an endocardial and epicardial ablation. A focal VT source was found in the apical lateral left ventricle. Due to proximity of the phrenic nerve to the site, no ablations were performed. However, due to recurrence of arrhythmia, she was taken back to the lab for a third ablation in the epicardial area with resulting success. Antiarrhythmics were changed to Flecainide which has since suppressed her VT. Patient has been maintained on Methotrexate, Hydroxychloroquine, and Prednisone for continued sarcoid therapy. We are using periodic F-FDG PET imaging to monitor the severity of myocardial inflammation. Based on patient\u27s clinical status and PET imaging, we have determined the time to wean immunosuppressant agents. Conclusion: Cardiac sarcoidosis affects at least 25% of sarcoidosis patients and accounts for substantial mortality and morbidity.Ventricular arrhythmias may be the presenting symptom of cardiac sarcoidosis and are challenging to treat. Risk stratification through proposed techniques such as advanced cardiac imaging and EP studies is integral in this population. Recognition of sarcoidosis as a possible etiology of arrhythmias through integration of clinical and imaging findings can lead to appropriate lifesaving treatments