Abstract 13232: Reverse Atrial Electrical Remodeling Induced by Continuous Positive Airway Pressure in Patients with Severe Obstructive Sleep Apnea
Background: Obstructive sleep apnea (OSA) has been associated with atrial enlargement in response to high arterial and pulmonary pressures and increased sympathetic tone. Continuous positive airway pressure (CPAP) is the gold standard treatment for OSA although its impact on atrial electrical remodeling has not been investigated. Signal average P-wave (SAPW) is a non-invasive quantitative method to determine P-wave duration, an accepted marker for atrial electrical remodeling. Our objective was to determine whether CPAP induces reverse atrial electrical remodeling in patients with severe OSA.
Methods: Prospective study in consecutive patients attending the Sleep Clinic at our institution. All patients underwent full polysomnography. OSA-negative and severe OSA were defined as apnea-hypopnea index (AHI) < 5 events/hour and AHI ≥ 30 events/hour, respectively. In severe OSA patients, SAPW was determined pre- and post-intervention with CPAP. In OSA-negative controls, SAPW was recorded at baseline and 4-6 weeks thereafter without any intervention.
Results: A total of 20 severe OSA patients and 10 controls were included in the analysis. Mean AHI and minimum O2 saturation were 40.9 ± 11.1 events/hour and 80.3 ± 6.5% in severe OSA patients and 2.8 ± 1.2 events/hour and 91.4 ± 2.1% in controls. Baseline BMI was different between severe OSA patients and controls (35.2 ± 4.7 vs 26.6 ± 4.6 kg/m2; p < 0.0001). At baseline, severe OSA patients had a greater SAPW duration than controls (131.2 ± 10.8 vs 122.8 ± 10.5 ms; p < 0.05). After CPAP intervention, there was a significant reduction of SAPW duration in severe OSA patients (126.3 ± 9.2 vs 131.2 ± 10.8 ms; p < 0.0001). In controls, SAPW duration did not change within 4-6 weeks.
Conclusion: CPAP induced reverse atrial electrical remodeling in patients with severe OSA as represented by a significant reduction in P-wave duration.
- © 2011 by American Heart Association, Inc.