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Biomedical subjects

R Ketelhut

Publications and source records attributed to R Ketelhut.

At least 19 recordsLinked to original sources
PubMed1996

[Decreasing the antihypertensive dosage during longterm treatment and complete regression of left ventricular hypertrophy].

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.

Adult↗
PubMed1994

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.)

Adult↗
PubMed1994

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.

Adult↗
PubMed1993

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.

Antihypertensive Agents↗
PubMed1992

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.

Aged↗
PubMed1992

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.

Adrenergic beta-Antagonists↗
PubMed1992

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.

Adrenergic beta-Antagonists↗
PubMed1992

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.

Adult↗
PubMed1991

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%).

Capsules↗
PubMed1991

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.

Adrenergic beta-Antagonists↗
PubMed1991

Long-term studies on regression of left ventricular hypertrophy.

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.

Adult↗
PubMed1991

Impaired left ventricular function during exercise in hypertensive patients with normal coronary arteriograms.

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.

Blood Pressure↗
PubMed1991

Left ventricular hypertrophy: an independent 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 six- to eightfold with the presence 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 disorders that cause an increase in the hemodynamic burden can lead to LVH. Left ventricular hypertrophy and its sequelae can be reduced by specific antihypertensive therapy but, despite these promising findings, future epidemiological studies are necessary to document the clinical benefits of a reduction of LVH.

Cardiomegaly↗
PubMed1991

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.

Antihypertensive Agents↗
PubMed1990

[Regression of left ventricular hypertrophy in hypertensive patients under long-term therapy with antihypertensive agents].

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.

Acebutolol↗
PubMed1989

Regression of left ventricular hypertrophy by acebutolol and nifedipine.

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.

Acebutolol↗
PubMed1989

[Regression of left heart hypertrophy in hypertensive patients as a result of antihypertensive therapy].

In a previous study (1) we could show a significantly more pronounced reversal of LVH with metoprolol than with gallopamil, whereas the combined therapy with atenolol and nifedipine was even more effective. We now report in 121 previously untreated hypertensive patients the longterm effect of the beta-blocker metoprolol (200 mg/die); 25 patients, mean age 43.6 yrs., follow-up 32.1 +/- 3.5 months, group A); the calcium antagonist gallopamil, 26 patients, mean age 49.7 yrs., follow-up 36.2 +/- 2.6 months, group B); the combined therapy with 50 mg atenolol and 20 mg nifedipine, 35 patients, mean age 44.5 yrs., follow-up 31.7 +/- 1.1 months, group C); 200 mg acebutolol and 20 mg nifedipine, mean age 52.1 yrs., follow-up 31.8 +/- 1.8 months, group D); 50 mg atenolol and 10 mg enalapril, mean age 43.3 yrs., follow-up 31.9 +/- 1.3 months, group E). Similar results were obtained for intraventricular septal and posterior wall thickness. Left ventricular enddiastolic dimensions remained unchanged but fractional shortenings were significantly (p less than 0.05-p less than 0.01) increased after 32 months of treatment.

Acebutolol↗