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Effect of beta blockade with betaxolol on left ventricular systolic function in chronic stable angina pectoris and
Insights
Beta blockade with betaxolol effectively reduces angina and improves exercise capacity in patients with stable angina and LV dysfunction. Importantly, it does not significantly impair left ventricular systolic function or cause heart failure.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Stable angina pectoris often coexists with left ventricular (LV) dysfunction.
- Beta-adrenergic blocking agents are a cornerstone in managing angina and improving outcomes in cardiovascular diseases.
Purpose of the Study:
- To evaluate the impact of cardioselective beta-blockade with betaxolol on LV performance in patients experiencing stable angina pectoris and LV dysfunction.
- To determine if optimal beta blockade therapy affects LV systolic function or precipitates heart failure.
Main Methods:
- A placebo-controlled study involving 18 patients with stable angina and LV dysfunction.
- Incremental doses of betaxolol were administered until optimal clinical beta blockade was achieved (resting heart rate 50-60 bpm, limited heart rate increase during exercise).
- Left ventricular ejection fraction (LVEF) was assessed at rest and during symptom-limited treadmill exercise using radionuclide ventriculography.
Main Results:
- Optimal beta blockade significantly decreased angina episodes (6.8 to 0.7 per week, p<0.0005) and increased exercise capacity (3.1 to 7.7 minutes, p<0.0005).
- Mean LVEF showed no statistically significant changes at rest (39% vs. 43%) or peak exercise (40% vs. 45%) between placebo and betaxolol therapy.
- No patients exhibited clinical or radiographic evidence of LV failure.
Conclusions:
- Optimal clinical beta blockade with betaxolol effectively manages symptoms and improves exercise tolerance in patients with stable angina and mild-to-moderate LV systolic dysfunction.
- This therapeutic approach does not lead to significant deterioration of LV systolic function or induce heart failure.
Abstract:
To assess the effect of beta blockade on left ventricular (LV) performance in patients with LV dysfunction and stable angina pectoris, 18 subjects taking a placebo followed by incremental doses of the cardioselective beta-adrenergic blocking agent betaxolol (5, 10, 20, 40 and 80 mg/day) were studied. The study ended with the achievement of optimal clinical beta blockade (heart rate at rest 50 to 60 beats/min, a 20% or smaller increase in heart rate during stage 1 of symptom-limited treadmill exercise using the modified Bruce protocol). Optimal clinical beta blockade produced a decrease in mean frequency of angina, from 6.8 +/- 1.7 to 0.7 +/- 0.8 episodes per week (p less than 0.0005) and an increase in mean treadmill exercise capacity, from 3.1 +/- 1.7 to 7.7 +/- 2.8 minutes (p less than 0.0005). LV systolic function was assessed at rest and during symptom-limited exercise with radionuclide left ventriculography. Mean LV ejection fraction (EF) during therapy with placebo was 39 +/- 7% at rest and 40 +/- 8% at peak exercise. Mean LVEF during optimal clinical beta blockade was 43 +/- 11% at rest and 45 +/- 10% at peak exercise. Neither of these changes was statistically significant. No patient had clinical or radiographic signs of LV failure. The results suggest that optimal clinical beta blockade with betaxolol, in doses sufficient to significantly reduce the frequency of angina and improve exercise capacity in patients with stable angina pectoris and mild to moderate LV systolic dysfunction, does not cause significant deterioration of LV systolic function or produce LV failure.