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Calcium antagonists like nifedipine show short-term benefits in heart failure but not sustained effects with daily use. Acute doses of verapamil, diltiazem, and nifedipine improve hemodynamics in pulmonary hypertension.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Clinical use of calcium antagonists in heart failure is limited, primarily involving nifedipine.
- Limited data exists for diltiazem and verapamil in congestive heart failure.
Purpose of the Study:
- To review the clinical experience and hemodynamic effects of calcium antagonists in congestive heart failure and pulmonary hypertension.
Main Methods:
- Review of existing clinical data and hemodynamic studies on nifedipine, diltiazem, and verapamil.
- Analysis of acute and chronic administration effects in patients with heart failure, aortic regurgitation, and pulmonary hypertension.
Main Results:
- Single-dose nifedipine decreased vascular resistance and improved cardiac output in acute heart failure.
- Sustained daily nifedipine (80 mg) did not show significant improvements in chronic heart failure.
- Acute administration of verapamil, diltiazem, and nifedipine demonstrated favorable hemodynamic effects in pulmonary hypertension.
Conclusions:
- Nifedipine offers acute hemodynamic benefits in heart failure but lacks sustained efficacy.
- Calcium antagonists may be beneficial in pulmonary hypertension, with potential for long-term use in select cases.
Abstract:
Clinical experience with calcium antagonists in congestive heart failure has, to date, been mainly restricted to the use of nifedipine but there is either no or only a limited extent of information available on diltiazem and verapamil. In patients with acute and chronic congestive heart failure, single-dose administration of nifedipine was seen to lead to a decrease in systemic vascular resistance, left ventricular filling pressure and ventricular volumes as well as to an increase in stroke volume, ejection fraction and mean velocity of circumferential fiber shortening. These favorable effects could not be detected in eight patients during a three-week treatment phase with 80 mg nifedipine daily: resting blood pressure, cardiac volumes, echocardiographically-dimensions and exercise tolerance were unchanged as compared with placebo. In patients with ischemic heart disease and impaired ventricular function, in addition to an improvement in systolic function, single-dose nifedipine administration led to favorable effects on diastolic function with a shift of the diastolic pressure-volume relationship downward and to the diastolic pressure-volume relationship downward and to the left. In patients with severe aortic regurgitation, the observed increase in effective cardiac output affected by nifedipine was primarily attributable to an increase in heart rate. In the presence of an initially-elevated systemic vascular resistance, the regurgitation fraction decreased. In pulmonary hypertension, favorable hemodynamic effects have been reported after acute administration of verapamil as well as diltiazem and nifedipine. In individual cases, promising results in patients with primary pulmonary hypertension have been reported during long-term therapy with nifedipine provided that a favorable initial response could be documented.