Sleep-disordered breathing in heart failure patients was associated with significantly lower vascular responses during hypoxia (P<0.01) and hypercapnia (P<0.001) compared to those without SDB.
Observational (n=41)
Does sleep-disordered breathing exacerbate muscle vasoconstriction and sympathetic neural activation in response to hypoxia and hypercapnia in patients with systolic heart failure?
In patients with systolic heart failure, the presence of sleep-disordered breathing is associated with exaggerated muscle vasoconstriction and sympathetic neural activation during hypoxia and hypercapnia.
p-value: p=<0.01
Background— Sleep-disordered breathing (SDB) is common in patients with heart failure (HF), and hypoxia and hypercapnia episodes activate chemoreceptors stimulating autonomic reflex responses. We tested the hypothesis that muscle vasoconstriction and muscle sympathetic nerve activity (MSNA) in response to hypoxia and hypercapnia would be more pronounced in patients with HF and SDB than in patients with HF without SDB (NoSBD). Methods and Results— Ninety consecutive patients with HF, New York Heart Association functional class II–III, and left ventricular ejection fraction ≤40% were screened for the study. Forty-one patients were enrolled: NoSDB (n=13, 46 39–53 years) and SDB (n=28, 57 54–61 years). SDB was characterized by apnea–hypopnea index ≥15 events per hour (polysomnography). Peripheral (10% O 2 and 90% N 2 , with CO 2 titrated) and central (7% CO 2 and 93% O 2 ) chemoreceptors were stimulated for 3 minutes. Forearm and calf blood flow were evaluated by venous occlusion plethysmography, MSNA by microneurography, and blood pressure by beat-to-beat noninvasive technique. Baseline forearm blood flow, forearm vascular conductance, calf blood flow, and calf vascular conductance were similar between groups. MSNA was higher in the SDB group. During hypoxia, the vascular responses (forearm blood flow, forearm vascular conductance, calf blood flow, and calf vascular conductance) were significantly lower in the SDB group compared with the NoSDB group ( P <0.01 to all comparisons). Similarly, during hypercapnia, the vascular responses (forearm blood flow, forearm vascular conductance, calf blood flow, and calf vascular conductance) were significantly lower in the SDB group compared with the NoSDB group ( P <0.001 to all comparisons). MSNA were higher in response to hypoxia ( P =0.024) and tended to be higher to hypercapnia ( P =0.066) in the SDB group. Conclusions— Patients with HF and SDB have more severe muscle vasoconstriction during hypoxia and hypercapnia than HF patients without SDB, which seems to be associated with endothelial dysfunction and, in part, increased MSNA response.
Lobo et al. (Tue,) conducted a observational in Systolic Heart Failure (n=41). Sleep-disordered breathing vs. No sleep-disordered breathing was evaluated on Vascular responses (forearm and calf blood flow and vascular conductance) during hypoxia and hypercapnia (p=<0.01). Sleep-disordered breathing in heart failure patients was associated with significantly lower vascular responses during hypoxia (P<0.01) and hypercapnia (P<0.001) compared to those without SDB.