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Evaluation of Endothelial Dysfunction and Inflammatory Vasculopathy After SARS-CoV-2 Infection-A Cross-Sectional
Philipp Jud1, Paul Gressenberger1, Viktoria Muster1
1Division of Angiology, Department of Internal Medicine, Medical University of Graz, Graz, Austria.
Insights
COVID-19 can cause lasting vascular injury, affecting arterial stiffness and capillary structure. These changes contribute to endothelial dysfunction and inflammation, similar to atherosclerotic cardiovascular disease.
Area of Science:
- Cardiovascular Medicine
- Infectious Diseases
- Pathology
Background:
- Emerging evidence links COVID-19 to vascular endothelium damage.
- Mechanisms behind COVID-19-induced endothelial dysfunction and vasculopathy remain unclear.
Purpose of the Study:
- To assess COVID-19's contribution to persistent vascular injury.
- To identify factors associated with COVID-19-related endothelial dysfunction and vasculopathy.
Main Methods:
- Cross-sectional study comparing post-COVID-19 patients, atherosclerotic cardiovascular disease (ASCVD) patients, and healthy controls.
- Evaluated flow-mediated dilation (FMD), nitroglycerine-related dilation (NMD), pulse-wave velocity (PWV), augmentation index, intima-media thickness (IMT), arginine/kynurenine metabolism, homocysteine, von Willebrand factor (vWF), endothelial microparticles (EMP), antibodies, inflammatory markers, and nailfold capillary morphology.
Main Results:
- Post-COVID-19 patients exhibited elevated PWV, augmentation index, IMT, dimethylarginines, vWF, homocysteine, EMPs, C-reactive protein, erythrocyte sedimentation rate, interleukin-6, and beta-2-glycoprotein antibodies.
- Lower levels of homoarginine and tryptophan were noted in post-COVID-19 patients.
- Significant alterations in capillary morphology and a higher microangiopathy score were observed in post-COVID-19 patients.
- Endothelial dysfunction and inflammation markers were comparable between post-COVID-19 and ASCVD patients.
Conclusions:
- COVID-19 impacts arterial stiffness, capillary structure, EMPs, and metabolism of arginine, kynurenine, and homocysteine.
- These effects contribute to endothelial dysfunction and inflammatory vasculopathy post-COVID-19.
- The vascular damage observed in post-COVID-19 patients resembles that seen in ASCVD.
Abstract:
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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