Патоморфологические особенности миокарда у пациентов с вирусной инфекцией COVID-19

Abstract

Coronavirus disease 2019 (COVID-19) is responsible for high mortality rates worldwide. Although myocardial injury has been demonstrated in critically ill COVID-19 patients, the mechanism of injury as well as morphological changes remain poorly understood. The purpose of the study was to study the morphology of the myocardium according to autopsy data in patients with established COVID-19 infection depending on the troponin level during hospitalization. Aim. To study autopsy myocardial morphology in patients with established COVID-19 infection, depending on the level of troponin during hospitalization. Design. Retrospective non-randomized cohort study. Materials and methods. The medical histories of 66 deceased patients diagnosed with coronavirus infection who were treated at the clinic of I.I. Mechnikov North-Western State Medical University from 05/01/2020 to 07/31/2020. Depending on the level of troponin T taken intravitally, the patients were divided into two groups: the first group — TnT+, which included patients who had an intravitally recorded increase in troponin T of more than 100,000 pg/ml (reference value in our laboratory), and the second group TnT–, it included individuals who did not have a significant increase in troponin T levels. In 22 patients, troponin was not determined, and they were included in the general group of deceased. Clinical manifestations of COVID-19 were analyzed (symptoms, physical examination data, volume of lung damage according to computed tomography, severity of respiratory failure), laboratory parameters, the presence of concomitant pathology, and autopsy results. The autopsy was performed according to a standard protocol, with histological examination of microslides of the lungs, myocardium, liver, kidneys, pancreas and spleen. Results. A comparative analysis of the TnT+ and TnT– groups showed that patients with elevated troponin levels more often developed disseminated intravascular coagulation (9 and 1, respectively (p = 0.05)), pulmonary embolism (6 and 0, respectively (p = 0, 05)), and thrombosis of other localizations was also detected (6 and 0, respectively (p = 0.05)). In addition, in the TnT+ group, paroxysm of atrial fibrillation developed for the first time during hospitalization against the background of COVID-19 pneumonia. A macroscopic examination of the myocardium of all deceased patients revealed a high prevalence of hypertrophy (56 (84.8%) people) and dilatation (31 (46.9%) people) of the left ventricle. Microscopic examination revealed perivascular fibrosis in 51 (77.3%) patients, intermuscular fibrosis in 38 (57.6%), interstitial edema was diagnosed in 40 (60.6%) people. Signs of damage to medium-sized vessels and microvasculature with the presence of stasis, microthrombosis of intramural myocardial vessels were determined in 10 (15.1%) people. When comparing the results of myocardial autopsy in patients with signs of acute myocardial injury (TnT+ group) and without it (TnT– group), no differences were found. At the same time, in the TnT+ group, signs of endothelitis were more common (p = 0.48), accompanied by microthrombosis and hemorrhages into the myocardium, but the differences were not statistically significant (p = 0.13 and p = 0.64, respectively), which may be due to a small sample of patients. Conclusion. Which substrate determines the increase in troponins in acute myocardial injury remains unclear, since the compared groups did not differ significantly according to the results of histological examination of the myocardium. Further research using modern diagnostic methods is required. Key words: myocardial injury, covid-19, autopsy, endotheliitis