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Usefulness of calcium antagonists for congestive heart failure
Insights
Calcium channel blockers like nifedipine can improve heart function in congestive heart failure (CHF) patients. However, verapamil is not tolerated, and some agents may depress left ventricular function, especially with beta-blockers.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Congestive heart failure (CHF) from dilated cardiomyopathy presents challenges in treatment.
- Calcium channel blockers (CCBs) are a class of drugs with varying effects on cardiac function.
Purpose of the Study:
- To review the effects of various calcium channel blockers on left ventricular function in patients with CHF.
- To compare the vascular and myocardial actions of CCBs.
Main Methods:
- Review of existing literature on CCB use in CHF patients.
- Comparative analysis of CCB effects on arterial pressure, contractility, and coronary blood flow.
Main Results:
- Nifedipine, diltiazem, and newer CCBs improve left ventricular function in CHF.
- Verapamil is generally not tolerated due to negative inotropic and chronotropic effects.
- Nifedipine primarily affects arterial vasculature but can cause myocardial depression, especially with beta-blockers.
Conclusions:
- CCBs have diverse effects on cardiac and vascular function in CHF.
- Further research is needed to understand the long-term effects and myocardial actions of newer CCBs.
Abstract:
In patients with congestive heart failure (CHF) due to dilated cardiomyopathy, nifedipine, diltiazem and several of the newer calcium antagonists including nicardipine, nitrendipine, felodipine and PN 200-110 (isradipine) improve left ventricular function. Because of its relatively more pronounced negative inotropic and chronotropic actions, verapamil is generally not tolerated by patients with left ventricular failure. In addition, even relatively vascular-selective agents such as nifedipine can occasionally cause significant left ventricular depression, particularly if combined with beta-adrenergic blocking agents. Comparative studies using nitroprusside to cause an equivalent decrease in arterial pressure indicate that nifedipine acts predominantly on the arterial vasculature, and that a small but significant decrease in contractility occurs, apparently due to a direct myocardial action. Although diltiazem causes a depression in myocardial contractility in dogs with volume overload heart failure, limited data show no significant negative inotropic action in patients with heart failure. The negative inotropic effects, if any, of newer and possibly more vascular-selective agents are not yet known. Calcium antagonists appear to act predominantly on the limb and coronary vasculature, with relatively less effect on renal and hepatic vessels. In patients with CHF, nifedipine causes an increase in coronary blood flow and a decrease in the aorto-coronary sinus oxygen difference indicating an improvement in myocardial energetics. Although nifedipine causes an increase in cardiac index and decreases in systemic vascular resistance and pulmonary capillary wedge pressure during exercise, the limited data available fail to show a short- or long-term increase in exercise capacity. Nifedipine causes an increase in plasma renin activity, possibly due to a direct action on the kidney.(ABSTRACT TRUNCATED AT 250 WORDS)