Circulation, Vol 67, 1178-1185, Copyright © 1983 by American Heart Association
MJ Kern, P Ganz, JD Horowitz, J Gaspar, WH Barry, BH Lorell, W Grossman and GH Mudge Jr
Although beta-adrenergic blocking agents reduce myocardial oxygen
consumption and symptoms of myocardial ischemia in patients with coronary
artery disease (CAD), propranolol has been reported to exacerbate coronary
artery spasm in some patients with variant angina. To determine whether
increased coronary vasomotor tone can be induced by beta-adrenergic
blockade, we measured the changes in coronary vascular resistance (CVR)
during cold pressor testing (CPT) in 15 patients, nine with severe CAD and
six with normal left coronary anatomy, before and after i.v. propranolol
(0.1 mg/kg). Coronary blood flow was measured by coronary sinus
thermodilution. CVR was calculated as mean arterial pressure divided by
coronary sinus blood flow. Heart rate was maintained constant at a paced
subanginal rate of 95 +/- 5 beats/min. Before propranolol, CPT induced
significant increases in coronary vascular resistance in patients with CAD
(15.0 +/- 2.2%, p less than 0.02), but no increase in CVR in the normal
patients. After propranolol, the CVR change during CPT was augmented for
patients with CAD (29 +/- 6%, p less than 0.01) and for the normal
population (9 +/- 5%, NS). The potentiated increase in CVR occurred without
significant changes in resting CVR or in the magnitude of the hypertensive
response to CPT. We conclude that beta-adrenergic blockade with propranolol
can potentiate coronary artery vasoconstriction in some patients with CAD,
possibly mediated by unopposed alpha-adrenergic vasomotor tone. These
changes may be important in patients in whom intense adrenergic stimulation
may increase coronary artery tone and adversely influence the balance
between myocardial oxygen supply and demand.
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