Coexisting sleep apnea in heart failure patients significantly increased daytime muscle sympathetic nerve activity compared to those without sleep apnea (76 vs 63 bursts per 100 heartbeats, P=0.005).
Observational (n=60)
Does coexisting sleep apnea increase daytime muscle sympathetic nerve activity in patients with systolic heart failure?
Coexisting sleep apnea in heart failure patients is associated with increased daytime sympathetic nerve activity, suggesting a potential mechanism for accelerated HF progression.
Absolute Event Rate: 76% vs 63%
p-value: p=0.005
Sympathetic activation and sleep apnea are present in most patients with symptomatic systolic heart failure (HF). Acutely, obstructive and central apneas increase muscle sympathetic activity (MSNA) during sleep by eliciting recurrent hypoxia, hypercapnia, and arousal. In obstructive sleep apnea patients with normal systolic function, this increase persists after waking. Whether coexisting sleep apnea augments daytime MSNA in HF is unknown. We tested the hypothesis that its presence exerts additive effects on MSNA during wakefulness. Overnight sleep studies and morning MSNA recordings were performed on 60 subjects with ejection fraction or =15 per hour. Subjects with and subjects without sleep apnea were similar for age, ejection fraction, HF etiology, body mass index, blood pressure, and heart rate. Daytime MSNA was significantly higher in those with sleep apnea (76+/-2 versus 63+/-4 bursts per 100 heartbeats mean+/-SEM, P=0.005; 58+/-2 versus 50+/-3 bursts/min, P=0.037), irrespective of its etiology (the mean difference for central sleep apnea was 17 bursts per 100 heartbeats; n=14; P=0.006; and for obstructive sleep apnea, 11 bursts per 100 heartbeats; n=29; P=0.032). In a subgroup (n=8), treatment of obstructive sleep apnea lowered MSNA by 12 bursts per 100 heartbeats (P=0.003). Convergence of independent excitatory influences of HF and sleep apnea on central sympathetic neurons results in higher MSNA during wakefulness in HF patients with coexisting sleep apnea. This additional stimulus to central sympathetic outflow may accelerate the progression of HF; its attenuation by treatment of sleep apnea represents a novel nonpharmacological opportunity.
Spaak et al. (Mon,) conducted a observational in Heart Failure (n=60). Sleep apnea vs. No sleep apnea was evaluated on Daytime muscle sympathetic nerve activity (MSNA) in bursts per 100 heartbeats (p=0.005). Coexisting sleep apnea in heart failure patients significantly increased daytime muscle sympathetic nerve activity compared to those without sleep apnea (76 vs 63 bursts per 100 heartbeats, P=0.005).