Acute effects of beta 1-selective and nonselective beta-adrenergic receptor blockade on cardiac sympathetic activity in congestive heart failure
Newton, G.E.; Parker, J.D.
Circulation 94(3): 353-358
1996
ISSN/ISBN: 0009-7322 PMID: 8759076 Document Number: 463903
Background: beta-Blockers may reduce cardiac sympathetic activity in patients with heart failure by antagonizing beta-adrenergic receptors that facilitate sympathetic outflow to the heart. To explore this possible effect of beta-blockade, we measured cardiac norepinephrine spillover responses in patients with heart failure after the acute administration of either propranolol, a nonselective beta-blocker, or metoprolol, a beta-1-selective agent. Methods and Results: Eighteen patients were studied. Repeated intravenous doses of propranolol (0.5 mg; nine patients; left ventricular ejection fraction, 14 +- 2%) or metoprolol (1.0 mg; nine patients; left ventricular ejection fraction, 18+-2%) were administered until one of the following end points was reached. a 15% decrease in heart rate, left ventricular +dP/dt, or mean arterial blood pressure or a 5 mm Hg increase in left ventricular end-diastolic pressure. Propranolol (mean dose, 2.0 mg) and metoprolol (mean dose, 3.6 mg) caused similar reductions in heart rate, +dP/dt, and coronary sinus plasma flow, Cardiac norepinephrine spillover was reduced after propranolol (277+-55 to 262+-53 pmol/min, P lt .05) but was after metoprolol (233+-57 to 296+-82 pmol/min, P lt .05). In a comparison of the two groups, the decrease in spillover after propranolol was significantly different than the increase seen after metoprolol (P lt .01). Conclusions: The administration of a beta-1-selective antagonist was associated with increased cardiac norepinephrine spillover. In contrast, the administration of a nonselective beta-blocker until similar hemodynamic end points were reached caused a reduction in norepinephrine spillover. This suggests that in patients with heart failure, nonselective beta-blockade may have favorable inhibitory effects on cardiac sympathetic activity.