SummaryBrrckgmui7d: Epidemiologic evidence suggests that an elevated heart rate (HR) is an adverse and independent prognostic factor in arterial hypertension and other cardiovascular diseases. Although diltiazem is characterized as an HR-lowering calcium antagonist, no studies have quantified the magnitude of HR changes in patients with angina or hypertension.Hypothesis: The study was undertaken to explore the magnitude of proportional HR reduction at varying levels of resting HR with the sustained-release formulation of diltiazem (SR diltiazem) at the usual clinical doses of 200 or 300 mg once daily.Morlzods: This meta-analysis was conducted on six comparative double-blind studies including 77 1 patients with angina or hypertension in which SR diltiazem 200-300 mg once daily was compared either with placebo or with other agents known not to influence HR (angiotensin-converting enzyme inhibitors, diuretics). Sustained-release diltiazem decreases elevated baseline HR, with an increasing effect at higher initial rates.Results: Multiple comparisons by baseline HR category showed a significant difference between both groups for baseline HR of 74-84 beats/min and 2 85 beatdmin (p = 0.001 ). Sustained-release diltiazem had no significant HR-decreasing effect on baseline HR 1 7 4 beats/min but appears to have a genuine regulating effect on HR: it reduces tachycardia without inducing excessive bradycardia. These findings are in contrast to those with dihydropyridine calcium antagonists, which tend to increase HR and have been associated with an adverse outcome in acute cardiovascularconditions. At the same time, there is evidence to suggest that HR-lowering calcium-channel blockers decrease cardiovascularevent rates following myocardial infarction.Conclusion: When calcium antagonists are indicated for use in patients with angina or hypertension, an HR-lowering agent, that is, diltiazem rather than dihydropyridine, should be recommended.
The use of beta-blockers in heart failure for a long time was regarded as contra-indicated because of their negative inotropic effects. Nevertheless, there is growing evidence that beta-blockers slow down the progression of left ventricular dilatation that characterizes heart failure. In addition changes in left ventricular ejection fraction after several months of beta-blocker treatment appears to have predictive value for survival. This beneficial effect of beta-blockade in chronic heart failure needs to be assessed further. The presumed benefit of beta-blockade with betaxolol (CAS 63659-18-7), a highly selective beta-blocker with long duration of action in chronic heart failure (CHF) will be assessed in BETACAR, a comparative study versus carvedilol (CAS 72956-09-3). The design of this study is provided in this article.
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