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Calcium antagonists in patients with left ventricular dysfunction: back on the bridge?
1Department of Cardiology, Lady Davis Carmel Medical Center, Technion-Israel Institute of Technology, Haifa, Israel.
Insights
Newer calcium antagonists offer benefits in heart failure management. Long-acting formulations improve outcomes, especially in non-ischemic heart failure, though mechanisms require further study.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Calcium antagonists provide vasodilation but can depress myocardial function.
- First-generation drugs may worsen heart failure due to myocardial depression and blood pressure changes.
- Newer slow-release and long-acting calcium antagonists aim to mitigate these adverse effects.
Purpose of the Study:
- To review the current data on calcium antagonists in cardiac disease management.
- To emphasize the role of newer slow-release and long-acting formulations.
- To assess their impact on ventricular dysfunction and heart failure outcomes.
Main Methods:
- Review of available clinical data and trial results.
- Emphasis on studies involving newer calcium antagonist formulations.
- Analysis of effects on coronary/systemic vasodilation, diastolic function, and heart failure outcomes.
Main Results:
- Nisoldipine improved diastolic function and reduced ischemia in post-MI patients.
- Felodipine showed no benefit in exercise capacity or survival for Class 2-3 heart failure.
- Amlodipine demonstrated a significant mortality reduction in non-ischemic heart failure (PRAISE study).
Conclusions:
- Long-acting calcium antagonists may improve outcomes in ventricular dysfunction when used with standard therapies.
- Amlodipine shows a specific survival benefit in non-ischemic heart failure, warranting further investigation.
- Mechanisms behind amlodipine's benefit in non-ischemic heart failure remain to be elucidated.
Abstract:
Calcium antagonists have a useful role in the management of patients with cardiac disease, producing coronary and systemic vasodilatation and an additional possibly beneficial effect on ventricular diastolic function. On the other hand, the myocardial depressant effect of the first-generation drugs and the abrupt changes in blood pressure, with neurohormonal activation, have been associated with worsening heart failure in certain patients. The present review summarizes the data currently available, with emphasis on the newer slow-release and long-acting calcium antagonists. Use of these drugs minimizes the peak and trough effect associated with short-acting preparations, and particularly when administered against a background of digoxin, diuretic and angiotensin converting enzyme inhibitors, may be associated with better long-term results in patients with ventricular dysfunction. The DEFIANT studies, using nisoldipine-coat core, showed that nisoldipine-CC improved diastolic ventricular function and had a significant anti-ischemic effect in patients with mild-moderate ventricular dysfunction after acute myocardial infarction. The VHeFT III trial showed that felodipine had no effect on exercise capacity or survival in patients with Class 2-3 heart failure. In the PRAISE study of Class 3-4 patients, amlodipine was neutral in patients with ischemic disease, but a strikingly beneficial effect was observed in non-ischemic heart failure (45% decrease in mortality). The precise mechanism for the beneficial effect of amlodipine in these patients is unknown. Further studies are needed to examine the issue of survival benefit in patients with non-ischemic heart failure and the mechanisms involved.