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.
Highlights
COVID-19 caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has evolved into a pandemic since it was detected in the end of 2019
Post-COVID-19 patients had a higher rate of pathologic aortic pulse-wave velocity (PWV) with >10 m/s (p = 0.001) and higher values of aortic PWV, augmentation index, intima-media thickness (IMT) of the common carotid, axillary and superficial femoral artery, asymmetric dimethylarginine (ADMA), symmetric dimethylarginine (SDMA), kynurenine/tryptophan ratio, von Willebrand factor (vWF) antigen and activity, homocysteine and CD31+/CD42b– endothelial microparticles (EMP) compared to healthy controls (p < 0.001; p = 0.009; p < 0.001; p < 0.001; p < 0.001; p = 0.001; p = 0.043; p = 0.001; p = 0.002; p = 0.004; p = 0.004; p = 0.020, respectively)
In the group of post-COVID-19 patients, values of those respective parameters were comparable to patients with atherosclerotic cardiovascular diseases (ASCVD) without significant differences, except for IMT of the axillary artery, which was lower (p = 0.017), and for CD31+/CD42b– EMP, which were higher (p = 0.012) in the COVID-19 group
Summary
COVID-19 caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has evolved into a pandemic since it was detected in the end of 2019. Endothelial microparticles (EMP), which are released during apoptosis or activation of endothelial cells, as Abbreviations: ACP, anti-citrullinated protein; ADMA, asymmetric dimethylarginine; AECA, antiendothelial cell antibodies; ANA, antinuclear antibodies; ANCA, anti-neutrophil cytoplasmic antibodies; ASCVD, atherosclerotic cardiovascular diseases; CRP, C-reactive protein; CSURI, capillaroscopic skin ulcer risk index; ELISA, enzyme-linked immunosorbent assay; EMP, endothelial microparticles; ENA, extractable nuclear antigen; ESR, erythrocyte sedimentation rate; FMD, flow-mediated dilation; GAB, global arginine bioavailability; Ig, immunoglobulin; IL-6, interleukin 6; IMT, intimamedia thickness; LEAD, lower extremity arterial disease; MES, microangiopathy evolution score; NMD, nitroglycerine-related dilation; NVC, nailfold video capillaroscopy; PCR, polymerase chain reaction; PWV, pulse-wave velocity; SAA, serum amyloid A; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2; SD, standard deviation; SDMA, symmetric dimethylarginine; UEAD, upper extremity arterial disease; vWF, von Willebrand factor. 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
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
