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Oxygen Uptake Kinetics and Cardiopulmonary Performance in Lone Atrial Fibrillation and the Effects of Sotalol FREE TO VIEW

Ngai-Sang Lok; Chu-Pak Lau
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From the Division of Cardiology, Department of Medicine, University of Hong Kong, Queen Mary Hospital, Hong Kong

1997 by the American College of Chest Physicians

Chest. 1997;111(4):934-940. doi:10.1378/chest.111.4.934
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Background: Atrial fibrillation (AF) is associated with impaired exercise capacity. Oxygen uptake (VO2) kinetics determines cardiopulmonary performance during submaximal exercise, which may be impaired in patients with AF.

Aim: To study oxygen kinetics and cardiopulmonary performance in patients with AF without structural heart disease and the effects of oral sotalol on these parameters.

Patients and methods: Twenty consecutive patients (mean age, 56±8 years) with chronic AF were recruited. The protocol design was a randomized, single-blinded, and placebo-controlled trial. Patients received either sotalol or placebo for an 8-week study period, and the alternative treatment in the subsequent period. Cardiopulmonary function tests using constant workload and incremental workload protocols were performed at the end of each phase. Sixteen age-matched normal subjects were included as control subjects.

Results: During constant submaximal exercise, patients with AF had a larger oxygen deficit (425±140 mL vs 289±80 mL in normal subjects; p<0.05) and the time for achieving 63% of VO2 (mean response time) was also delayed (46±15 s vs 33±10 s; p<0.05). Compared with normal subjects, patients with chronic AF had a higher maximal exercise heart rate (180±34 beats/min vs 153±22 beats/min; p<0.05), but a lower maximal VO2 (20±4 mL/kg/min vs 26±6 mL/kg/min; p<0.05). Oral sotalol lowered the resting (72±15 beats/min vs 93±22 beats/min; p<0.05) and exercise heart rate compared with placebo (125±27 beats/min vs 180±34 beats/min; p<0.05, respectively), and normalized oxygen pulse and the heart rate to minute ventilation ratio during maximal exercise. There was no significant difference between those receiving sotalol and those receiving placebo in oxygen deficit (502±150 mL vs 425±140 mL; p=0.38), maximal VO2 (17.2±4.9 mL/kg/min vs 20.4±4.7 mL/kg/min; p=0.17), and other gas exchange variables. In patients with AF, oxygen deficit has a fair correlation with VO2 at the anaerobic threshold (r2=0.43; p<0.05) and at maximal exercise (r2=0.45; p<0.05).

Conclusion: In addition to maximal exercise capacity and cardiopulmonary performance, patients with chronic AF without significant structural heart disease had impaired submaximal exercise performance as assessed by VO2 kinetics. These parameters were not significantly affected by sotalol used for rate control.




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