The article reviews the current understanding of the interaction between COVID-19 and the cardiovascular system, focusing on both basic mechanisms and clinical perspectives. COVID-19, caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has become a global pandemic affecting billions of individuals. Pre-existing cardiovascular diseases (CVDs) are linked with worse outcomes and increased risk of death in patients with COVID-19, while the virus can also induce myocardial injury, arrhythmias, acute coronary syndrome, and venous thromboembolism. The article discusses the biological features of SARS-CoV-2, including its genome, genes, and proteins, and highlights the role of angiotensin-converting enzyme 2 (ACE2) in viral entry and potential therapeutic targets. It also explores the diverse cardiovascular manifestations of COVID-19, such as myocardial injury, acute coronary syndrome, heart failure, arrhythmias, and coagulation abnormalities. The article emphasizes the bidirectional interaction between COVID-19 and the cardiovascular system and suggests that systemic inflammation may accelerate the development of subclinical disorders or cause de novo cardiovascular damage. Additionally, it discusses the potential impact of common cardiovascular drugs on susceptibility to COVID-19 and the cardiovascular effects of treatments for COVID-19. The review concludes by highlighting the need for further research to improve our understanding of the pathophysiology of COVID-19 and to develop effective preventive and therapeutic solutions.The article reviews the current understanding of the interaction between COVID-19 and the cardiovascular system, focusing on both basic mechanisms and clinical perspectives. COVID-19, caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has become a global pandemic affecting billions of individuals. Pre-existing cardiovascular diseases (CVDs) are linked with worse outcomes and increased risk of death in patients with COVID-19, while the virus can also induce myocardial injury, arrhythmias, acute coronary syndrome, and venous thromboembolism. The article discusses the biological features of SARS-CoV-2, including its genome, genes, and proteins, and highlights the role of angiotensin-converting enzyme 2 (ACE2) in viral entry and potential therapeutic targets. It also explores the diverse cardiovascular manifestations of COVID-19, such as myocardial injury, acute coronary syndrome, heart failure, arrhythmias, and coagulation abnormalities. The article emphasizes the bidirectional interaction between COVID-19 and the cardiovascular system and suggests that systemic inflammation may accelerate the development of subclinical disorders or cause de novo cardiovascular damage. Additionally, it discusses the potential impact of common cardiovascular drugs on susceptibility to COVID-19 and the cardiovascular effects of treatments for COVID-19. The review concludes by highlighting the need for further research to improve our understanding of the pathophysiology of COVID-19 and to develop effective preventive and therapeutic solutions.