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[Treatment of heart failure with calcium antagonists]
D Hall1, J Dirschinger, F Kraus
1Klinik für Herz- und Kreislauferkrankungen, Deutsches Herzzentrum München.
Insights
Calcium channel blockers can treat heart failure, but their use depends on left ventricular function. Verapamil may worsen severe heart failure due to its negative inotropic effects.
Area of Science:
- Cardiology
- Pharmacology
Context:
- Vasodilators are established treatments for congestive heart failure.
- Calcium channel blockers (CCBs) are considered for heart failure, especially when ischemic heart disease is the cause.
- Left ventricular dysfunction affects 60-70% of heart failure patients, often due to ischemic heart disease.
Purpose:
- To evaluate the hemodynamic effects of calcium channel blockers in heart failure patients.
- To determine the balance between negative inotropy and vasodilation from CCBs.
- To identify patient subgroups who may benefit or experience adverse effects from CCBs.
Summary:
- CCB administration results in opposing hemodynamic actions: negative inotropy and systemic vasodilation with sympathetic stimulation.
- The net effect depends on the patient's cardiovascular status; mild dysfunction may tolerate negative inotropy, while severe dysfunction can deteriorate.
- Verapamil has the strongest negative inotropic effect; benefits are seen with ejection fraction 30-40% and pulmonary capillary pressure ~20 mm Hg, beyond which heart failure may worsen.
Impact:
- CCBs require careful patient selection in heart failure management.
- Understanding the hemodynamic balance is crucial for optimizing CCB therapy.
- Identifying thresholds for adverse effects guides clinical decision-making for verapamil in heart failure.
Abstract:
Vasodilators have a well-established role in the treatment of congestive heart failure. By virtue of their vasodilating properties, the calcium channel blockers have been advocated for use in the treatment of heart failure, in particular, in consideration of the fact that the left ventricular dysfunction in 60 to 70% of the patients with this condition is due to ischemic heart disease, the primary disorder for which the calcium channel blockers are intended to treat. The net hemodynamic effect of calcium channel blockade is the result of two opposing actions: negative inotropy and systemic vasodilation with reflex-induced sympathetic stimulation. The balance is dependent on the prevailing cardiovascular status prior to administration of the drug. In the presence of no or only mild-to-moderate left ventricular dysfunction and intact adrenergic reflexes, a small amount of negative inotropy is readily offset by afterload reduction and adrenergic stimulation. In the presence of severe left ventricular dysfunction sufficiently extensive to lead to heart failure, a condition in which homeostatic reflexes are already attenuated, even a slight amount of negative inotropy can lead to unequivocal deterioration of hemodynamics. Of the three conventional calcium channel blockers, verapamil exerts the most marked negative inotropic effects. Even verapamil, however, has been shown to lead to hemodynamic improvement in some patients, at least after acute administration. Apparently, the cut-off point between beneficial and adverse actions lies at an ejection fraction between 30 and 40% and a pulmonary capillary pressure of about 20 mm Hg. In patients beyond these limits, if treated with verapamil, worsening of heart failure is not uncommon.(ABSTRACT TRUNCATED AT 250 WORDS)