Cardiovascular Manifestations of COVID-19 Infection
Top Cited Papers
Open Access
- 19 November 2020
- Vol. 9 (11), 2508
- https://doi.org/10.3390/cells9112508
Abstract
SARS-CoV-2 induced the novel coronavirus disease (COVID-19) outbreak, the most significant medical challenge in the last century. COVID-19 is associated with notable increases in morbidity and death worldwide. Preexisting conditions, like cardiovascular disease (CVD), diabetes, hypertension, and obesity, are correlated with higher severity and a significant increase in the fatality rate of COVID-19. COVID-19 induces multiple cardiovascular complexities, such as cardiac arrest, myocarditis, acute myocardial injury, stress-induced cardiomyopathy, cardiogenic shock, arrhythmias and, subsequently, heart failure (HF). The precise mechanisms of how SARS-CoV-2 may cause myocardial complications are not clearly understood. The proposed mechanisms of myocardial injury based on current knowledge are the direct viral entry of the virus and damage to the myocardium, systemic inflammation, hypoxia, cytokine storm, interferon-mediated immune response, and plaque destabilization. The virus enters the cell through the angiotensin-converting enzyme-2 (ACE2) receptor and plays a central function in the virus’s pathogenesis. A systematic understanding of cardiovascular effects of SARS-CoV2 is needed to develop novel therapeutic tools to target the virus-induced cardiac damage as a potential strategy to minimize permanent damage to the cardiovascular system and reduce the morbidity. In this review, we discuss our current understanding of COVID-19 mediated damage to the cardiovascular system.This publication has 156 references indexed in Scilit:
- Influenza and SARS-Coronavirus Activating Proteases TMPRSS2 and HAT Are Expressed at Multiple Sites in Human Respiratory and Gastrointestinal TractsPLOS ONE, 2012
- Prevention of Angiotensin II–Mediated Renal Oxidative Stress, Inflammation, and Fibrosis by Angiotensin-Converting Enzyme 2Hypertension, 2011
- Angiotensin-Converting Enzyme 2 Suppresses Pathological Hypertrophy, Myocardial Fibrosis, and Cardiac DysfunctionCirculation, 2010
- Circulating Rather Than Cardiac Angiotensin-(1-7) Stimulates Cardioprotection After Myocardial InfarctionCirculation: Heart Failure, 2010
- Multiple organ infection and the pathogenesis of SARSThe Journal of Experimental Medicine, 2005
- Cytokine Responses in Severe Acute Respiratory Syndrome Coronavirus-Infected Macrophages In Vitro: Possible Relevance to PathogenesisJournal of Virology, 2005
- Myocardial infarction increases ACE2 expression in rat and humansEuropean Heart Journal, 2005
- A Human Homolog of Angiotensin-converting EnzymeOnline Journal of Public Health Informatics, 2000
- Traffic signals for lymphocyte recirculation and leukocyte emigration: The multistep paradigmCell, 1994
- A Clinicopathological Study on Cardiac Lesions in 64 Cases of Disseminated Intravascular CoagulationJapanese Heart Journal, 1977