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Beta(2) adrenergic receptors mediate important electrophysiological effects in human ventricular myocardium
M D Lowe1, E Rowland, M J Brown
1Department of Cardiology, Papworth Hospital, Papworth Everard, Cambridge CB3 8RE, UK.
Objective:
To define the effects of beta(2) adrenergic receptor stimulation on ventricular repolarisation in vivo.
Design:
Prospective study.
Setting:
Tertiary referral centre.
Patients:
85 patients with coronary artery disease and 22 normal controls.
Interventions:
Intravenous and intracoronary salbutamol (a beta(2) adrenergic receptor selective agonist; 10-30 microg/min and 1-10 microg/min), and intravenous isoprenaline (a mixed beta(1)/beta(2) adrenergic receptor agonist; 1-5 microg/min), infused during fixed atrial pacing.
Main Outcome Measures:
QT intervals, QT dispersion, monophasic action potential duration.
Results:
In patients with coronary artery disease, salbutamol decreased QT(onset) and QT(peak) but increased QT(end) duration; QT(onset)-QT(peak) and QT(peak)-QT(end) intervals increased, resulting in T wave prolongation (mean (SEM): 201 (2) ms to 233 (2) ms; p < 0.01). There was a large increase in dispersion of QT(onset), QT(peak), and QT(end) which was more pronounced in patients with coronary artery disease-for example, QT(end) dispersion: 50 (2) ms baseline v 98 (4) ms salbutamol (controls), and 70 (1) ms baseline v 108 (3) ms salbutamol (coronary artery disease); p < 0.001. Similar responses were obtained with isoprenaline. Monophasic action potential duration at 90% repolarisation shortened during intracoronary infusion of salbutamol, from 278 (4.1) ms to 257 (3.8) ms (p < 0.05).
Conclusions:
beta(2) adrenergic receptors mediate important electrophysiological effects in human ventricular myocardium. The increase in dispersion of repolarisation provides a mechanism whereby catecholamines acting through this receptor subtype may trigger ventricular arrhythmias.