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1 Department of Allergy Immunology and Respiratory Medicine, Alfred Hospital, Melbourne Australia 2 Department of Medicine, Monash University, Melbourne Australia 3 Department of Cardiology, Alfred Hospital, Melbourne Australia 4 Baker Heart Research Institute, Melbourne Australia
m.naughton{at}alfred.org.au
Abstract
BackgroundHeart Failure (HF) is often associated with interstitial pulmonary edema and structural changes resulting in thickening of the alveolar-capillary membrane and reductions in transfer capacity for carbon monoxide (DLCO). Reduced DLCO reflects impaired efficiency of gas exchange which may increase plant gain, influence ventilatory control stability and result in central sleep apnea (CSA). In this study we test the hypothesis that reductions in DLCO would be associated with increased apnea-hypopnea index (AHI) in patients with CSA.
MethodsOvernight polysomnography, pulmonary function and arterial blood gas analyses were performed in 45 patients with chronic stable HF. Univariate and multivariate regression analyses were performed in those with predominantly CSA, to test which variables were associated with AHI.
Results: (Mean±SD) Age=52.7±8.9 years, LVEF=26.5±9.9 %, AHI=22.0±17.4 events/hr. In CSA, DLCO and PaO2 both correlated with total AHI (r=-0.43, p=0.046 and r=-0.53, p=0.011 respectively) and with supine AHI (r=-0.56, p=0.009 and r=-0.60, p=0.004 respectively). In a forward stepwise estimation model DLCO, PaO2 and BMI were independent predictors of total AHI explaining 51% of variability; as well as supine AHI explaining 64% of variability. DLCO and PaO2 accounted for 37% of the variability in total AHI and 49% of the variability in supine AHI.
ConclusionsIn HF and CSA, reductions in DLCO and PaO2 are independently associated with respiratory disturbance during sleep. The increase in ventilatory instability may be due to plant gain effects.
Key Words: plant gain central sleep apnea heart failure
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