Vasculitis and aortitis: COVID-19 challenging complications

Some pathophysiologic observations about thrombosis in small/medium sized arteries in coronavirus disease-19 (COVID-19) are of interest in study from Bellosta et al.¹ This complication can be correlated with two main processes. The first is an acute endotheliitis, where endothelial cells, inhabited by virions, become infiltrated by neutrophils and mononuclear elements, leading to an accelerated apoptosis and a lymphocytic endotheliitis, and to an inflammatory/prothrombotic milieu.² This correlates with a cell-mediated immune response. Second, in the same arteries in later stages of the disease, there is peri/panarteritis, consisting of an extended infiltration by the same inflammatory elements, followed by an accelerated karyolysis, accumulation of apoptotic bodies, caspase proteic granules, and fibrinoid substances, indicating a leukocytoclastic vasculitis. Interestingly, this inflammatory reaction is followed by deposition of polyclonal antigen-antibody immune complexes IgG, prevalent, IgA and IgM, of C3 complement fraction proteins, suggesting a type III hypersensitive acute vasculitis, equally predisposing to thrombosis.³ This finding indicates a host's dysregulated humoral response.

We have observed that an equivalent pathology can involve large-sized arteries as well, typically the aorta, with parietal thromboses often incidentally discovered and not always amenable to the sole blood hypercoagulability. In the absence of adequate histopathologic data, some aspects can be explained translating elements from the mechanisms presented in this letter, namely, the lymphocytic endotheliitis. In fact, we interpret an aortic parietal thrombosis in the course of COVID-19 as an infectious aortitis occurring during its viremic phase, when the aortic endothelium, largely provided of angiotensin-converting enzyme-2 receptors, is directly attacked by virions, leading to an endotheliitis that could later by complicated by a hypersensitive vasculitis.⁴ This process can be favored by a preexisting pathology, typically atherosclerotic plaques, mainly if ulcerated, or, more generally, by a basal condition of endothelial dysfunction.⁵ However, we do not exclude the importance of coexisting facilitating hemodynamic conditions, such as a turbulent flow and a reduced parietal elasticity, which are common in the aorta of elderly patients or after endovascular procedures. To our knowledge, this active inflammatory and non-necrotic/degenerative pathology did not cause intramural hematomas or dissections. However, we suggest further research about possible complications, such as extended thrombosis or secondary aneurysm.