Cardiovascular Disease Risk in Young Adults Following Covid-19

Introduction: SARS-CoV-2, the virus responsible for COVID-19, may cause a dysregulated systemic inflammatory response that could lead to cardiovascular damage and cause individuals recovering from COVID-19 to be at an increased risk for future cardiovascular disease (CVD). Physical activity (PA) is inversely associated with systemic inflammation and CVD risk, which may make it a useful cardioprotective lifestyle factor for individuals recovering from COVID-19. Purpose: 1) Compare arterial stiffness and systemic inflammatory levels between individuals recovering from COVID-19 and uninfected controls, 2) explore systemic inflammation as a predictor of arterial stiffness, and 3) explore PA as a mediator for the relationship for COVID-19 history with arterial stiffness and systemic inflammation. Methods: Cross-sectional analysis was performed on 23 SARS-CoV-2 participants (8M/15F, 25.0±8.9 years, 24.1±3.5 kg/m2) and 32 uninfected controls (14M/18F, 24.4±6.5 years, 25.1±3.5 kg/m2). Arterial stiffness, as a proxy for CVD risk, was estimated as pulse wave velocity (PWV) during 24-hour ambulatory blood pressure monitoring using an oscillometric blood pressure device. Systemic inflammation was assessed as salivary cytokine and C-reactive protein (CRP) levels collected using the passive drool method. PA was objectively measured via accelerometry and assessed as moderate-to-vigorous physical activity (MVPA). An independent samples t-test was used to compare measures of arterial stiffness and systemic inflammation between the SARS-CoV-2 and control groups. Simultaneous multiple regression was used to assess how well proinflammatory cytokine and CRP levels predicted arterial stiffness. Mediational analysis was used to determine whether there is a significant indirect effect of COVID-19 history through MVPA on arterial stiffness and CRP levels. Results: Participants recovering from COVID-19 were studied, on average, 111.6±118.3 days after testing positive, experienced 5.2±3.8 symptoms, and had mild COVID-19 disease severity. The results from independent samples t-test showed no significant differences (all p>0.05) between the SARS-CoV-2 and control group in PWV (5.0±0.5 m/s vs 5.1±0.5 m/s) , IL-8 (821.1±772.6 pg/mL vs 843.8±958.4 pg/mL), IL-1β (126.3±102.2 pg/mL vs 143.6±157.9 pg/mL), IL-6 (11.7±25.4 pg/mL vs 5.9±7.9 pg/mL), TNF-α (4.8±3.9 pg/mL vs 5.1±5.9 pg/mL), or CRP (765.4±672.9 pg/mL vs 526.3±674.8 pg/mL). Additionally, the combination of IL-8, IL-1β, IL-6, TNF-α, and CRP were not found to significantly predict PWV, with no individual measure of systemic inflammation significantly contributing to the regression equation (all p>0.05). Finally, mediational analysis did not find a significant indirect effect of COVID-19 history through MVPA on PWV (estimate = 0.0220, 95% CI = -0.0488 – 0.2427) or of COVID-19 history through MVPA on CRP levels (estimate = 0.0254, 95% CI = -0.0675 – 0.1646). Conclusion: This investigation found no differences in arterial stiffness and systemic inflammation between young adults recovering from COVID-19 and uninfected controls. Additionally, systemic inflammation was not found to be a significant predictor of arterial stiffness. Finally, MVPA was not found to significantly mediate the relationship for COVID-19 history with arterial stiffness and systemic inflammation.