SLEEP PATTERNS AND LIKELIHOOD OF STROKE AND CAROTID ATHEROSCLEROSIS

Abstract

85 BACKGROUND AND PURPOSE: Sleep patterns may independently affect morbidity and mortality. However, the effect of habitual sleep patterns on the risk for stroke and carotid atherosclerosis is undetermined. METHODS: We evaluated the association of nocturnal snoring, sleep duration, and daytime somnolence with stroke and carotid artery stenosis in 1,348 adults who participated in a stroke screening program in Buffalo, New York. A standard questionnaire was used for each person to report sleep habits and cardiovascular risk factors. Each participant underwent carotid Doppler ultrasound testing and an interview by a neurologist or neurosurgeon to determine the presence of carotid stenosis or history of stroke. Logistic regression analyses were used to examine these relationships. RESULTS: Of the 1348 persons evaluated, 82 (6%) had a previous stroke and 96 (7.1%) had significant carotid stenosis (stenosis > 60%). The frequency of prior stroke was higher in individuals who routinely slept for more than 8 hours per night (14%) than in those who either slept for 6–8 hours (5.4%) or less than 6 hours (5.4%). Persons who experienced daytime somnolence regularly had a higher frequency of stroke (14%) than those who did not (4%). After adjusting for differences in age, race, gender, cigarette smoking, hyperlipidemia, hypertension, and diabetes mellitus, the risk for stroke was significantly associated with daytime somnolence (Wald s chi-square test 11.8, p=0.018), average hours of sleep (Wald s chi-square test 14.7, p=0.002), and frequency of nocturnal snoring (Wald s chi-square test 13.3, p=0.009). After adjusting for other cardiovascular risk factors, daytime somnolence, average hours of sleep, and frequency of nocturnal snoring were not associated with carotid atherosclerosis. CONCLUSIONS: Daytime somnolence, sleeping more than 8 hours per night, and frequent nocturnal snoring increase the likelihood for stroke but not carotid atherosclerosis. This increased likelihood for stroke appears to be independent of atherosclerotic mechanisms and other cardiovascular risk factors.