Nitric Oxide‐dependent Cutaneous Vasodilation is not Altered in Adults Following SARS‐CoV‐2 Infection

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Cardiovascular complications are part of the clinical sequelae following SARS‐CoV‐2 infection. Vascular dysfunction, one of the earliest indicators of cardiovascular disease (CVD), has been reported in adults who have recovered from COVID‐19. To date, no studies have investigated the underlying mechanisms of persistent COVID‐19‐associated vascular dysfunction. Additionally, physical activity (PA) status has not been accounted for when examining vascular function in COVID‐19 recovered (CR) adults.PURPOSETo directly quantify nitric oxide (NO)‐dependent vasodilation in the microcirculation in adults who have recovered from SARS‐CoV‐2 infection. Using the skin as a model circulation, we hypothesized that CR adults would have impaired NO‐mediated vasodilation compared to appropriate controls, and PA would be positively associated with NO‐dependent vasodilation in CR.METHODSWe performed a cross‐sectional study including: 10 (5M/5W, 24 ± 4yrs) healthy control (HC) adults who were unvaccinated for COVID‐19, 11 (4M/7W, 25 ± 6yrs) healthy vaccinated (HV) adults, and 12 (5M/7W, 22 ± 3yrs) CR (19 ± 14 weeks post‐diagnosis) adults. COVID‐19 symptoms severity (survey) and PA (accelerometer) for 7 days prior to the experimental visit were assessed. A standardized 39°C local heating protocol was used to induce eNOS‐dependent vasodilation, quantified via perfusion (intradermal microdialysis) of 15 mM NG‐nitro‐l‐arginine methyl ester during the plateau of the heating response. Red blood cell flux was measured (laser‐Doppler flowmetry) and cutaneous vascular conductance (CVC = flux/mmHg) was expressed as a percentage of maximum (28mM sodium nitroprusside + 43°C). All data are means ± standard error.RESULTSThe local heating plateau (HC: 61 ± 20 %CVCmax, HV: 60 ± 19 %CVCmax, CR: 67 ± 19 %CVCmax, p=0.80) and NO‐dependent vasodilation (HC: 77 ± 9%, HV: 71 ± 7%, CR: 70 ± 10%, p=0.36) were not different among groups. In the CR group neither peak symptom severity (25 ± 12 AU) nor time since diagnosis correlated with NO‐dependent vasodilation (R2=0.21, p=0.13 and R2=0.17, p=0.19, respectively). PA was not different among groups (see Table). PA did not correlate with the NO‐dependent vasodilation in CR (sedentary: R2<0.01, p=0.89; light: R2=0.04, p=0.63; moderate‐to‐very vigorous: R2=0.35, p=0.16).CONCLUSIONOtherwise healthy young adults who have had COVID‐19 did not have impaired NO‐dependent cutaneous vasodilation. Additionally, in this cohort of CR adults, symptomology and physical activity was not related to microvascular function. As such, investigations in adults who have had more severe COVID‐19 cases are necessary. Discovering the underlying mechanisms linking SARS‐CoV‐2 infection and cardiovascular consequences are important for identifying additional treatment strategies for long haul COVID‐19.