Background Coronavirus disease 2019 (COVID-19) has high infectivity and causes extensive morbidity and mortality. Cardiovascular disease is a risk factor for adverse outcomes in COVID-19, but baseline left ventricular ejection fraction (LVEF) in particular has not been evaluated thoroughly in this context. Methods We analyzed patients in our state's largest health system who were diagnosed with COVID-19 between March 20 and May 15, 2020. Inclusion required an available echocardiogram within one year prior to diagnosis. The primary outcome was all-cause mortality. LVEF was analyzed both as a continuous variable and using a cutoff of 40%. Results Among 396 patients (67±16 years, 191 [48%] male, 235 [59%] Black, 59 [15%] LVEF ≤40%), 289 (73%) required hospital admission, and 116 (29%) died during 85±63 days of follow-up. Echocardiograms, performed a median of 57 (IQR 11-122) days prior to COVID-19 diagnosis, showed a similar distribution of LVEF between survivors and decedents (p=0.84). Receiver operator characteristic analysis revealed no predictive ability of LVEF for mortality, and there was no difference in survival among those with LVEF ≤40% vs. >40% (p=0.49). Multivariable analysis did not change these relationships. Similarly, there was no difference in LVEF based on whether the patient required hospital admission (56±13 vs. 55±13, p=0.38), and patients with a depressed LVEF did not require admission more frequently than their preserved-LVEF peers (p=0.87). A premorbid history of dyspnea consistent with symptomatic heart failure was not associated with mortality (p=0.74). Conclusions Among patients diagnosed with COVID-19, pre-COVID-19 LVEF was not a risk factor for death or hospitalization.

Background: Spontaneous bacterial peritonitis (SBP) is a life-threatening condition classically found as a complication of cirrhotic ascites, but it has rarely been documented in a case of nonportal hypertensive ascites. Case Report: We report the case of a 54-year-old male with SBP arising from nonportal hypertensive ascites in the setting of end-stage renal disease and restrictive cardiomyopathy, both secondary to primary amyloidosis (AL type, kappa light chain). Peritoneal fluid analysis showed a serum-ascites albumin gradient of 1.1 g/dL and total fluid protein of 3.6 g/dL consistent with nonportal hypertensive etiology. The patient was managed empirically with intravenous ceftriaxone and intravenous albumin. Additional workup was nondiagnostic for other causes of ascites, and the patient was discharged after a 7-day hospital course. Conclusion: Patients presenting with refractory ascites in the setting of end-stage renal disease, cardiomyopathy, and long-standing immunosuppressive therapy may be at increased risk for SBP despite a high ascitic fluid protein.

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