The laboratory and radiologic findings are shown in Table 1. In the overall study population of 416 patients, median (IQR) levels of C-reactive protein (4.5 [1.4-8.5] mg/dL; to convert to milligrams per liter, multiply by 10) and procalcitonin (0.07 [0.04-0.15] ng/L) were elevated, while the median values of other laboratory indicators were within the normal range, such as counts of leukocytes, lymphocytes, platelets, erythrocytes; hemoglobin level; cardiac indicators

In terms of laboratory findings, patients with cardiac injury compared with patients without cardiac injury showed higher median leukocyte count (median [IQR], 9400 [6900-13 800] cells/μL vs 5500 [4200-7400] cells/μL), and levels of C-reactive protein (median [IQR], 10.2 [6.4-17.0] mg/dL vs 3.7 [1.0-7.3] mg/dL), procalcitonin (median [IQR], 0.27 [0.10-1.22] ng/mL vs 0.06 [0.03-0.10] ng/mL), CK-MB (median [IQR], 3.2 [1.8-6.2] ng/mL vs 0.9 [0.6-1.3] ng/mL), myohemoglobin (median [IQR], 128 [68-305] μg/L vs 39 [27-65] μg/L), hs-TNI (median [IQR], 0.19 [0.08-1.12] μg/L vs <0.006 [<0.006-0.009] μg/L), N-terminal pro-B-type natriuretic peptide (NT-proBNP) (median [IQR], 1689 [698-3327] pg/mL vs 139 [51-335] pg/mL),

for those without underlying CVD but elevated TnT levels, and 69.44% (25 of 36) for those with underlying CVD and elevated TnTs.

Plasma TnT levels demonstrated a high and significantly positive linear correlation with plasma high-sensitivity C-reactive protein levels (β = 0.530, P < .001) and N-terminal pro–brain natriuretic peptide (NT-proBNP) levels (β = 0.613, P < .001). Plasma TnT and NT-proBNP levels during hospitalization (median [interquartile range (IQR)], 0.307 [0.094-0.600]; 1902.00 [728.35-8100.00]) and impending death (median [IQR], 0.141 [0.058-0.860]; 5375 [1179.50-25695.25]) increased significantly compared with admission values (median [IQR], 0.0355 [0.015-0.102]; 796.90 [401.93-1742.25]) in patients who died (P = .001; P < .001), while no significant dynamic changes of TnT (median [IQR], 0.010 [0.007-0.019]; 0.013 [0.007-0.022]; 0.011 [0.007-0.016]) and NT-proBNP (median [IQR], 352.20 [174.70-636.70]; 433.80 [155.80-1272.60]; 145.40 [63.4-526.50]) was observed in survivors

During hospitalization, patients with elevated TnT levels had more frequent malignant arrhythmias, and the use of glucocorticoid therapy (37 [71.2%] vs 69 [51.1%]) and mechanical ventilation (41 [59.6%] vs 14 [10.4%]) were higher compared with patients with normal TnT levels.

that the levels of the last test of neutrophils (14/16, 87.5%), PCT (11/11, 100%), CRP (11/13, 84.6%), cTnI (7/9, 77.8%),

Itis likely that cardiac troponin measurements wererequested in those who were more unwell or where there wasreasonable suspicion of myocardial ischemia or myocardial dysfunction. Only systematic testing of both symptomatic and asymptomatic patients infected with SARS-CoV-2 will provide an accurate estimate of the prevalence of myocardial injuryin this condition.

In a cohort of 191 patients with confirmed COVID-19 based on SARS-CoV-2 RNA detection, the univariable odds ratio for death when hs-cTnI concentrations were above the 99thpercentile upper reference limit was 80.1 (95% confidence interval [CI]10.3 to 620.4, P<0.0001).[4]This was higher than the odds ratios observed for all other biomarkerstested,including D-Dimer and lymphocyte count.

Creatine kinase, U/L≤1851 (ref)......>1852·56 (1·03–6·36)0·043....High-sensitivity cardiac troponin I, pg/mL≤281 (ref)......>2880·07 (10·34–620·36)<0·0001....

In this study, increased high-sensitivity cardiac troponin I during hospitalisation was found in more than half of those who died.

A raised troponin (hypersensitive-troponin I (hs-cTnI)) was detected in five patients, possibly suggestive of virus-associated myocardial injury.