Abstract:

COVID-19 disease, which emerged in Wuhan, China on November 17, 2019, was declared a global epidemic by the World Health Organization (WHO) on March 11, 2020. This virus, which causes severe disease and many deaths worldwide, has been named severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2). Although all age groups are susceptible to the disease, it has been observed that the probability of developing a serious disease is higher in elderly individuals and those with underlying diseases such as cardiovascular disease, diabetes, chronic respiratory disease or cancer. Spike (S) protein, which is one of the proteins on the surface of the SARS-CoV-2 virus, binds to angiotensin converting enzyme2 (ACE2) receptors in the epithelial cells of the lower respiratory tract, leaving its own genome in the cytoplasm of the cell, thus performing the synthesis of new virus particles. In studies, it has been stated that various hematological and hemorheological parameters change in COVID-19 disease. Some hematological parameters frequently observed in this disease are lymphopenia, neutrophilia, and thrombocytopenia. Platelet activation and endothelial dysfunction were detected depending on the increase in inflammation and thrombosis formation due to stasis. Studies on COVID-19 coagulopathy have shown high levels of D-dimer. It has also been found that increased fibrinogen causes erythrocyte hyperaggregation in COVID-19 patients, which is associated with the development of blood coagulation. Decreased deformability of erythrocytes results in an increase in erythrocyte rigidity. It has been suggested that the increase in hemorheological parameters such as D-dimer, blood viscosity, erythrocyte aggregation and deformability as a result of the deterioration in the coagulation/fibrinolytic system in COVID-19 disease is associated with the prognosis of the disease. The purpose of our review was to evaluate the roles of hemorheological parameters in the etiopathogenesis of COVID-19.