Vascular "Long COVID": A New Vessel Disease?

Abstract

Vascular sequelae following (SARS-CoV-2 coronavirus disease) (COVID)-19 infection are considered as "Long Covid (LC)" disease, when occurring 12 weeks after the original infection. The paucity of specific data can be obviated by translating pathophysiological elements from the original Severe Acute Respiratory Syndrome-Corona Virus (SARS-CoV-2) infection (In a microcirculatory system, a first "endotheliitis," is often followed by production of "Neutrophil Extracellular Trap," and can evolve into a more complex leukocytoklastic-like and hyperimmune vasculitis. In medium/large-sized vessels, this corresponds to endothelial dysfunction, leading to an accelerated progression of pre-existing atherosclerotic plaques through an increased deposition of platelets, circulating inflammatory cells and proteins. Associated dysregulated immune and pro-coagulant conditions can directly cause thrombo-embolic arterial or venous complications. In order to implement appropriate treatment, physicians need to consider vascular pathologies observed after SARS-Cov-2 infections as possible "LC" disease.

Keywords: COVID-19; arterial thrombosis; inflammation; long COVID; vascular complications; vasculitis.

Figure 1.

Diagram describing the pathway from acute COVID-19 infection to microvascular thrombosis and risk of worsening of atherosclerosis.

Figure 2.

Thrombosis of the extra-parenchymal splenic artery in a COVID-19 patient (Hematoxylin-Eosin staining). (A) The external part of the medial layer, infiltrated by inflammatory circulating cells, indicates an acute arteritis; inside a recent, non-recanalized thrombus [10X]. (B) Cordons of inflammatory cells, intercalated with bands of smooth muscle cells, containing lymphocytes, macrophages, and mainly neutrophils [40X].

Figure 3.

Diagram suggesting the pathway leading to vascular thrombosis and aortic aneurysm worsening in Long Covid.