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Cardiovascular diseases continue to be the main cause of hospital mortality and lead to great disability of the working population. Numerous clinical and experimental studies have shown that inflammation is the main factor causing the growth and progression of atherosclerosis. Despite significant progress in basic therapy aimed at both preventing the development of heart failure (HF) and treating it, the prognosis in patients after their first hospitalization remains extremely unfavorable. HF is the leading cause of morbidity and mortality worldwide. Various stimuli at different stages of HF pathophysiology trigger a cascade of proinflammatory reactions with the release of interleukins, the formation of reactive oxygen species, mitochondrial DNA damage and the induction of autophagy. Based on the presented results from experimental and clinical studies, it can be expected that a better understanding of the molecular aspects in the pathophysiology of HF will open opportunities for the development of new therapeutic monoclonal antibodies.

Patients with concomitant cardiovascular diseases and traditional cardiovascular risk factors (age, male gender, arterial hypertension, diabetes mellitus and obesity) belong to a particularly vulnerable cohort characterized by progressive severe COVID-19 and high hospital mortality. Thorough screening strategies, standardized guidelines, and center-level protocols are needed to identify patients who are at greater risk of postoperative complications and mortality. Therefore, in this review, we consider the possible impact of COVID-19 on the patency of bypass vessels in the coronary arteries, mainly in relation to venous shunts. However, this hypothesis needs to be confirmed and further studied in the framework of clinical randomized trials.