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I W Franz

Publications and source records attributed to I W Franz.

At least 37 records · Page 2Linked 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↗
PubMed1996

Blood pressure measurement during ergometric stress testing.

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.

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↗
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

[Disordered 24-hour blood pressure rhythm in normotensive and hypertensive asthma patients].

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.

Asthma↗
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

Blood pressure response to exercise in normotensives and hypertensives.

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.

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↗
PubMed1988

Regression of left ventricular hypertrophy during combined atenolol and nifedipine treatment.

36 patients with previously untreated essential hypertension and left ventricular hypertrophy were treated with a fixed dose combination of atenolol 50 mg and sustained release nifedipine 20 mg once daily for a mean period of 12.1 months. Echocardiography showed a significant decrease after a mean period of 7.9 months in interventricular septal thickness (13.6%, p less than 0.01), posterior wall thickness (12.6%, p less than 0.001) and left ventricular mass index (18.3%). After 12.1 months the reductions were 20.7% (p less than 0.001), 22.5% (p less than 0.001) and 30.8% (p less than 0.001), respectively. Posterior wall thickness was significantly reduced, but left ventricular end-systolic and end-diastolic dimensions and fractional shortening remained unchanged. Treatment significantly reduced resting blood pressure from 153/105 mm Hg to 122/79 mm Hg (p less than 0.001), and exercise blood pressure at 100W from 189/109 to 157/93 mm Hg (p less than 0.001). Thus, nifedipine in combination with atenolol produces significant blood pressure reduction accompanied by regression of left ventricular hypertrophy without noticeable changes in left ventricular function.

Adult↗