Hypertension and COVID-19 — current state and prospects

Abstract

New coronavirus disease (COVID-19) caused by SARS-CoV-2 is associated with a high mortality rate and is a major public health problem worldwide. In publications from the early months of the COVID-19 pandemic, the authors reported that hypertension (HTN) is associated with higher susceptibility to SARS-CoV-2 infection, severe disease, and increased mortality associated with COVID-19. The risk of more severe clinical manifestations of COVID-19 is higher in men and increases dramatically with age. However, according to the results of multivariate analyses with the inclusion of data on age, risk factors (RF) of cardiovascular diseases (CVD), diabetes mellitus, the independent role of HTN in the development and outcome of COVID-19 was not confirmed, while age turned out to be the most significant factor. The authors made the conclusion that HTN may not play an independent role in SARS-CoV-2 infection and the course of COVID-19, and the formation of adverse outcomes is influenced by old age. However, age-related changes include accumulated chronic diseases, their RF, target organ damage etc. Morphofunctional changes caused by a long course of HTN, the development of associated clinical conditions can increase the susceptibility of the cardiovascular system to the damaging effects of SARS-CoV-2, as well as contribute to the formation of adverse outcomes of COVID-19. In addition, diabetes mellitus, obesity, and other metabolic disorders associated with HTN negatively contribute to the course of COVID-19 and the risk of mortality. A more severe course of COVID-19 in HTN patients, especially the elderly, may be facilitated by the mechanisms of cellular and immune inflammation common in these diseases. The endothelial monolayer plays an important role. Endothelial injury and endothelial dysfunction in HTN and endothelitis in COVID-19 may reinforce each other, increasing the likelihood of cardiovascular events in patients with COVID-19. An important pathogenetic mechanism of HTN — the renin-angiotensin- aldosterone system (RAAS) activation — plays a significant role in the genesis of COVID-19. Angiotensin-converting enzyme 2 (ACE) is a key receptor for SARS-CoV-2 entry into human cells, providing a link between COVID-19 and RAAS. In this regard, it was expected that ACE inhibitors and angiotensin II receptor blockers (ARB), which modulate the RAAS, may increase the risk of SARS-CoV-2 infection and worsen outcomes in COVID-19. However, in further experimental and clinical studies, these assumptions were not confirmed. Moreover, currently international experts strongly recommend that ACE inhibitors or ARB be continued in HTN patients with COVID-19, as they protect against cardiovascular complications and improve prognosis. Observations have shown that COVID-19 significantly increases the likelihood of developing HTN, acute coronary syndrome, cardiac arrhythmias, right ventricular dysfunction, myocardial fibrosis, heart failure, and also increases the risk of death from CVD. Further clinical and long-term prospective studies are needed to evaluate the role of past COVID-19 as a RF for CVD and mortality.