Increasing cardiac troponin-I level as a cardiac injury index correlates with in-hospital mortality and biofactors in severe hospitalised COVID-19 patients.

backgroundSevere acute respiratory syndrome coronavirus-2 raised in 2019 (COVID-19) affects the lung tissue and other organs, specifically the heart.

methodsThe current study evaluated 120 hospitalised patients with severe COVID-19 between March 2021 and February 2022. Patients' demographics, vital signs, electrocardiogram abnormalities, clinical laboratory tests, including troponin I (TPI), mortality, and discharge type, were recorded.

resultsAmong the 120 hospitalised patients with severe COVID-19, 54 (45.0%) patients were male, with an average age of 63.2 ± 1.4. Many patients have chronic comorbidities, including hypertension (51.6%), diabetes mellitus (34.1%), and ischemic heart disease (17.5%). The in-hospital and six months after the discharge mortality were 45.8% and 21.5%, respectively. Cardiac injury was observed in 14 (11.7%) patients with a mean TPI level of 8.386 ± 17.89 μg/L, and patients with cardiac injury had higher mortality than those without cardiac injury (P < 0.001). Furthermore, the cardiac injury was meaningfully correlated with age (ρ = 0.182, P = 0.019), history of ischemic heart disease (ρ = 0.176, P = 0.05), hospitalisation result and mortality (ρ = 0.261, P = 0.004), inpatient in ICU (ρ = 0.219, P = 0.016), and serum levels of urea (ρ = 0.244, P = 0.008) and creatinine (ρ = 0.197, P = 0.033). Additionally, the discharge results were significantly correlated with oxygen saturation with (ρ = -0.23, P = 0.02) and without (ρ = -0.3, P = 0.001) oxygen therapy, D-dimer (ρ = 0.328, P = 0.019), LDH (ρ = 0.308, P = 0.003), urea (ρ = 0.2, P = 0.03), and creatinine (ρ = 0.17, P = 0.06) levels.

conclusionElevated TPI levels are associated with increased mortality in severe COVID-19 patients. Therefore, TPI may be a beneficial biofactor for early diagnosis of cardiac injury and preventing a high mortality rate.