Abstract

Introduction: Heart failure with preserved ejection fraction (HFpEF) is often accompanied by obstructive sleep apnea (OSA). The effects of HFpEF on OSA pathophysiology remain relatively unexplored. Pulmonary congestion and sympathetic nervous activity (SNA) may drive ventilatory control instability (high loop gain [LG]). Elevated SNA also theoretically predisposes sleep to easier interruption by breathing events of OSA, reflected by low arousal threshold (ArTH). Hypothesis: In comparison to patients with OSA alone, patients with both OSA and HFpEF have higher LG and lower ArTH. Methods: We reviewed records to include patients with 1) transthoracic echocardiography with EF>40% and left ventricular diastolic dysfunction by decreased age-adjusted e’ and/or left atrial volume index >28 mL/m 2 ; 2) OSA by apnea-hypopnea index (AHI3A) ≥15 events/hour; and 3) raw polysomnography (PSG) data available for advanced signal analysis. LG and ArTH were estimated by Phenotyping Using Polysomnography (PUP), a MATLAB algorithm that quantifies pathophysiologic mechanisms of OSA using PSG data. Values in HFpEF+OSA patients were compared to values from research volunteers with OSA alone. Results: The HFpEF+OSA group included 21 patients. The OSA alone group included 43 research volunteers. LG was lower for HFpEF+OSA (0.63±18) compared to OSA alone (0.69±18), but the difference was not statistically significant. ArTH was significantly lower for HFpEF+OSA (117.0±15.9 %eupnea) compared to OSA alone (152.8±54.8 %eupnea, p = <0.001) and remained significant after adjustment for age, sex, and body mass index. ArTH was correlated with sleep efficiency (R = 0.43, p = <0.001) and negatively correlated with wake after sleep onset (R = -0.35, p =0.005). Conclusions: HFpEF is associated with low arousal threshold, which may contribute to sleep fragmentation. Our data did not confirm the hypothesis of greater breathing instability in patients with HFpEF and OSA compared to OSA alone.

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