Epicardial fat accumulation is an independent marker of impaired heart rate recovery in obese patients with obstructive sleep apnea

Sympathetic nervous system activation plays a pivotal role in obese patients with obstructive sleep apnea (OSA), contributing to increased cardiovascular risk. Epicardial adipose tissue (EAT) activates cardiac autonomic nervous system. Our main study objective was to investigate effects of these autonomic dysfunction factors on post-exercise heart rate recovery (HRR).

36 patients, referred for clinical assessment of obesity (BMI > 30 kg/m²), underwent overnight polysomnography, transthoracic echocardiography and cardiopulmonary exercise testing.

Compared to non-OSA patients, OSA patients were older and displayed reduced body weight-indexed peak VO₂. Cardiac output at peak exercise was similar among groups. Peak exercise arterio-venous oxygen content difference D[a-v]O₂ was lower in OSA patients. In univariate linear analysis, age, AHI, EAT thickness, peak VO₂ and diabetes were associated with blunted HRR. Multiple linear regression analysis showed that increased EAT thickness, AHI and diabetes were independently associated with lower HRR. For identical AHI value and diabetes status, HRR significantly decreased by 61.7% for every 1 mm increase of EAT volume (p = 0.011). If HRR was treated as a categorical variable, EAT [odds ratio (OR) 1.78 (95% confidence interval [CI] 1.19–2.66); p = 0.005], and type 2 diabetes [OR 8.97 (95% CI 1.16–69.10); p = 0.035] were the only independent predictors of blunted HRR.

Aerobic capacity and peak exercise D[a-v]O₂ are impaired in obese OSA patients, suggesting abnormal peripheral oxygen extraction. EAT thickness is an independent marker of post-exercise HRR, which is a noninvasive marker of autonomic nerve dysfunction accompanying poor cardiovascular prognosis in obese patients.