At the end of 2019, a new SARS-CoV-2 virus appeared in the Chinese province of Wuhan, and the World Health Organization soon declared it a pandemic. The disease caused by the corona virus, COVID-19, can manifest itself with mild flu-like symptoms or more severe ones that can lead to death. The main way the virus enters the host cell is through the ACE2 receptor, which is expressed on alveolar epithelial cells, the heart, kidneys, lungs, etc. Coagulopathy caused by COVID-19 (CAC) is a life-threatening condition in which the immune system, vascular endothelium dysfunction and hypercoagulability are involved. The parameters used to assess hemostasis and the course and progression of the disease are PV, fibrinogen, fibrinogen degradation products, platelet count, protein C concentration, and D-dimer concentration proved to be the most reliable marker. Risk factors for CAC and cardiovascular diseases are genetic predispositions such as ITGB3 PIA1/PIA2 and ꞵ-Fbg gene polymorphisms, as well as the presence of hypertension and diabetes. Complications that are often present are micro- and macrothrombosis, disseminated intravascular coagulation, myocarditis, arrhythmias and heart failure. In anticoagulant therapy, low-molecular-weight heparin proved to be the best, while direct oral anticoagulants and platelet aggregation inhibitors should be used with caution due to numerous interactions, primarily with antivirals. Also, it is recommended to use nafamostat, if possible in combination with heparin. With the advent of the vaccine against SARS-CoV-2 and its widespread use, numerous side effects and the emergence of autoimmune diseases have been observed, such as autoimmune-acquired factor XIII deficiency.