**Abstract**

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a pro-inflammatory and prothrombogenic virus with a high mutagenic profile, which produces active infection of variable duration in various organs and systems, and it has been observed that patients who have already suffered from the disease, especially in its more severe forms such as bilateral pneumonia or respiratory distress, present symptoms and signs of chronic multi-organ involvement. However, little is known about the molecular mechanisms that generate endothelial damage (chronic reactive endotheliitis) and subsequent thrombosis in SARS-CoV-2 infection are still not sufficiently elucidated, and in this chapter, we explore these mechanisms and therapeutic options to reduce prothrombosis and multiple vascular involvement that cause morbidity and mortality in this disease. In particular, we will evaluate heparin doses according to the stage of infection and its correlation with improved survival.

**Keywords:** thrombosis, COVID-19, pathophysiology, heparin, mortality
