Serious intense respiratory disorder coronavirus 2 (SARS-CoV-2) taints have cells taking after authoritative with the cell surface ACE2 receptors, subsequently driving to coronavirus illness 2019 (COVID-19). SARS-CoV-2 causes viral pneumonia with extra extrapulmonary appearances and major complications, counting intense myocardial harm, arrhythmia, and stun primarily in elderly patients. Besides, patients with existing cardiovascular comorbidities, such as hypertension and coronary heart malady, have a more regrettable clinical result taking after compression of the viral sickness. A striking include of COVID-19 pandemics is the tall rate of fatalities in progressed matured patients: this could be due to the predominance of slightness and cardiovascular illness increment with age due to endothelial brokenness and misfortune of endogenous cardioprotective components. In spite of the fact that exploratory prove on this point is still at its earliest stages, the point of this position paper is to hypothesize and talk about more suggestive cellular and atomic instruments whereby SARS-CoV-2 may lead to hindering results to the cardiovascular framework. We are going center on maturing, cytokine storm, NLRP3/inflammasome, hypoxemia, and discuss contamination, which is an rising cardiovascular hazard calculate associated with rapid urbanization and globalization. We are going at last examine the affect of clinically accessible CV drugs on the clinical course of COVID-19 patients. Understanding the part played by SARS-CoV2 on the CV framework is in fact required to induce encourage experiences into COVID-19 pathogenesis and to plan a restorative methodology of cardio-protection for slight patients.