We injected acetylcholine (ACh), the neurotransmitter of the parasympathetic nervous system, into the coronary arteries of 28 patients with variant angina. Injection of 10 to 80 gg ACh into the coronary artery responsible for the attack induced spasm together with chest pain and ST segment elevation or depression on the electrocardiogram in 30 of the 32 arteries of 25 of the 27 patients. The injection of 20 to 100 gg ACh into the coronary artery not responsible for the attack in 18 patients resulted in various degrees of constriction in most of them, but no spasm in any of them. After intravenous injection of 1.0 to 1.5 mg atropine sulfate, the injection of ACh into the coronary artery responsible for the attack did not induce spasm or attack in any of the nine coronary arteries injected in eight patients. We conclude that the intracoronary injection of ACh induces coronary spasm and attack in patients with variant angina and that the activity of the parasympathetic nervous system may play a role in the pathogenesis of coronary spasm. We also conclude that the intracoronary injection of ACh is a useful test for provocation of coronary spasm. Circulation 74, No. 5, 955-963, 1986. IT IS NOW widely accepted that spasm of an epicardial coronary artery (coronary spasm) plays an important role in the pathogenesis, not only of variant angina, but also of other forms of resting angina, some types of exertional angina, and types of acute myocardial infarction. quently Endo et al.'0 confirmed our results. On the basis of this fact and the fact that the activity of the parasympathetic nervous system is enhanced at rest and is suppressed by physical activity," we postulated that the activity of parasympathetic nervous system might be related to the pathogenesis of variant angina or coronary spasm.7 It has been shown that stimulation of the parasympathetic (vagus) nerve or intracoronary injection of ACh causes coronary vasodilatation, as demonstrated by an increase in coronary blood flow in dogs,'2-'5 and that ACh dilates isolated epicardial coronary arteries in dogs'6 and monkeys. 17 In humans subcutaneous injection of methacholine causes profound dilatation of systemic vasculature, resulting in a transient fall in blood pressure and compensatory tachycardia due to reflex sympathetic discharge.7 We therefore speculated that coronary spasm might be induced by sympathetic discharge by way of a-adrenergic stimulation.7 Recently, however, reports have appeared that show that ACh contracts strips of human coronary arteries obtained from hearts of transplant recipients'8 or cadav-955

Multivessel coronary spasm has been described but its incidence in patients with variant angina still remains unclear. Thirty-three patients with variant angina were studied during coronary angiographic examination with selective intracoronary injection of acetylcholine (ACh). In all but three patients, the location of ischemia during attack was determined by the electrocardiographic findings, by exercise 201Tl myocardial scintigraphy, and by two-dimensional echocardiography during a hyperventilation test, and the coronary artery (or arteries) responsible for the attack was predicted before the study. ACh induced spasm of at least one coronary artery in all but one patient. ACh induced spasm of both the left and right coronary arteries (i.e., multivessel coronary spasm) in 24 patients: in two of the four patients who were predicted to have spasm of the left coronary artery, in six of the 11 predicted to have spasm of the right coronary artery, in 13 of the 15 predicted to have spasm of both the left and right coronary arteries, and in three of the three in whom coronary artery responsible for attack had not been predicted. This ACh-induced spasm of the left and right coronary arteries occurred separately and no patients showed hemodynamic instability during attack. In one patient in whom multivessel coronary spasm had been predicted and ACh failed to induice coronary spasm, ergonovine maleate (0.2 mg) induced spasm of both the left and right coronary arteries simultaneously, resulting in severe prolonged hypotension. Nineteen of the 25 patients in whom multivessel coronary spasm was documented showed angiographically normal or nearly normal coronary arteries after administration of nitroglycerin.(ABSTRACT TRUNCATED AT 250 WORDS)

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74, No. 2, 374-380, 1986. EXERTIONAL ANGINA has been explained on the basis of increased myocardial oxygen demand in the presence of fixed stenosis of coronary arteries.1 2 Thus, ,3-adrenergic-blocking drugs that decrease myocardial oxygen demand have been widely used in its treatment.2> Recently, acute reduction of myocardial blood flow or oxygen supply due to coronary artery spasm has been shown to play an important role in the pathogenesis of exercise-induced attack not only in patients with variant angina,5 but also in patients with classic exertional angina.8 In these patients, the drugs of choice for the treatment of exercise-induced attack would be calcium antagonists, which suppress coronary artery spasm, rather than ,3-adrenergic-blocking

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By intravenous administration of isoproterenol, 0.5 micrograms/min, a catecholamine-sensitive bypass tract was confirmed in two patients with exercise-induced Wolff-Parkinson-White syndrome. In a 24 year old woman, an intravenous bolus injection of 5 mg of verapamil suddenly blocked conduction over a catecholamine-sensitive bypass tract. In a 62 year old man, the exercise-induced Wolff-Parkinson-White syndrome disappeared after 3 days of oral administration of verapamil (120 mg/day). These observations suggest that a slow inward calcium current plays an important role in conduction over a catecholamine-sensitive bypass tract in exercise-induced Wolff-Parkinson-White syndrome.

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