Abstract 13778: Peripheral Chemoreflex Activation Contributes to Increased Sympathetic Nerve Activity Through Sympathetic Baroreflex Impairement in Heart Failure
Chemoreflex-mediated sympathetic activation contributes to both initiation and progression of chronic heart failure (CHF).
Aims: to study the direct role of increased peripheral chemosensitivity in reducing sympathetic baroreflex function in CHF patients.
Methods and results: we compared sympathetic baroreflex function assessed by the slope of the relationship between muscle sympathetic nerve activity (MSNA) and diastolic blood pressure in CHF patients with augmented (n=18) and normal (n=20) peripheral chemosensitivity. Using a double-blind, randomized, vehicle-controlled study we examined the effect of chemoreflex deactivation (by breathing 100% oxygen for 15 min) on sympathetic baroreflex function in CHF patients with elevated and with normal chemosensitivity. Baseline MSNA was elevated (60.6 ± 3.2 versus 48.9 ± 3.7 bursts/min; P<0.05) and sympathetic baroreflex function impaired (3.06 ± 0.55 vs 5.51 ± 0.69 % bursts/mmHg, P<0.05) in CHF patients with augmented peripheral chemosensitivity compared with controls. Administration of 100% oxygen led to a significant decrease in MSNA (from 60.5 ± 3.2 to 52.6 ± 3.2 bursts/min; P<0.001) and increase in sympathetic baroreflex (from 2.95 ± 0.56 to 6.18 ± 0.77; P<0.001) in CHF patients with enhanced chemoreflex sensitivity. In contrast, neither room air nor 100% oxygen changed MSNA, hemodynamics or sympathetic baroreflex function in CHF patients with normal chemosensitivity.
Conclusion, we report for the first time that increased peripheral chemoreflex sensitivity directly decrease sympathetic baroreflex function in CHF patients. This interaction contributes to sympathetic overactivity and blunted sympathetic baroreflex function of CHF patients and may explain how chemoreceptors contribute to the bad prognosis of CHF patients.
- © 2011 by American Heart Association, Inc.