Cardiac And Inflammatory Biomarkers And New Or Worsening Heart Failure In High-risk Patients With COVID-19

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IntroductionConsequences of COVID-19 on the cardiovascular (CV) system are broad and have encompassed conditions including cardiomyopathies and acute coronary syndrome. Inciting triggers are likely multifactorial, with reported mechanisms ranging from a pro-inflammatory cytokine storm to microvascular ischemia. Elevated inflammatory markers including high sensitivity C-reactive protein (hsCRP), d-dimer, and interleukin-6 (IL-6) have been associated with adverse outcomes in COVID-19. We sought to identify the association of cardiac and inflammatory biomarkers with new or worsening HF in patients admitted with COVID-19.MethodsWe performed a single-centered prospective cohort study of patients who were hospitalized with COVID-19 from September 2020 through April 2021. Blood serum specimens from enrolled patients were collected upon hospital admission, weekly and upon discharge for quantification of troponin T, B-natriuretic peptide (BNP), and inflammatory biomarkers, including immune cell subtypes, cell activation markers, and plasma cytokines. New or worsening HF was defined as any new left ventricular (LV) systolic dysfunction, decrease in ejection fraction >5% or a decompensated state in those with a prior history of HF.ResultsTwelve of the 41 patients who were enrolled presented with new or worsening HF. Of this subgroup, 6 had new or worsening LV systolic function, 7 had concomitant myocardial injury represented by elevated troponin and there were no biopsy-confirmed cases of myocarditis. The average age of this subgroup was 65.8 years (interquartile range [IQR] 55.6-76.0) and 67% were male. All patients had at least 3 CV risk factors upon presentation and 75% had a prior diagnosis of HF (p < 0.01). Clinical profiles were otherwise similar between groups, and there were no significant differences in acute medical management. Among those with new or worsening HF, median BNP was elevated (345, IQR 184-509 vs 95, IQR 38.5-171 pg/nl, p = 0.01), as was median troponin (201, IQR 30-620 vs 16, IQR 0-56.5 ng/L, p = 0.02). Otherwise, there were no significant differences noted in baseline or follow-up biochemical markers of inflammation, including hsCRP, IL-6 and d-dimer, between patients with and without new or worsening HF.ConclusionPatients admitted with COVID-19 who experience new or worsening HF syndrome have elevated BNP and troponin levels, but similar CV risk factors compared to those who do not. Baseline measures of inflammation are not greater in those who develop HF syndrome in the setting of COVID-19.