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Satoshi Hoshide

Publications and source records attributed to Satoshi Hoshide.

At least 19 recordsLinked to original sources

Impact of blood pressure vs. glycemic factors on target organ damage in patients with type 2 diabetes mellitus.

The hypothesis that three measures of target organ damage in type 2 diabetics would be more closely related to blood pressure (BP) than to glycemic factors was tested by recording 24-hour ambulatory BP and glycosylated hemoglobin. The prevalence of silent cerebral infarcts with brain magnetic resonance imaging, left ventricular mass index with cardiac ultrasonography, and albuminuria in 244 asymptomatic diabetics (mean age, 65.4+/-9 years; 122 men and 122 women; hypertension, 73%) were evaluated. Multivariate analysis showed that age (standard partial regression coefficient: b=0.299; p<0.001), duration of hypertension (b=0.176; p=0.007), and 24-hour systolic BP (b=0.195; p=0.004) were significantly associated with the number of silent cerebral infarcts, but glycosylated hemoglobin (b=0.104; p=0.109) and duration of diabetes were not. Left ventricular mass index was associated with 24-hour systolic BP (b=0.377; p<0.001) and male sex (b=0.172; p=0.019). Presence of albuminuria was significantly associated with 24-hour systolic BP (b=0.209; p=0.003), duration of diabetes (b=0.154; p=0.022), cholesterol (b=0.132; p=0.042), and insulin use (b=0.150; p=0.026). In conclusion, all three measures of target organ damage were related to 24-hour BP, but only albuminuria was related to glycosylated hemoglobin in type 2 diabetics. BP may be more important than glycemic factors for predicting future cardiovascular complications.

Age Factors↗

The Japan Morning Surge-1 (JMS-1) study: protocol description.

Morning blood pressure is reported to be more closely related to hypertensive organ damages such as left ventricular mass index, microalbuminuria and silent cerebral infarcts, than blood pressure at other times of the day. Morning blood pressure may play an important role in the pathogenesis of hypertensive target organ damage. Increased sympathetic nerve activity is reported to be one of the mechanisms of morning hypertension; however, there are no available data that show whether strict home blood pressure control, especially in the morning period, can reduce target organ damage. The Japan Morning Surge-1 (JMS-1) study includes hypertensive outpatients with elevated morning systolic blood pressure (>or=135 mmHg) as assessed by self-measured blood pressure monitoring at home. All enrolled patients are under stable antihypertensive medication status. Exclusion criteria are arrhythmia, chronic inflammatory disease, and taking alpha-blockers or beta-blockers. The target number of patients to be enrolled in the JMS-1 study is 600, and the aim is to evaluate differences in the markers of hypertensive target organ damage, such as brain natriuretic peptide and the urinary albumin excretion/creatinine ratio. All of the patients are randomized to an experimental group or a control group, with randomization to be carried out by telephone interviews with the patients' physicians. In the experimental group, patients begin taking additional antihypertensive medication just before going to bed. This consists of doxazosin 1 mg/day, which then is increased to 2 mg/day and 4 mg/day, with a beta-blocker added after a 1-month interval until the morning systolic blood pressure is controlled to less than 135 mmHg. Patients in the control group continue the treatment they are receiving at the enrollment for 6 months. Blood pressure levels, adverse effects, and hypertensive target organ damage before and after the study are evaluated. In the JMS-1 study, we will evaluate whether strict morning blood pressure control by sympathetic nervous system blockade using an alpha-blocker, doxazosin, and with the addition of a beta-blocker if needed, can reduce hypertensive target organ damage.

Albuminuria↗

Morning hypertension: the strongest independent risk factor for stroke in elderly hypertensive patients.

Stroke occurs most frequently in the morning hours, but the impact of the morning blood pressure (BP) level on stroke risk has not been fully investigated in hypertensives. We studied stroke prognosis in 519 older hypertensives in whom ambulatory BP monitoring was performed, and who were followed prospectively. During an average duration of 41 months (range: 1-68 months), 44 stroke events occurred. The morning systolic BP (SBP) was the strongest independent predictor for stroke events among clinic, 24-h, awake, sleep, evening, and pre-awake BPs, with a 10 mmHg increase in morning SBP corresponding to a relative risk (RR) of 1.44 (p<0.0001). The average of the morning and evening SBP (Av-ME-SBP; 10 mmHg increase: RR=1.41, p=0.0001), and the difference between the morning and evening SBP (Di-ME-SBP; 10 mmHg increase: RR=1.24, p=0.0025) were associated with stroke risks independently of each other. The RR of morning hypertension (Av-ME-SBP > or = 135 mmHg and Di-ME-SBP > or = 20 mmHg) vs. sustained hypertension (Av-ME-SBP > = 135 mmHg and Di-ME-SBP < or = 20 mmHg) for stoke events was 3.1 after controlling for other risk factors (p=0.01). In conclusion, morning hypertension is the strongest independent predictor for future clinical stroke events in elderly hypertensive patients, and morning and evening BPs should be monitored in the home as a first step in the treatment of hypertensive patients.

Aged↗

Diabetic brain damage in hypertension: role of renin-angiotensin system.

Diabetes and hypertension are potent risk factors for cerebrovascular disease. We studied the effects of an angiotensin II type 1 receptor blockade (ARB) on brain damage in hypertensives in relation to diabetes. We studied cerebral metabolism (by proton magnetic resonance spectroscopy) and hemodynamics (by phase-contrast magnetic resonance angiography) before and 3 to 4 months after candesartan therapy in 20 diabetic hypertensives (DHTs) and 20 matched nondiabetic hypertensives (HTs). Silent multiple cerebral infarcts detected by brain MRI were more common in DHTs than in HTs (50% versus 25%). Cerebral N-acetyl aspartate (NAA; an indicator of functional neuronal mass) was lower in DHTs than in HTs (8.35 versus 9.58 mmol/kg; P=0.007). Baseline quantitative volume flow in the internal carotid arteries (ICAs) and the middle cerebral arteries (MCAs) was comparable between the 2 groups, whereas cerebrovascular reserve (CVR) assessed using acetazolamide (a cerebral arteriolar dilator) in ICAs (25% versus 35%; P=0.03) and MCAs (20% versus 31%; P=0.01) was lower in DHTs than in HTs. These baseline CVR and NAA values of DHT group were lower than those of 12 matched normotensives (CVR: 44% for ICA; 41% for MCA; NAA: 10.5 mmol/kg; all P<0.005). After candesartan therapy, CVR in ICAs and MCAs was significantly increased (P=0.001) independently of the reduction of the 24-hour blood pressure level, whereas the cerebral NAA level did not change. In conclusion, brain damage is advanced in DHTs. ARB partly improved the impaired cerebral microvascular function in DHTs.

Aged↗

Type 2 diabetes is associated with left ventricular concentric remodeling in hypertensive patients.

BACKGROUND: Left ventricular (LV) geometric remodeling is associated with cardiovascular prognosis in hypertensive patients. It is uncertain how LV remodeling is modulated by diabetes in hypertensive patients. In this study, we investigated the impact of diabetes and ambulatory blood pressure (BP) on LV geometric remodeling in hyptensives with/without diabetes. METHODS: Ambulatory BP monitoring and echocardiography were performed to compare 24-h BP levels and LV measurements in 400 uncomplicated hypertensives (mean age, 67 years, 152 men and 248 women) between diabetic (n = 161) and nondiabetic (n = 239) patients. RESULTS: The age (67 v 68 years), percentage of men (43% v 34%), body mass index (24.5 v 24.0 kg/m(2)), 24-h systolic BP (144/80 v 144/82 mm Hg), LV mass index (128 v 130 g/m(2)) were similar between the groups. Diabetic patients had higher relative wall thickness (0.50 v 0.44, P < .001) and higher prevalence of concentric LV hypertrophy (39.4% v 26.8%, P < .001) than nondiabetic patients. The presence of diabetes (odds ratio [OR] = 2.76; 95% confidence interval [CI] = 1.73-4.41, P < .001) and 24-h systolic BP (OR for 10 mm Hg increase = 1.17; 95% CI = 1.01-1.37, P < .05) were independently associated with the higher relative wall thickness (>/=0.45). On the other hand, 24-h systolic BP was independently associated with LV hypertrophy (OR for 10 mm Hg increase = 1.32; 95% CI = 1.14-1.52, P < .05). CONCLUSIONS: Among hypertensive patients, type 2 diabetes was associated with concentric LV geometry independent of ambulatory BP.

Adult↗

Determinants of exaggerated difference in morning and evening blood pressure measured by self-measured blood pressure monitoring in medicated hypertensive patients: Jichi Morning Hypertension Research (J-MORE) Study.

BACKGROUND: Morning blood pressure (BP) surge in ambulatory BP monitoring was a risk factor for stroke in our previous study. We studied the determinants of the morning minus evening systolic BP difference (ME difference) in self-measured BP monitoring, as a possible risk factor for stroke in medicated hypertensive patients. METHODS: Nine hundred sixty-nine hypertensive outpatients receiving stable antihypertensive drug treatment were studied using self-measured BP monitoring in the morning and evening. RESULTS: The ME difference ranged from -37.3 to 53.3 mm Hg (mean 7.9 mm Hg). The highest quartile (Q4) of the ME difference group (>15.0 mm Hg) had older age (68.0+/-9.8 years v 66.2+/-10.3 years, P=.01) and higher prevalence of men (48.3% v 39.9%, P=.02), regular alcohol drinkers (34.7% v 26.0%, P=.01) and beta-blocker use (26.9% v 19.9%, P=.03) than the other quartile groups (Q1 to Q3), whereas there was no significant difference in the average of morning and evening (ME average) BP. In logistic regression analysis controlling for ME average and other confounding factors, independent risks for Q4 of ME difference were older age (10 years older: odds ratio [OR] 1.21, P=.01, 95% confidence interval (CI) 1.04-1.42), regular alcohol drinker (OR 1.51, P=.04, 95% CI 1.01-2.26), and beta-blocker use (OR 1.50, P=.02, 95% CI 1.06-2.12). CONCLUSIONS: Older age, beta-blocker use, and regular alcohol drinking were significant determinants of the exaggerated ME difference in medicated hypertensive patients.

Adrenergic beta-Antagonists↗

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

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.

Adult↗

Morning blood pressure hyper-reactivity is an independent predictor for hypertensive cardiac hypertrophy in a community-dwelling population.

BACKGROUND: Morning blood pressure (BP) surge seems to be a risk factor for cardiovascular events. Although physical activity after arising significantly affects morning BP surge, it has remained unclear whether morning BP surge after controlling for physical activity (morning BP reactivity) is associated with target organ damage. METHODS: We performed ambulatory BP monitoring with simultaneous actigraphy and echocardiography in 120 community-dwelling Japanese subjects. We determined the waking time by actigraphy, and defined morning BP surge (MBPS) as the average of systolic BP during the 2 h after awakening minus the average of systolic BPs during the 1 h that included the lowest sleep BP. The ratio of MBPS/(sum of the 2-h physical activity after the arising time)0.5 was calculated as the morning BP reactivity (MBPR). RESULTS: In all the subjects studied (n = 120), MBPR was positively associated with left ventricular (LV) mass index (r = 0.30, P = .001). The MBPR had a positive association with both 24-h BP variability (SD) (r = 0.373, P < .001) and awake BP variability (r = 0.20, P < .05). The MBP hyper-reactive group (the highest quartile [Q4] of MBPR: n = 30) had significantly higher LV mass index than the nonreactive group (the other quartiles [Q1 to 3]: n = 90) (140 v 113 g/m(2), P < .001). Even after controlling for age, body mass index, gender, and 24-h systolic BP, the MBP hyper-reactive status still remained a strong predictor for LV hypertrophy. CONCLUSIONS: Exaggerated MBPS, adjusted for physical activity, is associated with cardiac hypertrophy independent of ambulatory BP level in a community-dwelling population.

Age Factors↗

Comparison of the effects of cilnidipine and amlodipine on ambulatory blood pressure.

Cilnidipine is a novel and unique 1,4-dydropyridine derivative calcium antagonist that exerts potent inhibitory actions not only on L-type but also on N-type voltage-dependent calcium channels. Blockade of the neural N-type calcium channel inhibits the secretion of norepinephrine from peripheral neural terminals and depresses sympathetic nervous system activity. The purpose of this study was to assess the effect of cilnidipine and amlodipine on ambulatory blood pressure (BP) levels. We performed 24-h ambulatory BP monitoring before and after once-daily use of cilnidipine (n=55) and amlodipine (n=55) in 110 hypertensive patients. Both drugs significantly reduced clinic and 24-h systolic BP (SBP) and diastolic BP (DBP) (p < 0.005). However, the reductions of 24-h (-1.19+/-6.78 vs. 1.55+/-6.13 bpm, p=0.03), daytime (-1.58+/-6.72 vs. 1.68+/-7.34 bpm, p=0.02) and nighttime (-1.19+/-5.72 vs. 1.89+/-6.56 bpm, p=0.01) pulse rate (PR) were significantly greater in the cilnidipine group than the amlodipine group. There was no correlation between the degree of daytime SBP change and that of daytime PR change after amlodipine treatment (r=-0.08, n.s.), but there was a significant negative correlation between the degree of daytime SBP change and that of day-time PR change after cilnidipine treatment (r=-0.27, p<0.05). N-type calcium channel blockade by cilnidipine may not cause reflex tachycardia, and may be useful for hypertensive treatment.

Aged↗

Altered aortic properties in elderly orthostatic hypertension.

To investigate the impact of arterial properties on orthostatic blood pressure (BP) dysregulation in older hypertensives, orthostatic BP dysregulation, a common phenomenon in elderly hypertensives, is associated with target organ damage and falls. However, the mechanism of orthostatic BP dysregulation remains unclear. The pulse wave velocity (PWV), related arterial stiffness, and the augmentation index (AI), a measure of arterial wave reflection, were measured in 365 older hypertensives. We classified the study patients into an orthostatic hypertension (OHT) group with orthostatic increase of systolic BP (SBP) of > or = 220 mmHg (n = 27) and an orthostatic normotension (ONT) group with an orthostatic increase of SBP of < 20 mmHg and orthostatic SBP decrease of < 20 mmHg (n = 338). Orthostatic AI was significantly greater in the OHT group than in the ONT group (OHT: 6.5 +/- 12% vs. ONT: -5.6 +/- 12%, p < 0.001), while supine AI and supine and orthostatic pulse rate were comparable between the two groups. There was no significant difference in the PWV between the OHT and ONT groups. Orthostatic hypertension was affected by altered aortic properties and associated with augmented wave reflection of arterial pressure.

Aged↗

Smoking and antihypertensive medication: interaction between blood pressure reduction and arterial stiffness.

To investigate how cigarette smoking and antihypertensive drug therapy may interact to affect cardiovascular disease, in this prospective study we administered amlodipine to hypertensive smokers and non-smokers and compared blood pressure reduction and indices of arterial stiffness. We measured blood pressure (BP), heart rate (HR), brachial-ankle pulse wave velocity (baPWV), and the carotid augmentation index (AIx) by using a non-invasive automated device in 101 hypertensive patients at baseline and at 1, 3, and 6 months of amlodipine administration (5.0 mg). At baseline, the AIx was significantly lower in smokers (n=27) than in non-smokers (n=74) (27.3% +/- 13.3% vs. 33.3% +/- 11.4%). After amlodipine administration, in both the groups, the mean BP, baPWV, and AIx were significantly reduced; however, the HR did not show a statistically significant difference. The reduction in the baPWV (cm/s) at 1 and 3 months was less marked in smokers than in non-smokers (mean +/- SD: -186.6 +/- 36.5 vs. -283.6 +/- 24.5 at 1 month; -136.6 +/- 42.2 vs. -280.1 +/- 29.6 at 3 months, respectively, both p<0.05). At 6 months, these intergroup differences in the reductions of baPWV disappeared. The blunted reduction of baPWV, particularly at 3 months, was significantly associated with the extent of smoking (lifetime pack-years smoked). Changes observed in the AIx and mean BP were similar between groups throughout the study period. In the short term, cigarette smoking blunts the effect of amlodipine on the reduction of arterial stiffness, independently of the mean BP level.

Aged↗

Collagen metabolism in extracellular matrix may be involved in arterial stiffness in older hypertensive patients with left ventricular hypertrophy.

Collagen metabolism in the extracellular matrix (ECM) is related to the pathogenesis of cardiovascular stiffness and remodeling in hypertension. We evaluated the association between collagen metabolism markers and the newly developed parameter, brachial-ankle pulse wave velocity (baPWV), in older hypertensive patients with left ventricular hypertrophy (LVH). We performed echocardiography and baPWV measurement using a new device, form PWV/ABI (Colin Medical Technology, Komaki, Japan), and measured plasma levels of markers of collagen metabolism such as procollagen type I C-terminal propeptide (PICP: a marker of collagen synthesis), collagen type I pyridinoline cross-linked C-terminal telopeptide (ICTP: a marker of collagen type I degradation), matrix metalloproteinase-1 (MMP-1: a marker of collagen degradation) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) in 46 hypertensive patients with LVH. BaPWV was correlated with the plasma level of PICP (r=0.33, p=0.03) and ICTP (r=0.29, p=0.05) and the total TIMP-1/MMP-1 ratio (an index of collagen turnover; r=0.30, p=0.04). BaPWV was negatively correlated with the E/A ratio of left ventricular inflow (r=-0.36, p<0.05), while baPWV was not correlated with left ventricular mass index (LVMI; r=-0.175, p=0.25) or deceleration time of the mitral E wave (DCT; r=0.15, p=0.31). The measures of hypertensive heart disease, such as the E/A ratio, DCT or LVMI were not correlated with any collagen markers in this study. In multiple regression analysis adjusted for confounding factors such as age, sex, pulse pressure, mean blood pressure, pulse rate, LVMI, E/A ratio and DCT, the positive correlation between baPWV and total TIMP-1/MMP-1 ratio remained significant (p<0.05). In conclusion, arterial stiffness in high-risk older hypertensive patients may involve ECM collagen metabolism.

Aged↗

Comparison of valsartan and amlodipine on ambulatory and morning blood pressure in hypertensive patients.

BACKGROUND: Cardiovascular events occur most frequently in the morning. We aimed to study the effects of monotherapy with the long-acting angiotensin II receptor blocker valsartan compared with the long-acting calcium antagonist amlodipine on ambulatory and morning blood pressure (BP). METHODS: We performed ambulatory BP monitoring before and after once-daily dose of valsartan (valsartan group, n = 38) and amlodipine (amlodipine group, n = 38) therapy in 76 hypertensive patients. To achieve the target BP of < or =140/90 mm Hg, valsartan was titrated from 40 mg/day to 160 mg/day (mean dose 124 mg/day) and amlodipine was titrated from 2.5 mg/day to 10 mg/day (mean dose 6.4 mg/day). RESULTS: Both drugs significantly reduced clinic and 24-h systolic BP (SBP) and diastolic BP (DBP) (P <.002). However, the antihypertensive effect of amlodipine was superior to that of valsartan in clinical SBP (-26 mm Hg v -13 mm Hg, P =.001) and 24-h SBP (-14 mm Hg v -7 mm Hg, P =.008). In addition, morning SBP was significantly reduced by amlodipine from 156 to 142 mm Hg (P <.001) but not by valsartan. Both agents reduced lowest night SBP to a similar extent (amlodipine 121 to 112 mm Hg, P <.001; valsartan 123 to 114 mm Hg, P <.002). Reduction in morning SBP surge (morning SBP minus lowest night SBP) was significantly greater in patients treated with amlodipine compared with those treated with valsartan (-6.1 mm Hg v +4.5 mm Hg, P <.02). CONCLUSIONS: Amlodipine monotherapy was more effective than valsartan monotherapy in controlling 24-h ambulatory BP and morning BP in hypertensive patients.

Aged↗

Sleep pulse pressure and awake mean pressure as independent predictors for stroke in older hypertensive patients.

BACKGROUND: It remains uncertain which is the stronger predictor for stroke in older hypertensives, ambulatory pulse pressure (PP) or mean blood pressure (MBP). METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Aged↗

Morning blood pressure surge and hypertensive cerebrovascular disease: role of the alpha adrenergic sympathetic nervous system.

BACKGROUND: The morning surge of blood pressure (BP) is associated with alpha-adrenergic activity. We studied the association between the alpha-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 alpha1-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 alpha-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 > or = 45 mm Hg, n = 24) than in the Nonsurge group (MBPS < 45 mm Hg, n = 74) (54% v 31%, P = .04), and in the higher alpha-adrenergic surge group (top quartile: alpha-adrenergic MBPS > or = 28 mm Hg, n = 25) than in the lower alpha-adrenergic surge group (< 28 mm Hg, n = 73) (68% v 26%, P < .0001). In the Surge group, subjects with higher alpha-adrenergic surge (n = 17) had a markedly higher frequency of multiple SCI, whereas none in the lower alpha-adrenergic surge group had multiple SCI (n = 7) (77% v 0%, P = .001). The alpha-adrenergic MBPS was closely associated with multiple SCI (10 mm Hg increase: OR = 1.96, P = .006), independently of age, MBPS, 24-h systolic BP, and other confounding factors. CONCLUSION: The morning BP surge, particularly that dependent on alpha-adrenergic activity, is closely associated with advanced silent hypertensive cerebrovascular disease in elderly individuals.

Adrenergic alpha-Antagonists↗