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Biomedical subjects

Satoshi Hoshide

Publications and source records attributed to Satoshi Hoshide.

27 records · Page 2Linked to original sources

Effects of bedtime vs. morning administration of the long-acting lipophilic angiotensin-converting enzyme inhibitor trandolapril on morning blood pressure in hypertensive patients.

Cardiovascular events occur most frequently in the morning. To study the effects of the long-acting lipophilic angiotensin-converting enzyme (ACE) inhibitor trandolapril on morning blood pressure (BP), we performed ambulatory BP monitoring (ABPM) before and after administration of trandolapril just before going to bed (bedtime-administered group: n=17) or in the morning (morning-administered group: n=20) in 37 hypertensive patients. Both sets of ABPM data were available in 30 patients. The 24-h systolic BP (SBP) levels were significantly decreased by 7.2 mmHg in the morning-administered group (p=0.02) and by 5.2 mmHg in the bedtime-administered group (p=0.04). In the bedtime-administered group, prewaking SBP (the average of the 2-h SBP values just before waking) and morning SBP (the average of the 2-h SBP values just after waking) were significantly decreased by 11 mmHg (p=0.005) and by 8.4 mmHg (p=0.03), respectively. On the other hand, in the morning-administered group, the reduction of prewaking SBP (3.9 mmHg, n.s.) and morning SBP (6.6 mmHg, n.s.) did not reach the level of statistical significance. However, the differences in the reductions of prewaking and morning SBPs between the two groups were not statistically significant. There was no additional reduction of the nighttime lowest BP in either administration group. In conclusion, bedtime administration of the long-acting ACE inhibitor trandolapril seems to be a safe and effective means of controlling morning BP in hypertensive patients without an excessive fall in nocturnal BP.

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Greater change of orthostatic blood pressure is related to silent cerebral infarct and cardiac overload in hypertensive subjects.

Greater change of postural blood pressure (BP) is often seen in elderly hypertensives and is recognized as a risk factor for cognitive decline and poorer cerebrovascular outcome, but its clinical significance still remains to be clarified. We performed a head-up tilting test, ambulatory BP monitoring, and brain MRI in 59 hypertensives and 27 normotensive subjects. We measured plasma atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) levels at rest to assess cardiac burden. The 59 hypertensive patients were classified into 3 groups: an orthostatic hypertension (OHT) group with orthostatic increase in systolic BP (SBP) > or = 10 mmHg (n=16); an orthostatic hypotension (OHYPO) group with orthostatic SBP decrease < or = -10 mmHg (n=18); and an orthostatic normotension (ONT) group with neither of these two patterns (n=25). A group of 27 normotensive subjects (NT) was also included as a control. Plasma BNP (72 +/- 92 vs. 29 +/- 24 pg/ml, p < 0.05) and BNP/ANP ratio (4.6 +/- 3.3 vs. 2.4 +/- 1.5, p < 0.05) were significantly higher in the OHYPO than in the NT group. The BNP/ANP ratio was also higher in the OHT than in the NT group (5.1 +/- 3.9 vs. 2.4 +/- 1.5, p < 0.01). The number of silent cerebral infarct (SCI), prevalence of SCI and number of multiple SCIs was the highest in the OHT group, followed in order by the OHYPO, ONT and NT groups. Blood pressure and left ventricular mass index were not significantly different among the 3 hypertensive groups. In conclusion, hypertensive patients with greater change of postural BP (OHT and OHYPO) were shown to have increased risk of advanced silent brain lesions and greater cardiac burden.

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Smoking is associated with silent cerebrovascular disease in a high-risk Japanese community-dwelling population.

We aimed to investigate the relationships between smoking and silent cerebrovascular damage. We performed brain MRI to evaluate silent cerebral infarct (SCI) and periventricular hyperintensity (PVH), and carotid-ultrasonography to investigate carotid atherosclerotic plaque in 170 high-risk community-dwelling subjects (mean age: 67.2 years; men: 28.7%) who met more than 3 of the following 9 criteria: 1) high blood pressure (BP); 2) hypercholesterolemia; 3) left ventricular hypertrophy; 4) high hemoglobin A1c; 5) proteinuria; 6) high waist-to-hip ratio; 7) smoking > or =30 cigarettes/day; 8) heavy alcohol intake; 9) family history of stroke. The subjects with SCI (SCI group) were older (70 years vs. 66 years, p=0.004) and had higher systolic BP (SBP) (160 vs. 148 mmHg, p <0.001) and higher carotid plaque score (2.3 vs. 1.5/person, p <0.05) than those without SCI. Among the variables, smoking status (r =0.34, p <0.001), SBP (r =0.28, p <0.001), male gender (r =0.29, p <0.001), left ventricular mass index (r =0.25, p =0.001), and serum creatinine (r =0.20, p =0.006) were significantly correlated with the number of SCIs. Among smokers, the number of SCIs was significantly higher in current smokers than in past smokers (1.9+/-2.2 vs. 0.5+/-0.8, p <0.01). In multiple regression analysis, smoking status (beta =0.183, p =0.045) and SBP (beta =0.196, p =0.011) were independent determinants of the increased number of SCIs. In conclusion, smoking status was an independent determinant of multiple SCIs in a high-risk Japanese community-dwelling population.

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Reproducibility of arterial stiffness indices (pulse wave velocity and augmentation index) simultaneously assessed by automated pulse wave analysis and their associated risk factors in essential hypertensive patients.

Arterial stiffness is a strong determinant of cardiovascular risk. Pulse wave velocity (PWV) and the augmentation index (AIx) are widely used as arterial stiffness indices. We studied the reproducibility of these indices and their association with cardiovascular risk factors in hypertensives. We measured brachial blood pressure (BP), brachial-ankle PWV (baPWV) and carotid AIx (cAIx) twice (at the baseline and 4 weeks after the baseline) using an automatic device in 103 hypertensives. The mean intraobserver-intersession difference was 29.0 cm/s with an SD of 201.6 cm/s for baPWV, and 0.5% with an SD of 5.9% for cAIx, and the Bland-Altman plots demonstrated the good reproducibility of baPWV and cAIx. Both baPWV and cAIx (the average of the 1st and the 2nd measurements) were significantly correlated with age, systolic BP (SBP), and pulse pressure (all, p <0.005); however, these factors were not correlated with each other (r =0.06, NS). cAIx was correlated with height, heart rate (HR), total cholesterol, and low density lipoprotein cholesterol (LDL-C) (all, p <0.05). In multiple regression analysis, age, SBP, and HR emerged as significant independent predictors of baPWV (adjusted R(2)=0.43, p <0.0001), while height, SBP, HR, and LDL-C emerged as significant independent predictors of cAIx (adjusted R(2)=0.58, p <0.0001). Both PWV and AIx measured using an automatic device were fairly reproducible, and their associated risk factors appeared to be different. Automated simultaneous measurement of these arterial stiffness indices may be useful for risk stratification of hypertensives.

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Morning surge in blood pressure as a predictor of silent and clinical cerebrovascular disease in elderly hypertensives: a prospective study.

BACKGROUND: Cardiovascular events occur most frequently in the morning hours. We prospectively studied the association between the morning blood pressure (BP) surge and stroke in elderly hypertensives. METHODS AND RESULTS: We studied stroke prognosis in 519 older hypertensives in whom ambulatory BP monitoring was performed and silent cerebral infarct was assessed by brain MRI and who were followed up prospectively. The morning BP surge (MS) was calculated as follows: mean systolic BP during the 2 hours after awakening minus mean systolic BP during the 1 hour that included the lowest sleep BP. During an average duration of 41 months (range 1 to 68 months), 44 stroke events occurred. When the patients were divided into 2 groups according to MS, those in the top decile (MS group; MS > or =55 mm Hg, n=53) had a higher baseline prevalence of multiple infarcts (57% versus 33%, P=0.001) and a higher stroke incidence (19% versus 7.3%, P=0.004) during the follow-up period than the others (non-MS group; MS <55 mm Hg, n=466). After they were matched for age and 24-hour BP, the relative risk of the MS group versus the non-MS group remained significant (relative risk=2.7, P=0.04). The MS was associated with stroke events independently of 24-hour BP, nocturnal BP dipping status, and baseline prevalence of silent infarct (P=0.008). CONCLUSIONS: In older hypertensives, a higher morning BP surge is associated with stroke risk independently of ambulatory BP, nocturnal BP falls, and silent infarct. Reduction of the MS could thus be a new therapeutic target for preventing target organ damage and subsequent cardiovascular events in hypertensive patients.

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Associations between nondipping of nocturnal blood pressure decrease and cardiovascular target organ damage in strictly selected community-dwelling normotensives.

BACKGROUND: In hypertensives, nondippers are more likely than dippers to suffer silent, as well as overt, hypertensive target organ damage. In this study, we investigated whether a nondipper status was associated with target organ damage in normotensives. METHODS: We performed ambulatory blood pressure (BP) monitoring, echocardiography, and carotid ultrasonography and measured natriuretic peptides and urinary albumin (UAE) in 74 normotensive subjects with the following criteria: 1) clinical BP <140/90 mm Hg; 2) average 24-h ambulatory BP <125/80 mm Hg. RESULTS: The left ventricular mass index (LVMI) and the relative wall thickness (RWT) measured by echocardiography were greater in nondippers than dippers (LVMI: 103 +/- 26 v 118 +/- 34 g/m(2), P <.05; RWT: 0.38 +/- 0.07 v 0.43 +/- 0.09, P <.01). Plasma atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) were higher in nondippers than dippers (ANP: 14 +/- 10 v 36 +/- 63 pg/mL, P <.01; BNP: 16 +/- 12 v 62 +/- 153 pg/mL, P <.05). There were no significant differences in UAE and intima-media thickness measured by carotid ultrasonography. CONCLUSIONS: Normotensive nondipping may not reflect renal damage, but may have a predominant effect on cardiac damage. Nondipping of nocturnal BP seems to be a determinant of cardiac hypertrophy and remodeling, and may result in a cardiovascular risk independent of ambulatory BP levels in normotensives.

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U-curve relationship between orthostatic blood pressure change and silent cerebrovascular disease in elderly hypertensives: orthostatic hypertension as a new cardiovascular risk factor.

OBJECTIVES: The study investigated the clinical significance and mechanism of orthostatic blood pressure (BP) dysregulation in elderly hypertensive patients. BACKGROUND: Although orthostatic hypotension (OHYPO), often found in elderly hypertensive patients, has been recognized as a risk factor for syncope and cardiovascular disease, both the clinical significance and the mechanism of orthostatic hypertension (OHT) remain unclear. METHODS: We performed a head-up tilting test and brain magnetic resonance imaging (MRI) in 241 elderly subjects with sustained hypertension as indicated by ambulatory BP monitoring. We classified the patients into an OHT group with orthostatic increase of systolic blood pressure (SBP) of >or=20 mm Hg (n = 26), an OHYPO group with orthostatic SBP decrease of >or=20 mm Hg (n = 23), and a normal group with neither of these two patterns (n = 192). RESULTS: Silent cerebral infarcts were more common in the OHT (3.4/person, p < 0.0001) and OHYPO groups (2.7/person, p = 0.04) than in the normal group (1.4/person). Morning SBP was higher in the OHT group than in the normal group (159 vs. 149 mm Hg, p = 0.007), while there were no significant differences of these ambulatory BPs between the two groups during other periods. The OHT (21 mm Hg, p < 0.0001) and OHYPO (20 mm Hg, p = 0.01) groups had higher BP variability (standard deviation of awake SBP) than the normal group (17 mm Hg). The associations between orthostatic BP change and silent cerebrovascular disease remained significant after controlling for confounders, including ambulatory BP. The orthostatic BP increase was selectively abolished by alpha-adrenergic blocking, indicating that alpha-adrenergic activity is the predominant pathophysiologic mechanism of OHT. CONCLUSIONS: Silent cerebrovascular disease is advanced in elderly hypertensives having OHT. Elderly hypertensives with OHT or OHYPO may have an elevated risk of developing hypertensive cerebrovascular disease.

Adrenergic alpha-Antagonists↗

Incomplete benefit of antihypertensive therapy on stroke reduction in older hypertensives with abnormal nocturnal blood pressure dipping (extreme-dippers and reverse-dippers).

To determine whether the benefits of antihypertensive treatment vary according to dipper status, 811 asymptomatic elderly Japanese hypertensives underwent 24-h ambulatory blood pressure monitoring. During a mean follow-up period of 41 months, 32 stroke events were observed in patients who remained nonmedicated (n = 385), and in 27 patients in the medicated group (n = 426), indicating a 24% lower rate of stroke as a result of antihypertensive therapy. Patients were divided into a white-coat hypertensive (WCHT) group (ambulatory blood pressure <130/80 mm Hg; n = 236) and a sustained hypertensive (SHT) group (n = 575). Sixty-one percent of SHT and 32% of WCHT patients were being medicated. In the SHT group, the stroke rates were 12.4% in nonmedicated and 7.4% in medicated group (P =.04), whereas in the WCHT group the stroke rates were 2.5% in nonmedicated and 1.3% in medicated group (P = not significant). The SHT were further classified according to their nocturnal systolic blood pressure (BP) decrease, as follows: 97 extreme-dippers with >20% nocturnal systolic BP decrease; 230 dippers with >10% but <20% decrease; 185 nondippers with >0% but <10% decrease; 63 reverse-dippers with <0% decrease. In the dipping groups of SHT, the stroke rates were similar according to medication versus no-medication in extreme-dippers (12% v 13%), and reverse-dippers (23% v 22%), but in nondippers there was a significantly lower rate (by 65%, P =.038) in the medicated (4.4%) than the nonmedicated (13%) groups. In dippers, the stroke rate was also lower in the medicated than the nonmedicated patients (4.7% v 8.8%), a decrease of 47% (P =.217), although the difference was not significant. In conclusion, in older SHT subjects, antihypertensive therapy using clinic BP may be less effective for the groups with extremely abnormal diurnal BP patterns (extreme-dippers and reverse-dippers) than those with relatively normal patterns (dippers and nondippers). Patients with WCHT also showed no benefit.

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[Silent and clinically overt stroke in older Japanese subjects with white-coat and sustained hypertension].

BACKGROUND: Whether white-coat hypertension in older subjects is a benign condition or is associated with an increased risk for stroke remains uncertain. White-coat hypertension as a risk factor for stroke was investigated in relation to silent cerebral infarct in the older Japanese population. METHODS: The prognosis for stroke was studied in 958 older Japanese subjects [147 normotensives (NT), 236 white-coat hypertensives (WCHT), and 575 sustained hypertensives (SHT)] in whom ambulatory blood pressure monitoring was performed in the absence of antihypertensive treatment. Silent cerebral infarct was also assessed using brain magnetic resonance imaging in 585 subjects (61%). RESULTS: Silent cerebral infarcts were found in 36% of NT (n = 70), 42% of WCHT (n = 154), and 53% of SHT (n = 361), and multiple silent cerebral infarcts(presence of > or = 2 silent cerebral infarcts) were found in 24% of NT, 25% of WCHT, and 39% of SHT. During a mean 42-month-follow-up period, clinically overt strokes occurred in 62 subjects [NT 3(2.0%), WCHT 5(2.1%), SHT 54(9.4%)], with 14 fatal cases [NT 1(0.7%), WCHT 0(0%), SHT 13 (2.3%)]. Cox regression analysis showed that age (p = 0.0001) and SHT [RR(95% confidence interval): 4.3 (1.3-14.2), p = 0.018] were independent stroke predictors, whereas WCHT was not significant. Adding presence/absence of silent cerebral infarct at baseline into this model, the RR (95% confidence interval) for silent cerebral infarct was 4.6 (2.0-10.5) (p = 0.003), and that of SHT was 5.5 (1.8-18.9) vs WCHT (p = 0.004) and 3.8 (0.88-16.7) vs NT (p = 0.07). CONCLUSIONS: The incidence of stroke in WCHT is similar to that of NT, and one fourth the risk in SHT in older subjects. Although silent cerebral infarct is a strong predictor of stroke, the difference in stroke prognosis between SHT and WCHT was independent of silent cerebral infarct. It is clinically important to distinguish WCHT from SHT even after assessment of target organ damage in the elderly.

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