The blood pressure and heart rate during sauna bath correspond to cardiac responses during submaximal dynamic exercise.

OBJECTIVES: In the present study, the reaction of blood pressure and heart rate are examined during and after a single acute sauna application. DESIGN: In 19 healthy adult volunteers (7 women, aged 46.4±10.2 years, BMI 24.4±2 kg /m2), blood pressure (BP) and heart rate (HR) were measured during a 25-minute sauna session (93°C, 13 % humidity) and during a subsequent 30-minute rest period. The parameters obtained were compared with the BP and HR responses during submaximal dynamic exercise testing. RESULTS: The heat exposure resulted in a significant (p<0.01) and progressive increase in systolic and diastolic BP. After the sauna bath, BP decreased and showed significantly (p<0.001) lower values compared to baseline. HR also increased continuously during heat application (p<0.001), resulting in a significant increase (p<0.001) in systolic BP x HR as a measure of myocardial oxygen consumption. After the end of the sauna session, both the BP and the HR decreased steadily (p<0.001).When comparing BP and HR during the sauna session with the reaction during a dynamic exercise test, sauna bathing was equivalent to an exercise load of about 60-100 watts. CONCLUSIONS: Contrary to popular belief, acute sauna use does not lead to a reduction, but to an increase in BP and HR with a consequent increase in myocardial oxygen consumption. The cardiac load during the sauna use corresponds to a moderate physical load of 60-100 watts.

[Endurance training in hypertension is effective. Which form of sports, frequency and intensity of training? When should adjuvant chemotherapy be considered?]. / Ausdauertraining in der Hypertoniebehandlung erfolgreich. Welche Sportart, Trainingshäufigkeit und -intensität? Wann adjuvante medikamentöse Therapie?

Physical activity in the form of endurance training is highly recommendable for hypertensives. Both suitable and unsuitable forms of sports are identified. From various points of view, two one-hour sessions per week would appear to be optimal. The intensity of the activity should be oriented to the heart rate, and, for safety's sake, prior ergometric evaluation should be carried out. As a rule of thumb, the heart rate should not exceed 70% of the maximum rate during exercise. If the blood pressure should nevertheless increase too much, appropriate pharmacological treatment is indicated.

Efficacy and position of endurance training as a non-drug therapy in the treatment of arterial hypertension.

Regular conditioning has been well documented to exert a beneficial effect on cardiovascular risk factors and to improve overall cardiovascular health and to reduce the incidence of coronary disease. There are conflicting results concerning the effect of physical exercise on blood pressure (BP) in hypertensive patients and its importance in the treatment of hypertension. Therefore 10 male patients with mild arterial hypertension were studied in order to define the BP response to long-term aerobic training (60 min twice a week) under resting conditions, during standardised ergometric workload, during isometric exercise, during cold pressor testing and during 24-h BP monitoring. After 18 months of regular training there were significant reductions in arterial pressures at rest, during and after standardised ergometry and during isometric and cold pressor testing when compared with pre-training. The heart rate also decreased significantly during exercise testing thus implying a decrease in myocardial oxygen consumption. After long-term training, a reduction in systolic and diastolic BP could also be shown during 24-h ambulatory BP monitoring. These results demonstrate that long-term aerobic training leads to a decrease in systolic and diastolic BP at rest, during exercise and during 24-h BP monitoring and imply a beneficial effect in the management of hypertension that is nearly comparable to that of drug therapy.

Systemic and regional hemodynamic effects of gallopamil in patients with essential hypertension.

Systemic and regional hemodynamics were assessed in 10 patients with uncomplicated mild to moderate essential hypertension before and during gallopamil therapy. Cardiac output was measured in triplicate with indocyanine dye. Plasma volume and renal blood flow were measured radioisotopically. Immediately following the initial dose of a slow-release (SR) formulation of gallopamil, a significant fall in arterial pressure associated with a decreased total peripheral resistance and a reflex increase in heart rate and cardiac output were seen. Then, after 8-12 weeks of treatment, arterial pressure and total peripheral resistance remained reduced, but heart rate and cardiac output returned to pretreatment levels. Gallopamil also produced significant reductions in renal and splanchnic vascular resistance. Plasma volume and total blood volume did not change. Thus, gallopamil reduced arterial pressure and vascular resistances without fluid retention or prolonged reflexive changes.

[Decreasing the antihypertensive dosage during longterm treatment and complete regression of left ventricular hypertrophy]. / Verringerung der Antihypertonika-Dosis während Langzeitbehandlung und kompletter Rückbildung einer linksventrikulären Hypertrophie.

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.

Fitness in the fit: does physical conditioning affect cardiovascular risk factors in middle-aged marathon runners?

OBJECTIVE: The study was designed to assess cardiovascular risk factors in marathon runners with different degrees of fitness. DESIGN: A total of 30 male middle-aged marathon runners were divided according to their marathon running time into fit (265 +/- 8 min), fitter (222 +/- 5 min) and fittest (178 +/-12 min). The three groups of 10 runners each were comparable in age, weight, and body surface area. Cardiovascular risk factors were assessed by measuring arterial pressure before and during exercise (150 watts) and determination of plasma lipoproteins, uric acid, glucose and white blood cell count before and after a marathon run. RESULTS: All measured laboratory values such as high-density lipoprotein cholesterol (P < 0.05), low-density lipoprotein cholesterol (P < 0.05), total cholesterol (non-significant), triglycerides (non-significant), blood sugar (non-significant), uric acid (P < 0.01) and white blood cell count (P < 0.05) indicated a lower cardiovascular risk in the fastest when compared with the slowest runners. Resting blood pressure was similar in the three groups but consistently lower at all levels of exercise in the fittest when compared with the less fit runners. The fittest runners also showed greater increases in high-density lipoprotein cholesterol after the marathon run (14% vs 8% in the slowest runners, P < 0.005). CONCLUSIONS: We conclude that even at the extreme end of a continuum such as represented by well-conditioned, middle-aged marathon runners, cardiovascular risk factors are related to the degree of fitness, as measured by the marathon running time.

Time course of reduction in left ventricular mass during long-term antihypertensive therapy.

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.

Is a decrease in arterial pressure during long-term aerobic exercise caused by a fall in cardiac pump function?

Ten healthy normotensive volunteers demonstrated a progressive decrease (p < 0.01) in systolic and diastolic pressures during 1 hour of aerobic exercise. Cardiac function and structure were assessed by M-mode echocardiography before exercise and, at the same heart rate, after 5 minutes of exercise and after 60 minutes of exercise. After 5 minutes of exercise, heart rate, cardiac output, ejection fraction, fractional fiber shortening, and contractility index significantly increased (p < 0.01, p < 0.05, respectively) and total peripheral resistance decreased (p < 0.01) compared with resting values. When compared with the values at minute 5, there was a decrease (p < 0.01) in cardiac output, ejection fraction, fractional fiber shortening, and contractility index (p < 0.05) and an increase (p < 0.05) in total peripheral resistance after 60 minutes of exercise. We conclude that the gradual decrease in arterial pressure seen with prolonged aerobic exercise is the result of a fall in cardiac pump function (as measured by cardiac output, ejection fraction, fractional fiber shortening, and contractility index), possibly indicating cardiac fatigue.)

Left ventricular hypertrophy: a pressure-independent cardiovascular risk factor.

Left ventricular hypertrophy (LVH), an increase in the muscle mass of the left ventricle, has been identified as a powerful risk factor for future cardiovascular morbidity and mortality. The risk of acute myocardial infarction, congestive heart failure, sudden death, and other cardiovascular events increases sixfold to eightfold with the occurrence of LVH. The increase in myocardial mass lowers coronary reserve and enhances cardiac oxygen requirements, gives rise to ventricular ectopy, and impairs left ventricular filling and contractility. Hypertension, obesity, advanced age, valvular heart disease, and other pathologic disorders that cause an increase in the hemodynamic burden can lead to LVH. LVH and its sequelae can be reduced by specific antihypertensive therapy, but despite these promising findings, future epidemiologic studies are necessary to document the clinical benefits of a reduction in LVH.

Preserved ventricular pump function after a marked reduction of 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.

Depressed systolic and diastolic cardiac function after prolonged aerobic exercise in healthy subjects.

We studied 11 healthy untrained volunteers (aged 28.9 +/- 4.6 years) during 60 minutes of aerobic ergometric exercise with constant heart rates of 130 to 140 beats/minute. We found a continuous and significant decrease in systolic and diastolic pressure from 175 +/- 18/77 +/- 7 mmHg in the 5th minute to 144 +/- 14/68 +/- 6 mmHg in the 60th minute of exercise. Cardiac function and structure were assessed by M-mode echocardiography before exercise, after 5 minutes and after 60 minutes of exercise at comparable heart rates. The results demonstrated significant decreases in cardiac output, ejection fraction, and diastolic posterior wall velocity and an increase in total peripheral resistance after 60 minutes of exercise. We conclude that the decrease in blood pressure during long-term aerobic exercise in healthy untrained subjects might be at least influenced by a decrease in left ventricular filling and contractility, possibly indicating cardiac fatigue.

Comparison of the antihypertensive effects of carvedilol and metoprolol on resting and exercise blood pressure.

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.

Hemodynamic and metabolic effects of intravenous clentiazem in hypertensive patients.

To determine the hemodynamic and certain metabolic effects of clentiazem, a diltiazem congener, 10 untreated essential hypertensive patients were given the calcium antagonist in 3 successive doses totaling 1.0 mg/kg intravenously. Mean arterial pressure and total peripheral resistance progressively declined from 121 +/- 3 mm Hg and 47 +/- 2 U (mean) to 110 +/- 3 mm Hg and 33 +/- 1 U, respectively (p less than 0.05); heart rate remained unchanged. Cardiac output increased as a result of augmented cardiopulmonary volume (p less than 0.05) produced by peripheral venoconstriction and norepinephrine release (from 258 +/- 41 to 319 +/- 42 pg/ml; p less than 0.01). Surprisingly, there was an immediate reduction in plasma aldosterone (10.4 +/- 1.2 to 6.5 +/- 1.0 ng/dl; p less than 0.01), serum potassium (4.3 +/- 0.1 to 3.6 +/- 0.1 mEq/dl; p less than 0.001) and calcium (9.5 +/- 0.1 to 8.8 +/- 0.1 mg/dl; p less than 0.001) concentrations, whereas epinephrine increased (21.2 +/- 3.3 to 45.8 +/- 5.9 pg/ml; p less than 0.002). Previous studies with diltiazem, conducted similarly, did not show these changes. Therefore, clentiazem reduced mean arterial pressure through a decrease in total peripheral resistance, and released epinephrine was associated with intracellular potassium influx (urinary potassium did not change). The inhibited aldosterone release was not compensated by altered renal blood flow, glomerular filtration or increased plasma renin activity. These findings underscore the concept that calcium antagonists are a remarkably heterogeneous antihypertensive group.

Hemodynamic comparison of two nifedipine formulations in patients with essential hypertension.

The hemodynamic and humoral effects and trough-to-peak 24-hour blood pressure responses of 2 nifedipine formulations, capsules and continuous-release once-daily formulation tablets, were evaluated in 10 patients with mild to moderate essential hypertension. Both formulations reduced mean arterial pressure similarly from 120 +/- 3 (baseline) to 107 +/- 2 (p less than 0.005) and 105 +/- 2 mm Hg (p less than 0.005) and total peripheral resistance index from 65 +/- 9 (baseline) to 47 +/- 4 (p less than 0.05) and 45 +/- 3 U/m2 (p less than 0.05), respectively. Renal, splanchnic and total forearm (including skin and skeletal muscle) blood flows were maintained or even increased slightly associated with reductions in regional vascular resistances. Decreases in renal, total forearm and skeletal muscle resistances were significant (p less than 0.05) with the capsules, but the decrease was only significant in renal resistance with the long-acting tablets. Intravascular volume did not expand with reduction in arterial pressure. This antihypertensive effect was not related to baseline plasma renin activity levels or age. Nifedipine tablets provided a better control of mean arterial pressure (66%) than did capsules (44%).

Hypertension: left ventricular hypertrophy, ventricular ectopy, and sudden death.

Left ventricular hypertrophy (LVH) has been identified as a significant risk factor for future cardiovascular morbidity and mortality. LVH and its sequelae such as myocardial ischemia, impaired filling and contractility, ventricular arrhythmias, and congestive heart failure can be reduced by specific antihypertensive agents. Future clinical trials will determine whether a reduction of LVH will ultimately improve its inherent ominous prognosis.

Hemodynamic effects of celiprolol in essential hypertension.

The immediate and short-term (2 week) hemodynamic and humoral effects of the beta-1 antagonist, beta-2 agonist, celiprolol, were compared with those of more prolonged atenolol therapy in 12 patients with essential hypertension. Celiprolol produced an immediate dose-dependent decrease in mean arterial pressure (113 +/- 3 to 102 +/- 2 mm Hg; p less than 0.001) and total peripheral resistance (49 +/- 3 to 38 +/- 1 U/m2; p less than 0.005) that was associated with an increased heart rate (67 +/- 1 to 73 +/- 2 beats/min; p less than 0.01) and cardiac index (2,347 +/- 129 to 2,708 +/- 111 ml/min/m2; p less than 0.01). Both celiprolol and atenolol reduced mean arterial pressure with short-term treatment (p less than 0.01); this was associated with a reduced total peripheral resistance with celiprolol (from 24 +/- 1 to 21 +/- 1 U/m2; p less than 0.02) and was not observed with atenolol. Moreover, in contrast with atenolol, celiprolol did not change heart rate or stroke and cardiac indexes. Splanchnic and forearm vascular resistances decreased with celiprolol (p less than 0.05) but not with atenolol; neither beta-blocking drug altered renal blood flow. These results demonstrate that the hemodynamic effects of celiprolol were strikingly different from atenolol; celiprolol reduced arterial pressure and total peripheral and certain vascular resistances without altering heart rate, cardiac index or regional blood flows. These effects may be explained by celiprolol's cardiac beta-1 receptor inhibitory and peripheral beta-2 receptor agonistic effects.