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Objective There is a paucity of data on how race affects the clinical presentation and short-term outcome among hospitalized patients with SARS-CoV-2, the 2019 coronavirus (COVID-19). Methods Hospitalized patients ≥ 18 years, testing positive for COVID-19 from March 13, 2020 to May 13, 2020 in a United States (U.S.) integrated healthcare system with multiple facilities in two states were evaluated. We documented racial differences in clinical presentation, disposition, and in-hospital outcomes for hospitalized patients with COIVD-19. Multivariable regression analysis was utilized to evaluate independent predictors of outcomes by race. Results During the study period, 3678 patients tested positive for COVID-19, among which 866 were hospitalized (55.4% self-identified as Caucasian, 29.5% as Black, 3.3% as Hispanics, and 4.7% as other racial groups). Hospitalization rates were highest for Black patients (36.6%), followed by other (28.3%), Caucasian patients (24.4%), then Hispanic patients (10.7%) (p

Background Certain echocardiographic parameters may serve as early predictors of adverse events in patients with hemodynamically compromising pulmonary embolism (PE). Methods and Results An observational analysis was conducted for patients with acute pulmonary embolism evaluated by a Pulmonary Embolism Response Team (PERT) between 2014 and 2020. The performance of clinical prediction algorithms including the Pulmonary Embolism Severity Index and Carl Bova score were compared using a ratio of right ventricle and left ventricle hemodynamics by dividing the pulmonary artery systolic pressure by the left ventricle stroke volume. The primary outcome of in‐hospital mortality, cardiac arrest, and the need for advanced therapies was evaluated by univariate and multivariable analyses. Of the 343 patients meeting the inclusion criteria, 215 had complete data. Pulmonary artery systolic pressure/left ventricle stroke volume was a clear predictor of the primary end point (odds ratio [OR], 2.31; P =0.005), performing as well or better than the Pulmonary Embolism Severity Index (OR, 1.43; P =0.06) or the Bova score (OR, 1.28; P =0.01). Conclusions This study is the first study to demonstrate the utility of early pulmonary artery systolic pressure/left ventricle stroke volume in predicting adverse clinical events in patients with acute pulmonary embolism. Pulmonary artery systolic pressure/left ventricle stroke volume may be a surrogate marker of ventricular asynchrony in high‐risk pulmonary embolism and should be prognostically evaluated.

Coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 is an ongoing viral pandemic marked by increased risk of thrombotic events. However, the role of platelets in the elevated observed thrombotic risk in COVID-19 and utility of antiplatelet agents in attenuating thrombosis is unknown. We aimed to determine if the antiplatelet effect of aspirin may mitigate risk of myocardial infarction, cerebrovascular accident, and venous thromboembolism in COVID-19. We evaluated 22,072 symptomatic patients tested for COVID-19. Propensity-matched analyses were performed to determine if treatment with aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) affected thrombotic outcomes in COVID-19. Neither aspirin nor NSAIDs affected mortality in COVID-19. Thus, aspirin does not appear to prevent thrombosis and death in COVID-19. The mechanisms of thrombosis in COVID-19, therefore, appear distinct and the role of platelets as direct mediators of SARS-CoV-2-mediated thrombosis warrants further investigation.

Introduction: Risk stratification tools including the Pulmonary Embolism Severity Index (PESI) and BOVA rely on complicated calculations that give less attention to hemodynamic parameters predictive of cardiogenic shock in acute pulmonary embolism (PE). We explored the possibility that simultaneous measurement of right sided and left sided non-invasive hemodynamic parameters by echocardiography may predict adverse sequelae in the context of acute PE. Methods: We retrospectively reviewed all Pulmonary Embolism Response Team (PERT) activations between 2014 and 2020. The PESI and BOVA scores were calculated and their performance in predicting adverse events was compared to pulmonary artery elastance (PAE). PAE (mmHg/mL) was calculated by dividing the Pulmonary Artery Systolic pressure (PASP) by the LV Stroke (SV). Blood biomarkers (troponin T, NT-proBNP, and lactate) were recorded. The composite primary outcome was: 1) need for advanced intervention, 2) cardiac arrest, and 3) in-hospital mortality. Multivariate and univariate regression was used to analyze outcomes. Results: 215 of 343 patients met inclusion criteria. Baseline characteristics were similar in patients with PAE Conclusion: In the context of acute high risk PE, PAE ≥ 1.0 is a novel and independent predictor of adverse cardiovascular events and mortality that should be prospectively validated.

Coronavirus disease-2019 (COVID-19) caused by SARS-CoV-2 is an ongoing viral pandemic marked by increased risk of thrombotic events. However, the role of platelets in the elevated observed thrombotic risk in COVID-19 and utility of anti-platelet agents in attenuating thrombosis is unknown. We aimed to determine if human platelets express the known SARS-CoV-2 receptor-protease axis on their cell surface and assess whether the anti-platelet effect of aspirin may mitigate risk of myocardial infarction (MI), cerebrovascular accident (CVA), and venous thromboembolism (VTE) in COVID-19. Expression of ACE2 and TMPRSS2 on human platelets were detected by immunoblotting and confirmed by confocal microscopy. We evaluated 22,072 symptomatic patients tested for COVID-19. Propensity-matched analyses were performed to determine if treatment with aspirin or non-steroidal anti-inflammatory drugs (NSAIDs) affected thrombotic outcomes in COVID-19. Neither aspirin nor NSAIDs affected mortality in COVID-19. However, both aspirin and NSAID therapies were associated with increased risk of the combined thrombotic endpoint of (MI), (CVA), and (VTE). Thus, while platelets clearly express ACE2-TMPRSS2 receptor-protease axis for SARS-CoV-2 infection, aspirin does not prevent thrombosis and death in COVID-19. The mechanisms of thrombosis in COVID-19, therefore, appears distinct and the role of platelets as direct mediators of SARS-CoV-2-mediated thrombosis warrants further investigation.