BACKGROUND: Heart failure (HF) is often associated with interstitial pulmonary edema and structural changes, resulting in thickening of the alveolar-capillary membrane and reductions in diffusing capacity of the lung for carbon monoxide (Dlco). Reduced Dlco reflects an 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. METHODS: Overnight polysomnography, pulmonary function tests, and arterial blood gas analyses were performed in 45 patients with chronic, stable HF. Univariate and multivariate regression analyses were performed in those patients with predominant CSA to test which variables were associated with AHI. RESULTS: Patients had a mean (+/-SD) age of 52.7+/-8.9 years, a mean left ventricular ejection fraction of 26.5+/-9.9%, and a mean AHI of 22.0+/-17.4 events per hour. In CSA patients, 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 body mass index were independent predictors of total AHI, explaining 51% of variability, as was 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. CONCLUSIONS: In patients with 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.
BACKGROUND:Heart failure (HF) is often associated with interstitial pulmonary edema and structural changes, resulting in thickening of the alveolar-capillary membrane and reductions in diffusing capacity of the lung for carbon monoxide (Dlco). Reduced Dlco reflects an 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. METHODS: Overnight polysomnography, pulmonary function tests, and arterial blood gas analyses were performed in 45 patients with chronic, stable HF. Univariate and multivariate regression analyses were performed in those patients with predominant CSA to test which variables were associated with AHI. RESULTS:Patients had a mean (+/-SD) age of 52.7+/-8.9 years, a mean left ventricular ejection fraction of 26.5+/-9.9%, and a mean AHI of 22.0+/-17.4 events per hour. In CSA patients, 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 body mass index were independent predictors of total AHI, explaining 51% of variability, as was 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. CONCLUSIONS: In patients with 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.