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F X Kleber

Publications and source records attributed to F X Kleber.

At least 73 records · Page 4Linked to original sources
PubMed1992

Impact of converting enzyme inhibition on progression of chronic heart failure: results of the Munich Mild Heart Failure Trial.

OBJECTIVE: Neurohormonal activation has major impact on the pathophysiology of congestive heart failure. The Munich Mild Heart Failure Trial was designed to test the hypothesis that interference with the renin-angiotensin system by angiotensin converting enzyme inhibition favourably influences the natural history of heart failure. DESIGN AND PATIENTS: 170 patients, median New York Heart Association (NYHA) class II, were randomised to double blind treatment with 25 mg captopril twice a day or placebo in addition to standard treatment for a median observation period of 2.7 years. MAIN OUTCOME MEASURES: Progression of heart failure to NYHA class IV on an optimally adjusted standard treatment, death due to progressive heart failure, and sudden death. RESULTS: Heart failure progressed to class IV in nine patients (10.8%) treated with captopril and in 23 patients (26.4%) treated with placebo (p = 0.01). The mean survival time until this end point was 223 days longer in the captopril group (Kaplan-Meier life table analysis; p = 0.02). Also, progressive deterioration to severe heart failure was a powerful predictor of total mortality and death from heart failure; 80% of deaths due to progressive heart failure occurred after this end point. There were fewer deaths caused by progressive heart failure in the captopril group than in the placebo group (4 v 11; p = 0.10) but similar numbers of sudden deaths (11 v 10). Progressive heart failure was the cause of death in 18.2% of all deaths in the captopril group and 50% in the placebo group. Total heart failure events (the end point on which power calculation was based) were also more common in the placebo group (19 v 32 events) but not significantly so. Total mortality was similar to both groups (22 of 83 v 22 of 87). CONCLUSIONS: Angiotensin converting enzyme inhibition in conjunction with standard therapy early in the course of congestive heart failure slowed the progress of heart failure and thus favourably altered the natural history of the disease.

Adolescent↗
PubMed1992

Ibopamine as a valuable adjunct and substitute for dopamine in bridging therapy before heart transplantation.

Ibopamine is an active dopamine analogue leading to improved renal perfusion and afterload reduction in heart failure. This report describes casuistic experiences in patients with severe heart failure awaiting heart transplantation. All patients could be stabilized, intravenous catecholamines be discontinued, and diuretics be reduced. Six of seven patients could be successfully transplanted. No major side effects were noted. Thus ibopamine can be a suitable adjunct for patients with endstage heart failure.

Adult↗
PubMed1992

Mechanisms involved in cardiac enlargement and congestive heart failure development after acute myocardial infarction.

For 3 months, we followed up 40 patients with acute myocardial infarction, 20 were randomly assigned to treatment with captopril and 20 to placebo, to elucidate mechanisms inducing left ventricular volume enlargement and development of congestive heart failure. Echocardiographic follow-up could be obtained in 28 patients, 11 of whom showed more than a 10% increase in left ventricular systolic and/or diastolic volumes (captopril n = 3/15, placebo n = 8/13, p = 0.05). Volume increase was significantly associated with an impairment in exercise capacity (VO2 max in patients with vs. without volume enlargement 24.7 +/- 1.7 vs. 29.5 +/- 1.9 ml O2/kg/min; p < 0.05). Plasma renin activity, angiotensin II and catecholamines were normal in the acute and chronic postinfarction phase in patients on placebo as well as in patients 12-24 h after captopril intake. Plasma atrial natriuretic peptide concentration (ANP) was increased immediately after myocardial infarction, but ANP levels almost normalized in patients with captopril treatment, while they continued to be elevated in patients on placebo. The only technical parameter able to predict left ventricular volume increases was the sphericity index (28.7 vs. 35.7; p = 0.07). We concluded that morphologic deformation and filling pressures as estimated from elevated ANP levels are major factors promoting remodelling following myocardial infarction. ACE inhibitors might exert their favorable effect predominantly by reducing filling pressure.

Atrial Natriuretic Factor↗
PubMed1991

Influence of severity of heart failure on the efficacy of angiotensin-converting enzyme inhibition.

Angiotensin-converting enzyme (ACE) inhibition slowed the progression of congestive heart failure (CHF) in 170 patients who were randomly assigned to either captopril or placebo in the Munich Mild Heart Failure Trial. The two major end points were progression from New York Heart Association (NYHA) functional classes I, II, or III to class IV, despite optimal, adjusted standard therapy, and death due to CHF. The relative risk for progressive CHF with captopril therapy was 0.34 (95% confidence interval = 0.17-0.68; p = 0.01). A total of 52 prerandomization variables were tested to determine their contribution to disease progression. Logistic regression analysis revealed 5 independent risk factors for progressive CHF: NYHA class, left ventricular end-systolic diameter, need for diuretic, age, and cardiothoracic ratio. The presence of greater than 2 of these risk factors increased the odds ratio for progression to 8.13 (p less than 0.001) compared with the presence of 0-2 risk factors. However, the effectiveness of captopril in preventing progression was higher within the subgroup of patients who had less severe CHF: the odds ratio was 0.12 (95% confidence interval = 0.03-0.45; p less than 0.01) for patients in NYHA class I or II on captopril and was 0.83 for those in class III. We conclude that the severity of CHF, as represented by the above-defined risk factors, is directly related to the likelihood for the development of progressive heart failure. However, the less severe the heart failure, the more effective the treatment with captopril will be in preventing disease progression. Thus, ACE inhibition has considerable potential for improving the prognosis of patients with mild heart failure.

Age Factors↗
PubMed1991

Therapeutic alternatives in dilated cardiomyopathy--a review of current options.

In addition to the underlying pathophysiological processes that cause myocarditis and dilated cardiomyopathy, structural, biochemical, neurohormonal and haemodynamic influences and interrelations promote progression of the heart failure syndrome. Independent of their symptomatic benefits, diuretics, digitalis, ACE inhibitors, PDE inhibitors and dopamine agonists exert specific influences on factors that retard or accelerate progression of congestive heart failure (CHF). Important factors that indicate or promote progression of CHF are discussed here, with special emphasis on therapeutic options. Interference with baroreceptor function (digitalis, ACE inhibitors), the RAA system (ACE inhibitors), the sympathetic nerve system (dopamine agonists, ACE inhibitors, digitalis) can potentially retard progression of CHF, while other therapeutic options, such as PDE inhibitors and diuretics, might accelerate progression of left ventricular dysfunction and CHF.

Adrenergic beta-Antagonists↗
PubMed1991

[Ibopamine--clinical results].

Recently, major advances have been made in the therapy of chronic congestive heart failure. New vasodilatory and positive inotropic drugs as well as specific antagonists to activated neurohormones have added new therapeutic dimensions. Dopaminergic stimulation, which has been used in acute heart failure for many years has now been introduced with the new substance ibopamine into the therapy of chronic heart failure. The therapeutic efficacy of new drugs in the treatment of chronic congestive heart failure has to be evaluated in terms of their prognostic and therapeutic impact for improvement and symptomatology, which sometimes does not necessarily lead to improvement of prognosis. Ibopamine has potential in improving prognosis by its major effects: vasodilatation, decrease in vasoactive hormones and improvement in renal blood flow and water diuresis. In the long-term therapy of chronic congestive heart failure ibopamine has been useful in mobilization of edema in acute decompensation, improvement of symptoms according to the New York Heart Classification and of exercise tolerance. In addition improvement of hemodynamics with an increase in cardiac output, a decrease in filling pressures and in peripheral resistance has been demonstrated. Efficacy of diuretics is improved and ibopamine has been a valuable adjunct in the pre-operative therapy before cardiac transplantation. Major positive inotropic effects in the usual dose of 100 mg tid, as well as other potentially dangerous effects of beta-receptor-stimulation (such as malignant, ventricular arrhythmias) can be largely excluded. Historically, controls of patients with heart failure of similar severity do not suggest any unfavorable effect of this drug on prognosis.

Cardiotonic Agents↗
PubMed1991

[Prognosis of mild chronic heart failure: effects of the ACE inhibitor captopril].

UNLABELLED: The Munich Mild Heart Failure Trial (MHFT) investigated the influences of ACE-inhibition on progression of congestive heart failure (CHF). Major end points were progression of CHF from New York Heart Association (NYHA) functional classes I to III to NYHA functional class IV despite optimal adjusted standard therapy and death due to congestive heart failure, i.e. death due to pump failure or sudden death. 170 patients were randomly assigned to treatment with either captopril (n = 83) 25 mg b.i.d. or placebo in addition to standard therapy for a median observation period of 2.7 years. The major result of this trial was the decrease in the relative risk for progressive heart failure by captopril therapy to 34% (95% confidence interval 17 to 68%; p = 0.01). Though total mortality was not reduced, death due to pump failure was found considerably less often on captopril than on placebo (18.2 vs 50% of total deaths in each group). In addition this report describes influences of captopril therapy on left ventricular size and function, heart size on X-ray, influences on symptomatology, electrolytes, ventricular arrhythmias, on concomitant therapy as well as effects in various subgroups. The major finding of the trial--the influence on progression of CHF--was independent of the underlying cardiac disease and was consistent in subgroups with different etiology of heart failure. Captopril blunted the increase in norepinephrine levels usually seen with increasing severity of congestive heart failure. There was a significant increase in serum sodium and potassium levels in the captopril treated group. Left ventricular size and function were well preserved in the patients still on randomized therapy after two years. No effects of therapy on ventricular ectopic activity were found in a subgroup of 93 patients that had had Holter monitoring. IN CONCLUSION: Captopril has marked effects on progression of disease and reduces the likelihood of progressive heart failure in patients with mild symptoms. Several indices of unfavourable prognosis are either improved (sodium, norepinephrine, angiotensin II) or stabilized (left ventricular function). Thus ACE-inhibitors are to be considered for all patients requiring medical therapy for congestive heart failure.

Captopril↗
PubMed1990

Persistent atrioventricular block in Lyme borreliosis.

Cardiac manifestations are reported in 0.3%-4.0% of European patients with Borrelia burgdorferi (B.b.) infection. Usually symptoms disappear within 6 weeks. We report a case with persistent impairment of atrioventricular (AV) conduction. Diagnosis was confirmed by demonstration of IgM antibodies and increase of IgG antibody titers against B.b. in serum, by isolation of the spirochete from skin biopsy material and by the typical clinical combination of erythema migrans, Bannwarth syndrome (meningoradiculitis), and complete heart block. Despite immediate antibiotic therapy with ceftriaxone, first degree AV block and second degree block Wenckebach with atrial pacing at 100 beats/minute persisted for 2 years. We conclude, that Lyme carditis can cause long-standing or irreversible AV conduction defects despite adequate and early antimicrobial therapy.

Adult↗
PubMed1990

[Heart insufficiency and life expectancy--the role of ACE inhibitors].

Before efficacy of therapy has been proven in large populations years or decades may pass. Meanwhile the medical profession has to rely on probabilities. This holds true regarding improvement of prognosis of CHF by ACE inhibition. While symptomatic improvement of CHF by addition of ACE-inhibition. While symptomatic improvement of CHF by addition of ACE-inhibitors has been demonstrated in numerous studies, improvement of prognosis has not yet been demonstrated entirely sufficiently. Only one trial has been published so far in a severely ill but not very exactly defined population (66). Animal studies and several small or interim published trials, however, show that the positive influence of ACE-inhibitors on CHF pathophysiology and symptomatology might favourable affect the prognosis as well. The SAVE trial and the SOLVD trial - both have randomized several thousand patients - will give answers concerning the influence of Captopril and Enalapril on prognosis of symptomatic as well as asymptomatic left ventricular dysfunction and on progression of left ventricular dilatation. The VHEFT II trial will compare the effect of ACE-inhibitors with the combination of ISDN and Hydralazine. Results will be available within the first few years of this decade.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1990

Treatment of mild chronic congestive heart failure with ibopamine, hydrochlorothiazide, ibopamine plus hydrochlorothiazide or placebo. A double-blind comparative study.

This multicentre, double-blind, double-dummy, randomised parallel group study in 247 patients with mild chronic congestive heart failure compared the efficacy and tolerability of ibopamine, hydrochlorothiazide (HCTZ), ibopamine plus HCTZ and placebo during an 8-week treatment period. The combination of ibopamine and HCTZ resulted in a significantly greater reduction in body weight (p less than 0.05) than HCTZ alone. Trends in favour of the combination as compared to ibopamine or HCTZ alone and in favour of ibopamine as compared to HCTZ were observed. All active treatments were superior to placebo. All active treatments were well tolerated. There was a trend towards a higher incidence of hypokalemia in patients treated with HCTZ, alone or in combination, compared to those receiving ibopamine alone or placebo.

Adult↗
PubMed1990

Ibopamine versus digoxin in the treatment of mild congestive heart failure. A double-blind, randomized, placebo-controlled trial.

We describe a randomized double-blind 4-week study on the efficacy of monotherapy with ibopamine 200 mg b.i.d. in comparison to placebo and open titrated digoxin in patients with mild congestive heart failure NYHA class I and II. A total of 60 patients (22 males and 38 females) were evaluated for body weight, signs and symptoms score and the need for additional diuretic treatment for adequate symptom control. Mean decreases in body weight in the ibopamine group exceeded mean decreases in body weight in the placebo group (3.03 kg). The signs and symptoms score was improved in 7 out of 20 patients in the placebo group, in all patients treated with ibopamine and in 21 of 22 patients of the digoxin subgroup while the patient-questionnaire score improved in 23.5% (placebo), 100% (ibopamine) and 81.2% (digoxin) of the cases, respectively. There were no treatment failures in the ibopamine and digoxin group. However, 8 of 20 patients receiving placebo had need of additional diuretic therapy. No adverse drug reactions were reported in the ibopamine-treated patients. We conclude that ibopamine monotherapy over 4 weeks has favourable effects on body weight and signs and symptoms of mild congestive heart failure without exerting major side effects. The efficacy is comparable to digoxin therapy.

Adult↗
PubMed1990

[Progressive left ventricular dilatation following anterior myocardial infarct as a determinant for the development of heart failure].

35 consecutive patients were studied prospectively with respect to echocardiographic left ventricular size after anterior myocardial infarction. In 25 patients sufficient follow-up was possible. Another 57 patients and volunteers were examined to prove accuracy in comparison to angiocardiography and nuclear magnetic resonance imaging and reproducibility as well as to define normal values. While two-thirds of all patients did not develop left ventricular dilation, one-third showed marked dilation with left ventricular size being 41% above mean normal value. All patients who subsequently developed congestive heart failure or died were in this group. Two-thirds showed no left ventricular dilation and had an uneventful follow-up. Mean left ventricular dilation for all infarcts was 22% within 4 weeks and 26% within 6.3 months, but some patients showed marked left ventricular dilation beyond 4 weeks. We conclude that serial echocardiography is very useful for stratification of risk for CHF after myocardial infarction, and left ventricular dilation is a major risk factor for CHF.

Adult↗
PubMed1987

Congestive heart failure due to mitochondrial cardiomyopathy in Kearns-Sayre syndrome.

Despite extensive analysis of the ultrastructural changes in skeletal muscle fibers in chronic progressive external ophthalmoplegia (CPEO), similar changes in the heart muscle fibers of patients with cardiac involvement in CPEO, called Kearns-Sayre syndrome, have not been described in detail. We report the clinical long-term course in a patient with Kearns-Sayre syndrome in whom mitochondrial cardiomyopathy was suspected in vivo and was confirmed at autopsy as the underlying cause of severe dilative cardiomyopathy. Enlarged, abnormally structured, excessively augmented mitochondria and loss of myofibrils could be shown both in skeletal and heart muscle cells.

Adult↗
PubMed1987

[Effect of captopril on the life expectancy of patients with chronic heart failure].

UNLABELLED: Since the introduction of vasodilator therapy, progress has been realized in the management of advanced congestive heart failure (CHF) of different etiologies. The most encouraging influences on hemodynamics, exercise tolerance and symptomatology have been reported with ACE-inhibitors. While hemodynamic parameters do correlate with prognosis in CHF [11, 14, 27], the overall prognosis in CHF is very poor [19], and there is no tight correlation between symptomatology, hemodynamics and prognosis [13]. A powerful influence of ACE-inhibitors has been demonstrated not only on hemodynamics and on the neuro-endocrine activation in CHF [10], but also on left ventricular hypertrophy [22] and myocardial morphology [16, 23]. On the background of these therapeutic options, we designed a double-blind, randomized, placebo controlled trial on the efficacy of captopril on mortality and morbidity in chronic CHF. The basic population studied consists of patients of a large community, university-affiliated hospital, with five sub-specialized divisions in internal medicine, and about 600 medical beds. All patients considered for participation live in the greater Munich area. INCLUSION CRITERIA: With slight modifications, the criteria used in the Framingham Study were used as entrance criteria [19]. Patients were randomized if they were on stable therapy for their chronic congestive heart failure usually on digitalis and diuretics. Endpoints for the double-blind treatment period were either death or severe (with digitalis and diuretics) untractable heart failure NYHA Class IV. Follow-up examinations comprised office visits of the patients every three months for a precise cardiac history over the last three months based on a questionnaire. Captopril was used in a dose of 25 mg b.i.d.(ABSTRACT TRUNCATED AT 250 WORDS)

Captopril↗
PubMed1982

Alterations in the electrocardiogram of spontaneously hypertensive rats by chronic antihypertensive therapy with captopril.

To determine whether the electrocardiogram (ECG) could detect a reduction in ventricular mass with chronic antihypertensive therapy, ECGs were obtained in two year old female normotensive (NR) and spontaneously hypertensive rats (SHR) following nine months of treatment with captopril or water. The ECG of untreated SHR was considerably different than that of age- and sex-matched NR. The notable differences were the increased voltage, left axis deviation, a delay in the intrinsicoid deflection, and the increased frequency of left atrial abnormalities. Chronic captopril therapy produced a substantial reduction in left ventricular mass in the SHR (NR, 0.63 +/- 0.01; SHR, 1.08 +/- 0.03; captopril SHR, 0.80 +/- 0.04 g). The ECG reflected this regression of left ventricular hypertrophy since the voltage and axis of the treated SHR were no longer different than those of NR. Thus, the ECG may be effective in evaluating the regression of cardiac hypertrophy in response to chronic therapy in experimental hypertension.

Animals↗