The role of comorbid conditions in the pathogenesis and severity of Covid-19

Abstract

The article presents a generalized analysis of modern scientific data on the role of comorbid conditions in the pathogenesis and formation of severe COVID-19. It is shown that the presence of comorbidity is one of the leading factors determining the clinical course of SARS-CoV-2 infection, the frequency of hospitalization, the development of complications and mortality. According to clinical studies, up to 75% of hospitalized patients with COVID-19 have at least one comorbid disease. The most common comorbid conditions are arterial hypertension, coronary heart disease and type 2 diabetes; chronic lung diseases, renal dysfunction, oncological pathology and diseases of the digestive system also account for a significant proportion. The paper analyzes the results of international and domestic studies demonstrating a statistically significant relationship between cardiovascular diseases and the risk of severe COVID-19. It was found that arterial hypertension is associated with an increased risk of developing severe forms of infection by more than 2 times. The pathogenetic basis of this relationship is the interaction of the virus with the spike protein of the angiotensin-converting enzyme type 2 receptor (ACE2), which is involved in the regulation of the renin-angiotensin system. After SARS-CoV-2 penetrates the cell, the expression of ACE2 decreases, which leads to the loss of its vasodilating, anti-inflammatory and antifibrotic effects and contributes to damage to the cardiovascular system, lungs and kidneys. Special attention is paid to the role of coronary heart disease as a comorbid condition in the formation of acute coronary syndrome in COVID-19. It has been shown that the mechanisms of its development include endothelial dysfunction, hypercoagulable state, inflammatory response with the formation of a “cytokine storm”, destabilization of atherosclerotic plaques, direct viral invasion of cardiomyocytes through ACE2 and the development of tachyarrhythmias. The combination of these factors leads to a high risk of thrombotic complications and myocardial damage. The article also discusses the controversial issue of the influence of ACE inhibitors and angiotensin receptor blockers on the course of COVID-19. Despite the assumptions about the possible increase in ACE2 expression under the influence of these drugs, clinical studies do not provide unambiguous confirmation of their negative impact on the prognosis of the disease.
Thus, comorbid conditions, primarily cardiovascular pathology, play a key role in determining the severity of the course of COVID-19. Their influence is realized through complex mechanisms of disruption of vascular homeostasis, coagulation balance and inflammatory response. Further studies are needed to clearly define the independent contribution of individual comorbidities and optimize approaches to managing patients with COVID-19 in the context of comorbidity.