Key result
Intravenous propranolol did not facilitate coronary spasm in patients with Prinzmetal's angina, as coronary narrowings invariably dilated after administration.
Why the study?
Does intravenous propranolol facilitate coronary spasm in patients with Prinzmetal's angina?
Does intravenous propranolol facilitate coronary spasm in patients with Prinzmetal's angina?
Intravenous propranolol does not facilitate coronary spasm in patients with Prinzmetal's angina, suggesting different coronary contractility mechanisms compared to classic angina.
Beta-blockers do not appear to provoke spasm in Prinzmetal angina; leaves open need for larger randomized trials before changing practice.
BACKGROUND: Alpha-adrenergic activation enhances coronary vascular tone; beta-blockade leaves alpha-adrenergic vasoconstriction unopposed. Whether beta-adrenergic blockade facilitates coronary spasm in patients with Prinzmetal's angina is unknown. METHODS: Using quantitative angiography, we evaluated the response of normal and narrowed coronary arteries to intravenous propranolol, a cold pressor test (an alpha-stimulus), 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 right ventricular ejection times, we derived the tension-time index per minute as a measure of the oxygen need (O2 demand) of the whole heart. RESULTS: In group 1, cold invariably constricted normal and diseased vessels, and in two patients elicited spasm at sites of significant lesions; these changes did not correlate with those in O2 demand. In group 2, the vasomotor reaction of normal and narrowed vessels in response to cold correlated with the modifications in O2 demand. After propranolol administration, (1) in normal vessels in both groups, the baseline luminal diameter varied in parallel with the changes in myocardial O2 demand; (2) narrowings in group 1 patients invariably dilated and in group 2 the caliber varied according to changes in O2 demand; (3) during cold stimulation, luminal narrowing in group 1 varied in parallel with O2 demand, and, in group 2, vessels were uniformly constricted. CONCLUSION: These results do not support the facilitation of coronary spasm by propranolol in Prinzmetal's angina and support the hypothesis that the contractility of coronary vessels in patients with this form of angina is different from that in the classic form.
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Cesare et al. (1994) studied Prinzmetal's angina and classic angina (n=34). Intravenous propranolol and cold pressor test vs. Classic angina patients was evaluated on Vasomotor reaction of normal and narrowed coronary arteries and correlation with myocardial O2 demand. Intravenous propranolol did not facilitate coronary spasm in patients with Prinzmetal's angina, as coronary narrowings invariably dilated after administration.