The thromboembolic effect of COVID-19

Currently available evidence suggests that coronavirus disease 2019 (COVID-19) cannot be considered exclusively a respiratory disease, because the adverse effects of this viral infection extend far beyond the lung tissue. The biochemical and biological disturbances frequently seen in patients with COVID-19, particularly those with more aggressive forms, have led some authors to use the term “thromboinflammation” to describe the pathophysiological continuum of events that link the activation of hemostasis and the development of blood clots in various arterial and venous districts. Specific to this chapter, a handful of studies have been published that conclude that the risk of developing venous thromboembolism (VTE) is increased in patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, especially in the early (i.e., acute) phase of COVID-19. This risk appears to be higher in men, older persons, in those with obesity and history of venous thrombosis and/or thrombophilia. Other predisposing factors include the early phase of SARS-CoV-2 infection; severe COVID-19 illness especially leading to hospitalization, mechanical ventilation, and/or admission to an intensive care unit; increased values of d-dimer and inflammatory biomarkers; and unvaccinated status. Although the acute phase of illness is characterized by higher odds of developing VTE, a persistent increased risk (especially for pulmonary embolism) has also been demonstrated in the post-COVID period, up to nearly 1 year afterward.