Abstract

The aim – to investigate the clinical and pathomorphological features of the heart damagein patients who died due to COVID-19 pneumonia.Materials and methods. A retrospective analysis of the medical records of 556 patients,hospitalized to Lviv Clinical Emergency Care Hospital in January- February 2021, witha diagnosis of COVID-19 pneumonia and 90 reports of pathological examination ofthe causes of death of patients with COVID-19 pneumonia was carried out. Clinicalparameters (demographic data, comorbidities, presence of COVID-19 pneumoniacomplications, complaints, medical history, results of physical examination andadditional laboratory and instrumental investigations, performed during hospitalization,including levels of NT-proBNP and troponin, determined by immunofluorescence method)and results of pathological examination were evaluated.The results. During life, most patients who died due to COVID-19 pneumonia werediagnosed with acute respiratory distress syndrome (ARDS), the development of multipleorgan failure, rarely PE. They showed significantly lower capillary blood oxygensaturation indicators compared to similar indicators of recovered patients, as well asan increase in markers of systemic inflammation (level of leukocytes and interleukin-6),fibrin degradation products (D-dimers) and markers of multiorgan failure (creatinine,NT-proBNP, troponin I). The most frequent pathomorphological signs of heartdamage in patients with COVID-19 were interstitial edema with hyperemia (63.5 %) and fragmentation of cardiomyocytes (34.1 %). Every fourth patient had mononuclear cell infiltration, which was associated with increased level of NTproBNP, oxygen saturationdecrease in capillary blood, and increase in aspartate aminotransferase. Myocardialinfarction, pericarditis, and myocarditis occurred more rarely in patients with COVID-19.Conclusions. The variety of clinical scenarios of heart damage requires a high level ofsuspicion in the early stages of the disease and the use of appropriate investigations toidentify its cause.

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