Journal of the American College of Cardiology
Volume 8, Issue 6, June 2020
DOI: 10.1016/j.jchf.2020.04.001
Volume 8, Issue 6, June 2020
DOI: 10.1016/j.jchf.2020.04.001
Quote:
Four hospitalized patients with severe heart failure were retrospectively included who had been infected with COVID-19 between January 7, 2020, and March 15, 2020, in the authors' department. All patients were transferred to an isolation ward since the diagnosis was confirmed or highly suspected. Three patients were suspected of having received hospital-related transmission because they were once in the same ward. None of the patients had fever during the illness, and they had just mild cough or fatigue at the time of diagnosis. Significantly enlarged left ventricle (Figure 1) and reduced left ventricular ejection fraction were observed in 4 patients, and all had New York Heart Association functional class IV. Interestingly, Patient #1 was had negative results for 2 consecutive nucleic acid tests but positive result for serum antibodies (immunoglobulin M [IgM] 69.12 AU/ml). Only 2 patients had typical ground-glass imaging changes on lung computed tomography scans (Figure 1). With exacerbations, Patient #3 and #4 were transferred to intensive care units, and both died 10 days after the first positive nucleic acid test result. Three patients had elevated troponin I (TNI) in the later period, especially in Patients #3 and #4, TNI increased significantly a few days before death. Moreover, the levels of C-reactive protein (CRP) and brain natriuretic peptide in patients 3 and 4 were significantly higher than those in the remaining 2 patients. It is also worth mentioning that testing results for patient 2 turned positive again after 2 consecutive negative test results for nucleic acid. The detailed information and treatment of patients are shown in Table 1.
Quote:
The most novel finding was that the TNI levels of the 2 critically ill patients were 20-fold increased, indicating myocardial injury. Although there have been previous reports of myocardial damage in COVID-19 patients (4,5), those reports chose mainly nonspecific indicators such as creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH), which could be confounded by many other factors in clinic. In addition, CK-MB and LDH were not, in fact, significantly increased in those reports. The present findings provided definitely stronger evidence of myocardial injury by COVID-19.
