Oral beta-adrenergic blockade with metoprolol in chronic severe dilated cardiomyopathy

Abstract

A double-blind crossover trial was performed to assess the effect of metoprolol in 10 patients (mean age 55 years) with severe dilated cardiomyopathy. All patients clinically had idiopathic dilated cardiomyopathy; however, at coronary angiography, four had occult coronary disease. All were in New York Heart Association functional class III with a left ventricular ejection fraction less than 35% as assessed by rest radionuclide ventriculography. Studies were performed before treatment, after 4 weeks of metoprolol therapy and after 4 weeks of placebo administration. Erect bicycle sprint exercise was used to determine maximal work load. Hemodynamic variables and radionuclide left ventricular ejection fraction were recorded at rest and during graded supine bicycle exercise. Cardiac medications were unchanged throughout the trial. The mean (+/- standard error of the mean) dose of metoprolol was 130 +/- 13 mg/day. Metoprolol did not change symptoms, chest X-ray findings or exercise tolerance (baseline 700 +/- 73, placebo 690 +/- 85, metoprolol 710 +/- 81 kilopond-meters [kpm]/min). Metoprolol produced a significant decrease in heart rate at rest and during exercise (p less than 0.001). Mean blood pressure and left ventricular filling pressure did not differ significantly in the baseline, placebo and metoprolol studies. There was a slight, but significant (p less than 0.05) decrease in cardiac index with metoprolol compared with placebo and baseline studies. The small, but significant increase in left ventricular ejection fraction from baseline to the metoprolol and placebo studies (p less than 0.001) was considered a result of spontaneous improvement rather than of therapy. No significant differences were found between the patients with and without coronary disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Beta-blocker treatment of dilated cardiomyopathy. Beneficial effect of carteolol in mice.

“…The difference may be due to differences in the strain of mice, the virus, or the /3-adrenergic blocker. 30 A variety of mechanisms of the effect of f3-adrenergic blockers have been suggested, including 1) decreased myocardial energy demand, 2) improved diastolic relaxation, filling, and compliance, 3) protection of myocytes against the direct toxic effects of catecholamines, 4) inhibition of sympathetically mediated vasoconstriction through the release of prostaglandins and renin, 5) upregulation of 83-adrenergic receptors,33,34 and 6) anti-ischemic and antiarrhythmic effects. Another recently suggested mechanism is that the immune function is regulated in part by the sympathetic nervous system.3536 In view of the evidence for impaired cellular and humoral immunity in dilated cardiomyopathy such as defective natural killer and suppressor cell activities3738 and of the existence of autoantibodies against the cardiac /3-adrenergic receptors,39 it is certainly possible that inhibiting the effect of catecholamines on the immune system by ,B-adrenergic blockers may lead to reversal of some of these immune abnormalities.…”

“…To investigate the effect of carteolol on virus replication, BALB/c mice were given carteolol at a dose of 1 (n=10), 10 (n=10), 30 (n=11), or 100 mg/kg (n=9), or distilled water (n=23). Treatment was performed by daily subcutaneous injection starting on the day of inoculation.…”

Update on Pharmacological Heart Failure Therapies in Children

“…Early trials of β-blockers in adult heart failure patients failed to meet the primary end point of improvement in exercise tolerance, although an improvement in ejection fraction was noted. 22,23 Although it may be tempting to conclude that an improvement in symptoms or exercise tolerance from a medication would be sufficient to reasonably conclude that mortality would also be improved, this should be done with caution. Inotropic medications such as dobutamine and milrinone improve cardiac output and heart failure symptoms.…”

<![CDATA[<B>I Diretrizes do Grupo de Estudos em Cardiogeriatria</B> <B>da Sociedade Brasileira de Cardiologia</B>]]>

“…A redução da freqüência cardíaca diminui o consumo de oxigênio miocárdico e pode aumentar o tempo de perfusão coronariana pelo prolongamento da diástole, com efeitos favoráveis na isquemia miocárdica. A pressão arterial sistó-lica tende a cair no início do tratamento, porém estabiliza-se ou mesmo eleva-se posteriormente 69 .…”