Clinical features and characteristics of myocardial injure in COVID-19 (data from multicenter studies

Research article: Clinical features and characteristics of myocardial injure in COVID-19 (data from multicenter studies)

Authors: T.M. Cavadova*, G.M. Dadashova, M.N. Azimova, N.N. Qabiyeva

Scientific Research Institute of Cardiology named after academician J. Abdullayev; 85 Fatali Khan Xoyski Str., Baku AZ1072, Azerbaijan

*For correspondence: tmagayeva@gmail.com

Received 21 November 2020; Received in revised form 31 November 2020; Accepted 01 December 2020

Abstract:

In patients with COVID-19 caused by coronavirus-2 (SARS-CoV-2) and proceeding with the severe acute respiratory syndrome, studies were carried out to study myocardial damage, determine its na- ture and clinical significance. In an international, multicenter study, cardiovascular pathologists as- sessed cardiac tissue after necropsies in 21 COVID-19 patients. The presence of myocarditis was determined by the identification of multiple foci of inflammation with associated damage to myocytes, and the composition of the inflammatory cells was analyzed using immunohistochemistry. Other forms of acute damage and inflammation of myocytes, as well as damage to the coronary arteries, endocardium and pericardium, have also been described. Lymphocytic myocarditis occurred in 3 (14%) cases. Increased infiltration of interstitial macrophages was observed in 18 (86%) cases. In four cases, there was mild pericarditis. Acute damage to right ventricular myocytes, most likely due to stress/overload, occurred in four cases. In COVID-19, myocardial damage has been reported, in- cluding elevated serum troponin levels and acute heart failure with decreased ejection fraction. There was a slight trend towards higher serum troponin levels in patients with myocarditis compared with patients without myocarditis. With SARS-CoV-2, interstitial macrophages increase in most cases, and in a small proportion of cases, multifocal lymphocytic myocarditis. Other forms of myocardial injury may also occur. The risk of hospital death among patients with severe COVID-19 can be pre- dicted from markers of myocardial damage and has been significantly associated with older age, inflammatory response, and concomitant cardiovascular disease.

Keywords: Coronavirus Disease 2019 (COVID-19), SARS-CoV-2, myocardial injury, myocarditis, lactate dehydrogenase, cardiac troponin I, creatine kinase (-MB), myoglobin

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