TY - JOUR
T1 - Effect of betaxolol on the hemodynamic, gas exchange, and cardiac output response to exercise in chronic atrial fibrillation
AU - Atwood, J. Edwin
AU - Myers, Jonathan
AU - Quaglietti, Susan
AU - Grumet, Jill
AU - Gianrossi, Renato
AU - Umman, Tianna
PY - 1999
Y1 - 1999
N2 - Background: β-blockade controls the ventricular response to exercise in chronic atrial fibrillation (AF), but the effects of β-blockers on exercise capacity in AF have been debated. Methods: Twelve men with AF (65 ± 8 years) participated in a randomized, double-blind, placebo-controlled study of betaxolol (20 mg daily). Patients underwent maximal exercise testing with ventilatory gas exchange analysis, and a separate, submaximal test (50% of maximum) during which cardiac output was measured by a CO2 rebreathing technique. Results: After betaxolol therapy, heart rate was reduced both at rest (92 ± 27 vs 62 ± 12 beats/min; p < 0.001) and at peak exercise (173 ± 22 vs 116 ± 24 beats/min; p < 0.001). Maximal oxygen uptake (VO2) was reduced by 19% after betaxolol (21.8 ± 5.3 with placebo vs 17.6 ± 5.1 mL/kg/min with betaxolol; p < 0.05), with similar reductions observed for maximal exercise time, minute ventilation, and CO2 production. VO2 was reduced by a similar extent (19%) at the ventilatory threshold. Submaximal cardiac output was reduced by 15% during betaxolol therapy (12.9 ± 2.3 vs 10.9 ± 1.3 L/min; p < 0.05), and stroke volume was higher (88.0 ± 21 vs 105.6 ± 19 mL/beat; p < 0.05). Conclusion: Betaxolol therapy in patients with AF effectively controlled the ventricular rate at rest and during exercise, but also caused considerable reductions in maximal VO2 and cardiac output during exercise. The observed increase in stroke volume could not adequately compensate for reduced heart rate to maintain VO2 during exercise.
AB - Background: β-blockade controls the ventricular response to exercise in chronic atrial fibrillation (AF), but the effects of β-blockers on exercise capacity in AF have been debated. Methods: Twelve men with AF (65 ± 8 years) participated in a randomized, double-blind, placebo-controlled study of betaxolol (20 mg daily). Patients underwent maximal exercise testing with ventilatory gas exchange analysis, and a separate, submaximal test (50% of maximum) during which cardiac output was measured by a CO2 rebreathing technique. Results: After betaxolol therapy, heart rate was reduced both at rest (92 ± 27 vs 62 ± 12 beats/min; p < 0.001) and at peak exercise (173 ± 22 vs 116 ± 24 beats/min; p < 0.001). Maximal oxygen uptake (VO2) was reduced by 19% after betaxolol (21.8 ± 5.3 with placebo vs 17.6 ± 5.1 mL/kg/min with betaxolol; p < 0.05), with similar reductions observed for maximal exercise time, minute ventilation, and CO2 production. VO2 was reduced by a similar extent (19%) at the ventilatory threshold. Submaximal cardiac output was reduced by 15% during betaxolol therapy (12.9 ± 2.3 vs 10.9 ± 1.3 L/min; p < 0.05), and stroke volume was higher (88.0 ± 21 vs 105.6 ± 19 mL/beat; p < 0.05). Conclusion: Betaxolol therapy in patients with AF effectively controlled the ventricular rate at rest and during exercise, but also caused considerable reductions in maximal VO2 and cardiac output during exercise. The observed increase in stroke volume could not adequately compensate for reduced heart rate to maintain VO2 during exercise.
KW - Atrial fibrillation
KW - Beta blockade
KW - Exercise capacity
KW - Oxygen uptake
UR - http://www.scopus.com/inward/record.url?scp=0032932332&partnerID=8YFLogxK
U2 - 10.1378/chest.115.4.1175
DO - 10.1378/chest.115.4.1175
M3 - Article
C2 - 10208225
AN - SCOPUS:0032932332
SN - 0012-3692
VL - 115
SP - 1175
EP - 1180
JO - Chest
JF - Chest
IS - 4
ER -