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The present study characterized large-artery properties in patients with isolated systolic hypertension (ISH) and determined the efficacy of exercise training in modifying these properties. Twenty patients (10 male and 10 female) with stage I ISH and 20 age- and gender-matched control subjects were recruited, and large-artery properties were assessed noninvasively. Ten ISH patients (5 male and 5 female) were enrolled in a randomized crossover study comparing 8 weeks of moderate intensity cycling with 8 weeks of sedentary activity. Brachial and carotid systolic, diastolic, mean, and pulse pressures were higher in the ISH group than in the control group. Systemic arterial compliance (0.43+/-0.04 versus 0.29+/-0.02 arbitrary compliance units for the control versus ISH groups, respectively; P=0.01) was lower, and carotid-to-femoral pulse-wave velocity (9.67+/-0.36 versus 11.43+/-0.51 m. s(-1) for the control versus ISH groups, respectively; P=0.007), input impedance (2.39+/-0.19 versus 3.27+/-0.34 mm Hg. s. cm(-1) for the control versus ISH groups, respectively; P=0.04), and characteristic impedance (1.67+/-0.17 versus 2.34+/-0.27 mm Hg. s. cm(-1) for the control versus ISH groups, respectively; P=0.05) were higher in the ISH group than in the control group. Training increased maximal oxygen consumption by 13+/-5% (P=0.04) and maximum workload by 8+/-4% (P=0.05); however, there was no effect on arterial mechanical properties, blood lipids, or left ventricular mass or function. These results suggest that the large-artery stiffening associated with ISH is resistant to modification through short-term aerobic training.

Carotid augmentation index (AI) is used as a surrogate measure of arterial stiffness. Although arterial stiffness has been shown to either remain unchanged or increase with an increase in heart rate, AI decreases as heart rate increases. This study aimed to quantify this confounding effect of heart rate on AI. We investigated 873 hypertensives, mean age 72 +/- 5 years, 44% men, mean brachial blood pressure 161 +/- 21/82 +/- 11 mm Hg. Carotid artery tonometry with simultaneous continuous wave Doppler measurement of ascending aortic blood flow was performed. AI was calculated from the carotid pressure waveform. Waveforms were decomposed into their forward and backward components and the time to reflection between the maxima of the forward and backward pressure waves was measured. AI showed a stronger (P < .001) association with ejection time (r = 0.48, P < .001) than with heart rate (r = -0.28, P < .001). Although AI is strongly related to the time to reflection (r = -0.51, P < .001), only a weak association was seen between time to reflection and heart rate (r = 0.16, P < .001) or ejection time (r = -0.12, P < .001). Our analysis in an elderly cohort of patients with essential hypertension demonstrates that AI is related to the time to reflection. It also reiterates that AI is confounded by heart rate without any underlying heart rate-dependent change in wave reflection. In population-based studies the confounding effect of heart rate can potentially be corrected. AI remains strongly (r = -0.52) related to time to reflection after correction for the effects of ejection time on AI.

1. Both microalbuminuria and left ventricular hypertrophy may reflect target organ damage in essential hypertension. Both are related to the prevailing level of blood pressure and both are associated with an increase in morbidity and mortality. 2. The database of the Hypertension Diagnostic Service, a multicentre secondary referral clinic for patients with essential hypertension, was analysed in order to clarify the level of association between microalbuminuria and left ventricular hypertrophy, which might explain the observed increase in morbidity and mortality in patients with microalbuminuria. Microalbuminuria was measured semiquantitatively by urine dip-stix. After the exclusion of patients with potential secondary hypertension, renal disease and diabetes mellitus, patients with complete data for microalbuminuria, left ventricular mass (LVM) and 24 h blood pressure monitoring were selected. 3. Data were complete for 704 patients (47% male, age 51 +/- 12 years) and 42% tested positive for microalbuminuria. Microalbuminuria was positively related to 24 h systolic blood pressure and weight and was negatively related to age. Left ventricular mass was higher in patients with microalbuminuria (men, 265 +/- 69 g; women, 207 +/- 61 g) than in those without (men, 250 +/- 64 g, P < 0.05; women, 185 +/- 50 g, P < 0.001). After correction for the effects of gender, body mass index and 24 h systolic blood pressure, the presence of microalbuminuria was associated with an increase in LVM of 10 g (P < 0.05, 95% confidence interval, 2-19 g).

1. Arterial compliance is a major determinant of left ventricular afterload. In keeping with earlier experimental data obtained in isolated arterial segments, it has recently been shown in the rat that arterial compliance decreases with an increase in heart rate (HR) induced by atrial pacing. 2. To elucidate the potential relevance of this effect in humans, we investigated nine male volunteers (age 20-30 years; mean 26 years). Systemic arterial compliance (SAC) was measured with the diastolic area method and carotid-to-femoral and femoral-to-dorsalis pedis pulse wave velocities (PWV) were measured to determine regional changes in compliance. Heart rate was first lowered with intravenous metoprolol to 56 +/- 2 b.p.m. and then increased by transoesophageal atrial pacing to 80 and 100 b.p.m. 3. Increasing HR from 56 +/- 2 to 80 b.p.m. by pacing increased mean arterial pressure (MAP) from 78 +/- 2 to 98 +/- 1 mmHg (P < 0.001) and then to 102 +/- 2 mmHg (P = NS). Systemic arterial compliance fell from 0.48 +/- 0.06 to 0.33 +/- 0.04 arbitrary compliance units (ACU; P < 0.01), carotid-to-femoral PWV increased from 6.1 +/- 0.3 to 6.8 +/- 0.4 m/s (P < 0.001) and femoral-to-dorsalis pedis PWV increased from 8.9 +/- 0.4 to 10.1 +/- 0.5 m/s (P < 0.001). Pacing at 100 b.p.m did not change MAP, but did lead to a further decrease in SAC (to 0.24 +/- 0.03 ACU; P < 0.05) and further increases in carotid-to-femoral (7.3 +/- 0.4 m/s; P = NS) and femoral-to-dorsalis pedis PWV (11.3 +/- 0.4 m/s; P < 0.001). 4. We conclude that systemic, central and peripheral compliances decrease in vivo with an increase in HR induced by atrial pacing.

In hypertensive disease, the extent of target organ damage determines the prognosis. We conducted a 6-month, double-blind randomized study to compare the effects of an alpha1-adrenoreceptor blocker (bunazosin) with those of a beta1-adrenoreceptor blocker (metoprolol) on early hypertensive target organ damage at a similar level of blood pressure reduction. The study consisted of 43 patients (29 men and 14 women) of varying ages (mean age 52 +/- 9 years) with essential hypertension World Health Organization stage I-II. Both the alpha- and the beta-blocker lowered blood pressure to a similar extent measured by 24-h blood pressure monitoring. The left ventricular mass was comparably reduced in both cohorts (alpha-blocker 284 +/- 80 v 259 +/- 67 g, P < .05, beta-blocker 282 +/- 74 v 254 +/- 70 g, P < .05). Treatment with the alpha-blocker led to reduced total peripheral resistance (22.9 +/- 8.0 v 19.9 +/- 5.3 U, P < .05), whereas therapy with the beta-blocker resulted in an elevated total peripheral resistance (25.5 +/- 8.4 v 28.5 +/- 9.3 U, P < .10; P < .05 for the difference in both groups). Renal plasma flow remained constant in the alpha-blocker treated group but decreased in the beta-blocker treated group (508 +/- 141 v 477 +/- 134 mL/min/1.73 m2, P < .05). Glomerular filtration rate as measured by inulin clearance tended to increase after treatment with the alpha-blocker (112 +/- 20 v 115 +/- 18 mL/min/1.73 m2, P < .10) in accordance with a decrease of serum creatinine (1.00 +/- 0.14 v 0.93 +/- 0.12 mg/dL, P < .001). Plasma cholesterol and LDL cholesterol was lowered after treatment with the alpha-blocker (238 +/- 48 v 312 +/- 37 mg/dL; P < .001, and 153 +/- 32 v 130 +/- 25 mg/dL; P < .05) while remaining unchanged in group treated with the beta-blocker. Left ventricular hypertrophy was similarily reduced with alpha- and with beta-blockade at a comparable reduction of 24-h blood pressure. Alpha-blockers effected a more favorable renal and systemic hemodynamic profile than beta-blockers, but only long-term prospective studies will answer the question whether these hemodynamic effects result into a better cardiovascular prognosis.

Objective: To evaluate anthropometric, haemodynamic and biochemical risk markers for coronary heart disease (CHD) in the Polynesian population of Western Samoa in a case-control study of 43 cases of CHD compared with 90 age- (mean 53 years) and sex-matched controls., Methods: Cases were identified on the basis of a 12-lead electrocardiogram and clinical history., Results: More than 60% of the participants had a body mass index > or =30 kg/m2 and nearly 80% had central obesity. Both diabetes mellitus (17%) and impaired glucose tolerance (9%) were also common in this population. Nineteen per cent of the population were hypertensive and both antihypertensive therapy (21 versus 1%, P<0.001, risk 23.6) and hypertension (35 versus 11%, P<0.01, risk 4.3) were significantly more common among cases than they were among controls. In addition, the plasma high-density lipoprotein cholesterol level was lower (1.00+/-0.09 versus 1.24+/-0.05 mmol/l, P<0.05) and the plasma urate level was higher (0.42+/-0.02 versus 0.37+/-0.01 mmol/l, P<0.05) in the female cases than they were in their respective controls. Low-density lipoprotein (LDL) particle sizing did not reveal an excess of small LDL particles to be a feature of CHD cases, but more than 70% both of cases and of controls had multiple LDL species. The response of the triglyceride level to a fat-rich meal was the same for CHD cases and controls., Conclusion: The population studied had a high prevalence of several risk factors for CHD, including obesity and non-insulin-dependent diabetes mellitus; however, the most prominent factor relating to CHD within the community was the presence of hypertension.

Antihypertensive therapy has been thought to be a life-long treatment. Nevertheless, antihypertensive medication may be discontinued in a substantial proportion of hypertensive patients at least for some time. The current study focused on predictors for the development of elevated blood pressure levels after discontinuation of antihypertensive drug therapy. In an open, prospective study, 88 white male patients with newly discovered essential hypertension (age 42 +/- 7 years) were tested at baseline. Blood pressure was measured in various situations (at work, at rest, before and during treatment, and at follow-up), and the hemodynamic profile at rest and cardiovascular response patterns during stress tests were evaluated. Left ventricular mass and other cardiovascular risk factors were also carefully determined. After 6 months of strict blood pressure control (< 140/90 mm Hg), they were treated by their primary care physician (mean duration of antihypertensive therapy 1.3 +/- 1.7 years). After 6 years, 37 patients were still on antihypertensive therapy, but 19 of the 37 had blood pressure values > or = 160/95 mm Hg. In 51 patients, therapy was discontinued: 29 were hypertensive, 15 were borderline hypertensive and 7 were normotensive. Relapse of hypertensive blood pressure in these 51 patients off therapy was predicted by resting blood pressure values before therapy (138 +/- 11/91 +/- 5 vs. 131 +/- 11/85 +/- 7 mm Hg, p < 0.05/0.01), cardiac output at rest (7.5 +/- 1.9 vs. 6.2 +/- 2.1 l/min, p < 0.05), total peripheral resistance (20 +/- 9 vs. 14 +/- 4 U, p < 0.05), increased heart rate during ergometry (50 +/- 8 vs. 44 +/- 6 b.p.m., p < 0.05) and left ventricular mass determined by echocardiography (212 +/- 60 vs. 189 +/- 44 g, p < 0.01). There was no difference in age, blood pressure levels before and during treatment, the number of consultations with the primary care physician or cardiovascular risk factor profiles. In conclusion, intermittent rather than life-long antihypertensive treatment may be possible in hypertensive patients with low resting blood pressure, high cardiac output, low total peripheral resistance and low left ventricular mass.

Background: Urinary sodium excretion and angiotensin II (Ang II), which are linked in a physiological feedback mechanism, have both been described to be blood pressure-independent determinants of left ventricular hypertrophy in essential hypertension. We conducted a study to investigate the interaction of sodium excretion with Ang II and its potential impact on myocardial hypertrophy., Methods and Results: Sixty-eight patients (46 men and 22 women; mean age, 52 +/- 10 years) with untreated World Health Organization stage I to II essential hypertension were examined in a cross-sectional study. Left ventricular structure and function (two-dimensionally guided M-mode echocardiography), dietary sodium intake (as estimated by 24-hour urinary sodium excretion), and noninvasive ambulatory blood pressure over 24 hours (Spacelab 90207) were determined in parallel with plasma renin activity and plasma Ang II and serum aldosterone concentrations (radioimmunoassay). Twenty-four-hour urinary sodium excretion emerged as a strong correlate of relative wall thickness independent of 24-hour ambulatory blood pressure (partial r = .49, P < .001). Ang II concentrations were weakly correlated with septal wall thickness (r = .27, P < .05) and left ventricular mass (r = .25, P < .05). Patients with high Ang II concentrations in relation to sodium excretion had a greater left ventricular mass (318 +/- 77 versus 257 +/- 54 g, P < .02), posterior wall thickness (11.8 +/- 1.9 versus 10.5 +/- 0.8 mm, P < .02), and septal wall thickness (13.6 +/- 1.8 versus 11.9 +/- 1.3 mm, P < .01) than those with "relatively low" Ang II levels in relation to sodium excretion., Conclusions: Impaired suppression of the renin-Ang II system appeared to act as a stimulus for myocardial hypertrophy in hypertensive patients.

Most patients with secondary hypertension due to renal disease or on maintenance hemodialysis have lost the physiologic fall of blood pressure during sleep. To test the notion that kidney transplantation normalizes the blood pressure profile, we monitored ambulatory blood pressure over 24 hr in 45 patients (29 males and 16 females) after successful renal transplantation. The longer the time after renal transplantation, the more marked was the decrease of blood pressure during sleep (r = 0.38, P < 0.01). This effect of time after renal transplantation on the fall of blood pressure during sleep was independent of the prevailing level of 24-hr ambulatory blood pressure. The prevalence of dippers (defined by a fall in mean blood pressure during sleep of 10% or more of the awake mean) increased from 27% in the early phase (< 7 months) to 73% in the late phase (> or = 1 year) after renal transplantation (P < 0.01). Again, this effect was not attributable to the level of 24-hr ambulatory blood pressure and concomitant antihypertensive or immunosuppressive medication. We conclude that renal transplantation leads to a normalization of the circadian blood pressure profile with a marked decrease of blood pressure during sleep. As a consequence, the lower hemodynamic load imposed on the cardiovascular system may in turn lead to a reduction of cardiovascular morbidity and mortality.

Objective and Design: To identify predictors for the development of early hypertensive nephropathy, 88 previously untreated patients with mild-to-moderate essential hypertension (World Health Organization stage I or II) were re-examined after 6 years of follow-up. According to previous results, protein excretion, urinary excretion of N-acetyl-beta-glucosaminidase (NAG), serum NAG concentration and glomerular filtration rate (creatinine clearance) may predict the change in renal function., Results: Serum creatinine level increased significantly, but none of the patients developed serum creatinine of > 1.3 mg/dl. An elevated protein excretion between 200 and 500 mg/day at baseline (microproteinuria), urinary NAG excretion, serum NAG concentration and blood pressure control during treatment were not related to serum creatinine level at follow-up or change in serum creatinine level throughout the 6 years of follow-up. In contrast, a high creatinine clearance at baseline was related to a marked rise in serum creatinine level after 6 years. The patients with a clear-cut increase in serum creatinine level of > 0.2 mg/dl (n = 23) were characterized by a significantly higher pretreatment blood pressure at the worksite and a significantly greater initial creatinine clearance than the patients with no significant change in serum creatinine level. In the two groups age, blood pressure level during therapy, and the intensity and duration of blood pressure control were not different., Conclusion: In patients with uncomplicated essential hypertension, microproteinuria, NAG parameters and treatment blood pressure level did not predict the change in serum creatinine level in the first 6 years of follow-up. A high creatinine clearance (suggesting glomerular hyperfiltration) emerged as a clinical diagnostic marker of early hypertensive nephropathy.

Since left-ventricular hypertrophy (LVH) has been identified as a poor prognostic indicator in patients with secondary hypertension, we investigated 38 renal transplant recipients on antihypertensive medication with 24-h ambulatory blood-pressure measurement (SpaceLabs 90207) and determined their left-ventricular mass by two-dimensional guided M-mode echocardiography. An increased left-ventricular mass correlated with a reduced fall of diastolic blood pressure during sleep (r = 0.29; p less than 0.05), as well as with a reduced fall of mean arterial pressure during sleep (r = 0.31; p less than 0.05). Therefore, a less pronounced afterload during sleep is related to more severe left-ventricular hypertrophy, suggesting a worse cardiovascular prognosis.