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Apart from the well-known role of hypertension in cerebrovascular disease, visit-to-visit blood pressure (BP) variability is emerging as an independent risk factor for stroke. Although the underlying mechanism is not fully understood, artery remodeling is thought to be closely involved in the relationship between visit-to-visit BP variability and stroke. This review article summarizes the recent literature on these topics. Silent cerebral injury is considered to serve as a common pathophysiology in the relationship of visit-to-visit BP variability with cognitive impairment and stroke. Here we review visit-to-visit BP variability, some comparisons of the effects of antihypertensive agents on visit-to-visit BP variability, and an issue regarding the impact of these agents on stroke.

BACKGROUND Aging and hypertension are well-known risk factors for cerebral white matter lesions. Prothrombotic status has been shown to be a risk factor for cardiovascular disease. In this study, we investigated the relationships among prothrombotic status, ambulatory blood pressure (ABP), and white matter hyperintensity (WMH) in elderly hypertensives. METHODS Measurement of prothrombin fragments 1+2 (F1+2), von Willebrand Factor (vWF) and plasminogen activator inhibitor-1 (PAI-1), ABP monitoring (ABPM), and brain magnetic resonance imaging (MRI) were performed in 514 Japanese elderly hypertensives (72.3 years old, male 37%). WMH cases were further divided into deep subcortical white matter lesion (DWML) or periventricular hyperintensity (PVH). RESULTS Deep WMH (DWMH) had significant positive correlations with age, use of antiplatelet agents, log F1+2, log vWF, log PAI-1, and 24-h systolic BP (SBP). PVH had significant positive correlations with age, male gender, smoking, use of antiplatelet agents, white coat hypertension (WCH), log vWF, and 24-h SBP. Severe PVH had significant positive correlations with age, use of antiplatelet agents, WCH, and 24-h SBP, and that was marginally correlated with log F1+2. In the logistic linear regression analysis, log F1+2 was significantly associated with DWMH (P < 0.01) and severe PVH (P < 0.05) adjusted for age and 24-h SBP. Log PAI-1 was significantly associated with DWMH (P < 0.05) adjusted for age and 24-h SBP. CONCLUSIONS In the present study, F1+2 and PAI-1 were positively associated with WMH after adjustment for 24-h SBP in elderly hypertensives. In addition to the conventional risk factors, prothrombotic status might serve as a significant determinant for WMH.

Although hypertension is well known as a cause of vascular dementia (VaD), recent findings highlight the role of hypertension in the pathogenesis of Alzheimer's disease (AD) as well as mild cognitive impairment (MCI). Recent studies have shown that disruption of diurnal blood pressure (BP) variation is closely associated with cognitive impairment via injury of the small cerebral arteries indicating that long-standing hypertension constitutes a risk of brain matter atrophy or white matter lesions (WMLs). In several clinical trials, BP-lowering with antihypertensive agents was suggested to reduce the risk of dementia or cognitive decline. This review paper focuses on the role of hypertension as a risk factor for cognitive impairment, and summarizes current knowledge on the relationships between ambulatory BP monitoring (ABPM) and cognitive impairment. Finally, an overview of the impact of antihypertensive therapy on dementia prevention is provided.

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 (

BACKGROUND Recent studies have shown that short and long sleep durations and insomnia are associated with increased home-measured blood pressure (BP) variability, which in turn has a relationship with arterial stiffness. However, the determinants for visit-to-visit systolic blood pressure (SBP) variability have rarely been investigated in relation to sleep duration, insomnia, and carotid arterial stiffness. METHOD The subjects were 201 elderly individuals (79.9±6.4 years old) with one or more cardiovascular risks. Based on 12 visits, visit-to-visit BP variability (expressed as a coefficient of variation [CV]) and δ (maximum - minimum) BP were measured. Self-reported sleep duration and insomnia questionnaires were used to classify the patients according to sleep duration period and insomnia status. RESULTS After multivariable adjustment, long sleep duration (≥ 9 hours per night) had significant positive associations with SBP δ (P < 0.05), while persistent insomnia had significant positive associations with SBP CV (P < 0.05) and δ (P < 0.01). Additionally, significant interactions were found in terms of long sleep duration by carotid artery stiffness parameter β (P < 0.05), persistent insomnia by intima-media thickness (P < 0.01), and persistent insomnia by stiffness parameter β (P < 0.05) for SBP δ. CONCLUSION In elderly patients at high risk for cardiovascular disease, long sleep duration as well as persistent insomnia were significantly associated with higher visit-to-visit BP variability. Long sleep duration and persistent insomnia each had synergetic interactions with carotid artery stiffness and with visit-to-visit BP variability.

BACKGROUND Insular cortex (Ic) has been suggested to be a key site in limbic-autonomic integration. Association of Ic damage with disruption of diurnal blood pressure (BP) variation and higher serum level of noradrenaline has been reported. We examined the relationships of Ic volume with ambulatory BP measures and noradrenaline concentration. METHODS Ambulatory BP monitoring and brain magnetic resonance imaging (MRI) were performed in 55 elderly never-treated hypertensives. Ic volumes were measured using an intensity contour mapping algorithm. Serum adrenaline and noradrenaline concentrations were evaluated. RESULTS Subjects were classified into an Ic-atrophy group (n = 14) and non-Ic-atrophy group (n = 41) based on a total Ic volume (left and right side) of 12.6 cm(3) (lowest quartile). In the Ic-atrophy group, 24 h (145 mm Hg vs. 134 mm Hg, P < 0.05) and sleep (143 mm Hg vs. 127 mm Hg, P < 0.01) systolic BP (SBP) and nocturnal SBP dipping (1.30% vs. 8.54%, P < 0.05) were significantly different, and noradrenaline (373 pg/ml vs. 296 pg/ml, P = 0.08) was marginally different from those in the non-Ic-atrophy group. Left Ic volume was significantly correlated with 24 h (r = -0.277) and sleep (r = -0.499) SBP and nocturnal SBP dipping (r = 0.413), while right Ic volume was significantly correlated with 24 h (r = -0.261) and sleep (r = -0.430) SBP, nocturnal SBP dipping (r = 0.321) and noradrenaline (r = -0.335). In multiple linear regression analysis adjusted for age, gender and body mass index (BMI), left Ic volume was significantly negatively associated with sleep SBP (P < 0.01) and positively with nocturnal SBP dipping (P < 0.05). CONCLUSION Ic atrophy, specifically in the left side, may partly contribute to disruption of diurnal ambulatory BP rhythm via central autonomic nervous system (ANS) dysregulation.