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Background The morning surge of blood pressure (BP) is associated with α-adrenergic activity. We studied the association between the α-adrenergic morning surge in BP and silent cerebrovascular disease in elderly patients with hypertension. Methods We conducted ambulatory BP monitoring three times (twice at baseline and after nighttime dosing of the α1-blocker doxazosin) in 98 elderly hypertensive patients in whom the presence of silent cerebral infarcts (SCI) was assessed by brain magnetic resonance imaging. The morning BP surge (MBPS) was calculated as the mean systolic BP during the 2 h after waking minus the mean systolic BP during 1 h that included the lowest sleep BP. The α-adrenergic MBPS was calculated as the reduction of MBPS by doxazosin. Results The prevalence of multiple SCI was higher in the Surge group (top quartile: MBPS ≥45 mm Hg, n = 24) than in the Nonsurge group (MBPS Conclusion The morning BP surge, particularly that dependent on α-adrenergic activity, is closely associated with advanced silent hypertensive cerebrovascular disease in elderly individuals.

It remains uncertain which is the stronger predictor for stroke in older hypertensives, ambulatory pulse pressure (PP) or mean blood pressure (MBP).We studied the prognosis for stroke in 811 older hypertensives in whom ambulatory BP monitoring was performed. We also assessed silent cerebral infarct (SCI) by brain magnetic resonance imaging.Silent cerebral infarcts were found in 50% of 515 subjects (64% of the total population) in whom we assessed SCI using brain magnetic resonance imaging. During a mean of a 42-month follow-up period, stroke events occurred in 59 subjects. After adjustment for covariates, for each 10 mm Hg increase in sleep PP, there was an independent 43% (95% confidence interval [CI]:16%-75%, P =.001) increase in the stroke risk, and sleep MBP was not a significant factor after controlling for sleep PP. On the other hand, for each 10 mm Hg increase in awake MBP, there was an independent 48% (95% CI: 21%-81%, P =.0002) increase in the stroke risk, and awake PP was not a significant factor after controlling for awake MBP. After adjusting for SCI (a strong predictor, P.0001) at baseline, the effects of awake MBP (38% risk increase for each 10 mm Hg, P =.007) and sleep PP (32% risk increase for each 10 mm Hg, P =.016) remained significant.In older hypertensives, the impacts of PP and MBP on stroke risk are different during sleep and awake periods. Sleep PP and awake MBP are both predictors of stroke events independently of SCI.

BACKGROUND Sleep-disordered breathing (SDB) is recognized as a risk factor for cerebrovascular disease. The objective of this study was to investigate the relationship between nocturnal hypoxia and silent cerebral infarct (SCI) in the general population. METHODS In the 2001 annual health check in Nishiarita, Japan, 170 individuals at high risk were screened who met more than three of the following criteria: high blood pressure, hypercholesterolemia, left ventricular hypertrophy by electrocardiography, hemoglobinA(1)c >6.5%, proteinuria, central obesity, heavy smoking habit, heavy drinking, and family history of stroke. Overnight pulse oximetry, brain magnetic resonance imaging, and carotid/cardiac ultrasonography were performed in 146 (mean age 67.4 +/- 9.0 years) of the 170 individuals in whom pulse oximetry was successfully performed. RESULTS Subjects were classified into a nocturnal hypoxia group (n = 36) and a nonhypoxia group (n = 110) based on a 3% oxygen desaturation index (ODI) 5.6 times per hour during sleep (highest quartile) by pulse oximetry. The presence of silent cerebral infarct (SCI) (57% v 35%, P = .03) was significantly higher in the hypoxia group than in the nonhypoxia group. The number of SCI was positively correlated with age (r = 0.23, P < .01), systolic blood pressure (r = 0.196, P < .05), and 3% ODI (r = 0.318, P < .001). Even after adjustment for confounding factors using logistic regression analysis, nocturnal hypoxia (odds ratio = 2.2, 95% confidence interval = 1.10 to 5.30, P = .026) as well as systolic blood pressure and age (10-year increase: odds ratio = 1.22, 95% confidence interval 1.00 to 1.48, P = .048) were independently associated with SCI in the study subjects. CONCLUSIONS Based on the study results, SDB assessed by overnight pulse oximetry was associated with silent cerebral disease in a high-risk, community-dwelling Japanese population.

Congenital protein C deficiency is now widely recognized as a genetic risk for venous thrombosis. However, it remains uncertain whether this condition also confers risk for arterial thrombosis. We evaluated the association of congenital protein C deficiency with hypertension and silent cerebrovascular disease using brain magnetic resonance imaging (MRI) (T1- and T2-weighted and proton density images) in a large family pedigree of protein C deficiency diagnosed by gene analysis, compared with 46 non-pedigree related control subjects with normal protein C levels (≥ 75%) who were selected from among 55 asymptomatic hypertensive subjects matched for age and cardiovascular risk factors. Of the 58 living subjects in this pedigree, we measured plasma protein C levels in 45 subjects, and found 2 cerebral infarctions in the 24 heterozygotic subjects, whereas there was no stroke in the 21 normal homozygotic subjects. We performed brain MRI in 14 asymptomatic hypertensive subjects without any cardiovascular disease and in two patients with cerebral infarction, and found 28 cerebral infarcts (two corresponded to the patient neurologic deficits and 26 were silent). All were lacunar infarcts < 10 cm in size. A total of 25 silent lacunar infarcts were found in nine heterozygotic subjects, whereas only one was found in the seven normal homozygotic subjects (2.8 v 0.14 lacunes per person, P = .002). No advanced white matter hyperintense lesions in T2-weighted images were found in either group. The prevalence of silent lacunar infarcts in the heterozygotic subjects was also significantly higher than that in normal control subjects (1.0 per person, P = .01). Concerning the distribution of silent infarcts, the number of lacunes located in the basal ganglia was higher in the heterozygotic subjects (2.3 per person, P < .001) than in the seven normal homozygotic subjects (0.14 per person) or in the control group (0.28 per person), whereas the number of lacunes in the white matter was not different among the groups. In conclusion, congenital protein C deficiency may accelerate the progression of silent cerebral infarct formation in hypertension, particularly in the basal ganglia, and may be a potential risk for stroke or vascularly induced dementia.

The aim of the present study was to clarify the differences in the progression and the characteristics of silent cerebral infarcts (SCI) between patients with coronary artery disease (CAD) and hypertensive patients. Silent cerebral infarcts, a powerful prognostic indicator for stroke, are frequently found in patients with CAD and in hypertensives. However, the differences in the characteristics of SCI and related risk factors between CAD and hypertensive patients have not been thoroughly investigated. We evaluated the number of SCI and their distribution using brain magnetic resonance imaging (T1- and T2-weighted images) in 107 patients with CAD (validated by coronary angiography) and 101 hypertensive patients without history of clinical stroke. The prevalence of multiple SCI (three or more infarcts per person) in patients with CAD and with hypertension was significantly higher than in hypertensives without CAD (46% v 21%; P = .001), whereas that of patients with CAD without hypertension was intermediate (31%). The patients with multi- (two- or three-vessel) vessel diseases (VD) had a significantly higher prevalence of multiple SCI than the hypertensives and the no-stenosis or 1-VD group (68.1% in the 3-VD group, 52.0% in the 2-VD group, 26.8% in the 1-VD group, and 21.0% in the no-stenosis group). Multiple logistic regression analysis revealed that in the CAD group, the number of involved coronary arteries was an independent determinant of SCI (P < .005), whereas in the hypertensive group, age was an independent determinant of SCI (P < .005). When we investigated the distribution of SCI, in the CAD group, SCI in the deep perforator territory (the basal ganglia and the thalamus) were independently associated with the number of involved coronary arteries (P < .005), whereas SCI in the white matter were independently associated with age only (P < .005). In conclusion, SCI were more advanced in the patients with multivessel CAD than in the hypertensive patients, and were more common in patients with CAD and hypertension than in those without hypertension. Coronary atherosclerosis was independently and specifically associated with SCI located in the deep perferator territory but not of SCI located in the white matter. The CAD-atherosclerosis and hypertension may be independently involved in the pathologic process of SCI.

Recently, hyperinsulinemia or insulin resistance has been suggested to be a risk factor for cardiovascular diseases. We evaluated the role of insulin resistance in the occurrence of silent cerebral infarction in 28 patients with essential hypertension (40 to 75 years, 157 +/- 4/89 +/- 2 mm Hg). Patients with diabetes mellitus or obesity (BMI > or = 30) were excluded. Insulin resistance was evaluated by means of constant glucose infusion rate (M value) during euglycemic-hyperinsulinemic glucose clamp test. Infarction was defined as a focal area with prolonged T1 and T2 relaxation times that was > 5 mm in diameter on brain magnetic resonance imaging. The severity of periventricular hyperlucency was evaluated by the distribution of the high intensity area. The number of silent infarctions significantly correlated only with the M value (F = 7.58, R2 = 0.23, P = .01) in multiple regression analysis using all variables: age, blood pressure, smoking history, lipid profile, levels of plasma glucose and insulin on fasting, and total amounts during 75-g OGTT. However, the severity of periventricular hyperlucency did not show a correlation with any factors. The occurrence of cerebral infarction was significantly correlated with thickening of the intima-media complex (IMC) of the common carotid artery on B-mode ultrasonography (F = 8.43, R2 = 0.25, P < .01). In conclusion, insulin resistance and thickening of IMC show a close relationship with the occurrence of silent cerebral infarction. Therefore, it may be important to improve insulin resistance for prevention of cerebral infarction in essential hypertensives.

P-332 Key Words: Diabetic Hypertension, Cerebral Circulation, Angiotensin Receptor Blocker

P-80 Key Words: Diabetic Masked Hypertension, Stroke Risk, Silent Cerebral Infarct

OR-60 Key Words: Cerebral Infarcts, Diabetes Mellitus, Ambulatory Blood Pressure