The pathophysiology behind this could be attributed to (1) the repeated airway obstructions in OSA cause chronic intermittent hypoxia, which causes oxidative stress, endothelial dysfunction, and upregulates inflammatory cytokines such as interleukin 6 and 8, tumor necrosis factor-alpha, C-reactive proteins, intercellular adhesion molecule-1, vascular cell adhesion molecule 1, causing inflammation amplification [13]. Here, VCAM1 is linked to endothelial dysfunction.