The mechanisms involving these cardiovascular complications of COVID-19 may include direct myocardial injury, systemic inflammation and cytokine storm, downregulation of angiotensin-converting enzyme 2 (ACE2, EC 3.4.17.23) receptors, mismatch of myocardial oxygen demand-supply, atherosclerotic plaque rupture and coronary thrombosis, electrolyte imbalances, diffused endothelial damage, coagulation abnormalities characterized by hypercoagulation and microthrombosis, and adverse effects of COVID-19 therapies (Parvu et al. 2022; Zhao et al. 2023; Ozcan et al. 2023; Tangos et al. 2024). This evidence concerns the gene ACE2 and deep vein thrombosis.