Sleep-related breathing disorder is an independent risk factor for systemic hypertension

The exact influence of sleep-related breathing disorder (SRBD) on blood pressure control remains unknown. We investigated the influence of different degrees of SRBD on daytime blood pressure and its association to documented hypertension by examining 1,190 consecutive patients referred for diagnosis of SRBD. The protocol includes clinical interview, physical examination, office blood pressure measurement, cholesterol, and blood gas analysis. Unattended home monitoring of nocturnal breathing was performed for assessment of SRBD activity (respiratory disturbance index [RDI]). RDI was independently and linearly associated with systolic blood pressure (unstandardized coefficient [B] = 0.07 +/- 0.03, p = 0.03), diastolic blood pressure (B = 0.07 +/- 0.02, p = 0 < 0.001), and heart rate (B = 0.10 +/- 0.02, p < 0.001) at rest. The relative risk for hypertension (blood pressure >/= 160/95 mm Hg) increased with SRBD severity (odds ratio [OR], 4.15 for RDI >/= 40 versus < 5 [95% CI, 2.7 to 6.5]). This relative risk was also elevated in younger ( 50 yr) (OR, 7.15 versus 2.70 for RDI >/= 40 versus < 5). These cross-sectional clinical data suggest a relationship between SRBD severity and systolic blood pressure, diastolic blood pressure, and heart rate after control for confounders such as body mass index (BMI), age, alcohol/nicotine consumption, cholesterol level, and daytime PO(2) and PCO(2). SRBD is an independent risk factor for systemic hypertension with an increased likelihood in subjects 相似文献   

Sleep-related breathing disorder is an independent risk factor for uncontrolled hypertension

OBJECTIVE: To test the hypothesis that sleep-related breathing disorder (SRBD) is associated with poor blood pressure control in hypertensive patients independent from confounding factors such as age, body mass index, alcohol, smoking and daytime blood gases. DESIGN AND METHODS: This cross-sectional study of a sleep laboratory cohort was carried out at the University Hospital Sleep Disorders Centre, Marburg. The study comprised 599 patients referred for a sleep study, all of them with a documented history of systemic hypertension and/or previously initiated antihypertensive therapy. Data were obtained from a clinical interview, two unattended sleep studies and assessment of clinic blood pressure, cholesterol level, alcohol and nicotine consumption and daytime blood gases. The main outcome measure was a post hoc analysis of predictors for poor blood pressure control. RESULTS: Respiratory disturbance index (RDI) was significantly higher in patients with uncontrolled hypertension (blood pressure > or = 160 and/or 95 mmHg, n = 463) than in those with controlled hypertension (n = 136) (34.0 +/- 26.8 versus 27.0 +/- 23.5, P < 0.01). The relative proportion of patients with uncontrolled hypertension increased significantly as SRBD activity increased (chi2, P< 0.05). Body mass index was the only independent predictor (P = 0.006) of uncontrolled hypertension in the whole study sample. However, in the subset of patients aged < or = 50 years, RDI (P= 0.006) and age (P = 0.016) were the only independent predictors. The probability of uncontrolled hypertension increased by approximately 2% (B = 0.019, P= 0.006) for each RDI unit. CONCLUSION: SRBD should be considered, in addition to traditional confounders, as a risk factor for poor blood pressure control in younger hypertensive patients (< or = 50 years of age).     

The effects of continuous positive airway pressure on prehypertension and masked hypertension in men with severe obstructive sleep apnea

Obstructive sleep apnea and hypertension are common conditions that frequently coexist. Continuous positive airway pressure (CPAP) reduces blood pressure in patients with obstructive sleep apnea and sustained hypertension. However, the impact of CPAP on patients with obstructive sleep apnea and prehypertension and masked hypertension, conditions associated with increased cardiovascular risk, is unknown. Thirty-six male patients (age, 43 ± 7 years; body mass index, 28.8 ± 3.0 kg/m(2)) with untreated severe obstructive sleep apnea (apnea-hypopnea index, 56 ± 22 events/hr on polysomnography) with diagnostic criteria for prehypertension and/or masked hypertension, based on office and 24-hour ambulatory blood pressure monitoring, respectively, were studied. The patients randomized to no treatment (control; n=18) or CPAP (n=18) for 3 months had similar frequency of prehypertension and masked hypertension at study entry. There were no significant changes in blood pressure in patients randomized to the control group. In contrast, patients randomized to CPAP presented significant reduction in office systolic (from 126 ± 5 to 121 ± 7 mm Hg; P=0.001) and a trend for diastolic blood pressure (from 75 ±7 to 73 ± 8 mm Hg; P=0.08) as well as a significant decrease in daytime and nighttime systolic and diastolic blood pressure (P<0.05 for each comparison). There was a significant reduction in the frequency of prehypertension (from 94% to 55%; P=0.02) and masked hypertension (from 39% to 5%; P=0.04) only in the CPAP group. In conclusion, effective CPAP therapy promotes significant reduction in the frequency of prehypertension and masked hypertension by promoting significant blood pressure reductions in patients with severe obstructive sleep apnea.     

At 68 years, unrecognised sleep apnoea is associated with elevated ambulatory blood pressure

After the age of 65 yrs the specific impact of unrecognised sleep-related breathing disorders (SRBD) on 24-h blood pressure (BP) levels remains under debate. We tested the cross-sectional relationship between the severity of obstructive sleep apnoea/hypopnoea (OSAH) and the increase of BP using ambulatory BP monitoring (ABPM) in the PROOF (PROgnostic indicator OF cardiovascular and cerebrovascular events study)-SYNAPSE (Autonomic Nervous System Activity, Aging and Sleep Apnea/Hypopnea study) cohort. 470 subjects (aged 68 yrs) neither treated for hypertension nor diagnosed for SRBD were included. All subjects underwent ABPM, and unattended at-home polygraphic studies. OSAH was defined by an apnoea/hypopnoea index (AHI) >15·h(-1). The severity of the sleep apnoea was also quantified as the index of dips in oxyhaemoglobin saturation >3% (ODI). Results are expressed in per protocol analysis. Severe OSAH (AHI >30·h(-1), 17% of subjects) was associated with a significant 5 mmHg increase in both diurnal and nocturnal systolic BP (SBP), and with a nocturnal 3 mmHg increase in diastolic BP (DBP). Systolic (mean SBP >135 mmHg) or diastolic (mean DBP >80 mmHg) hypertension were more frequently encountered in subjects suffering from moderate (AHI 15-30) or severe OSAH. After adjustment, the independent association between severe OSAH and 24-h systolic hypertension remained significant (OR 2.42, 95% CI 1.1-5.4). The relationship was further reinforced when SRBD severity was expressed using ODI >10·h(-1). The impact of unrecognised SRBD on BP levels also exists at the age of 68 yrs. The hypoxaemic load appears to be the pathophysiological cornerstone for such a relationship.     

Comparison between office and ambulatory blood pressure in young and elderly subjects with isolated systolic hypertension

BACKGROUND: It has been claimed that isolated systolic hypertension (ISH) in the elderly is not a sustained condition but a short-lasting increase in office systolic blood pressure magnified by arterial stiffness. DESIGN: Office and ambulatory blood pressures werecompared at baseline and after 3 months of observation of young and elderly subjects with ISH. METHODS: The study was carried out in 39 young (mean age 27.1+/-9.8 years) and 37 elderly patients (mean age 72.5+/-5.7 years). Office blood pressure was defined as the mean of six readings. All subjects underwent two non-invasive 24 h blood pressure monitorings performed 3 months apart and echocardiography (n = 50). RESULTS: The difference between office and mean 24 h systolic/diastolic blood pressure was 27.9/8.2 mmHg in the young and 18.9/6.9 mmHg in the elderly patients (P < 0.01 for systolic blood pressure). Twenty-four-hour (P < 0.001), daytime (P = 0.001) and night-time (P < 0.001) systolic blood pressures were higher in the elderly and the difference between daytime and night-time systolic blood pressure was greater in the young (P < 0.05). Office and ambulatory heart rates were significantly higher in the young subjects. The elderly patients showed a greater left ventricular wall thickness ( P = 0.005 for posterior wall; P < 0.005 for septum), relative wall thickness (P = 0.01) and left ventricular mass index (P = 0.001) and impaired left ventricular filling rate ( P = 0.05), whereas systolic performance and stroke volume were no different in the two groups. Due to the higher heart rate, cardiac output was greater in the young (P = 0.03). CONCLUSION: These data show that larger differences between office and ambulatory systolic blood pressure are not unique to elderly patients with ISH. Increased ambulatory blood pressure levels and a decreased nocturnal blood pressure fall were associated with left ventricular structural and functional abnormalities in the elderly subjects.     

高血压合并阻塞性睡眠呼吸暂停患者的血压变异性

目的探讨高血压合并阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者的血压变异性特点。方法纳入疑似OSAHS的高血压患者217例,根据睡眠呼吸暂停低通气指数(AHI)分为4组:非OSAHS组(33例),轻度OSAHS组(57例),中度OSAHS组(68例),重度OSAHS组(59例),比较各组患者血生化指标、血压及血压变异性,分析AHI与血压变异性的关系。结果 4组患者的体质量指数(BMI)和血压变异性明显不同,随睡眠呼吸暂停的严重程度增加而增大(P<0.05)。以BMI进行分层后,超重及肥胖高血压患者的夜间血压变异性随睡眠呼吸暂停严重程度的增加而增大(P<0.05)。偏相关分析显示控制年龄、BMI、血压后,AHI与24h收缩压变异性、24h舒张压变异性、白昼收缩压变异性、白昼舒张压变异性、夜间收缩压变异性及夜间舒张压变异性呈正相关(分别r=0.346,0.414,0.263,0.324,0.445,0.570,均P<0.05)。结论 AHI与血压变异性相关,睡眠呼吸暂停对夜间血压变异性影响更为明显。     

Relationship between 24-H blood pressure and sleep disordered breathing in a normotensive community sample

Sleep disordered breathing (SDB) and hypertension are commonly associated. In this study, we assessed how longitudinal measures of SDB predict a 24-h ambulatory blood pressure monitoring (ABPM) profile. Participants (n = 82) were recruited from a community-based urban (26% African American) sample and included family members of patients with laboratory diagnosed SDB (cases) and family members of neighborhood control subjects evaluated at baseline and at 5 years. Nearly all participants were normotensive and were not receiving therapy for SDB. During both examinations, the respiratory distress index (RDI) was assessed with overnight in-home polysomnography. Seated blood pressure (BP) was assessed at a baseline examination (t₁) and after a 5-year follow-up period (t₅), when 24-h ABPM also was performed.The change in RDI (t₅−t₁) over 5 years was significantly associated with 24-h mean systolic blood pressure (SBP) (P = .04), 24-h maximum diastolic blood pressure (DBP) (P = .03), sleep mean SBP (P = .05), sleep mean DBP (P < .05), and sleep maximum SBP (P = .02). Regression analysis revealed that average 24-h mean arterial pressure (MAP) and mean 24-h DBP were each best predicted by change in RDI, explaining 5% of the variance in these 24-h BP readings, and by current smoking status. After accounting for these variables, BP was not predicted by any of the other potential confounders (all P > .10). Mean RDI (averaged between t₅ and t₁) was associated with mean MAP, mean SBP, and maximal SBP measured during sleep. This study documents for the first time the association between changes in sleep apnea activity and BP and in a community-based normotensive sample. Further long-term evaluation of the effects of these findings and the long-term consequences of hypertension are needed.     

Blood pressure load determines left ventricular mass in essential hypertension.

In a series of 35 newly diagnosed, previously untreated patients (mean age 46 years) with mild to moderate essential hypertension, office blood pressure measurements, 24-hour ambulatory blood pressure monitoring, and determination of left ventricular mass index by echocardiography according to the formula of Devereux were performed. We aimed at correlating left ventricular mass index with systolic and diastolic office blood pressure, mean 24-hour systolic and mean 24-hour diastolic blood pressure, systolic and diastolic load. Left ventricular mass index did not correlate with office systolic and office diastolic blood pressure. On the contrary, all correlations with ambulatory blood pressure parameters and left ventricular mass index turned out to be significant (mean 24-hour systolic blood pressure: r = 0.344, P = 0.026; systolic load: r = 0.408, P = 0.020; mean 24-hour diastolic blood pressure: r = 0.490, P = 0.004; diastolic load: r = 0.504, P = 0.003). These results clearly demonstrate that ambulatory blood pressure determinants but not the office blood pressure parameters are well correlated with left ventricular mass index in mild to moderate essential hypertension. Blood pressure load is as important as mean 24-hour blood pressure in this regard.     

睡眠障碍与高血压患者血压变异性及冠心病的相关性分析

目的探讨睡眠障碍对高血压患者血压变异性及冠状动脉粥样硬化性心脏病(冠心病)的影响。方法入选2015年7月至2018年6月于烟台市莱阳中心医院心内科住院高血压受试者242例,年龄36~72岁,由同一研究小组完成24 h动态血压监测,依据匹茨堡睡眠指数(PSQI)量表对受试者睡眠状况进行评估分组,PSQI≤7分为睡眠良好组(n=155),PSQI>7分为睡眠障碍组(n=87),分析两组动态血压参数的差异,并评价血压波动状况与冠心病的关系。结果睡眠障碍组体质量指数、空腹血糖、糖化血红蛋白(HbA1c)、冠心病比例高于睡眠良好组(P<0.05或P<0.01)。睡眠障碍组异常血压节律比例高于睡眠良好组(72.4%vs.52.3%,χ^2=9.395,P=0.002)。睡眠障碍组24 h平均收缩压(24 hSBP)、白天平均收缩压(dSBP)、夜间平均收缩压(nSBP)、白天收缩压平台、夜间收缩压平台、清晨收缩压上升速度水平[(15.0±8.8)vs.(11.1±9.2)mmHg/h]高于睡眠良好组(P均<0.01),而夜间舒张压下降速度慢于睡眠良好组(P<0.05)。单因素相关分析显示:24 hSBP、白天收缩压平台、夜间收缩压平台和清晨收缩压上升速度与PSQI评分密切相关(r=0.481,0.370,0.390,0.208,P均<0.05)。睡眠障碍冠心病的患病率要高于睡眠良好组(57.5%vs.31.6%,P<0.001),在校正相关因素后,Logistic回归分析显示:吸烟(OR=6.023,95%CI:3.108~11.672,P<0.001)、睡眠障碍(OR=2.970,95%CI:1.618~5.452,P<0.001)、清晨收缩压上升速度(OR=1.048,95%CI:1.015~1.083,P=0.004)是冠心病的独立危险因素。结论睡眠障碍会升高高血压患者血压水平,加剧清晨血压波动及减慢夜间血压下降速度,睡眠障碍和清晨收缩压上升速度加快可能是冠心病发生的危险因素。     

The effect of sibutramine-assisted weight loss in men with obstructive sleep apnoea

OBJECTIVE: Obstructive sleep apnoea (OSA) occurs frequently in obese patients and may be reversible with weight loss. Obstructive sleep apnoea and obesity are both independent risk factors for hypertension and increased sympathetic activity. Sibutramine has been increasingly used in the management of obesity, but is relatively contraindicated in patients with hypertension. No studies have investigated the effect of sibutramine on OSA, blood pressure and heart rate. We aimed to assess the changes in OSA and cardiovascular parameters in obese men with OSA enrolled in a sibutramine-assisted weight loss programme (SIB-WL). DESIGN: Open uncontrolled cohort study of obese male subjects with OSA in an SIB-WL. SUBJECTS: Eighty-seven obese (body mass index =34.2+/-2.8 kg/m(2)) middle-aged (46.3+/-9.3 years) male subjects with symptomatic OSA (Epworth score 13.4+/-3.6; respiratory disturbance index (RDI) 46.0+/-23.1 events/h) completed the study. RESULTS: At 6 months, there was significant weight loss (8.3+/-4.7 kg, P<0.0001), as well as a reduction in waist and neck circumference and sagittal height (all P<0.0001). These changes were accompanied by a reduction in OSA severity (RDI fell by 16.3+/-19.4 events/h and Epworth score by 4.5+/-4.6), both P<0.0001). There was no significant change to systolic (P=0.07) or diastolic blood pressure (P=0.87); however, there was a mild rise in resting heart rate (P<0.0001). CONCLUSION: Moderate (approximately 10%) weight loss with SIB-WL results in improvement in OSA severity without increase in blood pressure in closely monitored OSA subjects.     

Pulse pressure is more susceptible to the white coat effect than is systolic blood pressure: observations from real-life ambulatory blood pressure monitoring

BACKGROUND: Pulse pressure is a derivative of arterial stiffness. We have previously demonstrated ambulatory pulse pressure to be relatively independent from the blood pressure (BP) lowering during sleep, and thus of a neurogenic effect. On the other hand, white coat BP effects are thought to involve neurogenic activation. The aim of this work was to analyze white coat induced variability in pulse pressure. METHODS: Percent clinic-awake differences in systolic BP (SBP) and pulse pressure (white coat effects) were calculated for 688 consecutive subjects (mean age 60 +/- 16 years, 58% female). Of the subjects, 23% had controlled hypertension, 45% uncontrolled hypertension, 8% normotension, and 4% isolated office hypertension; all were referred to our unit for 24 h ambulatory BP monitoring. RESULTS: Pulse pressure highly correlated with SBP (r = 0.82, P <.00001). We found a larger white coat effect on pulse pressure than on SBP (8.3% and 5.2%, respectively, P < or =.0001). This was true in all subgroups except in normotensive subjects. Specifically, the magnitude of the white coat effect on pulse pressure was greater than on SBP in subjects with treated hypertension, untreated hypertension, and isolated office hypertension, and in young hypertensive subjects, older subjects, and those with diabetes. CONCLUSIONS: Although pulse pressure is related to the mechanical properties of large arteries, it is also influenced by the white coat effect, a neurogenic process. Furthermore, in hypertensive but not in normotensive subjects, the white coat effect on pulse pressure is significantly more pronounced than on SBP.     

Echocardiographic parameters in adolescents with sleep-related breathing disorders

Few data are known about the effects of sleep-related breathing disorders (SRBD) on the cardiovascular system in adolescents. Forty healthy adolescents (mean age, 13.7 +/- 1.6 years) answered a questionnaire regarding symptoms of sleep-related breathing disorders (SRBD) and underwent a cardiorespiratory polygraphy and echocardiography. Echocardiographic data in snorers with polygraphic abnormalities suggestive of SRBD (positive group, n = 29) were compared with the results in nonsnorers without polygraphic abnormalities (n = 11) who were included in the control group. Ventricular dimensions and indices of left ventricular systolic function were within normal limits and were not significantly different between the two groups. Indices of left ventricular diastolic function were also within normal limits, but isovolumetric relaxation time (IVRT) was significantly longer among the positive group (72.5 +/- 8.4 msec) than among the controls (65.1 +/- 7.9 msec) (P = 0.018). Multiple regression analysis showed that posterior wall thickness was predicted by a model that included cardiac events related with respiratory events and/or desaturations, and respiratory disturbance index (RDI) in supine position. Deceleration of early diastolic flow was predicted by RDI, percentage of total recording time with SaO(2) < 90% (CT(90)), and age; the variability of isovolumetric relaxation time was predicted by a model that included RDI in supine position. We found a significant relationship between polygraphic parameters suggestive of SRBD and echocardiographic measurements of ventricular dimensions and diastolic function. Also, echocardiographic parameters suggestive of some degree of left ventricular diastolic dysfunction were found in snoring adolescents with polygraphic abnormalities.     

Office hypertension: abnormal blood pressure regulation and increased sympathetic activity compared with normotension

BACKGROUND: The percentage of patients with office or white-coat hypertension has been reported in international studies to be 20-30% of the hypertensive population. These patients can be identified and distinguished from patients with established hypertension by ambulatory blood pressure monitoring (ABPM) or self-measurement. There is still no satisfactory explanation for the phenomenon of 'office hypertension' and there are no data available to show how the blood pressure behaviour of office hypertensives differs from that of normotensive subjects away from the physician's office or clinic environment. OBJECTIVE: To investigate the blood pressure behaviour of patients with office hypertension away from the clinical setting over a 24 h period and to compare it with that of normotensive subjects. DESIGN AND METHODS: The blood pressure and heart rate of 36 patients with office hyhpertension and 33 normotensive subjects matched for age and sex were measured in a hypertension outpatient clinic and over 24 h using ABPM. The ambulatory data were subjected both to conventional and to modern rhythm analysis. Urinary catecholamine excretion was measured as a marker of sympathetic activity. RESULTS: In the clinic, the patients with office hypertension had significantly (P < 0.01) higher blood pressure values (146/97 mmHg) than did the normotensive controls (128/81 mmHg). The conventional analysis as well as the rhythm analysis of the ABPM data revealed no difference between the two groups with respect to the 24 h, daytime or night-time mean values and SD. However, the rhythm analysis showed a higher maximum and a lower minimum value for systolic and diastolic blood pressures in the patients with office hypertension, resulting in a greater amplitude both of systolic and of diastolic blood pressure due to a significantly (P < 0.005 and P < 0.05) higher maximum minus minimum value (38/32 mmHg) compared with those of normotensive controls (29/28 mmHg). The early morning rise in systolic and diastolic blood pressures was significantly (P < 0.008 and P < 0.03) greater in the patients with office hypertension (11/9 versus 7/7 mmHg) and intersected the curve of the normotensive controls at approximately 0600 h. No significant differences in heart rate at any time were observed between the groups. The urinary excretion of noradrenaline and dopamine was significantly (P < 0.01 and P < 0.05) increased during daytime for the office hypertensives. CONCLUSION: Patients with office hypertension, who by definition do not yet have established hypertension, already exhibit abnormal regulation both of systolic and of diastolic blood pressure during the morning period and daytime, with a significantly greater early morning rise compared with normotensive subjects and a greater blood pressure amplitude (amplitude hypertension) due to lower blood pressure during night-time and higher blood pressure during the day with increased sympathetic activation. Office hypertension seems to be the earliest manifestation of hypertension.     

Effects of renal sympathetic denervation on blood pressure, sleep apnea course, and glycemic control in patients with resistant hypertension and sleep apnea

Percutaneous renal sympathetic denervation by radiofrequency energy has been reported to reduce blood pressure (BP) by the reduction of renal sympathetic efferent and afferent signaling. We evaluated the effects of this procedure on BP and sleep apnea severity in patients with resistant hypertension and sleep apnea. We studied 10 patients with refractory hypertension and sleep apnea (7 men and 3 women; median age: 49.5 years) who underwent renal denervation and completed 3-month and 6-month follow-up evaluations, including polysomnography and selected blood chemistries, and BP measurements. Antihypertensive regimens were not changed during the 6 months of follow-up. Three and 6 months after the denervation, decreases in office systolic and diastolic BPs were observed (median: -34/-13 mm Hg for systolic and diastolic BPs at 6 months; both P<0.01). Significant decreases were also observed in plasma glucose concentration 2 hours after glucose administration (median: 7.0 versus 6.4 mmol/L; P=0.05) and in hemoglobin A1C level (median: 6.1% versus 5.6%; P<0.05) at 6 months, as well as a decrease in apnea-hypopnea index at 6 months after renal denervation (median: 16.3 versus 4.5 events per hour; P=0.059). In conclusion, catheter-based renal sympathetic denervation lowered BP in patients with refractory hypertension and obstructive sleep apnea, which was accompanied by improvement of sleep apnea severity. Interestingly, there are also accompanying improvements in glucose tolerance. Renal sympathetic denervation may conceivably be a potentially useful option for patients with comorbid refractory hypertension, glucose intolerance, and obstructive sleep apnea, although further studies are needed to confirm these proof-of-concept data.     

Ambulatory blood pressure as an independent determinant of brain atrophy and cognitive function in elderly hypertension

OBJECTIVE: Recent studies have demonstrated a relationship between brain atrophy and hypertension. Systolic hypertension in the elderly has been found to be a risk factor for cognitive impairment. We studied the relationship of ambulatory blood pressure with brain atrophy and cognitive function. METHODS: We performed ambulatory blood pressure monitoring and brain magnetic resonance imaging in 55 unmedicated elderly hypertensive patients (72.7 +/- 6.0 years old). The volume of total brain matter was measured using an intensity contour-mapping algorithm. Cognitive function was assessed by mini-mental state examination score. RESULTS: Total brain matter volume and cognitive function were significantly correlated (r = 0.314, P = 0.02). Total brain matter volume was significantly negatively correlated with age (r = -0.365, P = 0.006), 24-h systolic blood pressure (r = -0.343, P = 0.01), awake systolic blood pressure (r = -0.278, P = 0.04) and sleep systolic blood pressure (r = -0.491, P = 0.0001), and significantly positively correlated with male sex (r = 0.493, P = 0.0001), body mass index (r = 0.282, P = 0.04) and nocturnal systolic blood pressure dipping (r = 0.323, P = 0.02). Mini-mental state examination score was significantly negatively correlated with age (r = -0.277, P = 0.04) and sleep systolic blood pressure (r = -0.360, P = 0.007), and significantly positively correlated with nocturnal systolic blood pressure dipping (r = 0.402, P = 0.002). In multiple linear regression analysis adjusted for age, sex, and body mass index, sleep systolic blood pressure (P = 0.009) was more significantly negatively associated with total brain matter volume than was either 24-h (P = 0.035) or awake (P = 0.020) systolic blood pressure. CONCLUSIONS: In elderly hypertensive patients, absolute ambulatory systolic blood pressure level (particularly during sleep) and nocturnal dipping in systolic blood pressure were strong indicators of brain matter volume and cognitive function.     

Telemedicine home blood pressure measurements and progression of albuminuria in elderly people with diabetes

We assessed whether home blood pressure monitoring improved the prediction of progression of albuminuria when added to office measurements and compared it with ambulatory blood pressure monitoring in a multiethnic cohort of older people (n=392) with diabetes mellitus, without macroalbuminuria, participating in the telemedicine arm of the Informatics for Diabetes Education and Telemedicine Study. Albuminuria was assessed by measuring the spot urine albumin:creatinine ratio at baseline and annually for 3 years. The ambulatory sleep:wake systolic blood pressure ratio was categorized as dipping (ratio: < or =0.9), nondipping (ratio: >0.9 to 1.0), and nocturnal rise (ratio: >1.0). In a repeated-measures mixed linear model, after adjustment that included office pulse pressure, home pulse pressure was independently associated with a higher follow-up albumin:creatinine ratio (P=0.001). That association persisted (P=0.01) after adjusting for 24-hour pulse pressure and nocturnal rise, which were also independent predictors (P=0.02 and P=0.03, respectively). Cox proportional hazards models examined the progression of albuminuria (n=74) as defined by cutoff values used by clinicians. After the adjustment for office pulse pressure, the hazards ratio (95% CI) per 10-mm Hg increment of home pulse pressure was 1.34 (range: 1.1 to 1.7; P=0.01). Home pulse pressure was not an independent predictor in the model including ambulatory monitoring data; a nocturnal rise was the only independent predictor (P=0.035). Cox models built separately for home pulse pressure and ambulatory monitoring exhibited similar calibration and discrimination. In conclusion, nocturnal blood pressure elevation was the strongest predictor of worsening albuminuria. Home blood pressure measurements added to office measurements and may constitute an adequate substitute for ambulatory monitoring.     

Influence of age and severity of hypertension on blood pressure response to isometric handgrip exercise.

The influence of age and severity of hypertension on the blood pressure response to isometric handgrip exercise (IHG) was studied in essential hypertensive patients (n = 122). The change in blood pressure during IHG in elderly patients with isolated systolic hypertension (ISH) (n = 12) was also studied. Left ventricular hypertrophy due to hypertension was used as an index of the severity of hypertension. The change in systolic blood pressure (SBP) during IHG was markedly greater in essential hypertensives than in normotensive subjects (n = 36). Among hypertensive patients, the change in SBP increased with increasing severity of hypertension. This change in SBP was not influenced by age. The change in SBP during IHG in patients with ISH was significantly smaller than that in essential hypertensive patients and was similar to that in normotensive subjects in the elderly. These results demonstrate that age does not affect the increased blood pressure response to IHG in essential hypertensive patients but the greater the severity of hypertension, the greater the increase in SBP during IHG. Elderly patients with ISH do not have an enhanced blood pressure response to IHG.     

广西地区打鼾人群血压状况分析

目的了解广西地区打鼾的发生率、打鼾人群血压状况及打鼾与高血压的相关性。方法2003年1月至2005年3月对广西桂南、桂中、桂北14岁及以上人群进行打鼾的流行病学调查。采用集中填写问卷辅以入户问卷调查的方法收集资料，同时检测受调查者血压、身高、体重等身体参数。结果共抽样调查2862户，11163人，年龄14—99岁，平均年龄（39．6±17．5）岁。其中2940人打鼾，打鼾发生率为27．3％（2940／10758）。非打鼾人群平均收缩压为（122．7±21．7）mmHg（1mmHg=0．133kPa），舒张压为（75．7±13．2）mmHg，高血压患病率为19．9％（1566／7860）。打鼾人群平均收缩压为（128．2±30．9）mmHg，舒张压为（79．3±12．4）mmHg，高血压患病率为31．5％（931／2940）。随着年龄的增加，打鼾的发生率逐渐升高（趋势X^2=592．613，P=0．000），高血压的患病率也逐渐升高（趋势X^2=1868．277，P=0．000）。非习惯性打鼾者高血压患病率为27．6％，习惯性打鼾者高血压患病率37．4％。轻度打鼾者高血压患病率为27．5％，中度为31．1％，重度为37．4％，同时合并（被发现）有睡眠呼吸暂停者为44．1％。可能影响高血压的诸多因素的单因素分析及logistic回归分析结果显示，年龄、民族、打鼾、体重指数、饮酒是高血压的危险因素。控制年龄、民族、体重指数、饮酒等因素后的偏相关分析结果显示，打鼾人群的打鼾程度与收缩压和舒张压均呈正相关。结论广西地区14岁及以上人群打鼾发生率为27．3％。打鼾人群收缩压与舒张压及高血压患病率明显高于非打鼾人群。高血压的患病率随打鼾程度的增加而增加。打鼾程度与收缩压和舒张压均呈正相关。打鼾是除年龄、体重指数、饮酒以外与高血压发生相关的危险因素。     

Assessment of blood pressure control in hypertensive stroke survivors: an ambulatory blood pressure monitoring study

BACKGROUND: We compared the sensitivity of office blood pressure and ambulatory blood pressure monitoring recordings in evaluating the effectiveness of antihypertensive treatment and identified factors related to inadequate blood pressure control among hypertensive stroke survivors. METHODS: Office blood pressure and ambulatory blood pressure monitoring measurements were performed at 120+/-30 days after ictus in 187 first-ever consecutive hypertensive stroke survivors who were receiving blood pressure-lowering medications according to international guidelines. Handicap was assessed by the modified Rankin Scale. Blood pressure was regarded as controlled if office and daytime ambulatory systolic and diastolic blood pressure values were <140/90 and <135/85 mmHg, respectively. Patients were subclassified according to the degree of their nocturnal systolic blood pressure fall [(mean daytime values-mean night-time values)100/mean daytime values] as dippers (>or=10%), nondippers (>or=0% and <10%) and reverse dippers (<0%). RESULTS: Effective blood pressure control was documented in significantly (P<0.001) fewer patients using ambulatory blood pressure monitoring (32.1%) than those using office recordings (43.3%), whereas in 16% of the study population a masked lack of per-treatment blood pressure control (elevated ambulatory blood pressure in the presence of normal office blood pressure levels) was identified. The distribution of dipping patterns differed significantly (P=0.01) between controlled hypertensive individuals (normal office and ambulatory measurements) and patients with isolated ambulatory hypertension (dippers: 31.3 vs. 10.0%; nondippers:56.9 vs. 53.3%; reverse dippers: 11.8 vs. 36.7%). Logistic regression analysis revealed diabetes mellitus and functional independency (modified Rankin Scale score<2) as independent predictors of inadequate blood pressure control. CONCLUSION: Ambulatory blood pressure monitoring detects a substantial number of treated hypertensive stroke survivors with a masked lack of per-treatment blood pressure control, who present a higher prevalence of abnormal circadian blood pressure patterns (reverse dipping). Diabetes mellitus and poststroke functional independency are the main factors contributing to inadequate blood pressure control.     

Recent advances in blood pressure measurement technology: normalized blood pressure measurement with a double-cuff sphygmotonometer

BACKGROUND: In our previous studies of 24-h blood pressure measurement, basal blood pressure (minimum sleep-time blood pressure) showed the strongest correlation with hypertensive target-organ damage. We have currently devised a new accurate method of blood pressure measurement that entails recording casual blood pressure waves by means of a double-cuff sphygmotonometer, and attempted to normalize casual blood pressure to basal blood pressure. METHODS: The double-cuff sphygmotonometer records the arterial pressure wave, from which, using the formula (P0 = phi(-1)(i) x Pi), we attempted a normalization of casual blood pressure (Pi) to values close to those of the basal blood pressure (P0). True basal blood pressure was measured by an indirect ambulatory blood pressure monitoring device (TM2425, A&D Co. Ltd., Tokyo, Japan). The subjects were 54 normotensive volunteers and 156 out-patients with essential hypertension [63 with World Health Organization (WHO)-II stage and 93 with WHO-I stage, including 47 subjects with white-coat hypertension] not receiving medication. RESULTS: The coefficient of correlation (r) between normalized diastolic blood pressure (Pd0') and true diastolic basal blood pressure (Pd0) was 0.82 (mean difference = 1 +/- 9.8 mmHg), that between normalized systolic blood pressure (Ps0') and true systolic basal blood pressure (Ps0) being 0.78 (1 +/- 13 mmHg) in 210 subjects. When an office mean blood pressure (MBP) of 116 mmHg was taken as the standard for identifying the WHO-I group, the sensitivity was 70% (65/93) and the specificity 67% (42/63), but when an MBP0 [MBP0' = (Ps0'-Pd0')/3 + Pd0'] of 89 mmHg was the standard, the sensitivity was 82% (76/93) and the specificity 90% (57/63), both significantly higher than the corresponding values for office MBP (P < 0.05). CONCLUSION: We devised a new double-cuff sphygmotonometer and normalizing function (phi(-1)) and, using these methods, calculated the normalized blood pressure in hypertensive out-patients, which may make it possible to identify degrees of severity of hypertension in terms of WHO stages.