There is important bidirectional interaction between COVID-19 and cardiovascular system. Pre-existing cardiovascular diseases increase susceptibility to serious SARSCoV-2 infection, associated with worse outcomes and higher risk of death. Although COVID-19 is primarily respiratory disease with viral pneumonia in severe cases, it can also induce cardiovascular manifestations including myocardial injury, myocarditis, heart failure, arrhythmias, acute coronary syndrome and arterial or venous thromboembolism (VTE). Risk factors for severe COVID-19 overlap with risk factors for thromboembolic events. Additionally, people who live in a nursing home or care facility, and who therefore may be less mobile, are at increased risk of both severe COVID-19 and thromboembolism. In patients with pneumonia, acute respiratory distress syndrome (ARDS) and sepsis, incidence of atrial fibrillation is high. Recent observational studies have shown that new-onset or recurrent atrial fibrillation may be triggered by COVID- 19, with a subsequent risk of cardioembolic stroke. Clinical observations of increased thromboembolic events in patients with COVID-19 suggest the presence of a hypercoagulable state. The proposed mechanisms are COVID-19- associated systemic inflammation, endothelial damage, coagulation activation, hypoxaemia and immobilization, in combination with underlying comorbidities. Venous thromboembolism, which includes deep vein thrombosis (DVT) and pulmonary embolism (PE), is common complication in severe COVID-19 patients. Therefore, anticoagulation with low molecular weight heparin at standard prophylactic doses should be considered for all patients admitted to the hospital with COVID-19. The diagnosis of acute PE may be difficult, because COVID-19 respiratory symptoms largely overlap with the presentation of acute PE, and may cause underdiagnosis. Even more, the specificity of D-dimer tests may be lower in patients with COVID-19 compared to other clinical settings, but it is still advised to follow diagnostic algorithms starting with pre-test probability and D-dimer testing. Every unexpected respiratory worsening, unexplained tachycardia, a fall in blood pressure not attributable to tachyarrhythmia, hypovolaemia or sepsis, ECG changes suggestive of PE, and signs of DVT on the lower extremities, should be suspicious for PE. The diagnostic tests for PE should not be ordered routinely, but only when it is clinically suspected, with a low threshold of suspicion. When thromboembolic event is confirmed, treatment should be guided by risk stratification in accordance with the current European Society of Cardiology Guidelines. Non- vitamin K antagonist oral anticoagulants (NOACs) provide advantages over vitamin K antagonists such as warfarin, due to the lack of the need for routine monitoring and minimization of patient contact with the healthcare environment, except in some special circumstances when warfarin is indicated (prosthetic heart valves, moderate-to-severe rheumatic mitral stenosis, antiphospholipid syndrome, negative interactions of some investigational COVID-19 drugs with NOACs).