Sleep deprivation potentiates activation of cardiovascular and catecholamine responses in abstinent alcoholics

Alcohol dependence is associated with an increased incidence of hypertension and cardiac arrhythmias, but the triggering mechanisms are not known. Sleep loss, common in alcohol-dependent patients, causes an activation of the sympathetic nervous system. To determine whether sleep deprivation induces differential cardiovascular and sympathetic responses in alcohol dependence, we measured heart rate, blood pressure, and circulating sympathetic catecholamines in 36 abstinent alcohol-dependent men and 36 age-, gender-, and ethnicity-matched controls after a baseline night of sleep, in the morning after early night partial sleep deprivation, and again after a full night of recovery sleep. Subjects were on average normotensive and none was being treated for hypertension. Baseline heart rate, blood pressure, and sympathetic catecholamines were similar in the 2 groups. Administration of partial night sleep deprivation induced greater increases of heart rate (P<0.01) and circulating levels of norepinephrine (P<0.05) and epinephrine (P<0.05) in the alcohol-dependent men as compared with responses in controls. Even after a full night of recovery sleep, elevations in heart rate (P<0.05) and circulating catecholamines (P<0.05) persisted in the alcoholic subjects. Partial night sleep deprivation induces elevated heart rate and sympathetic catecholamine responses in alcoholic subjects as compared with controls, and this sympathetic activation is sustained after nights of partial and recovery sleep. It is possible that modest habitual sleep loss could contribute to triggering cardiac arrhythmias or other cardiovascular events in alcohol dependence.