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Use of calcium antagonists in ventricular dysfunction
Insights
Calcium antagonists like verapamil, nifedipine, and diltiazem have varied hemodynamic effects. Caution is advised when using these agents in patients with impaired heart function.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Calcium antagonists are frequently prescribed for cardiocirculatory disorders.
- Many of these conditions involve impaired myocardial function.
Purpose of the Study:
- To evaluate the hemodynamic effects of calcium antagonists in patients with normal and depressed ventricular function.
- To determine the clinical relevance of these effects in various cardiac conditions.
Main Methods:
- Review of existing clinical data on verapamil, nifedipine, and diltiazem.
- Analysis of their impact on myocardial function and ventricular pressures.
Main Results:
- Verapamil, nifedipine, and diltiazem show minimal negative inotropic effects in normal hearts.
- Verapamil and diltiazem may increase left ventricular end-diastolic pressure.
- Nifedipine generally improves function in depressed hearts if sympathetic reflexes are intact, but deterioration is possible.
Conclusions:
- Calcium antagonists are not recommended as afterload-reducing agents in heart failure.
- Careful consideration is necessary when administering these drugs to patients with compromised ventricular performance.
Abstract:
Calcium antagonists are now widely used in a variety of cardiocirculatory disorders, many of which are associated with varying levels of depressed myocardial function. Thus, the hemodynamic effects of calcium antagonists in patients with normal as well as depressed ventricular function are clinically relevant. None of the 3 agents verapamil, nifedipine or diltiazem exerts significant negative inotropic effects in patients with relatively normal myocardial function, although increases in left ventricular end-diastolic pressure may occur with verapamil and possibly diltiazem. In a setting in which ischemia, hypertension or arrhythmias contribute to cardiac failure, all 3 agents may ameliorate myocardial decompensation if they reverse the precipitating causes. In patients with depressed myocardial function, the effects of diltiazem are not known; verapamil may depress myocardial function, especially if the ventricular filling pressure is increased. Nifedipine generally has little depressant action in this setting and usually improves cardiac function, especially if the sympathetic reflexes are intact. However, hemodynamic deterioration after nifedipine administration has been reported. Thus, the available data do not support the use of calcium antagonists as afterload-reducing agents in heart failure and suggest caution in the use of these agents in patients with impaired ventricular performance.