Severe acute respiratory syndrome coronavirus 2 and its resulting disease, COVID-19, remain a significant public health concern. Cardiovascular injury is the second most common complication, following respiratory disease, encompassing conditions such as myocarditis, acute myocardial injury, acute coronary syndrome, arrhythmia, and heart failure. It presents with high-troponin levels, reduced left ventricular systolic function, and/or electrocardiographic abnormalities. Cardiac involvement is an independent risk factor for worse clinical outcomes and higher mortality, particularly in the elderly patients. The debate continues regarding whether the cardiac manifestations of COVID-19 result from direct viral infection or indirect cellular injuries. The virus attaches directly to angiotensin-converting enzyme 2 receptor, which is extensively expressed in the heart, invades myocardial tissue, and triggers an excessive inflammatory response. Indirect mechanisms stem from endothelial damage, hypercoagulability and micro-thrombosis, cytokine storm, respiratory failure and hypoxia, and autoimmunity. The pathophysiology of cardiac injury in COVID-19 patients is important to frame the main pathways and biomarkers to encourage new therapeutic trials to improve the disease prognosis and to understand the course of the disease.