Reply

We thank Dr Roncati for reading and commenting¹ on our case reporting an acute aortic intramural hematoma (IMH) in a SARS-CoV-2 positive patient.² The author¹ suggests a combination of different pathophysiologic mechanisms of aortic injury in these patients, which is undoubtedly an interesting aspect to consider in the ever-growing association between SARS-CoV-2 infection and vascular disease.³ In the clinical setting, SARS-CoV-2 is associated with hypercoagulability leading to peripheral arterial and venous thrombosis, but some aortic phenomena have been described as well.^{3 , 4}

Historically, acute aortic syndromes and mostly IMHs have been associated with vasa vasorum degeneration and/or rupture.⁵ Roncati et al suggest a SARS-CoV-2-related vasa vasorum “endotheliitis” driven by the innate and adaptive immune systems and also involving platelet activation. This immunothrombosis ultimately leads to medial degeneration, the pillar of acute aortic syndrome pathogenesis. We believe that a pre-existing state of damaged vasa vasorum due to hypertension and advanced age have laid the foundation for the inflammatory degeneration that led to the IMH in our patient.

Aortic inflammation in relation to SARS-CoV-2 has to be further investigated from a histology, pathophysiology and clinical perspective. Even though it is difficult to demonstrate a direct link between aortic disease and SARS-CoV-2 infection, some studies suggest a potential association. However, it seems reasonable to assume that an endothelial inflammatory mechanism might incite acute aortic syndromes such as the one seen on our patient.