ABSTRACT
Introduction: In January 2020, a new coronavirus was identified as the source of a newly developing type of pneumonia (COVID-19) in China. The number of infected people has been rising swiftly throughout the world since then and it has been reported to affect multiple systems apart from causing usual atypical pneumonia, one of which being the cardiovascular system. The underlying mechanism leading to cardiac injury has been hypothesized to be linked to a cytokine storm with unbalanced response to T-cell subtypes or secondary hemophagocytic lympho-histiocytosis, direct cardiac injury through viral myocarditis or cardiomyopathy through the ACE2 receptor, oxygen supply/demand imbalance with or without coronary artery disease, hypoxemia, and positive pressure ventilation leading to increased right ventricular afterload due to respiratory acidosis. Case Presentation: A 49-year-old female with a non-notable medical history presented to the emergency department with the chief complaint of dyspnea, fever and chills, severe dry coughs, and diarrhea. COVID-19 was confirmed by chest Computed Tomography (CT) scan and Real-Time Polymerase Chain Reaction (RT-PCR). Due to high troponin levels, echocardiography was done, indicating that the patient had a reduced left ventricular ejection fraction with multiple large Left Ventricular (LV) clots, but she had no lesions in coronary angiography. Conclusions: The pathological mechanism by which SARS-COV-2 causes viral myocarditis is still uncertain. However, it may result in cardiac injury via multiple mechanisms. COVID-19 may also predispose the body to thromboembolism in different ways. The current data suggested the existence of a hyper-coagulability state in patients with COVID-19 and endotheliitis could explain the reason why these patients seem more prone to venous and arterial thrombosis. However, further studies are needed to determine the other causes of the cardiovascular complications of COVID19.