Abstract

We tested the hypothesis that muscle vasoconstriction in response to hypercapnia and hypoxia would be more pronounced in patients with chronic heart failure (CHF) and sleep apnea than patients with CHF alone. Ninety consecutive CHF patients, Functional Class II‐III NYHA, LVEF≤40% were selected to the study. Forty‐two patients who fulfilled all the inclusion criteria were enrolled in the study: No Sleep Disordered Breathing (NoSDB, n=13, 47±3y), Obstructive Sleep Apnea (OSA, n=22, 57±1y) and Central Sleep Apnea (CSA, n=07, 53±3y). Sleep apnea was characterized by apnea‐hypopnea index≥15 events/hour (polysomnography). Central (7%CO2 and 93%O2) and peripheral (10%O2 and 90%N2, with CO2 titrated) chemoreceptors were stimulated for 3 min. Muscle sympathetic nervous activity (MSNA) was evaluated by microneurography technique, forearm (FBF) and calf (CBF) blood flow by venous occlusion plethysmography, and blood pressure by beat‐to‐beat noninvasive technique. Baseline MSNA, FBF, forearm vascular conductance (FVC), CBF, and calf vascular conductance (CVC) were similar among groups. FBF (hypercapnia: P=0.001; and hypoxia: P=<0.001) and CBF (hypercapnia: P=<0.001; and hypoxia: P=0.002) responses were significantly lower in OSA and CSA groups compared to NoSDB group. FVC (hypercapnia: P=0.001; and hypoxia: P=<0.001) and CVC (hypercapnia: P=<0.001; and hypoxia: P=0.001) responses were also significantly lower in OSA and CSA groups compared to NoSDB group. MSNA responses were not different in all groups studied (hypercapnia: P=0.12; and hypoxia: P=0.17). Patients with CHF and obstructive or central sleep apnea have more severe muscle vasoconstriction during hypercapnia and hypoxia than patients with CHF alone. The similarities in MSNA suggest that these responses are associated with endothelial dysfunction.Support or Funding InformationCNPq #140265/2013‐9 and FAPESP #2010/50048‐1

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