Is there coronary vasoconstriction after intracoronary beta-adrenergic blockade in patients with coronary artery disease.

Vasomotility of normal and stenosed coronary arteries was studied at rest and during supine bicycle exercise in 10 patients with classical exercise-induced angina pectoris receiving 1 mg intracoronary propranolol before the exercise test (propranolol group). Normal and stenotic coronary lumen areas were determined from biplane coronary arteriograms using a computer-assisted system. Measurements were performed at rest, after 1 mg intracoronary propranolol, during supine exercise (89 W for 3.4 minutes) and 5 minutes after 1.6 mg sublingual nitroglycerin administered at the end of the exercise test. The results were compared with previously obtained data on the effect of dynamic exercise on coronary lumen area in 12 patients receiving no medication (control group) and in 6 patients receiving 0.1 mg intracoronary nitroglycerin before the exercise test (nitroglycerin group). In the control group, coronary stenosis area decreased during exercise to 71% of levels at rest (p less than 0.001) whereas normal coronary lumen area increased to 123% of control (p less than 0.01). In the propranolol group both normal (113%, p less than 0.05 versus rest) and stenotic coronary lumen area (122%, p less than 0.05 versus rest) increased during exercise. A similar increase in both normal and stenotic areas was observed during exercise after pretreatment with 0.1 mg intracoronary nitroglycerin (123%, p less than 0.01 and 114%, p = NS versus rest). Sublingual administration of 1.6 mg nitroglycerin at the end of exercise increased coronary stenosis area to 145% (p less than 0.01 versus rest) in the propranolol group and to 115% in the control group (p = NS versus rest). It is concluded that intracoronary administration of propranolol does not potentiate coronary vasoconstriction of the epicardial vessels at rest and during exercise. In contrast, intracoronary propranolol prevents exercise-induced stenosis narrowing either because of reduced myocardial oxygen demand with a lower coronary blood flow resulting in a smaller transstenotic pressure gradient and, thus, a smaller flow-induced fall in stenosis distending pressure; or because of "local" beta-receptor blockade with unopposed distal arteriolar alpha-receptor tone, resulting in a higher poststenotic pressure and, thus, in a greater stenosis distending pressure; or because of a local anesthetic effect of propranolol with a decrease in calcium influx to the coronary smooth musculature.