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J Am Coll Cardiol, 2003; 42:1605-1610, doi:10.1016/j.jacc.2003.07.004 © 2003 by the American College of Cardiology Foundation |
* Department of Cardiology, Erasme Hospital, Brussels, Belgium
Manuscript received November 25, 2002; revised manuscript received May 16, 2003, accepted July 7, 2003.
* Reprint requests and correspondence: Dr. Sonia Velez-Roa, Department of Cardiology, Erasme Hospital, 808 Lennik Road, 1070 Brussel, Belgium.
pvandebo{at}ulb.ac.be
OBJECTIVES: We assessed the effects of beta-adrenergic agonism on muscle sympathetic nerve activity (MSNA) in patients with congestive heart failure (CHF) and young and matched controls.
BACKGROUND: Myocardial response to beta-adrenergic stimulation decreases with aging and with CHF.
METHODS: In CHF patients, we measured cardiac hemodynamics and MSNA (microneurography) before, with short-term (n = 5), and after 48-h (n = 9) of dobutamine infusion (10 µg/kg/min). In eight young controls and nine controls matched to the CHF patients, we measured cardiac hemodynamics and MSNA during randomized short-term dobutamine (10 µg/kg/min) and placebo infusions.
RESULTS: In CHF patients, short-term dobutamine infusion did not modify mean blood pressure (MBP), MSNA, or heart rate (HR). Moreover, 48-h dobutamine infusion increased cardiac index (3.1 ± 0.2 vs. 2.2 ± 0.2 l/min/m2, p = 0.006), decreased mean pulmonary pressure (28 ± 7 vs. 38 ± 7 mm Hg, p = 0.0001) and peripheral resistance (1,099 ± 112 vs. 1,759 ± 263, p = 0.03), but did not change MBP, HR, or MSNA in the patients. In matched controls, dobutamine increased HR (87 ± 5 vs. 65 ± 2 beats/min, p = 0.0009) but did not change MBP or MSNA. In young controls, dobutamine increased MBP (102 ± 2 vs. 90 ± 2 mm Hg, p = 0.0003) and decreased MSNA (28 ± 5 vs. 35 ± 3 bursts/min, p = 0.03) but did not change HR (p = 0.054). In the controls, the largest increases in MBP with dobutamine were associated with the most marked reductions in MSNA (r = 0.49, p = 0.04) and the smallest increases in HR (r = 0.70, p = 0.001).
CONCLUSIONS: Arterial baroreceptor activation during increases in MBP inhibits MSNA and limits the HR response to dobutamine in controls. This mechanism, together with peripheral vasodilation, probably contributes to the absence of peripheral sympathetic withdrawal despite substantial hemodynamic improvements in CHF patients.
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