Introduction: The coronavirus 2019 (COVID-19) pandemic has significantly impacted the management of cardiovascular emergencies across the world. Early in the pandemic, an unforeseen decline in hospital admissions of patients with acute cardiovascular emergencies was noted. Furthermore, the overall reduction in respiratory infections and vigorous exercise related to social isolation may have contributed to a decrease in the incidence of acute coronary syndrome (ACS). However, a significant number of patients have presented with late-stage cardiac diseases, such as late-presenting ACS, and with serious cardiac complications including cardiac arrests and out-of-hospital death.\\
Material and Methods: A retrospective cross-sectional study of all consecutive COVID-19 infected ACS patients admitted during the period April 1st, 2021 to March 1st, 2022, at VIMSAR BURLA. The cases could be ACS patients shown to be COVID-19 positive during routine screening after admission or referred from elsewhere as COVID positive or ACS developing in the hospital after admission for the treatment of COVID-19 infection. All consecutive COVID-19 (RT-PCR) positive patients above the age of 18 years with ACS admitted to VIMSAR Burla. Data of patients with age and sex-matched COVID-19 free ACS patients treated in the same period in VIMSAR Burla was enrolled as the control group for comparison in a 1:3 ratio. Data about baseline characteristics, electrocardiographic findings, clinical findings, and outcomes of patients were compared between the case and control groups.
Results: Once ACS is suspected, medical therapy should be instituted immediately along with a decision on whether to proceed with an invasive strategy. Medical therapy for ACS in COVID-19 patients is identical to patients without COVID-19. This includes dual antiplatelet therapy (aspirin and a P2Y12 inhibitor), intravenous or subcutaneous anticoagulation, statins, and beta-blockers (if no contraindications). However, only one in vitro study has shown that SARS-CoV-2 downregulates the ACE2 expression, and further studies are needed to confirm this pathophysiological pathway.
Conclusion: Despite the overall reduction in cases admitted to the emergency departments during the early phase of the pandemic, ACS is a potential life-threatening complication of COVID-19. The pathophysiological mechanisms are multiple and include atherosclerotic plaque rupture, overactivation of the coagulation system, platelet hyperreactivity, abnormal systemic inflammatory response, and oxygen supply/demand imbalance. When compared to non-COVID-19 cases, patients with ACS and SARS-CoV-2 infection present distinctive clinical and anatomical features, including the absence of obstructive CAD, the higher burden of thrombus, and the angiographic evidence of multiple thrombotic lesions.
