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COVID-19, caused by SARS-CoV-2, is linked to both acute and lasting cardiovascular complications. This review synthesizes 165 studies from MEDLINE, Embase, and the Cochrane Library to summarize cardiovascular outcomes, underlying mechanisms, and implications for variant surveillance and vaccination. Clinical evidence reveals increased risks of arrhythmias, ischemic and inflammatory heart disease, heart failure, cerebrovascular events, and thromboembolic disorders even after the acute phase, including in non-hospitalized patients. These risks are higher following more severe infections. Proposed mechanisms include direct viral injury, endothelial dysfunction, complement activation, dysregulated inflammation and coagulation, and disruption of the renin–angiotensin–aldosterone system. Experimental studies show spike mutations alter viral entry and antibody escape, though their impact on cardiovascular outcomes is still unclear. Vaccination is associated with fewer cardiovascular events and post-acute sequelae, despite offering incomplete protection. Ongoing genomic surveillance, vaccination efforts, and cardiovascular follow-up are crucial to inform preventive strategies and manage the long-term cardiovascular burden of SARS-CoV-2 infection.
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Francesco Nappi (2026) studied this question.
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