RT Journal Article
SR Electronic
T1 Inhaled β-agonist does not modify sympathetic activity in patients with COPD
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP P2196
VO 44
IS Suppl 58
A1 Helge Haarmann
A1 Cordula Mohrlang
A1 Uta Tschiesner
A1 David Rubin
A1 Thore Bornemann
A1 Karin Rüter
A1 Slavtcho Bonev
A1 Tobias Raupach
A1 Gerd Hasenfuß
A1 Stefan Andreas
YR 2014
UL http://erj.ersjournals.com/content/44/Suppl_58/P2196.abstract
AB BackgroundNeurohumoral activation is present in patients with COPD and might provide a link between COPD and systemic effects, especially cardiovascular disease. We aimed to evaluate if inhaled therapy with the long-acting β-agonist (LABA) bronchodilator salmeterol modifies muscle sympathetic nerve activity (MSNA) as evaluated by microneurography.MethodsMSNA, heart rate, blood pressure, and respiration were continually measured as placebo and salmeterol were administered sequentially. The primary endpoint was the acute effect of salmeterol on MSNA/100 heart beats. Additionally, plasma catecholamine levels and arterial pulse wave velocity were evaluated. Following 4 weeks of treatment with salmeterol 50 µg twice daily, measurements were repeated without placebo administration.ResultsA total of 32 COPD patients were included. A valid MSNA signal for the primary endpoint was derived from 18 patients. After acute administration of salmeterol there was no significant change in MSNA/100 heart beats vs. placebo [72.96 ± 14.716 (SD) vs. 73.30 ± 10.767; p=0.5062]. Likewise, no changes in MSNA from baseline were observed after 4 weeks of salmeterol treatment. MSNA was positively correlated with plasma norepinephrine levels. Heart rate slightly increased as an acute and long-term effect, while blood pressure and arterial pulse wave velocity were unchanged. Treatment with salmeterol was safe and well tolerated.ConclusionBy using microneurography as a gold standard to evaluate sympathetic activity we found no change in MSNA following salmeterol inhalation. Thus a negative effect of β-agonists on sympathetic activation cannot be inferred by these data.