Key result
Previous SARS-CoV-2 is linked to increased arterial stiffness and inflammatory microvascular changes without affecting FMD.
Why the study?
The mechanisms promoting COVID-19-associated endothelial dysfunction and inflammatory vasculopathy are largely unknown, necessitating evaluation of vascular injury after COVID-19.
Does prior SARS-CoV-2 infection lead to persistent endothelial dysfunction and inflammatory vasculopathy compared to healthy controls and patients with ASCVD?
Cross-Sectional (n=42)
No
Does prior SARS-CoV-2 infection lead to persistent endothelial dysfunction and inflammatory vasculopathy compared to healthy controls and patients with ASCVD?
Absolute Event Rate: 4.44% vs 4.58%
Prior SARS-CoV-2 infection is associated with persistent endothelial dysfunction, arterial stiffness, and inflammatory vasculopathy comparable to that seen in patients with established atherosclerotic cardiovascular disease.
Should not yet inform post-COVID vascular risk assessment; leaves open whether stiffness and microvascular changes predict clinical events.
Background: Rising data suggest that COVID-19 affects vascular endothelium while the underlying mechanisms promoting COVID-19-associated endothelial dysfunction and inflammatory vasculopathy are largely unknown. The aim was to evaluate the contribution of COVID-19 to persisting vascular injury and to identify parameters linked to COVID-19-associated endothelial dysfunction and inflammatory vasculopathy. Methods: In a cross-sectional design, flow-mediated dilation (FMD), nitroglycerine-related dilation (NMD), pulse-wave velocity (PWV), augmentation index, intima-media thickness (IMT), compounds of the arginine and kynurenine metabolism, homocysteine, von Willebrand factor (vWF), endothelial microparticles (EMP), antiendothelial cell antibodies, inflammatory, and immunological parameters, as well as nailfold capillary morphology were measured in post-COVID-19 patients, patients with atherosclerotic cardiovascular diseases (ASCVD) and healthy controls without prior or recent SARS-CoV-2 infection. Results: Post-COVID-19 patients had higher values of PWV, augmentation index, IMT, asymmetric and symmetric dimethylarginine, vWF, homocysteine, CD31+/CD42b– EMP, C-reactive protein, erythrocyte sedimentation rate, interleukin-6, and β-2-glycoprotein antibodies as well as lower levels of homoarginine and tryptophan compared to healthy controls (all with p < 0.05). A higher total number of pathologically altered inflammatory conditions and higher rates of capillary ramifications, loss, caliber variability, elongations and bushy capillaries with an overall higher microangiopathy evolution score were also observed in post-COVID-19 patients (all with p < 0.05). Most parameters of endothelial dysfunction and inflammation were comparably altered in post-COVID-19 patients and patients with ASCVD, including FMD and NMD. Conclusion: COVID-19 may affect arterial stiffness, capillary morphology, EMP and selected parameters of arginine, kynurenine and homocysteine metabolism as well as of inflammation contributing to COVID-19-associated endothelial dysfunction and inflammatory vasculopathy.
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Jud et al. (2021) conducted a cross-sectional in SARS-CoV-2 infection (n=42). Previous SARS-CoV-2 infection vs. Healthy controls and patients with ASCVD was evaluated on Flow-mediated dilation (FMD). Previous SARS-CoV-2 infection did not significantly affect flow-mediated dilation compared to healthy controls, but was associated with increased arterial stiffness and inflammatory microvascular changes.
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