Contracting severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been observed to cause decrements in vascular function of young adults. However, less is known about the impact of SARS-CoV-2 on arterial stiffness and structure, which might have additional implications for cardiovascular health. The purpose of this study was to assess the carotid artery stiffness and structure using ultrasound and the aortic augmentation index (AIx) using applanation tonometry in young adults after they tested positive for SARS-CoV-2. We hypothesized that carotid artery stiffness, carotid intima-media thickness (cIMT) and aortic AIx would be elevated in young adults with SARS-CoV-2 compared with healthy young adults. We evaluated 15 young adults (six male and nine female; 20 ± 1 years of age; body mass index, 24 ± 3 kg m −2 ) 3-4 weeks after a positive SARS-CoV-2 test result compared with young healthy adults (five male and 10 female; 23 ± 1 years of age; body mass index, 22 ± 2 kg m −2 ) who were evaluated before the coronavirus 2019 pandemic. Carotid stiffness, Young's modulus and cIMT were assessed using ultrasound, whereas aortic AIx and aortic AIx standardized to 75 beats min −1 (AIx@HR75) were assessed from carotid pulse wave analysis using SphygmoCor. Group differences were observed for carotid stiffness (control, 5 ± 1 m s −1 ; SARS-CoV-2, 6 ± 1 m s −1 ), Young's modulus (control, 396 ± 120 kPa; SARS-CoV-2, 576 ± 224 kPa), aortic AIx (control, 3 ± 13%; SARS-CoV-2, 13 ± 9%) and aortic AIx@HR75 (control, −3 ± 16%; SARS-CoV-2, 10 ± 7%; P < 0.05). However, cIMT was similar between groups (control, 0.42 ± 0.06 mm; SARS-CoV-2, 0.44 ± 0.08 mm; P > 0.05). This cross-sectional analysis revealed higher carotid artery stiffness and aortic stiffness among young adults with SARS-CoV-2.These results provide further evidence of cardiovascular impairments among young adults recovering from SARS-CoV-2 infection, which should be considered for cardiovascular complications associated with SARS-CoV-2.

Introduction: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can increase arterial stiffness 3-4 weeks following infection, even among young, healthy adults. However, the long-term impacts of SARS-CoV-2 infection on cardiovascular health and the duration of recovery remains unknown. Purpose: The purpose of this study was to elucidate potential long-lasting effects of SARS-CoV-2 infection on markers of arterial stiffness among young adults during the six months following infection. Methods: Assessments were performed at months 1, 2, 3, 4, and ~6 following SARS-CoV-2 infection. Doppler ultrasound was utilized to measure carotid-femoral pulse wave velocity (cfPWV) and carotid stiffness, and arterial tonometry was used to measure central blood pressures and aortic augmentation index at a heart rate of 75 beats∙min-1 (AIx@HR75). Vascular (VCAM-1) and intracellular (ICAM-1) adhesion molecules were analyzed as circulating markers of arterial stiffness. Results: From months 1-6, a significant reduction in cfPWV was observed (month1: 5.70±0.73m·s-1; month6: 4.88±0.65m·s-1; p<0.05) without any change in carotid stiffness measures. Reductions in systolic blood pressure (month1: 123±8mmHg; month6: 112±11mmHg) and mean arterial pressure (month1: 97±6mmHg; month6: 86±7mmHg) were observed (p<0.05), although AIx@HR75 did not change over time. The month1-6 change in cfPWV and MAP were correlated (r=0.894; p<0.001). A reduction in VCAM-1 was observed at month 3 compared with month 1 (month1: 5575±2242pg·ml-1; month3: 4636±1621pg·ml-1; p<0.05) without a change in ICAM-1. Conclusion: A reduction in cfPWV was related with MAP, and some indicators of arterial stiffness remain elevated for several months following SARS-CoV-2 infection, possibly contributing to prolonged recovery and increased cardiovascular health risks.

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Cross‐sectional data indicate that acute SARS‐CoV‐2 infection increases resting muscle sympathetic nerve activity (MSNA) and alters hemodynamic responses to orthostasis in young adults. However, the longitudinal impact of contracting SARS‐CoV‐2 on autonomic function remains unclear. The aim of this study was to longitudinally track MSNA, sympathetic transduction to blood pressure (BP), and hemodynamics over 6 months following SARS‐CoV‐2 infection. Young adults positive with SARS‐CoV‐2 reported to the laboratory three times over 6 months (V1:41 ± 17, V2:108 ± 21, V3:173 ± 16 days post‐infection). MSNA, systolic (SBP) and diastolic (DBP) blood pressure, and heart rate (HR) were measured at rest, during a cold pressor test (CPT), and at 30° head‐up tilt (HUT). Basal SBP (p = 0.019) and DBP (p < 0.001) decreased throughout the 6 months, whereas basal MSNA and HR were not different. Basal sympathetic transduction to BP and estimates of baroreflex sensitivity did not change over time. SBP and DBP were lower during CPT (SBP: p = 0.016, DBP: p = 0.007) and HUT at V3 compared with V1 (SBP: p = 0.041, DBP: p = 0.017), with largely no changes in MSNA. There was a trend toward a visit‐by‐time interaction for burst incidence (p = 0.055) during HUT, wherein at baseline immediately prior to tilting, burst incidence was lower at V3 compared with V1 (p = 0.014), but there were no differences between visits in the 30 HUT position. These results support impairments to cardiovascular health, and potentially autonomic function, which may improve over time. However, the improvements in BP over 6 months recovery from mild SARS‐CoV‐2 infection are likely not a direct result of changes in sympathetic activity.

Elevated levels of brain injury biomarkers have been found primarily in middle-aged or older persons experiencing moderate-to-severe COVID-19 symptoms. However, there is little research in young adults, and there is concern that COVID-19 causes brain injury even in the absence of moderate-to-severe symptoms. Therefore, the purpose of our study was to investigate whether neurofilament light (NfL), glial fibrillary acidic protein (GFAP), tau, or ubiquitin carboxyl-terminal esterase L1 (UCHL1) are elevated in the plasma of young adults with mild COVID-19 symptoms. Twelve participants diagnosed with COVID-19 had plasma collected 1, 2, 3, and 4 months after diagnosis to determine whether NfL, GFAP, tau, and UCHL1 concentrations increased over time or whether plasma concentrations were elevated compared with COVID-19-naïve participants. We also compared plasma NfL, GFAP, tau, and UCHL1 concentrations between sexes. Our results showed no difference between NfL, GFAP, tau, and UCHL1 concentrations in COVID-19-naïve participants and COVID-19-positive participants at any of the four time points ( p = 0.771). Within the COVID-19-positive participants, UCHL1 levels were higher at month 3 after diagnosis compared to month 1 or month 2 ( p = 0.027). Between sexes, females were found to have higher UCHL1 ( p = 0.003) and NfL ( p = 0.037) plasma concentrations compared to males, whereas males had higher plasma tau concentrations than females ( p = 0.024). Based on our data, it appears that mild COVID-19 in young adults does not increase plasma NfL, GFAP, tau, or UCHL1.