新保 昌久

BACKGROUND Short sleep duration has been shown to be associated with cardio/cerebrovascular disease. White matter hyperintensities (WMH) have been associated with an increased risk of stroke. In addition to high ambulatory blood pressure (BP), chronic kidney disease (CKD) is a risk for WMH. In this study, we investigated the relationships among sleep duration, CKD, and WMH in elderly hypertensives. METHODS Ambulatory BP monitoring and brain magnetic resonance imaging were performed in 514 Japanese elderly hypertensives (mean age 72.3 years, males 37%). WMH cases were further divided into deep subcortical white matter lesion or periventricular hyperintensity (PVH). CKD (n = 193) was defined as estimated glomerular filtration rate less than 60 ml/min/1.73 m(2). RESULTS According to sleep duration (< 7.5, a parts per thousand yen7.5 to < 9.5, and a parts per thousand yen9.5 hour per night), significant associations of sleep duration were observed with WMH and PVH. In the regression analysis including age, gender, smoking, antiplatelet agents use, 24-hour systolic BP, nondipper, white coat hypertension and CKD, short sleep duration was significantly positively associated with WMH and PVH when subjects with mid-range sleep duration were used as a reference group. A significant interaction was found between short sleep duration and CKD for PVH. In the non-CKD group, short sleep duration had strong significant positive associations with WMH and PVH. CONCLUSIONS In the present study, short sleep duration was a positive significant determinant for WMH and PVH in elderly hypertensives. Sleep duration might serve as a strong determinant for white matter lesions especially in those without CKD.

Obstructive sleep apneas syndrome (OSAS) is associated with nocturnal hypertension with higher sleep blood pressure (BP) and its variability, both of which increase cardiovascular risk. In this crossover design study, the effect of nighttime single-dose administration of vasodilating (nifedipine 40mg) vs sympatholytic (carvedilol 20mg) antihypertensive agents on sleep BP in 11 hypertensive OSAS patients was evaluated. The authors recently developed a trigger sleep BP monitor with an oxygen-triggered function that initiates BP measurement when oxygen desaturation falls. The BP-lowering effects of nifedipine on the mean (P<.05) and minimum sleep systolic BPs (SBPs) (P<.01) were stronger than those of carvedilol. Sleep SBP surge (difference between the hypoxia-peak SBP measured by oxygen-triggered function and SBPs within 30minutes before and after the peak SBP) was only significantly reduced by carvedilol (P<.05). The nighttime dosing of both vasodilating and sympatholytic antihypertensive drugs is effective to reduce sleep BP but with different BP-lowering profiles.