Exercise tolerance, exercise hyperpnea and central chemosensitivity to carbon dioxide in sleep apnea syndrome in heart failure patients

Background Sleep apnea syndrome (SAS) and exercise hyperpnea are common in patients with chronic heart failure (CHF), and although it is not known whether they are both regulated by the same mechanisms, the hypothesis of the present study was that they are related to augmented central chemosensitivity. Methods and Results The oxygen desaturation index (ODI) was evaluated in 29 patients and those with ODI > 5 times/h underwent polysomnography. Patients with an apnea-hypopnea index (AHI) > 15/h without evidence of obstructive apnea were defined as central SAS (CSAS). Cardiopulmonary exercise testing was performed to determine peak oxygen uptake and the VE-VCO2 Slope. A hypercapnic gas mixture (7% CO2/93% O-2) was used to activate the central chemoreflex. Nine patients had central SAS (CHF-CSAS) and 20 did not have apnea (CHF-nonSAS). Patients with CHF-CSAS had a lower peak oxygen uptake than the CHF-nonSAS group (13.0 +/- 2.4 vs 16.9 +/- 4.3 ml (.) kg(-1) (.) min-, p < 0.05). There was a significant correlation between central chemosensitivity and the AHI. (r=0:63, p < 0.05), between central chemosensitivity and the VE-VCO2 slope (r=0.50, p < 0.01), whereas the VE-VCO2 slope showed an insignificant tendency to correlate with AHI (r=0.44, p=0.07). Conclusion CHF-CSAS is associated with impaired exercise tolerance and elevated central chemosensitivity is the responsible mechanism for CSAS and exercise hyperpnea.