Dose‐Dependent Arterial Stiffness Responses to Binge Alcohol Consumption

Abstract

Arterial stiffness is a known contributor to hypertension. While there is evidence that light to moderate alcohol consumption can decrease arterial stiffness, the impact of binge alcohol consumption on acute changes of arterial stiffness remains unknown. We tested the hypothesis that arterial stiffness would be increased after binge drinking. Participants (n=22; 50% women; age 24.5±1.1 years; BMI 26.8±0.9 kg/m2) arrived to the laboratory at 4:00 pm for baseline arterial stiffness measures, and provided a standardized meal verified by a registered dietitian. Three supine blood pressures were taken prior to each arterial stiffness recording. In a randomized order, separated by one month, participants received a binge alcohol dose or fluid control. Alcohol or fluid control doses were administered in two equally divided allocates at 8 and 9 pm, and participants were provided a 15 min consumption period. The entire binge alcohol session consisted of a 1:3 mixture of 190 proof grain ethanol and fruit juice based on body weight and sex (1g/kg men, 0.85g/kg women), while the fluid control was only fruit juice in equal volume. Thirty minutes post-consumption of each allocated beverage, arterial stiffness was recorded via applanation tonometry using a SphygmoCor system. Briefly, a tonometer was placed at the radial artery for pulse wave analysis. While gated to a three-lead electrocardiogram, a tonometer was placed at the carotid and femoral arteries for pulse wave velocity. Blood alcohol content (BAC) was estimated via breathalyzer at the 4 pm baseline, and 30 minutes after completion of each fluid consumption. Statistical analysis was performed using repeated measures ANOVA with a condition level of two (i.e., alcohol vs. fluid control) and three time points (i.e., baseline, 8pm post-drink, and 9pm post-drink). Means were considered significantly different when p<0.05. BAC was significantly and progressively elevated after the first (0.045±0.003%) and second (0.095±0.004%) alcohol doses. Mean arterial pressure was not significantly changed after alcohol or fluid control. However, aortic augmentation index normalized to 75 heart beats (AIx@75) was significantly different from baseline following the alcohol condition (time: p=0.004). Post-hoc paired t-tests revealed AIx@75 was significantly reduced after the first dose of alcohol consumption (Δ-7±2%, p<0.01), but was similar to baseline following the second dose of alcohol (p=0.29). Alcohol consumption did not change (time: p=0.147) carotid-femoral pulse wave velocity (cfPWV). Supine HR was changed after the binge alcohol and fluid control visit (condition × time: p<0.001). Specifically, HR was higher after the 2nd dose of alcohol (∆5±1 beats/min, p<0.001) and lower after the 2nd dose of fluid (∆-4±2 beats/min, p=0.030). In summary, our results indicate binge alcohol consumption depressed AIx@75 after the first dose in the evening and increased supine HR after the second dose. Our preliminary findings align with epidemiological evidence on chronic drinkers, and suggest that acute arterial stiffness and cardiovascular responses to alcohol are dose-dependent.