Introduction & Background literature: Viral infections persist globally, among all age groups, race, and gender.  Of particular importance is the SARS-CoV-2 (COVID-19), and its prevalence in communities infecting all patient populations with symptoms ranging from asymptomatic to severe complications and mortality.  Emerging data continues to link COVID-19 with cardiovascular impacts. The most common cardiovascular pathologies according to the World Health Organization include coronary heart disease, cerebrovascular disease, peripheral artery disease, rheumatic heart disease, congenital heart disease, deep vein thrombosis, and pulmonary embolism. Some common mechanisms of cardiovascular pathologies include arteriosclerosis and inflammation often seen with aging, obesity, infection, smoking, and alcohol use. After reviewing mechanisms of COVID-19, Hepatitis C, and HIV, we look to find a common pathway for cardiovascular implications in these viral disease states.

Hypothesis: There is a common mechanism between other viral disease states and COVID-19’s effects on the cardiovascular system.

Our goal / Aims:

1. Compare COVID-19-induced CVS dysfunction with other common viral associated CVS pathologies
2. What is the specific mechanism leading to cardiotoxicity and CVS pathologies in COVID-19?

Materials and Methods: Thus, PubMed, Scopus, Elsevier, and Google Scholar databases were examined up to May-2021, using suitable keywords.  Individual and pooled prevalence rates with 95% confidence intervals (CI) will be calculated using the fixed- or random-effects model as appropriate. Identification of the independent parameters based on age, sex, and illness to understand the effect of COVID-19 on the different disease states of the CVS will be carried out using the fixed and random-effects meta-analysis models as appropriate.

Results: Elevated interleukin-6 levels are associated with inflammation of cardiomyocytes particularly, with prolonged synthesis of IL-6 having detrimental effects on the heart. One proposed mechanism is that IL-6 promotes atherogenesis via recruitment of other inflammatory cells to further uptake and oxidize low density lipoproteins. COVID-19, Hepatitis C, and HIV have increased IL-6 levels in the blood which can lead to cardiovascular alterations. Acute COVID-19 cardiovascular syndrome is associated with cardiomyopathy, ventricular arrhythmias, and hemodynamic instability. The cause of acute COVID-19 cardiovascular syndrome is uncertain but is suspected to be related to systemic cytokine mediated injury. Hepatitis C viral infections lead to an increased cardiovascular risk, with the common understanding being that increased TNF alpha and IL-6 cause the cardiovascular alterations. HIV-infected patients are at an additional risk for cardiovascular events, with increased blood levels of IL-6 and D-dimer. These HIV-infected patients with elevated IL-6, high-sensitivity C-reactive protein, and D-dimer corresponds with increased all-cause mortality and predicted cardiovascular disease, independent of other risk factors. Increased IL-6 is seen with COVID-19, hepatitis C infections, and HIV infections, that lead to cardiovascular effects.