This review discusses the relationship between COVID-19 and cardiovascular disease (CVD), focusing on the biological mechanisms and clinical implications. SARS-CoV-2, the virus causing COVID-19, shares many biological features with SARS-CoV, including the use of ACE2 as a receptor for cell entry. The interaction between the viral spike (S) protein and ACE2 is likely involved in cardiovascular manifestations of COVID-19. Pre-existing CVD is associated with higher mortality in patients with COVID-19, while the virus itself can cause myocardial injury, arrhythmias, acute coronary syndrome, and venous thromboembolism. Potential drug-disease interactions are a concern for patients with both COVID-19 and CVD. The virus can cause coagulation abnormalities, leading to thromboembolic events. The SARS-CoV-2 genome is approximately 30 kb long and contains ten open reading frames (ORFs) that encode 24–27 genes. The S protein of SARS-CoV-2 has two distinctive features: a high binding affinity to ACE2 and an insertion of four amino acid residues that introduces a novel furin cleavage site. These features may contribute to the virus's high transmissibility and severity. The life cycle of SARS-CoV-2 involves binding to ACE2, followed by entry into host cells via fusion or endocytosis. The viral genome is then replicated, and new viral particles are assembled and released. The interaction between the S protein and ACE2 is a potential therapeutic target for vaccines, neutralizing antibodies, and antiviral compounds. The cardiovascular system is significantly affected by COVID-19, with a high prevalence of pre-existing CVD in patients. Myocardial injury is independently associated with high mortality, and some patients may present with cardiac symptoms as the first clinical manifestation. Myocarditis and acute coronary syndrome are also common manifestations. The mechanisms underlying these cardiovascular effects are not fully understood, but systemic inflammation and direct viral infection of cardiac cells are potential factors. The role of ACE2 in the cardiovascular system is crucial, as it is part of the renin-angiotensin-aldosterone system (RAAS) and is highly expressed in the heart. However, the interaction between SARS-CoV-2 and ACE2 may affect the cardiovascular system indirectly. The review also discusses the impact of immunosuppressive treatments on patients with CVD and the need for careful management of cancer patients during the pandemic. In conclusion, the relationship between COVID-19 and the cardiovascular system is complex, involving both direct and indirect mechanisms. Understanding these mechanisms is essential for developing effective preventative and therapeutic strategies.This review discusses the relationship between COVID-19 and cardiovascular disease (CVD), focusing on the biological mechanisms and clinical implications. SARS-CoV-2, the virus causing COVID-19, shares many biological features with SARS-CoV, including the use of ACE2 as a receptor for cell entry. The interaction between the viral spike (S) protein and ACE2 is likely involved in cardiovascular manifestations of COVID-19. Pre-existing CVD is associated with higher mortality in patients with COVID-19, while the virus itself can cause myocardial injury, arrhythmias, acute coronary syndrome, and venous thromboembolism. Potential drug-disease interactions are a concern for patients with both COVID-19 and CVD. The virus can cause coagulation abnormalities, leading to thromboembolic events. The SARS-CoV-2 genome is approximately 30 kb long and contains ten open reading frames (ORFs) that encode 24–27 genes. The S protein of SARS-CoV-2 has two distinctive features: a high binding affinity to ACE2 and an insertion of four amino acid residues that introduces a novel furin cleavage site. These features may contribute to the virus's high transmissibility and severity. The life cycle of SARS-CoV-2 involves binding to ACE2, followed by entry into host cells via fusion or endocytosis. The viral genome is then replicated, and new viral particles are assembled and released. The interaction between the S protein and ACE2 is a potential therapeutic target for vaccines, neutralizing antibodies, and antiviral compounds. The cardiovascular system is significantly affected by COVID-19, with a high prevalence of pre-existing CVD in patients. Myocardial injury is independently associated with high mortality, and some patients may present with cardiac symptoms as the first clinical manifestation. Myocarditis and acute coronary syndrome are also common manifestations. The mechanisms underlying these cardiovascular effects are not fully understood, but systemic inflammation and direct viral infection of cardiac cells are potential factors. The role of ACE2 in the cardiovascular system is crucial, as it is part of the renin-angiotensin-aldosterone system (RAAS) and is highly expressed in the heart. However, the interaction between SARS-CoV-2 and ACE2 may affect the cardiovascular system indirectly. The review also discusses the impact of immunosuppressive treatments on patients with CVD and the need for careful management of cancer patients during the pandemic. In conclusion, the relationship between COVID-19 and the cardiovascular system is complex, involving both direct and indirect mechanisms. Understanding these mechanisms is essential for developing effective preventative and therapeutic strategies.