Cardiovascular risk in COVID-19 infection

A few months ago a new coronavirus was identified in Cina officially named by the WHO as COVID-19. The thousands of patients who died showed pneumonia and alveolar damage, but actually, according to several authors in addition to the acute respiratory distress syndrome the virus can give rise to multiorgan failure. In fact, many people died equally despite being intubated and treated for respiratory failure. In this review, we especially wanted to describe the virus effects on the cardiovascular system, probably the leading cause of death of thousands of deceased patients. Therefore, mortality is indirectly induced by the virus through vascular inflammation and cardiovascular damage and patients with severe COVID-19 infection showed significantly increased levels of cardiac troponin I and inflammatory cytokines. The main activation of the signal pathways for the production of inflammatory cytokines are the toll-like receptors that recognize the presence of viral nucleic acids and the ACE-2 receptors, that the virus uses to infect the cells. The binding to ACE-2 also allows to promote high levels of angiotensin II by promoting high levels of blood pressure. High levels of IL-6,1L-113 and IL-8 have been associated with plaque instability and increased thrombotic risk. Furthermore IL-6 is involved in the stimulation of matrix-degrading enzymes such as matrix metalloproteinases, and may contribute to the development of acute coronary syndrome. In addition, TNF-alpha, IL-1 and IL-6 present in patients with severe COVID-19 are associated with coagulation activation and thrombin generation resulting in disseminated intravascular coagulation or thrombotic microangiopathy. Considering these pathological effects of the virus, anti-inflammatory and anticoagulant treatments are to be considered to avoid cardiovascular events. In this regard, heparin, in addition to its anticoagulant characteristics, has been shown to have good control over inflammation and to be a good anti-viral drug.