The increased risk and incidence of cardiovascular disease (CVD) in adults living with HIV-1 is not solely due to worsening of traditional CVD risk factors, but also involves ill-defined factors related to the virus and/or its therapies. More than 70% of adults living with HIV-1 report sleep problems, the most common malady being short nightly sleep duration (<7 h/night). Short nightly sleep duration is associated with increased CVD risk and events. An underlying mechanism for the sleep-related increase in CVD is a profound worsening in vascular endothelial function. The influence of insufficient sleep on vascular endothelial function in HIV-1-seropositive adults is unknown. We tested the hypotheses that: 1) short nightly sleep duration is associated with lower nitric oxide (NO)-mediated endothelium-dependent vasodilation in antiretroviral (ART)-treated adults living with HIV-1; and 2) the short sleep-related reduction in endothelial vasodilator function is due, at least in part, to increased oxidative stress.
Thirty-two sedentary, middle-aged HIV-1-seropositive adults on stable antiretroviral therapy were studied: 16 with normal nightly sleep duration (12M/4F; age: 50±2 yr; BMI: 25.4±0.7 kg/m2; sleep: 7.8±0.3 h/night) and 16 with short nightly sleep duration (14M/2F; 51±2 yr; 25.4±0.8 kg/m2; 5.6±0.3 h/night). Forearm blood flow (FBF) responses to intra-arterial infusion of acetylcholine (ACh), in the absence and presence of the endothelial NO synthase inhibitor NG-monomethyl-L-arginine (L-NMMA) and the antioxidant vitamin C were determined by venous occlusion plethysmography.
FBF responses to ACh were significantly lower (~20%) in the short sleep (from 4.5±0.3 to 12.4±0.6 mL/100 mL tissue/min) vs normal sleep adults (from 4.7±0.3 to 14.5±0.7 mL/100 mL tissue/min). L-NMMA significantly reduced (~15%) the FBF response to ACh in the normal sleep but not the short sleep group; whereas, vitamin C significantly increased (~30%) the vasodilator response to ACh in short sleep but not the normal sleep group.
Habitual short sleep duration is associated with lower endothelium-dependent vasodilation in adults living with HIV-1 due, in part, to increased oxidative stress. Reduced NO-mediated endothelium-dependent vasodilation may increase the CVD risk in adults living with HIV-1 who sleep < 7h/night.