Integrating the Metaverse Into Medical Practice: A Systematic Review of Its Potential and Applications.

Since emerging in late 2019 and now in its sixth year, SARS‐CoV‐2 is recognized as a systemic illness affecting multiple organs, including the cardiovascular system []. It manifests acutely and may persist during convalescence or beyond. Acute cardiac injury, a common extrapulmonary complication of COVID‐19, occurs in 8% to 62% of hospitalized patients and correlates with greater disease severity, including mechanical ventilation needs, higher mortality, and potential long‐term effects []. The dominant SARS‐CoV‐2 variants evolved over the pandemic, with the Delta variant (B.1.617.2), emerging in late 2020 and dominant by mid‐2021, associated with higher hospitalization and death risks than the Alpha variant and varying risks of major vascular events []. Few studies have examined post‐acute cardiovascular outcomes, primarily in hospitalized patients with limited follow‐up; comprehensive 12‐month assessments across care settings (non‐hospitalized, hospitalized, ICU) are lacking but essential for post‐acute care strategies [, ]. Longitudinal data indicate SARS‐CoV‐2 infection raises cardiovascular event risks by 30%–60% in survivors, even without prior heart disease []. Beyond 30 days post‐infection, survivors face elevated risks of arrhythmias (e.g., atrial fibrillation, sinus tachycardia, sinus bradycardia, ventricular arrhythmias, atrial flutter), inflammatory heart diseases (pericarditis, myocarditis), ischemic heart disease, heart failure, non‐ischemic cardiomyopathy, and thromboembolic events (pulmonary embolism, deep vein thrombosis, superficial vein thrombosis) []. Proposed mechanisms involve ACE2 (angiotensin‐converting enzyme 2), a key host factor for SARS‐CoV‐2 virulence and pathogenesis, with viral binding to ACE2 in endothelial cells, vascular smooth muscle cells, cardiomyocytes, cardiofibroblasts, pericytes, and epicardial adipose cells, conferring cardiac and vascular tropism []. Additional contributors include viral‐induced endothelial dysfunction, immune dysregulation, systemic inflammation (e.g., elevated CRP), and hypercoagulability (e.g., high ‐dimer), disrupting cardiovascular stability []. Severe COVID‐19 may induce immunothrombosis, where activated immune cells and platelets drive clotting in vessels, potentially exacerbating ARDS and organ dysfunction [].