Abstract 17981: Decreased Oscillatory Pattern of Sympathetic Nerve Activity is Associated With Arterial Baroreflex Dysfunction in Chronic Heart Failure Patients
Background: Sympathetic activation and arterial baroreflex (ABR) dysfunction typify chronic heart failure (CHF). In addition, decreased oscillatory pattern of muscle sympathetic nerve activity (MSNA, LFMSNA/HFMSNA) seems to contribute to sympathetic exacerbation in patients with CHF. Unknown is whether the LFMSNA/HFMSNA is associated with ABR dysfunction in CHF patients. To answer this question, we investigated the association between gain, latency and coupling of ABR function and LFMSNA/HFMSNA in CHF patients.
Methods and Results: Forty-three CHF patients, Functional Class II to III, NYHA, ejection fraction ≤40% were allocated into two groups according to the level of LFMSNA/HFMSNA index: 1) Higher LFMSNA/HFMSNA (n=21, 52±2 years) and 2) Lower LFMSNA/HFMSNA (n=22, 54±1 years). Blood pressure (BP, oscillometric beat-to-beat basis) and MSNA (microneurography technique) were recorded during 10 min at rest. Spectral and cross-spectral analyses of BP and MSNA variabilities were conducted to assess the LFMSNA/HFMSNA and the gain, latency and coupling between BP and MSNA of ABR function. Etiology, ejection fraction, gain and latency of ABR function were similar between groups. However, the patients with lower LFMSNA/HFMSNA had increased MSNA bursts frequency (53±2vs. 39±3 bursts/min, P<0.01) and total activity (180±15 vs. 126±17 a.u, P=0.03) compared to the patients with higher LFMSNA/HFMSNA. In contrast, the patients with lower LFMSNA/HFMSNA had reduced coupling of ABR function (69±3 vs. 80±2 %, P<0.01). Further analysis showed a significant association between the coupling of ABR function and LFMSNA/HFMSNA (R=0.36, P=0.02).
Conclusions: There is an inverse association between the LFMSNA/HFMSNA index and sympathetic nerve activity. In addition, there is a direct association between the LFMSNA/HFMSNA index and the coupling of ABR, which suggests that the ABR dysfunction explains, at least in part, the augmented sympathetic nerve activity in CHF patients.
Author Disclosures: E. Toschi-Dias: None. R.V. Groehs: None. L.M. Antunes-Correa: None. P.F. Trevizan: None. D.M. Lobo: None. P. Oliveira: None. M.N. Alves: None. D.R. Almeida: None. C. Negrao: None. M.P. Rondon: None.
- © 2015 by American Heart Association, Inc.