Key result
COVID-19 may trigger the progression of stable coronary artery disease to acute coronary syndrome through mechanisms including systemic inflammation, plaque rupture, cytotoxic T-cell dysregulation, and hypercoagulability.
Why the study?
Patients with underlying cardiovascular disease face increased mortality risk from COVID-19, and the virus enhances myocardial injury, suggesting a need to discuss how COVID-19 promotes progression of stable CAD to ACS.
COVID-19 may trigger the progression of stable coronary artery disease to acute coronary syndrome through multiple mechanisms including systemic inflammation, plaque rupture, and hypercoagulability, warranting close monitoring of these patients.
May warrant closer monitoring of stable CAD patients with COVID-19; leaves open prospective confirmation of mechanisms and clinical impact.
Since the beginning of the coronavirus disease 2019 (COVID-19) pandemic, the increased mortality risk of patients with underlying cardiovascular diseases and COVID-19 was raised. Besides, coronavirus itself enhances the incidence of myocardial injury, which suggests a two-sided relation. We aimed to discuss the role of COVID-19 in the progression of stable coronary artery disease (CAD) to acute coronary syndrome (ACS), which might lead to a greater rate of out-of-hospital cardiac arrest and a higher fatality rate of ACS during the pandemic. We briefly reviewed several mechanisms in this regard: Systemic inflammation and cytokine release in critical patients; Plaque rupture and coronary thrombosis; Dysregulation of cytotoxic T-cell lymphocytes; Malignant ventricular arrhythmias. We reinforce applying more attention to COVID-19 patients with stable CAD during follow-up to prevent progression to ACS. These individuals should seriously observe World Health Organization protocols to avoid virus transmission by carriers.
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Shafeghat et al. (2021) conducted a review in COVID-19 and Coronary Artery Disease. COVID-19 was evaluated. COVID-19 may trigger the progression of stable coronary artery disease to acute coronary syndrome through mechanisms including systemic inflammation, plaque rupture, cytotoxic T-cell dysregulation, and hypercoagulability.
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