FACILITATION OF CORONARY SPASM BY PROPRANOLOL IN PRINZMETALS ANGINA -FACT OR UNPROVED EXTRAPOLATION

Background: Alpha-adrenergic activation enhances coronary vascular ton e; beta-blockade leaves alpha-adrenergic vasoconstriction unopposed. W hether beta-adrenergic blockade facilitates coronary spasm in patients with Prinzmetal's angina is unknown. Methods: Using quantitative angi ography, we evaluated the response of normal and narrowed coronary art eries to intravenous propranolol, a cold presser test (an alpha-stimul us), and the combination of the two in 15 patients with Prinzmetal's ( group 1) and in 19 with classic (group 2) angina. From measurements of heart rate, systemic and pulmonary arterial pressures, and left and r ight ventricular ejection times, we derived the tension-time index per minute as a measure of the oxygen need (O-2 demand) of the whole hear t. Results: In group 1, cold invariably constricted normal and disease d vessels, and in two patients elicited spasm at sites of significant lesions; these changes did not correlate with those in O-2 demand. In group 2, the vasomotor reaction of normal and narrowed vessels in resp onse to cold correlated with the modifications in O-2 demand. After pr opranolol administration, (1) in normal vessels in both groups, the ba seline luminal diameter varied in parallel with the changes in myocard ial O-2 demand; (2) narrowings in group 1 patients invariably dilated and in group 2 the caliber varied according to changes in O-2 demand; (3) during cold stimulation, luminal narrowing in group 1 varied in pa rallel with O-2 demand, and, in group 2, vessels were uniformly constr icted. Conclusion: These results do not support the facilitation of co ronary spasm by propranolol in Prinzmetal's angina and support the hyp othesis that the contractility of coronary vessels in patients with th is form of angina is different from that in the classic form.