The World Health Organization declared the SARS-CoV-2 infection causing severe acute respiratory distress a global pandemic in March 2020. While respiratory features are commonly at the forefront of the disease, cardiovascular complications have been observed and associated with a poorer prognosis. The ACE2 enzyme intrinsically involved in the physiology of cardiac function and in the development of hypertension and diabetes has been identified as a functional receptor for SARS-CoV-2. It is difficult to highlight the precise mechanisms of cardiac damage because of its possible multiple implications, through direct damage from SARS-CoV-2 responsible for viral myocarditis or indirect damage from the state of exacerbated systemic inflammation associated with hypoxaemia. The treatments of the disease may also induce adverse effects such as an increase in QT segment duration. Measurements of cardiac biomarkers are required if myocardial damage is suspected and are part of a panel of arguments confronted with clinical features, ultrasonic monitoring and electrocardiogram. As the cardiac disorders increase post-hospital morbidity, risk stratification with cardiac MRI and prolonged follow-up are required.