P18 Focused longitudinal observational study to improve knowledge of COVID-19 (follow-COVID19)

Introduction COVID-19 is a complex multisystemic disease. Many studies have described the multifaceted role of the endothelium in the pathophysiology of COVID-19. Emerging evidence suggests that endotheliitis in arteries may be a contributing factor of morbidity and mortality in COVID-19. Methods In this study 89 participants infected with COVID-19 were categorised into two groups: non-hospitalised patients (N=33, mean age = 49±9.7 yrs) and hospitalised patients (N=56, mean age = 60±12.2 yrs). All participants underwent arterial stiffness assessment, endothelial function tests and microvascular function tests using non-invasive techniques such as SphygmoCor, EndoPAT and moorFLPI-2 respectively. These tests were performed at visit 1 (£3 months after infection) and visit 2 (³6 months after infection). Results The Carotid-Femoral Pulse Wave Velocity (cfPWV, a measure of arterial stiffness) was significantly higher in hospitalised patients than non-hospitalised patients at both visit 1 (hospitalised cfPWV: 8.1±1.3 m/s vs non-hospitalised cfPWV: 7.0±1.3 m/s, p=0.03) and visit 2 (hospitalised cfPWV: 8.7±1.4 m/s vs non-hospitalised cfPWV: 7.3±1.4 m/s, p=0.012). EndoPAT analysis revealed that hospitalised patients demonstrated poorer endothelial function compared to non-hospitalised patients (hospitalised: RHI = 2.0±0.8 vs non-hospitalised: RHI =2.4±0.7, p=0.028). Furthermore, moorFLPI-2 tests showed that hospitalised patients had higher baseline skin perfusion (p=0.035) and decreased responses to endothelial-dependent (acetylcholine (ACh), visit 1 p=0.019 and visit 2 p<0.001) and endothelial-independent (sodium nitroprusside (SNP), visit 1, p=0.026) vasodilators. Interestingly, hospitalised patients also displayed a progressive deterioration in vasodilatory response to ACh between visit 1 and visit 2 (p=0.036). Conclusion The results from this study illustrate that severe COVID-19 infections which require hospitalisation are associated with arterial stiffness and poor endothelial function. A limitation of this study which was considered when interpreting the results was age-matching as the hospitalised patients were significantly older compared to non-hospitalised patients. Nonetheless, the progressive deterioration of microvascular function seen in severely affected patients between visits was independent of age.