Ambulatory Blood Pressure Variability Is Increased in Diabetic Hypertensives

The purpose of this study was to examine the possible difference in the 24-hr BP profile—including short-term BP variability, assessed as the standard deviation—between diabetic and non-diabetic hypertensives. We measured 24-hr ambulatory BP in 11 diabetic hypertensives (diabetic HT) and 10 non-diabetic hypertensives (non-diabetic HT) who were hospitalized for the educational program in our hospital and were under stable salt intake. Renal function and sleep apnea were also estimated. There were no significant differences in 24-hr systolic BP (141 mmHg vs. 135 mmHg, ns), daytime systolic BP (143 mmHg vs. 138 mmHg, ns), and nighttime systolic BP (135 mmHg vs. 130 mmHg, ns) between diabetic HT and non-diabetic HT. The values of 24‐hr HR (69.7 beats/min vs. 65.2 beats/min, ns) and 24-hr HR variability (9.9 beats/min vs. 10.1 beats/min, ns) were also similar between the groups. Interestingly, diabetic HT had a significantly greater 24-hr systolic and diastolic BP variability than non-diabetic HT (18.2 mmHg vs. 14.5 mmHg, p < 0.05; 11.5 mmHg vs. 9.6 mmHg, p < 0.05, respectively). The values for creatinine clearance, urinary protein excretion, and apnea-hypopnea index were similar between the groups. Bivariate linear regression analysis demonstrated that fasting blood glucose was the primary determinant of 24-hr diastolic BP variability (r = 0.661, p < 0.01). Multiple stepwise regression analysis revealed that fasting blood glucose was a significant and independent contributor to 24-hr systolic BP variability (r = 0.501, p < 0.05). Taken together, these results demonstrate that BP variability is increased in diabetic hypertensives. Furthermore, it is possible that an elevation of fasting blood glucose may contribute to the enhanced BP variability in hypertensives.     

Ambulatory blood pressure and heart rate in hypertensives with renal failure: comparison between diabetic nephropathy and non-diabetic glomerulopathy

The purpose of this study was to examine a possible difference in the 24-h blood pressure (BP) profile between hypertensives with diabetic nephropathy (DN) and those with non-diabetic glomerulopathy (non-DN). We measured 24-h ambulatory BP in 34 type 2 DN and 34 non-DN patients who were hospitalized for the educational program in our hospital. There were no significant differences in 24-h and daytime systolic BP between DN (143 vs. 136 mmHg, NS for 24-h systolic BP) and non-DN (143 vs. 138 mmHg, NS for daytime systolic BP). Although both groups disclosed blunted nocturnal decrease in BP and were classified as "non-dipper" type, DN patients had a significantly higher nighttime systolic BP than patients with non-DN (142 vs. 132 mmHg, p = 0.0217). BP and heart rate (HR) variabilities were also estimated, and patients with DN showed a reduced nighttime HR variability than those with non-DN (4.8 vs. 6.6 beats/min, p = 0.0115). DN patients had an increase in urinary protein excretion (3.0 vs. 1.4 g/day, p = 0.0095) and a decrease in serum albumin concentration (3.1 vs. 3.7 mg/dl, p < 0.0001). Furthermore, urinary protein excretion was significantly correlated with nighttime systolic BP (r = 0.480, p = 0.0031) but not with nighttime HR variability. Taken together, these results demonstrate that the circadian rhythms of BP and HR are affected by underlying diseases and suggest that an elevated nighttime BP level may contribute to the enhanced urinary protein excretion in hypertensives with DN.     

Ambulatory Blood Pressure and Heart Rate in Hypertensives with Renal Failure: Comparison between Diabetic Nephropathy and Non-Diabetic Glomerulopathy

The purpose of this study was to examine a possible difference in the 24-h blood pressure (BP) profile between hypertensives with diabetic nephropathy (DN) and those with non-diabetic glomerulopathy (non-DN). We measured 24-h ambulatory BP in 34 type 2 DN and 34 non-DN patients who were hospitalized for the educational program in our hospital. There were no significant differences in 24-h and daytime systolic BP between DN (143 vs. 136 mmHg, NS for 24-h systolic BP) and non-DN (143 vs. 138 mmHg, NS for daytime systolic BP). Although both groups disclosed blunted nocturnal decrease in BP and were classified as “non-dipper” type, DN patients had a significantly higher nighttime systolic BP than patients with non-DN (142 vs. 132 mmHg, p?=?0.0217). BP and heart rate (HR) variabilities were also estimated, and patients with DN showed a reduced nighttime HR variability than those with non-DN (4.8 vs. 6.6 beats/min, p?=?0.0115). DN patients had an increase in urinary protein excretion (3.0 vs. 1.4 g/day, p?=?0.0095) and a decrease in serum albumin concentration (3.1 vs. 3.7 mg/dl, p < 0.0001). Furthermore, urinary protein excretion was significantly correlated with nighttime systolic BP (r?=?0.480, p?=?0.0031) but not with nighttime HR variability. Taken together, these results demonstrate that the circadian rhythms of BP and HR are affected by underlying diseases and suggest that an elevated nighttime BP level may contribute to the enhanced urinary protein excretion in hypertensives with DN.     

Sequelae of Acute Hypoglycaemia on 24 hour Blood Pressure and Metabolic Parameters in Normal and Type 1 (Insulin-dependent) Diabetic Individuals

This study was performed to assess possible delayed after-effects of acute hypoglycaemia on blood pressure (BP) and heart rate (HR) over a 24-h period. Eleven insulin-dependent diabetic patients and 11 sex, age, and body mass index matched non-diabetic subjects were studied. Blood pressure was measured using a non-invasive ambulatory blood pressure monitor following acutely induced hypoglycaemia in the morning. No significant differences were observed in 24-h systolic and diastolic BP and HR in either groups, between the day when hypoglycaemia was induced and the day when plasma glucose was kept normal. In diabetic patients, hypoglycaemia induced a temporary but significant fall in mean BP (-7 ± 1 mmHg vs -2 ± 2; p < 0.05). Plasma glucose levels were significantly higher in insulin-dependent diabetic patients following hypoglycaemia than in those observed during the reference test. This study demonstrates that acute hypoglycaemia in insulin-dependent diabetic subjects does not cause significant alterations in 24-h BP in either diabetic or normal subjects.     

Blood pressure and heart rate of students undergoing a medical licensing examination

AIMS: To assess the effect of a real life mental stress situation on blood pressure (BP) and heart rate (HR) in students undergoing a medical licensing examination. METHOD: Prospective observational study of 121 medical students taking the final licensing exam. BP and HR were taken before and after the exam. Additionally, BP was measured by ambulatory BP monitoring device and HR was recorded continuously by an HR monitor belt in 25 students throughout the examination. MAJOR FINDINGS: Diastolic BP (DBP) increased from 81 +/- 10 mmHg before the exam to 86 +/- 9 mmHg (p = 0.008) during the exam and to 88 +/- 11 mmHg, (p = 0.007) 15 min after the exam. Systolic BP (SBP) did not increase significantly during (from 131 +/- 14 before the exam to 136 +/- 18 mmHg) and after the exam (135 +/- 16 mmHg). HR decreased during (to 100 +/- 18 beats/min, p < 0.001), and after the exam (to 95 +/- 19 beats/min, p < 0.001) compared to values before the exam (114 +/- 19 beats/min). SBP was higher in male students compared to female students before (138 +/- 10 vs 125 +/- 18 mmHg) and after (126 +/- 18 vs 115 +/- 17 mmHg) the exam (p < 0.01). CONCLUSION: Only DBP increased during medical licensing examination, albeit within a small range. SBP did not change significantly and HR decreased during the exam. Male students showed a higher SBP compared to female students.     

Home ambulatory blood pressure readings do not differ from clinic readings taken at the same time of day

In most hypertensives clinic blood pressure (BP) is variably higher than home BP, but the underlying mechanisms are uncertain. We investigated whether the 24-hour ambulatory home BP profile as well as the office-home BP discrepancy could vary with the time of day of application of the recording system (from 08.00 h to 19.00 h) in 135 untreated hypertensives who underwent non-invasive home BP monitoring (ICR 5200). Neither systolic nor diastolic 24-hour home BP (average of daily readings, area-under-the-curve) varied significantly with the time of day of application of the system. Clinic BP was about 12% higher than 24-hour home BP in the whole population, mean values being 161.4/102.9 mmHg (office BP) vs 141.2/90.8 mmHg (average 24-hour home readings), as well as in each of the subcohorts based on the time of day of application of the system (all P less than 0.01). However, in none of the subcohorts were there any statistically significant differences between clinic BP and home BP readings taken at the same time of day as the clinic readings. No correlation was found between clinic heart rate and clinic-home discrepancy. We conclude that in essential hypertension 24-hr non-invasive ambulatory BP monitoring can begin indifferently from 08.00 h to 19.00 h with no expected influence of time of application on results and that clinic BP is not dissimilar from home BP at the same time of day.     

Blood pressure on arising, morning blood pressure surge and blood pressure variability in white coat hypertensives and in matched normotensives and sustained hypertensives.

INTRODUCTION: It is still controversial whether subjects with white-coat hypertension (WCHT) exhibit higher cardiovascular risk compared to normotensive subjects (NT). In subjects with WCHT it is not known whether the abnormal blood pressure (BP) reaction in the office also occurs at other times of day, particularly on arising and immediately after waking, i.e. the times at which the majority of cardiovascular events are reported to occur. OBJECTIVE AND METHODS: To evaluate with 24h ambulatory BP measurement the values of morning BP surge, BP on arising and BP variability in subjects with WCHT in comparison with age-, gender- and weight-matched normotensives (BP) and untreated sustained hypertensives (BP). RESULTS: Groups of BP, WCHT and BP were matched for age, gender and body weight: BP: n=69, age 49 +/- 7 years, 54 % female, BMI 26 +/- 1, casual BP 126/79 +/- 5/4 mmHg, daytime BP 124/80 +/- 6/6 mmHg; WCHT: n=74, age 52 +/- 8 years, 57% female, BMI 26 +/- 2, casual BP 152/95 +/- 7/7 mmHg, daytime BP 126/80 +/- 5/6 mmHg; HT: n=79, age 53 +/- 7 years, 56% female, BMI 27 +/- 2, casual BP 154/97 +/- 9/8 mmHg, daytime BP 143/89 +/- 12/10 mmHg. Of the three groups, subjects with WCHT exhibited BP on arising (121/81 +/- 13/8 mmHg) similar to that of NTs (120/80 +/- 13/9 mmHg, NS), both significantly lower than that of HTs (137/92 +/- 17/10 mmHg, p < 0.01), suggesting the absence of an alerting BP reaction in WCHT at that time. By contrast, subjects with WCHT showed higher values of systolic morning BP surge vs. NTs (25 +/- 10 vs. 22 +/- 11 mmHg, p < 0.05), both lower than that observed in hypertensives (33 +/- 11 mmHg, p < 0.01 vs. NT and WCHT) and greater daytime variability (systolic BP standard variation), i.e. 12 2 vs. 10 +/- 2 mmHg, p < 0.05, both lower than that observed in hypertensives (14 +/- 3 mmHg, p < 0.01 vs. NT and WCHT). CONCLUSIONS: Although subjects with WCHT did not show any alerting blood pressure reaction on arising, morning BP surge and BP variability were greater in these subjects than in control normotensives, although lower than sustained hypertensives. Although this is still speculative, we cannot exclude the possibility that even a slight increase in morning BP surge might in the long term constitute an additional load on the circulation that could increase cardiovascular risk in subjects with WCHT compared to matched normotensives.     

合并阻塞性睡眠呼吸暂停的高血压患者血压变异性和靶器官损害的研究

目的阻塞性睡眠呼吸暂停（OSA）引发睡眠期间血流动力学变化,增加夜间血压变异性,加重靶器官损害,但这种影响可能受年龄的干扰。方法143例多导睡眠诊断的OSA患者分为3组：〈60岁高血压组（62例）、〈60岁正常血压组（38例）和〉60岁正常血压组（43例）,全部进行24h动态血压监测,分析白天和夜间血压变化的标准差（SD）和变异系数（CV）,在排除年龄干扰因素外,判断OSA对血压变异性的影响及靶器官的损害情况。结果与〈60岁正常血压组相比,高血压组白天和夜间血压变化SD明显增加,白天收缩压18．5和10．6mmHg（P〈O．05）;白天舒张压13．8和10．6mmHg（P〈0．05）;夜间收缩压20．5和12．6mmHg（P〈0．01）;夜间舒张压17．8和12．6mmHg（P〈O．01）。血压CV也明显增加,白天收缩压0．119和0．078（P〈0．01）;白天舒张压0．139和0．118（P〈0．05）;夜间收缩压0．137和0．111（P〈0．01）;夜间舒张压0．195和0．177（P〈O．01）。与〉60岁正常血压组相比,高血压组白天和夜间血压变化SD明显增加,白天收缩压18．5和13．3mmHg（P〈O．05）;白天舒张压13．8和10．2mmHg（P〈O．05）;夜间收缩压20．5和15．2mmHg（P〈0．01）;夜间舒张压17．8和14．2mmHg（P〈0．01）。白天收缩压CV增加（0．119和0．093;P〈O．05）;夜间收缩压和舒张压CV增加（O．137和0．123;P〈0．01;0．195和0．179;P〈0．05）。与〈60岁正常血压组相比,〉60岁正常血压组白天收缩压CV增加（0．093和0．078;P〈O．05）。与〈60或〉60岁正常血压组相比,高血压组靶器官损害增加（P〈0．01）。与〈60岁正常血压组相比,〉60岁正常血压组靶器官损害也增加（P〈0．05）。结论尽管年龄可能影响血压变异性,但是OSA对血压变异性的影响明显超过年龄的作用,并加重靶器官损害。因此,对于合并OSA的老年高血压患者更应给予足够重视。     

Ambulatory blood pressure monitoring and clinical characteristics of the true and white-coat resistant hypertension

The resistant hypertension has been differentiated in true resistant hypertension and white-coat resistant hypertension by using ambulatory blood pressure monitoring. White-coat resistant hypertension was defined as high clinic blood pressure, despite triple treatment for at least 3 months, but day-time blood pressure values < 135/85 mmHg. The aim of this study was to evaluate the presence of different clinical characteristics between two types of resistant hypertension. The study group consisted of 49 patients with essential hypertension, resistant to an adequate and appropriate triple-drug therapy, that included a diuretic, with all 3 drugs prescribed in near maximal doses and that had persistently elevated clinic blood pressure (> 140/90 mm Hg), for at least 3 months. They represented the 2% of 2500 hypertensive outpatients that referred at our Hypertension Unit. Patients with white-coat resistant hypertension (n=19) were older (p<0.05) than those with true resistant hypertension (n=30). The sodium intake (p<0.05) and alcohol intake (p<0.05) were significantly higher in patients with true resistant hypertension than in those with white-coat resistant hypertension. The renin plasma activity and plasma aldosterone were higher (p<0.05) in patients with true resistant hypertension than in those with white-coat resistant hypertension with normal plasma electrolyte balance. There were no significant differences in mean values of office systolic and diastolic blood pressures between white coat resistant hypertensives and true resistant hypertensives (165+17 vs 172+28 and 98+12 vs 102+14 mmHg). Day-time and night-time ambulatory 24-h-systolic and diastolic blood pressures were significantly higher in the true resistant hypertensive patients when compared with white-coat resistant hypertensives (153+15 vs 124+10 mmHg and 97+9 vs 76+6 mmHg all p<0.001). Day-time and night-time ambulatory 24-h-heart rate were significantly higher in the true resistant hypertensive patients when compared with white-coat resistant hypertensives (79+11 vs 71+9 beats/min; p<0.01; 68+9 vs 60+6 beats/min, p<0.001). The ABP readings were analysed by a Fourier series with 4 harmonics. According to the runs test both two groups of patients showed a circadian rhythm for both systolic and diastolic blood pressure. The nocturnal fall in SBP, DBP and HR was not different in both groups of patients. In conclusion, our findings showed that true resistant hypertensive patients were characterized both by higher heart rate and higher plasma renin activity values as an expression of a possible increased sympathetic activity. Thus, the combination of ABPM with the assessment of the clinical characteristics allow to differentiate better the true drug-resistant hypertension from the white coat resistant hypertension.     

QT interval prolongation in association with impaired circadian variation of blood pressure and heart rate in adolescents with Type 1 diabetes.

AIMS: The aim of our study was to assess diurnal blood pressure (BP) and heart rate variability and their possible relationship to the duration of the QT interval in adolescents with Type 1 diabetes. METHODS: In 48 normotensive, normoalbuminuric diabetic adolescents, with a mean (+/- sd) age of 17.3 (+/- 4.1) years and a mean (+/- sd) diabetes duration of 8.5 (+/- 3.3) years, 24-h ambulatory BP was recorded. In addition, 24-h heart rate (HR) monitoring was performed and QT and corrected QT (QTc) intervals were estimated as indices of autonomic function. The patients were divided into two groups according to the absence of a decrease (non-dippers) or the presence of a decrease (dippers) in nocturnal diastolic BP (DBP). RESULTS: In comparison with the dippers, the non-dippers showed reduced mean 24-h HR (79.6 vs. 84.0 beats/min, P = 0.05) and reduced mean daytime HR (81.3 vs. 86.0 beats/min, P = 0.05). The QT interval was prolonged in the non-dippers (366.3 vs. 347.5 ms, P = 0.015), and end systolic (28.7 vs. 25.9 mm, P = 0.004) and end diastolic left ventricular diameters (47.8 vs. 45.5 mm, P = 0.037) were greater. In stepwise multiple regression, HR variables were the most important factors affecting DBP ratio or the duration of the QT interval. CONCLUSIONS: In conclusion, normotensive diabetic adolescents with impaired nocturnal BP reduction also have impaired autonomic function tests, in association with prolonged QT interval and increased left ventricular diameters. These findings suggest that diabetic adolescents who have the 'non-dipper' phenomenon may need close follow-up for the possible development of vascular complications, such as cardiac arrhythmias and left-ventricular hypertrophy.     

AMBULATORY BLOOD PRESSURE MONITORING AND CLINICAL CHARACTERISTICS OF THE TRUE AND WHITE-COAT RESISTANT HYPERTENSION

The resistant hypertension has been differentiated in true resistant hypertension and white-coat resistant hypertension by using ambulatory blood pressure monitoring. White-coat resistant hypertension was defined as high clinic blood pressure, despite triple treatment for at least 3 months, but day-time blood pressure values < 135/85 mmHg. The aim of this study was to evaluate the presence of different clinical characteristics between two types of resistant hypertension.

The study group consisted of 49 patients with essential hypertension, resistant to an adequate and appropriate triple-drug therapy, that included a diuretic, with all 3 drugs prescribed in near maximal doses and that had persistently elevated clinic blood pressure (>140/90 mm Hg), for at least 3 months. They represented the 2% of 2500 hypertensive outpatients that referred at our Hypertension Unit. Patients with white-coat resistant hypertension (n=19) were older (p<0.05) than those with true resistant hypertension (n=30). The sodium intake (p<0.05) and alcohol intake (p<0.05) were significantly higher in patients with true resistant hypertension than in those with white-coat resistant hypertension. The renin plasma activity and plasma aldosterone were higher (p<0.05) in patients with true resistant hypertension than in those with white-coat resistant hypertension with normal plasma electrolyte balance. There were no significant differences in mean values of office systolic and diastolic blood pressures between white coat resistant hypertensives and true resistant hypertensives (165+17 vs 172+28 and 98+12 vs 102+14 mmHg).

Day-time and night-time ambulatory 24-h-systolic and diastolic blood pressures were significantly higher in the true resistant hypertensive patients when compared with white-coat resistant hypertensives (153+15 vs 124+10 mmHg and 97+9 vs 76+6 mmHg all p<0.001). Day-time and night-time ambulatory 24-h-heart rate were significantly higher in the true resistant hypertensive patients when compared with white-coat resistant hypertensives (79+11 vs 71+9 beats/min;p<0.01; 68+9 vs 60+6 beats/min. p<0.001). The ABP readings were analysed by a Fourier series with 4 harmonics. According to the runs test both two groups of patients showed a circadian rhythm for both systolic and diastolic blood pressure. The nocturnal fall in SBP, DBP and HR was not different in both groups of patients.

In conclusion, our findings showed that true resistant hypertensive patients were characterized both by higher heart rate and higher plasma renin activity values as an expression of a possible increased sympathetic activity. Thus, the combination of ABPM with the assessment of the clinical characteristics allow to differentiate better the true drug-resistant hypertension from the white coat resistant hypertension.     

A possible relationship of nocturnal blood pressure variability with coronary artery disease in diabetic nephropathy

Evidence suggests a relationship between short-term blood pressure (BP) variability and cardiovascular target-organ damage. Although a blunted nocturnal decrease in BP and reduced heart rate variability have been shown to be associated with cardiovascular morbidity in diabetic patients, little information is available on short-term BP variability. In this study, short-term BP variability was assessed in 36 subjects with type 2 diabetes and overt nephropathy who underwent ambulatory BP monitoring, and the factors that correlated with short-term BP variability were examined. The incidence of coronary artery disease (CAD) was significantly greater in the patients with increased 24-h systolic BP variability (67% versus 11%; p < 0.0005), while that of cerebrovascular disease was not significantly affected (61% versus 50%). Multiple stepwise regression analysis revealed that serum cholesterol (cholesterol) and plasma norepinephrine (p-NE) were significant and independent contributors to nighttime systolic BP variability (partial R2 = 0.490, p < 0.001; partial R2 = 0.470, p < 0.001) and demonstrated that body mass index and p-NE were primary determinants of nighttime diastolic BP variability (partial R2 = 0.539, p < 0.0005; partial R2 = 0.304, p < 0.05). Diabetic nephropathy patients with CAD had significantly increased daytime systolic (17.8 mmHg versus 13.1 mmHg, p < 0.0005), nighttime systolic (17.4 mmHg versus 10.5 mmHg, p < 0.0001), and nighttime diastolic (10.4 mmHg versus 7.2 mmHg, p < 0.05) BP variability. Furthermore, logistic regression analysis demonstrated that nighttime systolic BP variability was an independent risk factor for CAD (odds ratio 3.13 [95% CI 1.02-9.61]; p < 0.05). The increase in nighttime BP variability is associated with a proportional sympathetic activation in diabetic nephropathy. Elevated short-term BP variability combined with relative sympathetic prevalence during the night might represent an important risk factor for cardiovascular events in the diabetic population.     

Effects of multiple factorial intervention on ambulatory BP profile and renal function in hypertensive type 2 diabetic patients with overt nephropathy - a pilot study

Accumulating evidence has shown that diabetic patients are increasing in number, and renal and cardiovascular complications are the most common cause of death in diabetic patients. Thus, it would be of considerable value to identify the mechanisms involved in the progression of renal impairment and cardiovascular injury associated with diabetes. Recent evidence also indicated that multifactorial intervention is able to reduce the risk of cardiovascular disease and death among patients with diabetes and microalbuninuria. In this pilot study, we examined the effects of intensified multifactorial intervention, with tight glucose regulation and the use of valsartan and fluvastatin on ambulatory blood pressure (BP) profile, estimated glomerular filtration rate (eGFR), and urinary albumin to creatinine ratio (UACR), in 20 hypertensive patients (16 male and 4 female) with type 2 diabetes mellitus and overt nephropathy. After 12 months of intensified treatment, office BP, fasting plasma glucose (FPG), and low-density lipoprotein cholesterol (LDLC) were significantly decreased compared to baseline (systolic blood pressure (SBP), 130 ± 2 vs. 150 ± 1 mmHg; diastolic blood pressure (DBP), 76 ± 1 vs. 86 ± 1 mmHg; FPG, 117 ± 5 vs. 153 ± 7 mg/dl; LDLC, 116 ± 8 vs. 162 ± 5 mg/dl, P < 0.0001). Also, compared to the baseline values, the daytime and nighttime ambulatory BP and short-term BP variability were significantly decreased after 12 months. Furthermore, while eGFR was not altered (44.3 ± 5.1 vs. 44.3 ± 6.5 ml/min/1.73 m(2), not significant (NS)), UACR showed a significant reduction after 12 months of intensified treatment (1228 ± 355 vs. 2340 ± 381 mg/g-cr, P < 0.05). These results suggest that the intensified multifactorial intervention is able to improve ambulatory BP profile, preserve renal function, and reduce urinary albumin excretion in type 2 diabetic hypertensive patients with overt nephropathy.     

How does deep breathing affect office blood pressure and pulse rate?

Little is known about the relation between deep breathing (DB) and blood pressure (BP). We studied the relationship between DB and BP in a large Japanese population. The subjects were recruited from randomly selected clinics and hospitals that were members of a medical association, and divided into two groups. In one group, BP was measured before and after taking 6 DB over a period of 30 s, and in the other group BP was measured before and after a 30-s rest in a sitting position without DB. Before these measurements, all patients rested 10 min or more in the waiting room and another 2 min or more in the doctor's office. Analyses were performed on data collected from 21,563 subjects. In both groups, systolic blood pressure (SBP), diastolic blood pressure (DBP) and pulse rate (PR) were significantly reduced after DB or a 30-s rest compared with the baseline measurements (p < 0.001). SBP reductions were greater in the DB group than in the 30-s rest group (normotensives: -6.4 +/- 8.3 vs. -3.0 +/- 7.4 mmHg, p < 0.001; untreated hypertensives: -9.6 +/- 10.2 vs. -5.9 +/- 9.1 mmHg, p < 0.001; treated hypertensives: -8.3 +/- 9.6 vs. -4.4 +/- 8.3 mmHg, p < 0.001). Greater BP reductions were found in patients with a higher baseline BP in both the DB and 30-s rest groups. In conclusion, the present study showed a baseline BP-dependent BP reduction by DB, suggesting that BP measurement should be done without DB in the office because DB lowers BP.     

Controlling systolic blood pressure is difficult in patients with diabetic kidney disease exhibiting moderate-to-severe reductions in renal function

This study compared the use of antihypertensive treatment and blood pressure (BP) controls between patients with diabetic kidney disease (DK+) and patients with non-diabetic kidney disease (DK-) exhibiting moderate-to-severe chronic renal failure who did not need renal replacement therapy. A cross-sectional survey included all renal patients with s-creatinine at ?200 micromol/l attending regular control sessions at six renal units in Norway. Of the 351 patients included, 73 (20.8%) were DK+. The proportion reaching a BP goal of <130/80 mmHg was similar in DK+ and DK- (14.1% vs 13.6%, p = 0.92), while 38% and 39% achieved a BP of <140/90 mmHg, respectively. The systolic BP goal was more difficult to achieve than the diastolic BP goal in DK+ patients (35% vs 15%) despite a mean of three different types of drugs being used. Loop diuretics and beta-adrenergic-receptor antagonists were the most frequently prescribed drugs, and the use of angiotensin-converting enzyme inhibitors or angiotensin-II-receptor antagonists declined when renal function deteriorated, from 80% to 0% and from 66% to 20% in the DK+ and DK- groups, respectively (p = 0.001). Thus, despite the use of multiple antihypertensive drugs, controlling BP - especially the systolic BP - is difficult in high-risk patients with chronic renal failure caused by diabetic kidney disease.     

Ambulatory blood pressure is still elevated in treated hypertensive diabetic subjects compared with untreated diabetic subjects with the same office blood pressure.

Ambulatory blood pressure, ABP, was determined every 15 min for 24 h (Spacelabs 5200 system) in 16 hypertensive diabetic subjects treated for high blood pressure. Office blood pressure (OBP) in these subjects (systolic BP greater than 160 mmHg and diastolic BP greater than 95 mmHg before treatment) had been reduced by treatment to the borderline range (systolic less than or equal to 160 mmHg and/or diastolic less than or equal to 95 mmHg). Sixty-five diabetic subjects with normal or borderline OBP were included as controls. The two groups had the same age (58 +/- 10 yrs in both groups), duration of diabetes (15 +/- 9 yrs), 24 hr microalbumin, and included the same percentage of subjects with moderate neuropathy (36% and 29%, NS). The two groups had the same OBP (138 +/- 16 mmHg and 140 +/- 16 mmHg systolic, NS, 84 +/- 9 mmHg and 84 +/- 13 mmHg diastolic, NS). In contrast, ambulatory BP was significantly higher in the treated group, when compared with the controls (123 +/- 13 mmHg and 133 +/- 23 mmHg systolic, P less than 0.025, 77 +/- 7 mmHg and 84 +/- 16 mmHg diastolic, P less than 0.015). The difference was significant both in daytime and in nighttime, and was more significant in nighttime (11 mmHg systolic, P less than 0.02, 9 mmHg diastolic, P less than 0.004) than in daytime (9 mmHg systolic, P less than 0.05 and 5 mmHg diastolic, P less than 0.05). Ambulatory heart rate was also significantly higher in the treated group, but only in daytime (7 b/min difference, P less than 0.02). The study demonstrated the need to survey and investigate ABP in treated hypertensive diabetic subjects.     

Blood pressure and sleep apnea: results of long-term nasal continuous positive airway pressure therapy

Arterial blood pressure patterns in 12 men with sleep apnea and arterial hypertension were studied at baseline and after 6 months' therapy with nasal continuous positive airway pressure (nCPAP). Preexisting antihypertensive medication was discontinued 1 week before baseline measurements. Weight did not change during the study period; body mass index was 29.3 (range, 25.4-38.5) vs. 29.3 (25.0-38.5). During therapy the apnea index decreased from 58 (range 30-73) to 2 (range 0-7) apneic episodes per hour (p less than 0.01). Intra-arterial systolic (BP sys.) and diastolic (BP dias.) blood pressure and heart rate decreased during therapy (p less than 0.001). Mean values +/- 95% confidence intervals were as follows: BP sys., 147.1 (+/- 1.6) mm Hg vs. 126.4 (+/- 1.5) mm Hg; BP dias., 81.6 (+/- 0.8) mm Hg vs. 69.4 (+/- 0.6) mm Hg; heart rate, 68.8 (+/- 0.7) beats/min vs. 65.4 (+/- 0.7) beats/min. Furthermore, the variability of these parameters decreased during therapy: variability BP sys., 53.8 (+/- 1.1) mm Hg vs. 25.6 (+/- 1.1) mm Hg; variability BP dias., 35.6 (+/- 0.7) mm Hg vs. 17.9 (+/- 0.7) mm Hg; variability of heart rate, 28.1 (+/- 0.7) beats/min vs. 14.9 (+/- 0.7) beats/min (p less than 0.001). During treatment we found that blood pressure scores already dropped during the awake phase, with a further decrease during non-REM and REM sleep (p less than 0.001). Our results, which demonstrate the reversibility of high blood pressure upon treatment of sleep apnea, indicate that sleep apnea can be an etiological factor in hypertension. Sleep apnea should therefore be considered in the differential diagnosis of arterial hypertension.     

Blood pressure surge on rising

OBJECTIVES: Since cardiovascular complications tend to occur more often in the morning, it is tempting to link this to the surge in blood pressure (BP) on rising. Our objective was to measure BP and heart rate (HR) on rising and compare values with those recorded immediately beforehand and seek variables related to marked changes in the two parameters in a cohort of initially untreated hypertensives. METHODS: The 24-h ambulatory BP measurement along with an accurate measurement of the BP on rising (either manually or automatically from the device coupled with a position sensor) was obtained in untreated hypertensives. Left ventricular mass was measured with echocardiography at baseline. Patients were then treated and followed by their general physician and news was obtained at regular intervals. RESULTS: A total of 507 patients with adequate recordings were included. Rising led to a mean increase of 14 mmHg in systolic blood pressure (SBP) and a 13 beats per minute (bpm) increase in HR. This elevation in BP on rising in the morning differed from the alteration in BP on normal changes in position. It was associated with left ventricular hypertrophy at baseline and an increased risk of future cardiovascular complications. CONCLUSIONS: Our study confirms the surge in BP on rising in the morning. This elevation in BP is accompanied by an acceleration in cardiac rhythm with no significant correlation between the two parameters. The increase in BP on rising was linked with the overall variability in BP, but was independent of the mean BP over 24 h. It was associated with an increased risk of cardiovascular complications independently of age and average 24-h SBP.     

Effects of cerivastatin on forearm vascular responses, blood pressure responsiveness and ambulatory blood pressure in type 2 diabetic men

OBJECTIVE: The objective of the study was to investigate the effects of cerivastatin therapy on forearm endothelial dependent acetylcholine (ACH) and independent (nitroprusside) vasodilator responses, blood pressure (BP) responses to intravenous infusions of angiotensin II (AII) and noradrenaline (NA) and on 24-h ambulatory BP recordings in type 2 diabetic men. DESIGN: Eleven type 2 diabetic men aged 59 +/- 9 years with total cholesterol levels of 5.0 +/- 1.26 mmol/l, triglycerides of 2.23 mmol/l and high-density lipoprotein cholesterol levels of 1.24 mmol/l completed a double-blind, randomized, crossover trial comparing 8 weeks of cerivastatin therapy (800 microg of nocte) with placebo. Forearm vascular resistance (FVR) responses to intrabrachial-arterial infusions of ACH (3-24 microg/min), nitroprusside (2-16 microg/min), the nitric oxide(NO) synthase inhibitor l-nitro-mono-methyl arginine (l-nmma) (8 micromol/min), ACH during l-NMMA infusion and BP responses to intravenous infusions of AII (12.5-50 ng/min) and NA (20-400 ng/min) were measured at the end of each treatment period. Twenty-four-hour ambulatory BP recordings were also performed. RESULTS: FVR responses to ACH during l-NMMA infusion were significantly (p = 0.026) greater during cerivastatin than during placebo therapy. In contrast, FVR responses to ACH in the absence of NO synthase inhibition did not differ significantly between cerivastatin and placebo therapies (p = 0.81). FVR increased by 31.4 +/- 57.3% in response to l-NMMA infusion during cerivastatin therapy compared with 6.1 +/- 41.2% during placebo therapy (p = 0.20). FVR responses to nitroprusside did not differ between cerivastatin and placebo therapies (p = 0.28), nor did BP responses to AII (systolic BP, p = 0.99; diastolic BP, p = 0.98) or NA (systolic BP, p = 0.21; diastolic BP, p = 0.48). Mean 24-h BP was similar during cerivastatin (123 +/- 10 or 70 +/- 7 mmHg) and placebo therapies (129 +/- 11 or 74 +/- 7 mmHg) (systolic BP, p = 0.26; diastolic BP, p = 0.41). CONCLUSION: Cerivastatin increases FVR responses to ACH in type 2 diabetic men with mild dyslipidaemia but only following NO synthase inhibition. This may indicate an improvement in endothelium-derived hyperpolarizing factor-mediated responses.     

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.