COVID-19 beyond the lungs: Unraveling its vascular impact and cardiovascular complications-mechanisms and therapeutic implications.

Abstract

COVID-19, caused by severe acute respiratory syndrome corona virus 2 (SARS-CoV-2), is primarily a respiratory illness but significantly affects the cardiovascular system as well. After entering the body through the respiratory tract, the virus directly and indirectly disrupts the vascular system. Vascular endothelial cells (ECs), which express ACE2 and TMPRSS2, are targets for viral invasion. However, the predominant cause of widespread vascular damage is the "cytokine storm" induced by the immune response. This leads to EC activation, inflammation, neutrophil activation, and neutrophil-platelet aggregation, causing endothelial injury. Additionally, increased expression of plasminogen activator inhibitor-1 disrupts the balance between prothrombotic and fibrinolytic processes, while activation of the renin-angiotensin-aldosterone system adds oxidative stress to the vascular endothelium. In the heart, SARS-CoV-2 invades ECs, leading to apoptosis and pyroptosis, exacerbated by inflammation and elevated catecholamines. These factors contribute to arrhythmias, strokes, and myocardial infarction in severe cases of COVID-19. This narrative review aims to explore the mechanisms by which SARS-CoV-2 affects the cardiovascular system and to highlight the resulting complications. It also identifies research gaps and discusses potential therapeutic strategies to mitigate the cardiovascular impacts of COVID-19.