Abstract

Introduction: COVID-19 has affected millions of people worldwide and is associated with cardiovascular complications like myocarditis, MI, pericarditis & stress-induced cardiomyopathy (Takotsubo cardiomyopathy). Hypothesis and aim: The aim of our study was to examine the outcomes of stress-induced cardiomyopathy in patients with COVID-19. Methods: Using TriNetX, which aggregates >100 million patients' charts, we identified adults (>18) between Jan. 2020 & Apr. 2023. We identified 2 groups: stress induced cardiomyopathy in the setting of COVID-19, & stress-induced cardiomyopathy without COVID-19. We performed 1:1 propensity score matching for demographics and co-morbidities like DM, HTN, HLD, IHD, CKD, obesity, PVD, COPD, liver cirrhosis, smoking & alcohol abuse. We conducted Kaplan-Meier survival analysis to assess all-cause mortality. Adjusted odds ratios (aOR) with 95% confidence interval (CI) were calculated to express the risk of each outcome. Results: We identified 1990 cases of stress-induced cardiomyopathy with COVID-19, and 27,702 patients with stress-induced cardiomyopathy without COVID-19. The majority were female gender and white race across the groups. Table 1 summarizes the demographics and characteristics of cohorts. After matching, stress-induced cardiomyopathy with COVID-19 were more likely to develop LV thrombus (aOR 1.41 [1.02-1.61]), cerebral infarction (aOR 1.25 [1.05-1.47]), acute respiratory failure (aOR 1.72 [1.53-1.94]), cardiogenic shock (aOR 1.37 [1.09-1.72]), and VTE (aOR 1.86 [1.61-2.14]). No difference was found in VT (aOR 0.89 [0.72-1.10]), or cardiac arrest (aOR [1.13 (0.88-1.45]), figure 1. All cause-mortality was worse in COVID-19 associated stress-induced cardiomyopathy (HR 1.17 [1.007-1.35]). Conclusions: Stress induced cardiomyopathy in the setting of COVID-19 was associated with a higher risk of adverse events and increased mortality compared to stress induced cardiomyopathy without COVID-19.

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