ABSTRACT
Purpose. To establish the features of laboratory indicators of inflammation and endothelial dysfunction in persons with new SARS-CoV-2 coronavirus infection and pulmonary artery thromboembolism verified by computed tomographic angiography. Materials and methods. The study enrolled 116 patients with the confirmed coronavirus infection SARS-CoV-2 who were treated in the health care institution "4th City Clinical Hospital named after N.E. Savchenko" of Minsk in whom computed tomographic angiography (CTA) was performed to verify the diagnosis of pulmonary embolism (PE). The median age of the subjects was 62.0 (52.0–70.0) years, the proportion of males was 45.7% (53), females – 54.3% (63). The study group consisted of patients with SARS-COV-2 and confirmed diagnosis of PE (n=37), comparison group included patients with SARS-COV-2 whose diagnosis of PE was excluded on CTA (n=79). The formed groups were comparable by gender, age, presence of diabetes mellitus, bad habits, degree of arterial hypertension, and severity of course of COVID-19. The serum levels of tumor necrosis factor alpha (TNF-a), interleukin-6 (IL-6), interleukin-1 beta (IL-1β), big endothelin-1 (Big ET-1), homocysteine were determined on the day when CTA was performed by enzyme immunoassay (EIA). A level of D-dimer on the day when CTA was performed was additionally analyzed. Results. In individuals with coronavirus infection and PE group mean values of IL-6, D-dimer, big ET-1, and homocysteine were significantly higher compared with the group without PE: 41.65 (21.84–136.36) versus 25.79 (15.93–36.17) pg/mL (U=135, p<0.05);2058.5 (826.0–4026.0) versus 982.5 (656.5–1936.0) ng/mL (U=141.5, p<0.05);0.34 (0.26– 0.51) versus 0.29 (0.07–0.38) pg/ml (U=137, p<0.05);19.55 (13.81–23.84) versus 16.01 (11.07–19.13) pg/ml (U=139, p<0.05) respectively. There were no significant differences between group mean values of TNF-a, interleukin-1β in the study and comparison groups. In the group of patients with PE and COVID-19 values of IL-6 and big ET-1 (ρ=0.66;p<0.05);TNF-a (ρ=0.62;p<0.05) were moderately positively correlated, values of IL-6 and D-dimer (ρ=0.78;p<0.05);interleukin-1β (ρ=0.80;p<0.05) were highly positively correlated. Conclusion. The obtained data demonstrates that in patients with COVID-19 and PE the course of the disease is accompanied by a more pronounced increase in serum levels of markers of inflammation (IL-6) and endothelial dysfunction (large endothelin-1, homocysteine). The correlation between the levels of IL-6 and big ET-1, D-dimer indicates the association of the activity of systemic inflammation with the level of endothelial dysfunction markers. © 2022, Professionalnye Izdaniya. All rights reserved.
ABSTRACT
The World Health Organization (WHO) officially announced the beginning of the COVID-19 pandemic in March 2020. So far, according to official WHO data, more than 195 million people worldwide have been infected with coronavirus infection, and the number of deaths has exceeded 4.1 million. At the beginning of the pandemic, the focus of the medical community was predominantly on the tropism of the virus to respiratory system, but the data accumulated today from national and foreign studies demonstrate the multiorgan nature of lesions in SARS-CoV-2, including atherothrombosis- associated cardiovascular diseases (CVDs). Patients with COVID-19 and concomitant cardiovascular disease and those who had cardiovascular events (CVE) are reported to have an increased risk of adverse outcomes. CVE in individuals infected with SARS-CoV-2 primarily consists of acute myocardial injury, acute myocardial infarction, myocarditis, rhythm disorders, heart failure, and thromboembolic events. The team of authors analyzed electronic medical records of 10 908 patients aged from 18 to 90 years, who were treated from June 01, 2020 to May 31, 2021 at the infectious disease departments of the 4th City Clinical Hospital named after N.E. Savchenko for patients with coronavirus infection (SARS-CoV-2). Individuals with rhythm disorders prevailed in this analysis - 13.38% (n=1460). The prevalence of persons with myocarditis and acute myocardial infarction developed on the background of SARS- CoV-2 infection was 0.29% (n=32) and 2.80% (n=305), respectively. The prevalence of patients with COVID-19 and thromboembolic events was 5.97% (n=651). SARS-CoV-2 can lead to CVE or decompensation of concomitant CVDs through direct or mediated mechanisms, including direct viral toxicity, excessive systemic inflammatory response, dysregulation of the renin-angiotensin- aldosterone system (RAAS), endothelial dysfunction and thrombosis, ventilation-perfusion failure, electrolyte imbalance, as well as on the background of ongoing therapy, which may potentially have cardiotoxic effects. The published article reviews the main proposed pathophysiological mechanisms and factors that lead to development of CVEs and provides the data on the contribution of CVEs to the course and outcomes in patients with COVID-19. Understanding the potential mechanisms underlying the pathophysiology of SARS-CoV-2 effects on the cardiovascular system is essential for providing comprehensive medical care for patients with CVDs and COVID-19. © 2021, Professionalnye Izdaniya. All rights reserved.