ABSTRACT
Purpose. To establish the factors influencing the progression of chronic coronary heart disease (CCHD) in patients with postinfarction cardiosclerosis after COVID-19 infection. Materials and methods. Included 45 patients with CCHD and postinfarction cardiosclerosis from among those who were under dynamic observation in the CCHD laboratory of the Republican Scientific and Practical Centre "Cardiology". All included in the study were divided into 2 groups: group I (31 patients) – after COVID-19, group II – patients with CCHD who did not have a COVID infection – 14. The I test was carried out in the pre-Covid period, the II test – within 1-3 months after documented COVID-19. Examination included echocardiography (EchoCG), computed tomographic angiography (CTA) of the coronary arteries (CA), magnetic resonance imaging. Results. Risk factors influenced on the progression of CCHD in patients after COVID-19 are: increased for more than 1 month levels of C-reactive protein (CRP), cardiac troponin, erythrocyte sedimentation rate (ESR), D-dimer. All mentioned factors contributed to the progression of coronary artery atherosclerosis. The coronavirus infection affected the enlargement of the left ventricle and the right parts of the heart, the deterioration of the systolic-diastolic function of both ventricles, including an increase in pressure in the pulmonary artery. The consequence of these changes was the progression of signs of heart failure according to echocardiography and the n-terminal fragment of the natriuretic peptide (NT-proBNP), an increase in the zones of myocardial ischemia compared with the pre-COVID period, and more frequent and significant ventricular arrhythmia. © 2022, Professionalnye Izdaniya. All rights reserved.
ABSTRACT
The coronavirus disease pandemic (coronavirus disease 2019 – COVID-19) has spread all over the world. With the tendency towards stabilization of the incidence rate in some European countries, the number of patients being hospitalized remains significant. The disease can be asymptomatic, however, the most dangerous manifestations are acute respiratory distress syndrome and fulminant pneumonia, which are most often the causes of death. More and more information is appearing in the press about the involvement of the cardiovascular system in the pathological process, both in persons, who previously suffered from circulatory system diseases and in patients, who had no cardiovascular pathology before they became infected with COVID-19. Possible mechanisms of the damaging effects of SARS-CoV-2 on the cardiovascular system are increasingly discussed. However, the accumulated data is not yet enough to draw global conclusions. New information appears almost every day. It was systematized in this review. The focus is on the damaging effects of SARS-CoV-2 on the heart. Methods. Literary data were searched using PubMed and Google search among Russian-language and English-language original articles, recommendations of national professional communities, expert comments published since the beginning of the COVID-19 pandemic. When searching, the terms “coronavirus”, “cardiac”, “cardiovascular”, “myocardial injury”, “myocardial infarction”, “troponin”, “myocarditis” were used. Conclusion. Currently, the mechanisms of heart damage with COVID-19 require further research. The question remains what prevails: the specific, typical only for the SARS-CoV-2 virus, action on the heart, blood vessels, and hemostasis, or changes in the cardiovascular system are non-specific, inherent in the presence of a systemic inflammatory reaction and acute respiratory distress syndrome. Preliminary evidence suggests that acute myocardial damage, accompanied by the increase of cardiac troponins, is by no means a rare condition associated with SARS-CoV-2 virus infection. The presence of acute myocardial damage with any mechanism of its development contributes to increase of nosocomial mortality, regardless of the presence of cardiovascular diseases before the development of COVID-19. © 2020, Professionalnye Izdaniya. All rights reserved.