Abstract 4365709: Obstructive Sleep Apnea, Adverse Cardiac Remodeling, and Inflammation

Abstract

Background: Obstructive sleep apnea (OSA) has been linked to increased cardiovascular risk, potentially contributing to adverse cardiac remodeling and arrhythmias through inflammation. However, its specific role in adverse cardicac remodeling and post-operative atrial fibrillation (POAF) in patients undergoing cardiac surgery remains understudied. Hypothesis: We hypothesized that OSA would be associated with adverse structural remodeling, elevated systemic inflammation, and a higher incidence of POAF in patients undergoing cardiac surgery. Methods: Sixty-five cardiac surgery patients (mean age 66 ± 8 years; 25% female) were included, with 13 having OSA and 52 without. Preoperative transthoracic echocardiography assessed cardiac structure and function, including left ventricular (LV) mass, wall thickness, and ejection fraction. Plasma proteomics using Olink proximity extension assays targeted inflammatory markers. POAF was defined as new-onset atrial fibrillation during hospitalization. Statistical comparisons used t-tests and chi-squared tests. Results: OSA and control groups were similar in age (66 ± 7 vs. 66 ± 9 years) and sex (15% vs. 27% female, p= 0.5). OSA patients had higher BMI (32.3 ± 5.2 vs. 28.9 ± 4.6 kg/m 2 , p= 0.035) and showed signs of adverse structural remodeling: increased interventricular septal thickness (1.17 ± 0.21 vs. 1.02 ± 0.21 cm, p= 0.017), posterior wall thickness (1.10 ± 0.19 vs. 0.99 ± 0.16 cm, p= 0.024), and LV mass (114 ± 27 vs. 90 ± 27 g, p= 0.005). Unexpectedly, POAF incidence was significantly lower in OSA patients (7.7% vs. 42%, p= 0.023). Proteomic profiling revealed no significant elevations in canonical inflammatory markers. In fact, CCL25 (8.30 ± 0.60 vs 7.91 ± 0.85, p= 0.0322) and hepatocyte growth factor (HGF) (13.08 ± 0.34 vs 12.93 ± 0.31, p= 0.0244) levels were significantly lower in the OSA group. Conclusions: OSA was associated with increased LV wall thickness and mass, consistent with adverse structural remodeling. Notably, these changes occurred without evidence of elevated systemic inflammation or an increased risk of POAF in our surgical cohort. These findings challenge the presumed link between OSA, inflammation, and post-operative atrial arrhythmias. They suggest that, at least in some surgical populations, OSA may not be accompanied by heightened inflammatory signaling. Further studies in larger and more diverse cohorts are warranted to better understand these complex relationships.