Abstract
Background-In patients with chronic heart failure (CHF), central sleep apnea (CSA) and enhanced ventilatory response ((V) over dot (E)/(V) over dot CO2 slope) to exercise are common. Both breathing disorders alone indicate poor prognosis in CHF. Although augmented chemosensitivity to CO2 is thought to be one important underlying mechanism for both breathing disorders, it is unclear whether both ...
Abstract
Background-In patients with chronic heart failure (CHF), central sleep apnea (CSA) and enhanced ventilatory response ((V) over dot (E)/(V) over dot CO2 slope) to exercise are common. Both breathing disorders alone indicate poor prognosis in CHF. Although augmented chemosensitivity to CO2 is thought to be one important underlying mechanism for both breathing disorders, it is unclear whether both breathing disorders are related closely in patients with CHF. Methods and Results-We investigated 20 CHF patients with clinically important CSA (apnea-hypopnea-index (AHI), number of episodes per hour greater than or equal to 15) and 10 CHF patients without CSA. Patients with and without CSA did not differ with respect to exercise capacity (peak (V) over dot O-2, 63.4+/-3.4% versus 60.8+/-4.4% of predicted value; P=0.746) and left ventricular ejection fraction (LVEF, 31+/-2% versus 31+/-3%; P=0.948). The AHI was not correlated with exercise capacity (peak (V) over dot O-2, percent of predicted value; P=0.260) and LVEF (percent, P=0.886). In contrast, the positive correlation of the (V) over dot (E)/(V) over dot CO2 slope, determined by cardiopulmonary exercise testing, with the AHI was highly significant (P<0.001). The (V) over dot (E)/(V) over dot CO2 slope was significantly increased in patients with CSA compared with those without CSA (29.7 versus 24.9; P<0.001). Conclusions-The ventilatory response to exercise is significantly augmented in CHF patients with CSA compared with those without. In contrast to peak (V) over dot O-2 and LVEF, the (V) over dot (E)/(V) over dot CO2 slope is strongly related to the severity of CSA in patients with CHF, which underscores an augmented chemosensitivity to CO as a common underlying pathophysiological mechanism.
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