Why the study?
Does captopril compared to nifedipine improve clinical symptoms and hemodynamics in patients with dilated cardiomyopathy?
Does captopril compared to nifedipine improve clinical symptoms and hemodynamics in patients with dilated cardiomyopathy?
In patients with dilated cardiomyopathy, captopril improves clinical symptoms and hemodynamics by reducing afterload, whereas nifedipine reduces muscle contractility and fails to improve symptoms.
Answers are grounded in this paper and cite their sources.
Captopril may be preferred to nifedipine for symptom relief and hemodynamics in dilated cardiomyopathy; reinforces afterload reduction over calcium-channel blockade in systolic HF.
Nifedipine and captopril are potent vasodilators and may be expected to help left ventricular failure by reducing afterload. Nifedipine (20 mg three times a day) and captopril (50 mg three times a day) were added to an optimal regimen of digitalis and diuretics in a double blind crossover trial in 18 cases of dilated cardiomyopathy. New York Heart Association functional class rating symptoms and exercise tolerance times improved on captopril but not on nifedipine. The reduction in pulmonary capillary wedge pressure and the increase of cardiac output on captopril indicated that the augmented functional capacity may have resulted in part from an improved performance of the left ventricle. Although there were comparable decreases in systemic vascular resistance and presumably in impedence to ejection by the left ventricle on both drugs, the dimensions of the ventricular cavity were found to be reduced by captopril and augmented by nifedipine, and only captopril reduced the afterload (wall stress). In addition, the force-length relation (between left ventricular end systolic stress and end systolic diameter) was shifted to the left of baseline by captopril and to the right by nifedipine, suggesting that muscle contractility was reduced by nifedipine and not by captopril. These results suggest that nifedipine and captopril have different effects on afterload and contractility and these may account for the different effects of these drugs on the performance of the heart and clinical responses.
No takes yet. Share an insight, caveat, or question.
Agostoni et al. (1986) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: