Effect of beta blockade with betaxolol on left ventricular systolic function in chronic stable angina pectoris and left ventricular dysfunction |
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Authors: | M A Alpert A Singh R A Holmes J F Sanfelippo G C Flaker D Villarreal V Mukerji R J Morgan |
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Affiliation: | 1. Department of Pharmacology, University of California Davis, Davis, CA, USA;2. Department of Bioengineering, University of California San Diego, La Jolla, CA, USA;3. Institute for Experimental Medicine, Oslo University Hospital Ullevål, Oslo, Norway;4. Simula Research Laboratory, Lysaker, Norway;1. Department of Medicine/Endocrinology, Division of Endocrinology, University of Tennessee Health Science Center, Memphis, Tennessee;2. Department of Research Services, Veterans Affairs Medical Center, Memphis, Tennessee;3. Department of Preventive Medicine, University of Tennessee Health Science Center, Memphis, Tennessee;1. Department of Medicine, Division of Cardiovascular Disease, The University of Alabam at Birmingham, Birmingham, AL 35233, United States of America;2. Department of Internal Medicine, Fuwai Hospital, Chinese Academy for Medical Science, National Center of Cardiovascular Disease, Beijing 100037, China;3. Department of Internal Medicine, Division of Cardiology, UT Southwestern Medical Center, 6000 Harry Hines Blvd. NB11.200, Dallas, United States of America;4. Department of Molecular Biology, UT Southwestern Medical Center, 6000 Harry Hines Blvd. NB11.200, Dallas, United States of America;1. Department of Comparative, Cellular and Molecular Biology, Universidad Favaloro, Buenos Aires, Argentina;2. Department of Neurobiology, Physiology and Behavior, University of California Davis, CA, USA;3. Department of Pharmacology, University of California Davis, CA, USA |
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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. |
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