Coronavirus disease of 2019 (COVID-19), which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is spreading rapidly the world over. The disease was declared "pandemic" by the World Health Organization. An approved therapy for patients with COVID-19 has yet to emerge; however, there are some medications used in the treatment of SARS-CoV-2 infection globally including hydroxychloroquine, remdesivir, dexamethasone, protease inhibitors, and anti-inflammatory agents. Patients with underlying cardiovascular disease are at increased risk of mortality and morbidity from COVID-19. Moreover, patients with chronic stable states and even otherwise healthy individuals might sustain acute cardiovascular problems due to COVID-19 infection. This article seeks to review the latest evidence with a view to explaining possible pharmacotherapies for the cardiovascular complications of COVID-19 including acute coronary syndrome, heart failure, myocarditis, arrhythmias, and venous thromboembolism, as well as possible interactions between these medications and those currently administered (or under evaluation) in the treatment of COVID-19.

World Health Organization has designated coronavirus disease 2019 (COVID-19) as a pandemic. During the past several weeks, a considerable burden has been imposed on the Iranian's healthcare system. The present document reviewed the latest evidence and expert opinion regarding the management of ST-segment-elevation myocardial infarction during the outbreak of COVID-19 and outlines a practical algorithm for it.

Background and objectives: We aimed to demonstrate the clinical utility of CHA2DS2-VASc score in risk assessment of patients with STEMI regarding adverse clinical outcomes particularly no-reflow phenomenon. Materials and Methods: We designed a retrospective cohort study using the data of Tehran Heart Center registry for acute coronary syndrome. The study included 1331 consecutive patients with STEMI who underwent primary angioplasty. Patients were divided into two groups according to low and high CHA2DS2-VASc score. Angiographic results of reperfusion were inspected to evaluate the association of high CHA2DS2-VASc score and the likelihood of suboptimal TIMI flow. The secondary endpoint of the study was short-term in-hospital mortality of all cause. Results: The present study confirmed that CHA2DS2-VASc model enables us to determine the risk of no-reflow and all-cause in-hospital mortality independently. Odds ratios were 1.59 (1.30–2.25) and 1.60 (1.17–2.19), respectively. Moreover, BMI, high thrombus grade, and cardiogenic shock were predictors of failed reperfusion (odds were 1.07 (1.01–1.35), 1.59 (1.28–1.76), and 8.65 (3.76–24.46), respectively). We showed that using a cut off value of ≥ two in CHA2DS2-VASc model provides a sensitivity of 69.7% and specificity of 64.4% for discrimination of increased mortality hazards. Area under the curve: 0.72 with 95% CI (0.62–0.81). Conclusions: Calculation of CHA2DS2-VASc score applied as a simple risk stratification tool before primary PCI affords great predictive power. Furthermore, incremental values are obtained by using both CHA2DS2-VASc and no-reflow regarding mortality risk assessment.