Ascending aortic thrombosis in COVID respiratory patient: the “perfect storm”

Abstract

COVID-19 spans from asymptomatic disease to severe respiratory insufficiency often associated with thrombotic complications. COVID-19 appears to cause a hypercoagulable state through mechanisms unique to SARS-CoV-2 infection, particularly dependent on the connection between thrombosis and inflammation. Patients with more severe disease may be affected by a generalized hypercoagulable state that results in macro- and microvascular thrombosis, not only limited to the lungs. The pathophysiology underlying the hypercoagulable state induced by the infection is not fully understood. Microvascular thrombotic mechanisms seem to be well explained by direct infection and injury of pulmonary endothelial cells, while the macrovascular arterial thrombotic mechanisms are less clear. The detailed mechanism of the etiology of aortic thrombosis is not entirely understood, particularly the thrombosis of the ascending tract is an extremely rare event, with potentially catastrophic complications. The identification of biomarkers of thrombosis and severe illness as D-dimer levels, platelet counts, coagulation assays and fibrinogen, can guide clinicians on early interventional strategies. Here we report the case of a patient affected by respiratory insufficiency due to COVID-19 pneumonia, who developed ascending aortic thrombosis. We assumed that this case could be the direct result of COVID-19-induced vascular damage in the context of a hypercoagulable state. This report advocates for a careful early assessment of this condition.