Effects of Short-Term Continuous Positive Airway Pressure on Myocardial Sympathetic Nerve Function and Energetics in Patients with Heart Failure and Obstructive Sleep Apnea: A Randomized Study
Background—Heart failure with reduced ejection fraction (HFrEF) and obstructive sleep apnea (OSA), two states of increased metabolic demand and sympathetic nervous system activation, often co-exist. Continuous Positive Airway Pressure (CPAP), which alleviates OSA, can improve ventricular function. It is unknown whether this is due to altered oxidative metabolism or pre-synaptic sympathetic nerve (SN) function. We hypothesized that short-term (6-8 weeks) CPAP in patients with OSA and HFrEF would improve myocardial SN function and energetics.
Methods and Results—Forty-five patients with OSA and HFrEF (LVEF 35.8±9.7%; mean±SD) were evaluated using echocardiography, 11C-acetate and 11C-hydroxyephedrine (HED) positron emission tomography (PET) before and approximately 6-8 weeks after randomization to receive short-term CPAP (N=22) or no CPAP (N=23). Work metabolic index (WMI), an estimate of myocardial efficiency, was calculated as: [stroke-volume-index × heart rate × systolic BP ÷ k-mono], where k-mono is the mono-exponential function fit to the myocardial 11C-acetate time-activity data, reflecting oxidative metabolism. Presynaptic SN function was measured using the 11C-HED retention index. CPAP significantly increased HED retention vs. No-CPAP (Δretention: +0.012 (0.002,0.021) vs. -0.006 (-0.013,0.005) min-1, p=0.003). There was no significant change in WMI between groups. However, in those with more severe OSA (Apnea Hypopnea Index >20 events/hr), CPAP significantly increased both WMI and systolic BP (p<0.05).
Conclusions—In patients with HFrEF and OSA, short-term CPAP increased HED retention, indicating improved myocardial SN function, but overall did not affect energetics. In those with more severe OSA, CPAP may improve cardiac efficiency. Further outcome-based investigation of the consequences of CPAP is warranted.
Clinical Trial Registration Information—clinicaltrials.gov. Identifier: NCT00756366.
- Received August 30, 2013.
- Revision received June 1, 2014.
- Accepted June 27, 2014.