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After entering the body through the respiratory tract, the virus directly and indirectly disrupts the vascular system. Vascular endothelial cells (ECs), which express ACE2 and TMPRSS2, are targets for viral invasion. However, the predominant cause of widespread vascular damage is the \u201ccytokine storm\u201d induced by the immune response. This leads to EC activation, inflammation, neutrophil activation, and neutrophil\u2013platelet aggregation, causing endothelial injury. Additionally, increased expression of plasminogen activator inhibitor-1 disrupts the balance between prothrombotic and fibrinolytic processes, while activation of the renin\u2013angiotensin\u2013aldosterone system adds oxidative stress to the vascular endothelium. In the heart, SARS-CoV-2 invades ECs, leading to apoptosis and pyroptosis, exacerbated by inflammation and elevated catecholamines. These factors contribute to arrhythmias, strokes, and myocardial infarction in severe cases of COVID-19. This narrative review aims to explore the mechanisms by which SARS-CoV-2 affects the cardiovascular system and to highlight the resulting complications. 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