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PURPOSE: Exercise has been well documented to exert a beneficial effect on cardiovascular health. The effective control of arterial pressure (BP) is essential from the standpoint of cardiovascular prevention. So far, no study has determined the long-term effect of regular training as a monotherapy on both BP at rest and during exercise. METHODS: Therefore, 10 subjects with hypertension (aged 43 +/- 3 yr) were studied in order to define BP response to long-term aerobic training. BP measurements were obtained at rest and during ergometry (50-100 W). Patients were instructed to exercise weekly (2 x 60 min aerobic exercise). RESULTS: BP during exercise (100 W) did fall already after 6 months of regular training from 184 +/- 10/107 +/- 6 to 170 +/- 10/100 +/- 7, and this was associated with a 14% decrease in the rate-pressure product (at 100 W). After 18 months of training, there were further reductions in BP, at rest from 139 +/- 9/96 +/- 6 to 133 +/- 14/91 +/- 7 (P < 0.05) and during ergometry (100 W) from 184 +/- 10/107 +/- 6 to 172 +/- 8/96 +/- 6 mm Hg (P < 0.001). During a 3-yr follow-up, BP continued to decrease significantly to 130 +/- 13/87 +/- 7 mm Hg at rest and 167 +/- 9/92 +/- 6 mm Hg during exercise. No significant changes in body weight were documented during the training period. CONCLUSION: The data demonstrate that long-term aerobic exercise is associated with a decrease in BP at rest and during exercise, which is comparable to that of drug therapies. This antihypertensive effect of regular training can be maintained as long as 3 yr. [ABSTRACT FROM AUTHOR]

Introduction: Left ventricular hypertrophy (LVH) can be successfully reduced by antihypertensive medication. Both hypertension and aerobic exercise can cause increases in left ventricular mass (LV-mass)., Aim: Therefore, hypertensive athletes with LVH were studied to investigate the effect of antihypertensive medication on LV-mass reduction despite continuing their regular intensive exercise programs., Methods: 14 previously untreated hypertensive male athletes (A) with LVH and a prolonged history of endurance training where included in the study. 50 previously untreated inactive comparable hypertensives with LVH served as controls (C). For both groups inclusion criteria were blood pressure (BP) at rest: > 140/90 mmHg, BP during ergometry (at 100 W): > 200/100 mmHg and. LV-mass-index > 125 g/m 2 . Echocardiography was performed to calculate LV-mass and function before and after 3 years of antihypertensive medication., Results: Despite regularly aerobic training throughout the treatment period, LV mass decreased from 164 ± 19 g/m 2 before to 97 ± 16 g/m 2 after 3 years of therapy (p < 0.001). Controls with identical pressures demonstrated a decrease from 149 ± 29 g/m 2 to 87 ± 15 g m 2 . There were similar decreases in LV wall thicknesses in both groups, whereas diastolic dimensions did not change significantly. Moreover, there was an increase in fractional fiber shortening as a measure of LV pump function in both groups of 15% in A and 11% in C, respectively., Conclusions: In hypertensive athletes LVH due to hypertension can be reduced and LV-function can be improved by long-term antihypertensive medication despite regular aerobic exercise. Therefore, exercise does not interfere with the regression of LVH on account of antihypertensive therapy in hypertensive subjects.

The diagnosis of hypertension is complicated by the fact that the blood pressure varies greatly, depending on physical and mental stresses. In the doctor's office in particular, measurements are often too high (white coat hypertension). A practicable and inexpensive supplementary method as a means of avoiding inaccurate measurements, is to have the patient take his/her own blood pressure. This approach enables numerous measurements to be obtained, which more accurately reflects the true situation than the one-off measurement in the physician's office. Furthermore, self-measurement can also reveal therapeutic effects more reliably, and has a greater predictive value for organic damage. Patients who measure their own blood pressure should first receive comprehensive instruction in the technique, and should be required to record their measurements.

Objective: The course of chronic diseases does not only depend on the patients' physical situation but also on their psychological state of mind. Therefore, inpatient medical rehabilitation has to aim at including psycho-social features present themselves at the beginning and at the end of inpatient rehabilitation - and, even more importantly, six months afterwards., Patients and Methods: For half a year all patients of an internistic rehabilitation clinic were taking part in a long- term baseline-study. They have been questioned about anxiety, susceptibility to depression, aspects of quality of life and about their body weight, using a standardized questionnaire. The analyzed total spot check (n = 1222) consisted of cardiological (n = 197; mean age 53,5 +/- 10,9 years), pulmonary (n = 709; mean age 47 +/- 11,2 years) and breast cancer patients (n = 277; mean age 54,2 +/- 8,8 years) and n = 39 could not be classified., Results: At the onset of rehabilitation all patients suffered significantly more from anxiety than from depression. Accordingly, of the cardiological and pulmonary group 12.2 % or 10.9 % respectively showed a clinically strong depression and 27.9 % or 27.1 % respectively revealed remarkable values in anxiety. Moreover, 17.8 % of the cardiological and 14.7 % of the pulmonary patients stated a remarkable restriction of their fitness. Unexpectedly, the statements of the breast cancer patients group showed lower rates in all these categories. Six months after termination of rehabilitation, a significant long-term improvement of anxiety could be observed, especially for those patients who had had the highest values before. This also applies to patients who had stated the highest depression values initially. In addition, there was also a significant improvement in the capability for fitness, pleasure, relaxation and contact - while the BMI benefited, too., Conclusion: The data show that the psychological comorbidity of patients in inpatient medical rehabilitation is much higher than that of the general population and that of the general population and the psycho-social situation, especially for psycho-social very stressed patients, improves considerably on a long-term basis.

Aim: To study whether an oat bran enriched diet has a specific effect in lowering total and low-density lipoprotein cholesterols, in addition to caloric and fat restriction., Methods: We performed a randomized, controlled, parallel-group, single-centre study in which 1,994 patients from the Wehrawald Hospital (Todtmoos, Germany) were screened and 235 met the criteria male gender, hypercholesterolemia, and overweight. All patients in the Wehrawald Hospital took part in a 4-week standardized inpatient lifestyle health program consisting of dietary intervention, increased physical activity, and health education. Caloric restriction, fat modification, and oat bran supplementation were part of the nutritional regimen within the lifestyle health program. Ninety-nine patients were randomized to a fat-modified diet with caloric restriction and a daily intake of 35-50 g oat bran and 136 patients to a fat-modified, oat bran-free diet with caloric restriction. Fifty-three male overweight but normocholesterolemic subjects were selected as controls., Results: The most significant decreases in total cholesterol (-67.7 +/- 37.2 mg/dl; p < 0.01), low-density lipoprotein cholesterol (-56.3 +/- 35.1 mg/dl; p < 0.01), and apolipoprotein B (-42.4 +/- 34.1 mg/dl; p < 0.01) were found with the combination of the fat-modified and oat bran enriched food., Conclusions: Added to a fat-modified diet, oat bran within a practical range of intake significantly reduces total cholesterol, low-density lipoprotein cholesterol, and apolipoprotein B. These beneficial effects occurred independent of covariables such as physical activity or caloric and fat restriction in the diet., (Copyright 2003 S. Karger AG, Basel)

Unlabelled: BACKGROUND AND PERSPECTIVE: Various parameters of the coagulation cascade and fibrinolysis are important predictors of myocardial infarction and stroke, for which hypertension is a risk factor. It is unclear whether an elevated blood pressure by itself can produce activated clotting., Patients and Methods: Coagulation tests were done on overweight hypertensive (n=40); aged 49 +/- 8 years; group 3), overweight normotensives (n=19; aged 51 +/- 8 years; group 2) and normal-weight normotensives (n=20; aged 51 +/- 8; group 1)., Results: Plasminogen-activator-inhibitor 1 (PAI-1), a measure of impaired fibrinolysis, was elevated in group 2 (20.5 +/- 11 U/ml; p < 0.001), compared with group 1 (11.6 +/- 6 U/ml), and was even higher in group 3 (27.5 +/- 9 U/ml; p < 0.05). Fibrinogen and factor VIII, parameters that promote clotting, were elevated in group 2 (360 +/- 61 mg/dl and 143 +/- 15 %, respectively; p < 0.001), and in group 3 (368 +/- 63 mg/dl and 146 +/- 18%; p < 0.001) compared to group 1 (304 +/- 40 mg/dl and 127 +/- 17%). Correspondingly, fibrin monometers, a measure of intravascular coagulation, were elevated in group 3 (p < 0.05) and partial thromboplastin time (PTT) decreased (p < 0.001). Pearson correlation showed a significant (p < 0.001) positive relationship between PAI-1 and body mass index (BMI) (0.539), triglycerides (0.512), blood pressure (0.388 to 0.534), fibrinogen (0.404, and a negative one with HDL-cholesterol (0.625). BMI also correlated with fibrinogen (0.509; p < 0.001) and factor VIII (0.337; p < 0.01)., Conclusions: Fibrinolysis and activated coagulation are reduced in hypertensive subjects: this favours the occurrence of myocardial infarction and stroke. In addition to the level of blood pressure, the extent of the changes are effected especially by BMI and metabolic risk factors.

The aim of the study was to investigate the pulmonary vasodilator effect of the dihydropyridine calcium channel blocker amlodipine in patients with clinically stable chronic obstructive pulmonary disease (COPD) and pulmonary hypertension (PH). Many patients with COPD develop chronic PH and this may predict mortality in this disorder. The treatment with calcium channel blockers is accepted as a therapeutic strategy for primary pulmonary hypertension. In twenty male patients (mean age 57+/-7 years) with clinically stable COPD and PH, we investigated whether amlodipine could effectively decrease pulmonary vascular resistance (PVR) and pulmonary arterial pressure (PAP) and improve right heart function. PAP was recorded by a balloon-tipped thermodilution catheter and cardiac output was determined in triplicate by thermodilution at rest and during exercise. In addition, blood gas values were determined from the capillary blood of the earlobe. All measurements were done under identical conditions before and after 18 days of chronic treatment: with 10 mg amlodipine once daily starting with 5mg in the first week. At a mean maximal achieved workload of 71.3+/-20 Watts, amlodipine achieved a significant reduction in PVR (-13.4%; p<0.01) and PAP (-12.1%; p<0.001) implying an improved right heart function assessed by a significant reduction in mean right atrial pressure (-20.6%; p<0.05). During the action of amlodipine there were no significant changes in pulmonary gas exchange and pulmonary capillary wedge pressure. Amlodipine given as a single daily oral dose of 10mg is a safe and effective pulmonary vasodilator in COPD patients with PH and leads to an improvement in right heart function.

A healthy diet has a positive impact both on elevated blood pressure and its associated cardiovascular risk. In particular the association between obesity and hypertension is beyond doubt. Accordingly, a calorie-controlled or low-calorie diet resulting in a reduction in weight, lowers raised blood pressure. Blood pressure is also determined by the composition of the diet. A substantial pressure-lowering effect has been shown to be associated with the regular ingestion of fish and olive oil. Evidence also points to a positive effect of a diet high in fruit and vegetables and low in fat. Also recommended for hypertensives is a low-salt and potassium-rich diet, and sparing use of alcohol. The impact of a healthy diet on the cardiovascular risk is particularly favorable when the patient also takes regular physical exercise.

Changes in lifestyle represent a rational, promising and low side effect means of lowering the blood pressure and reducing the cardiovascular risk in many hypertensives. The first measure in all over-weight hypertensives is weight reduction. Even when the ideal weight is not reached, this measure leads to a lasting decrease in blood pressure. Beyond a threshold of 30 mg alcohol per day in men (approximately three glasses of beer or two glasses of wine) and 20 mg alcohol per day in women, the consumption of alcohol leads to an increase in blood pressure. Although only some hypertensives respond to a restriction of salt, all hypertensives should limit their salt intake to 5 to 6 g daily. Endurance training is an important pillar of lifestyle change. That relaxation techniques lower blood pressure has not been confirmed by the results of relevant studies. What has been confirmed, however, is the benefit of extensive changes in lifestyle, including information on health, daily endurance training, healthy eating habits and reduction of alcohol intake.

Metaanalyses have indicated that ACE inhibitors are more effective than other first-line therapies in reducing left ventricular hypertrophy (LVH). The average treatment period, however, was only approximately 6 months. The aim of the present study, therefore, was to clarify the time course and degree of reversal, and primarily to find out in how many patients a complete normalization of LVH can be achieved. Secondly, we sought to determine whether atrial enlargement can be reduced. Previously untreated hypertensive patients (mean age 46.3 +/- 9 years, eight women, 15 men) with echocardiographically confirmed LVH (left ventricular mass index ([LVMI] > 125 g/m2 for men; > 110 g/m2 for women) were prospectively treated over a 3-year treatment period with quinapril. Nine patients received 10 mg quinapril, 12 received 20 mg of quinapril daily, and five patients additionally received 25 mg hydrochlorothiazide. The time course of changes in LVMI, relative wall thickness, left atrial size, fractional shortening, and diastolic function was evaluated and ambulatory blood pressure monitoring (ABPM) and an exercise test were performed every 6 months. After a mean treatment period of only 7.5 months, there was a significant (P < .001), 17.5% decrease in LVMI with a further continuous and significant (P < .001) decrease of 38.6% after 38.3 +/- 3 months of therapy. In 90.5% of the patients a complete reversal of LVH was achieved. Fractional shortening increased significantly, the maximum being 14.6% after 38.3 +/- 3 months. The peak early/atrial velocity (E/A) ratio increased significantly (P < .01) after just 7.5 +/- 3.1 months with no further changes during follow-up. There seemed to be a parallel change with the decrease in left atrial dimension, where the most important decrease occurred after only 7.5 +/- 3.1 months (P < .01), with a further continuous reduction. Our study clearly shows that maximum reversal of LVH is a time-consuming process and that an essential goal of antihypertensive therapy should be not only a reduction in LVH but also a normalization in LV mass, left atrial size, and in diastolic dysfunction.

Objective: Is heart function during exercise impaired in hypertensive patients with effort angina and ST-segment depression but normal coronary angiograms?, Methods and Results: In 12 hypertensive patients (group 1; aged 53 +/- 4 yrs), who had ST-segment depression during exercise, concomitant angina pectoris but normal coronary angiograms, and no LVH, left ventricular function at rest and during exercise was studied by cardiac catheterization and compared with 12 hypertensives with CAD (group 2; aged 56 +/- 5 yrs) and 12 hypertensives without ST-segment depression (group 3; aged 56 +/- 7 yrs) after discontinuation of all cardiac medications. PCWP was normal at rest and pathologically increased at 79.2 +/- 17.9 watts only in group 1 and 2 (30.2 +/- 6 mm Hg; 31.5 +/- 5 mm Hg, respectively) but not in group 3 (18.5 +/- 3 mm Hg; p < 0.001). Repeated measurements during exercise and 30 min after 10 mg nifedipine orally, showed a significant (p < 0.001) and nearly identical fall in MAP, an increase in CI (p < 0.01), and an unchanged HR x SBP in all groups. However there were significant differences in decrease of PCWP (group 1: -41.4%; group 2: -22.9%, p < 0.01; group 3: -25.4%, p < 0.01) with concomitant reduction in ST-segment depression (p < 0.01) in group 1 and 2 (-43.7% and -36% respectively)., Conclusions: ST-segment depression during exercise ECG with concomitant angina pectoris is not a false-positive finding in hypertensive patients with normal angiograms and without LVH but demonstrates myocardial ischemia, resulting in an impaired left ventricular heart function. This seems to be mainly caused by a functional changeable disorder of the coronary vascular bed as heart function is improved after nifedipine.

Evaluation of high blood pressure would be greatly facilitated by a standardized test procedure that could enable comparable and reproducible blood pressure determinations to be made. It would also be useful to have a standardized method for monitoring sympathetic activity, so that the occurrence and magnitude of inordinate stress responses could be assessed more accurately. One way to meet these requirements is through standardized ergometric testing at workloads of 50 to 100 watts using increments of 10 watts/min. or 25 watts/2 min. (cuff blood pressure measurements). Between the ages of 20 and 50 years the criteria for a hypertensive response during exercise are blood pressure values of more than 200/100 mmHg (mean + 1 SD of the normotensives) at a workload of 100 watts. In the recovery phase, blood pressure is considered as being hypertensive if a value of 140/90 mmHg ist exceeded in the fifth minute. There are several studies showing that the blood pressure response to ergometry predicts future hypertension in patients with normal resting blood pressure. Patients suffering from mild hypertension showed significantly higher blood pressures at 100 watts and after exercise than age-matched normotensives but significantly lower values than hypertensives with stable hypertension. Ergometric studies also assume a prognostic importance, with respect to prevention of acute and chronic complications of hypertension. Therefore we must require that antihypertensive drugs not only normalize the resting blood pressure, but also lower the blood pressure adequately in stressful situations.

Aim of Study: To discover whether in hypertensives with left ventricular hypertrophy (LVH) the increased muscle mass will completely regress under antihypertensive treatment and drug dosage can in consequence be reduced., Patients and Method: Prospectively 22 previously untreated hypertensives (20 men, 2 women; mean age 43.6 +/- 9 years) with echocardiographically confirmed LVH were investigated. The observation period was 102 +/- 5 months. All patients initially received metoprolol, 100 mg daily, after 14 days 200 mg daily (additionally hydrochlorothiazide in five patients). In all patients the blood pressure became normal at rest and on exercise within 6 weeks., Results: After one year the mean left ventricular muscle mass index (LVMI) had fallen from 151 +/- 29 to 117 +/- 26 g/m2 (P < 0.001), and after 7 years to 82 +/- 14 g/m2 (P < 0.001; - 45.7%). Complete remission of LVH was demonstrated in 21 Patients. The drug dosage could either be reduced or the drug completely discontinued in 11 patients (group 1): after 102 +/- 5 months four patients took no drug, while seven were on 100 mg metoprolol. This was not possible in the other 11 patients (group 2), five of whom had been on both metoprolol and hydrochlorothiazide. The two groups differed with respect to loss of body weight (group 1: from 81.+/- 12 to 79.1 +/- 13 kg; P < 0.05; group 2: 85.7 +/- 8 to 88.1 +/- 10 kg; P < 0.05), but not regarding reduction of LVMI and blood pressure., Conclusion: Antihypertensive treatment for several years leads to regression in LVH in nearly all patients. In half of them the drug dosage can be reduced or the drug even discontinued. Weight loss may play an important part in this development.

Evaluation of high blood pressure would be greatly facilitated by a standardized test procedure that could enable comparable and reproducible blood pressure determinations to be made. It would also be useful to have a standardized method for monitoring sympathetic activity, so that the occurrence and magnitude of inordinate stress responses could be assessed more accurately. One way to meet these requirements is through standardized ergometric testing at workloads of 50 to 100 watts using increments of 10 watts/ min or 25 watts/2 min (cuff blood pressure measurements). Between the ages of 20 and 50 years the criteria for a hypertensive response during exercise are blood pressure values of more than 200/100 mg Hg (mean + 1 SD of the normotensives) at a workload of 100 W. In the recovery phase, blood pressure is considered as being hypertensive if a value of 140/90 mm Hg is exceeded in the fifth minute. There are several studies showing that the blood pressure response to ergometry predicts future hypertension in patients with normal resting blood pressure. Patients suffering from mild hypertension showed significantly (p < 0.001) higher blood pressures (213 +/- 22/116 +/- 11 mm Hg) at 100 W and after exercise than age-matched normotensives (188 +/- 14/92 +/- 9 mm Hg) but significantly (p < 0.001) lower values than hypertensives with stable hypertension (225 +/- 22/126 +/- 11 mm Hg). Using the normal upper limits for blood pressure during and after ergometry, the ergometric procedure revealed that 50% of the patients with borderline hypertension at rest could be classified as hypertensives. Follow-up examinations several years (average 3.8 years) later subsequently showed that 97% of the ergometric-positive borderline hypertensives developed established hypertension. Ergometric studies also assume a prognostic importance, with respect to prevention of acute and chronic complications of hypertension. Therefore, we must require that antihypertensive drugs not only normalize the resting blood pressure, but also lower the blood pressure adequately in stressful situations. This requirement is by no means satisfied by all hypertensive drugs that are effective at rest.

Left ventricular mass sometimes decreases during treatment of hypertension but the effects are inconsistent and the response to long-term treatment is unknown. Therefore the long-term effects of antihypertensive therapy on echocardiographically-proven left ventricular hypertrophy (LVH) were prospectively investigated in 117 previously untreated hypertensive patients (mean age 46 +/- 9 years; 15 women and 102 men). Twenty-two patients received 100 mg of gallopamil daily, 24 patients received 200 mg of metoprolol, 35 patients received both 50 mg of atenolol and 20 mg of nifedipine (follow-up five years), 14 patients received 200 mg of acebutol plus 20 mg of nifedipine, and 21 patients received 50 mg of atenolol and 10 mg of enalapril daily (follow-up of four years). For the entire population, there was a significant (P < 0.001) decrease in left ventricular mass index (LVMI; measurements were performed blind by two observers) of 24.5% after one year, with a further continuous and significant (P < 0.001) reduction of 44.1% after five years of treatment. There was a significant (r = 0.61, P < 0.001) correlation between the extent of LVMI before therapy and the percentage of regression of LVMI after five years of treatment. In 82% of the patients, almost complete regression of LVH was achieved. Nevertheless, there was no significant change in ventricular end-diastolic dimension but fractional shortening increased by 16% (P < 0.001). It can be concluded that achieving maximum regression of LVH by antihypertensive therapy in previously untreated hypertensives takes a long time and depends not only on the drug regimen chosen but especially on the duration of treatment and the extent of pretreatment left ventricular mass.

Objectives: This study was designed to evaluate the long-term effects of combination therapy with an angiotensin-converting enzyme inhibitor and a beta-adrenergic blocking agent on the relation between the decrease in arterial pressure at rest and during exercise and the decrease in left ventricular mass., Background: A variety of antihypertensive drugs including angiotensin-converting enzyme inhibitors and beta-blockers have been shown to reduce ventricular hypertrophy, although little is known about combination therapy and the time course of such a reduction., Methods: Twenty-one patients with previously untreated essential hypertension were treated with a low dose combination of 50 mg of atenolol and 10 mg of enalapril once daily for 39 months. Cardiovascular findings were assessed by two-dimensionally guided M-mode echocardiography in the pretreatment phase and after 6 and 39 months of combination therapy., Results: Combination therapy reduced arterial pressure at rest from 161/108 to 130/86 mm Hg (p less than 0.001) and exercise arterial pressure at 100 W from 192/112 to 167/95 mm Hg (p less than 0.001). After 6 months of treatment, significant decreases in interventricular septal thickness (9%, p less than 0.001), posterior wall thickness (9%, p less than 0.001) and left ventricular mass index (16%, p less than 0.001) were demonstrated on the echocardiogram. After 39 months of therapy, reductions in these values were 28% (p less than 0.001), 29% (p less than 0.001) and 40% (p less than 0.001), respectively., Conclusions: Long-term treatment with combination therapy of atenolol and enalapril produced significant reductions in arterial pressure at rest and during exercise accompanied by a marked reduction of left ventricular mass. However, whereas arterial pressure decreased immediately and remained unchanged, left ventricular mass decreased more gradually and continued to decrease throughout the treatment period of greater than 3 years. Despite this marked reduction in left ventricular mass, left ventricular pump function was well preserved during rest and exercise.

The present study was conducted to assess the efficacy and safety of carvedilol 50 mg as compared to metoprolol 200 mg at rest and during and after a standardized bicycle ergometric exercise test. Carvedilol is a novel non-selective beta-blocker without intrinsic sympathomimetic activity possessing vasodilatory properties primarily due to an alpha 1-antagonism in the same dose range. Both drugs were effective in reducing systolic and diastolic blood pressure at rest and during and after exercise. The reduction of diastolic blood pressure was much stronger under carvedilol treatment than under metoprolol treatment at all measurement points. Carvedilol was even effective in the treatment of patients whose blood pressure was unsatisfactorily controlled by metoprolol. This shows the importance of the vasodilation component of carvedilol. No serious adverse events were observed. Carvedilol therefore promises very well as a powerful and safe drug for the treatment of essential arterial hypertension.

Asthmatic patients typically show a nocturnal increase in bronchial obstruction. In 100 asthmatic patients, we investigated if there is also a reduced decline of blood pressure; we used 24-h blood-pressure monitoring. The whole group consisted of 50 hypertensive asthmatic patients (group 1, 48.8 +/- 11 years, 30 females, 20 males), 25 normotensive asthmatic patients (group 2, 49.6 +/- 10 years, 22 females, 3 males) and 25 antihypertensive-treated asthmatic patients (group 3, 50.2 +/- 8 years, 15 females, 10 males). 52% of group 1, 52% of group 2, and 44% of group 3 patients showed no sufficient nocturnal systolic and diastolic blood pressure decline (less than - 15%). When we looked only for systolic blood pressure that was also the case in 82%, 92%, and 64% of the patient groups', respectively. There was no significant difference in daytime blood pressure between hypertensives (group 1) without (142 +/- 9/93 +/- 5 mmHg) and with 142 +/- 12/92 +/- 6 mmHg) sufficient nocturnal blood pressure decline, however, nighttime blood pressure (135 +/- 14/84 +/- 5 mmHg versus 123 +/- 14/72 +/- 6 mmHg) was significantly (p less than 0.0001) different. This was also true for the normotensive asthmatic patients (group 2). The results cannot be explained by differences in heart rate, degree of asthma, or in anti-obstructive medication.

Hypertensive patients have lower cardiac outputs and stroke volumes, higher heart rates, and a markedly higher peripheral resistance than normotensive individuals at the same intensity of exercise. Even patients with mildly elevated resting blood pressures have a markedly increased myocardial oxygen demand during exercise; since demand is determined not only by the pressure load but also by the degree of ventricular hypertrophy, three therapeutic inferences may be drawn: (a) Endurance training offers hypertensive patients a means of lowering exercise heart rate, reducing the systolic blood pressure and myocardial oxygen consumption, and also improving physical work capacity. (b) Besides avoiding isometric exercise, due to possible excessive peaks of blood pressure, all patients should be evaluated by ergometric testing before beginning an exercise training programme. (c) If ergometry reveals a marked rise in blood pressure at low levels of exertion, then appropriate antihypertensive medication (beta-blockers, calcium antagonists) should be prescribed prior to training.

The long-term effects of antihypertensive therapy on echocardiographically proven left ventricular hypertrophy (LVH) were investigated in 117 previously untreated hypertensive patients (mean age of 46 +/- 9 years; 15 women, 102 men). Twenty-two patients (group 1) received daily 100 mg of gallopamil, 25 (group 2) received 200 mg of metoprolol, 35 (group 3) received both 50 mg of atenolol and 20 mg of nifedipine (follow-up of 5 years), 14 (group 4) received 200 mg of acebutolol and 20 mg of nifedipine, and 21 (group 5) daily received 50 mg of atenolol and 10 mg of enalapril (follow-up of 4 years). For the entire population, there was a significant (p less than 0.001) decrease in left ventricular mass index (LVMI) of 24.5% after 1 year, which increased further to 44.1% after 5 years of treatment. In addition, fractional fiber shortening increased by 16% (p less than 0.001). In 82% of the patients, almost complete regression of LVH was achieved. However, the time course of regression of LVMI differed significantly between the five treatment groups, despite similar blood pressure reduction under resting conditions.

Patients with left ventricular hypertrophy (LVH) often exhibit manifestations of myocardial ischemia. In 17 hypertensive patients (group 1, mean age of 56 +/- 4 years, 10 females, 7 males) with ST-segment depression during the exercise electrocardiogram (ECG) and effort angina and normal coronary arteriograms, the left ventricular function at rest and during exercise was studied by heart catheterization. The results were compared with 17 hypertensive patients (group 2, mean age of 56 +/- 6 years, 6 females, 11 males) with coronary artery disease (CAD). The normal pulmonary wedge pressure at rest (group 1, 8.9 +/- 3 mm Hg; group 2, 8.9 +/- 3 mm Hg) was pathologically increased (p less than 0.001) in both groups (group 1, 27.1 +/- 5 mm Hg; group 2, 28.8 +/- 7 mm Hg) even at a work load of 50 W with a further increase at 75 W to 31 +/- 4 and 29.7 +/- 4 mm Hg, respectively. Cardiac output was normal. There was no significant correlation between ST-segment depression, pulmonary wedge pressure, LVH, and Holter ECG. Hypertensive patients without CAD may reveal a disturbed pump function due to ischemia even at low work loads, which does not differ significantly from patients with CAD. This may provoke subendocardial fibrosis and thereby contribute to the development of heart failure.

The effect of long-term therapy of hypertension with antihypertensive drugs was investigated in 117 previously untreated patients (15 women, 102 men; mean age 46.4 +/- 9 years) with echocardiographically proven left-ventricular hypertrophy. 22 patients (group 1) received 100 mg/d Gallopamil, 25 (group 2) received 200 mg/d Metoprolol, 35 daily received both 50 mg Atenolol and 20 mg Nifedipine (group 3), 14 received daily 200 mg Acebutolol plus 20 mg Nifedipine (group 4), and 21 (group 5) 50 mg Atenolol plus 10 mg Enalapril daily. The treatment period lasted a mean of 38 (36.2-42.3) months. Left-ventricular muscle mass index (LVMI) as well as septal and posterior-wall thickness decreased significantly after 12.8 and 38.5 months (P less than 0.001). After a mean of 38.5 months LVMI had decreased by 36.7% in group 1, 35.1% in group 2, 42.3% in group 3, 45% in group 4 and 39.6% in group 5. LVMI was within normal range (less than or equal to 95 g/m2) in 81 of the 117 patients (69.2%) at the end of the treatment period. There was, however, no significant increase of the end-diastolic dimension of the left ventricle, but a significant increase of "fractional shortening" as a measure of myocardial contractility.

Beta-receptor antagonists lower exercise heart rate and cardiac output, and can thus be expected to interfere with oxygen transport, and hence physical performance, particularly at higher levels of activity. Therefore, the effects of a 4-week and 15-month treatment period with the beta 1-selective receptor blocker acebutolol (500 mg daily) on oxygen uptake and plasma catecholamines during submaximal steady-state and maximal exercise and on maximal work load were studied in eight WHO stage 1 hypertensive men (mean age 36.4 years). Oxygen uptake, ventilation, and plasma noradrenaline, adrenaline, and dopamine concentrations during steady-state exercise were not significantly different from control conditions either after 4 weeks or after 15 months of receptor blockade, although heart rates were significantly (27% and 25%, respectively; P less than 0.01) reduced. After the 4-week treatment period, maximal oxygen uptake (3.9% reduction, NS) and maximal work load (2.4% reduction, NS) tended to be slightly lower after acebutolol compared with control values; maximal oxygen pulse was significantly (P less than 0.05) increased. However, after long-term treatment of 15 months, maximal oxygen uptake was virtually identical compared with pretreatment values, and maximal work load tended to be higher (5.2%, NS); plasma noradrenaline and adrenaline concentrations were significantly (P less than 0.05) enhanced. Since beta 1-selective receptor blockers do not affect maximal oxygen uptake and maximal work capacity after long-term treatment, they appear preferable for patients taking part in preventive and rehabilitative training programs.

1. Ergometric studies enable comparable and reproducible determinations of the cardio-pulmonary-corporeal performance. Prerequisite, however, is a well-based knowledge of the methodology and exercise-physiologic principles of ergometry. 2. With respect to the methodologic prerequisites, consideration must be given to the length of shaft displacement and the inertial mass of the ergometer. Additionally, at submaximal workloads, standardized performance at 50 revolutions/min must be ensured. This also holds true for r.p.m.-independent ergometers since the biologic capacity varies at differing r.p.m. values. Furthermore, the results of ergometric examinations are comparable only on standardization of workload and duration (for example, 10 watts/1 min, 25 watts/2 min). Consideration should also be given to ancillary determinants of exercise capacity such as environmental factors, previous physical exertion, nutrition, medications and other self-administered drugs or stimulants as well as the clothing worn at the time of examination. 3. Based on the limited equipment necessary and the good reproducibility, the physical working capacity 170 (the capacity in watts at a heart rate of 170 beats/6 min) is well-suited for assessment of cardio-pulmonary-corporeal performance. The results do not differ significantly at workloads of 25 watts/min or 50 watts/6 min. The decreasing maximal heart rate with increasing age (on the average 10 beats/min per decade; in the individual case, substantially more) may result in a marked misestimation in elderly subjects. This also applies to patients with coronary artery disease in whom, for example, a slow heart rate during ergometry is caused by ischemia and only mimics an economic circulatory function. Evaluation of the systolic and diastolic blood pressure during ergometry is, to some degree, indicative of the pump function in patients with coronary artery disease. Measurement of oxygen uptake alone at submaximal workloads does not permit differentiation between healthy and diseased subjects since the latter compensate for a reduced cardiac output by a more marked oxygen extraction with subsequently greater arterio-venous oxygen differences. On calculation of the oxygen uptake per stroke, however, in relation to the heart volume, a clinically relevant differentiation between healthy subjects and diseased patients can be established. Thus, in patients with heart disease, noninvasive parameters also enable assessment of the cardio-pulmonary-corporeal performance. 4. Under physiological conditions, there is a close relationship between invasively and noninvasively-measured parameters during ergometry. In patients with heart disease, however, the response of noninvasively-measured parameters is not a reliable indicator of pressure in the pulmonary circulation and the cardiac output.

1. Comparative measurements of the Tension-Time-Index during ergometric work and of the Physical Working Capacity 170 were carried out in patients with borderline (n = 24) and stable hypertension (n = 51) in comparison with normals (n = 47), aged 20-60 years. 2. The Tension-Time-Index which is generally accepted as an indirect estimation of the myocardial oxygen consumption was significantly (p < 0.001) higher in the borderline hypertensives (30.5%) and in the hypertensives (41.7%) already at the low work load of 50 watt. 3. The PWC170 which has been shown to be a reliable ergometric method for determination of the physical performance was 21.2% lower (p < 0.001) in the hypertensives with 2.71 +/- 0.74 W/kg body weight in comparison with 3.44 +/- 0.8 W/kg body weight of the normals. Already the borderline hypertensives had a reduced PWC170 of 2.93 +/- 0.7 W/kg body weight. 4. Therefore hypertensives should perform a dosed endurance training of middle intensity, which results in a reduction of heart rate, systolic blood pressure and consequently of the Tension-Time-Index and which improves the Physical Working Capacity. These favourable effects of training are of great benefit especially for those patients also suffering from ischemic heart disease because the myocardial oxygen consumption is the limiting factor of physical performance. 5. In order to prevent acute and chronic vascular complications caused by excessive blood pressure increases during physical activity in hypertensives, ergometric tests for dosage of training and if necessary an antihypertensive treatment should be applied before starting the training program.

In hypertensive patients physical exercise can induce considerable increases of blood pressure. This means particularly for elder patients a high risk of cardiovascular complications. Therefore we investigated in 13 elder patients suffering from arterial hypertension the effect of a hypotensive combined therapy with a diuretic and a beta-receptorblocker on elevated blood pressures during and after ergometric work. Apart from the reduction of the blood pressure at rest, especially the systolic and diastolic blood pressure during exercise was lowered significantly. In addition to a diuretic hypotensive therapy a beta-receptorblocker can be of great benefit also for elder patients particularly in order to reduce elevated exercise blood pressures.

On repeated measurement hypertensives have greater swings in resting blood pressure than those with normal pressures. In 20 untreated hypertensives (WHO stage I), average age 35.8 years, blood pressures were measured during and after ergometry (50-100 Watt) to see whether there were any variations during the day and whether repeat measurements were affected by adaptation. Blood pressure measurements repeated three times during ergometry, gave good agreement above 1 Watt/kg body weight, with a mean of 203/116 mm Hg at 8 a.m., 200/114 mm Hg at 10 a.m. and 203/113 mm Hg at 4 p.m., although resting blood pressures at times differed significantly. Even in patients with labile or borderline hypertension, blood pressure measurement during and after ergometry without exception made it possible to assign them to the hypertensive range, which would not have been possible or only to a limited extent at rest. Measurement of blood pressure during and after standardised ergometry is thus superior to resting blood pressure measurements in the identification of hypertensives.

Fourteen patients with previously untreated essential hypertension and left ventricular hypertrophy were treated with a fixed-dose combination of acebutolol 200 mg and nifedipine 20 mg once daily for a followup of 25.6 +/- 1.8 months. Echocardiography showed a significant decrease after a mean period of 6.6 months in interventricular septal thickness (14.8%, p less than 0.001), posterior wall thickness (14.8%, p less than 0.001), and left ventricular mass index (21.3%). After 25.6 months, the reductions were 29% (p less than 0.001), 28.1% (p less than 0.001), and 38.7% (p less than 0.001), respectively. Left wall thickness was significantly reduced, but left ventricular end-systolic and end-diastolic dimensions and fractional shortening remained unchanged. Treatment reduced resting blood pressure from 161/102 mmHg to 132/87 mmHg (p less than 0.001) and reduced exercise blood pressure at 100 W from 208/113 mmHg to 170/94 mmHg (p less than 0.001). Thus, nifedipine in combination with acebutolol produces significant blood-pressure reduction accompanied by regression of left ventricular hypertrophy without noticeable changes in left ventricular function.

The efficacy of nifedipine (40 mg, long-acting preparation), nitrendipine (20 mg) and acebutolol (400 mg) in reducing blood pressure at rest and during exercise was assessed in 35 hypertensive patients using a crossover study with 4-week treatment periods. In 20 patients the antihypertensive effect of the combination of nifedipine and acebutolol was also investigated. Both calcium antagonists nitrendipine and nifedipine and the beta-receptor blocker acebutolol resulted in a significant (p less than 0.001) and almost identical reduction in systolic and diastolic blood pressure at rest. This was also true for diastolic blood pressure during and after work. Both calcium antagonists also revealed a significant (p less than 0.01-p less than 0.001) reduction in systolic exercise blood pressure, however, this effect was more pronounced with acebutolol. The additional application of nifedipine significantly enhanced the antihypertensive effect of acebutolol under resting conditions (p less than 0.05), and particularly during (p less than 0.01) and after (p less than 0.001) exercise. No adverse reactions to the monotherapy or to the nifedipine and acebutolol combination were found, in particular no effect on PQ interval or on serum lipids. It is concluded that nifedipine and nitrendipine and their combination with betablockers appear to offer an alternative therapeutic approach in the management of arterial hypertension.

The efficacy of nifedipine (40 mg), nitrendipine (20 mg), and acebutolol (400 mg) in reducing blood pressure at rest and during exercise was assessed in 35 hypertensive patients using a crossover study with 4-week treatment periods. In 20 patients, the antihypertensive effect of the combination of nifedipine and acebutolol was investigated. Both the calcium antagonists nitrendipine and nifedipine and the beta-receptor blocker acebutolol led to a significant (p less than 0.001) and almost identical reduction in systolic and diastolic blood pressures at rest. This was also the case with the diastolic blood pressure during and after work. Both calcium antagonists also revealed a significant (p less than 0.01; p less than 0.001) reduction in systolic exercise blood pressure; however, this effect was more pronounced with acebutolol. The additional use of nifedipine significantly enhanced the antihypertensive effect of acebutolol under resting conditions (p less than 0.05) but particularly during (p less than 0.01) and after (p less than 0.001) exercise. No adverse reactions to the monotherapy or to the nifedipine and acebutolol combination were found, in particular no effect on the PQ interval or the serum lipids. It is concluded that nifedipine and nitrendipine and their combination with beta-blockers appear to offer an alternative therapeutic approach in the management of arterial hypertension.