A man of 81 years, with previous coronary artery disease, unrecognized myocardial infarction, carrier of implanted pacemaker, presented to the cardiology department for a scheduled hospitalization to treat shortness of breath and symptoms of heart failure. There was no chest pain, ECG poorly assessable for pacemaker-induced rhythm, cardiac troponin I of 35,879 ng/L (cut-off 20). Suspecting an acute coronary syndrome (ACS), the patient undergoes immediate coronary angiography that does not showed any change compared to a previous examination. Meanwhile SARS-CoV-2 research in nasopharyngeal swab by RT-PCR was positive and after a few hours fever appears.
The authors discussed the case and extensive monitoring of cardiac markers and intensive evaluation of clinical parameters were activated. Troponin I HS, CK-MB, Myoglobin (Beckman Coulter DxI), CK, AST, LDH are determined by routine methods (Beckman Coulter AU700), Troponin T (cTnT-hs Roche Diagnostics) on (Roche Cobas 8000).
All markers (except Troponin T) had the typical pattern of an ACS, in accordance with their characteristic half-life of an acute insult with development of a peak and subsequent decrease in a few days. The peaks recorded were cTnI 35,789 ng/L, CK-MB 72.6 ug/L, CK 800 U/L, AST 1,51U/L , Myoglobin 244 ng/ml, LDH 600 U/L, all at time 0. Troponin T was moderately increased at presentation (3700 ng/L, cut-off 10) followed by a peak of 3,872 after 2 hours stabilizing around 2,800 ng/L for the next days and decreasing after day 7. The final diagnosis was acute COVID-19-related myocarditis.
It has been described that the presentation of a SARS-CoV-2 infection can sometimes simulate a condition of ACS when there is an inflammatory involvement of the heart. In this case all the clinical data pointed towards an ischemic pathology which, however, was excluded in diagnostic imaging. A conclusive assessment with cardiac MRI was not possible due to the presence of the pacemaker, so the diagnosis was made as probable. Among the different markers, Troponin I was found to express a more intense signal and an earlier positive evolution than that of Troponin T. Our report highlights the different evolution of cardiac troponins in this disease.