Obesity is frequently associated with obstructive sleep apnea (OSA). Both conditions are proinflammatory and proposed to deteriorate cardiac function. We used a nested cohort study design to evaluate the long-term impact of bariatric surgery on OSA and how weight loss and OSA relate to inflammation and cardiac performance.
Design and Methods:
At 10-year follow-up in the Swedish Obese Subjects (SOS) study, we identified 19 obese subjects (BMI 31.2 ± 5.3 kg m−2), who following bariatric surgery at SOS-baseline had displayed sustained weight losses (surgery group), and 20 obese controls (BMI 42.0 ± 6.2 kg m−2), who during the same time-period had maintained stable weight (control group). All study participants underwent overnight polysomnography examination, echocardiography and analysis of inflammatory markers.
The surgery group displayed a lower apnea hypopnea index (AHI) (19.9 ± 21.5 vs. 37.8 ± 27.7 n/h, P = 0.013), lower inflammatory activity (hsCRP 2.3 ± 3.0 vs. 7.2 ± 5.0 mg L−1, P < 0.001), reduced left ventricular mass (165 ± 22 vs. 207 ± 22 g, P < 0.001) and superior left ventricular diastolic function (E/A ratio 1.24 ± 1.10 vs. 1.05 ± 0.20, P = 0.006) as compared with weight stable obese controls. In multiple regression analyses including all subjects (n = 39) and controlling for BMI, the AHI remained independently associated with hsCRP (β = 0.09, P < 0.001), TNF-α (β = 0.03, P = 0.031), IL-6 (β = 0.01, P = 0.007), IL 10 (β = −0.06; P = 0.018), left ventricular mass (β = 0.64, P < 0.001), left atrial area (β = 0.08, P = 0.002), pulmonary artery pressure (β = 0.08, P = 0.011) and E/Ea ratio (β = 0.04, P = 0.021).
Patients with sustained weight loss after bariatric surgery display less severe sleep apnea, reduced inflammatory activity, and enhanced cardiac function. Persisting sleep apnea appears to limit the beneficial effect of weight loss on inflammation and cardiac performance.