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To examine whether acute myocardial ischemia activates the coagulation system and platelet activation in the coronary circulation, we measured plasma levels of fibrinopeptide A and beta-thromboglobulin in the coronary sinus and the aortic root simultaneously in 15 patients with coronary spastic angina before and after the left coronary spasm induced by intracoronary injection of acetylcholine and in 15 patients with stable exertional angina before and after acute myocardial ischemia induced by rapid atrial pacing. Fifteen patients with chest pain but normal coronary arteries and no coronary spasm served as controls. The coronary sinus-arterial difference of fibrinopeptide A increased markedly (p less than 0.001) from 0.1 +/- 0.2 to 4.3 +/- 0.7 ng/ml after the anginal attacks in the coronary spastic angina group. However, fibrinopeptide A levels remained unchanged after the attacks in the stable exertional angina group and after intracoronary injection of acetylcholine in the control group. Plasma beta-thromboglobulin levels remained unchanged after the attacks in both patient groups and after acetylcholine in the control group. Our data indicate that coronary spasm induces thrombin generation and may lead to thrombus formation in the coronary artery involved, but pacing-induced ischemia does not activate the coagulation system.

Plasma levels of fibrinopeptide A (FPA), beta-thromboglobulin (BTG), and platelet factor 4 (PF4) were examined on venous plasma samples taken every 4 hours for 24 hours in 20 patients with variant angina and 20 patients with stable exertional angina together with 24-hour Holter recordings. The mean plasma FPA levels (ng/ml) at 2:00 PM, 6:00 PM, 10:00 PM, 2:00 AM, 6:00 AM, and 10:00 AM were 4.6 +/- 1.0, 3.1 +/- 0.5, 6.1 +/- 1.6, 9.9 +/- 2.4, 8.7 +/- 1.4, and 4.2 +/- 0.8 in patients with variant angina (p less than 0.01) and 1.8 +/- 0.2, 2.3 +/- 0.3, 1.9 +/- 0.3, and 2.3 +/- 0.2 in those with stable exertional angina. In seven patients with variant angina, we also examined the effects of heparin (3,000 units), given subcutaneously at 6:00 PM, 10:00 PM, and 2:00 AM, on the plasma FPA levels and the anginal attacks. Although heparin suppressed the elevation and circadian variation of plasma FPA levels, it did not suppress the attacks and their circadian variation in these patients. Plasma FPA levels increased significantly from 3.7 +/- 0.5 to 12.5 +/- 2.7 ng/ml during or immediately after an attack in the seven patients with no heparin. On the other hand, the plasma levels of BTG and PF4 were increased in patients with variant angina as compared with those with stable exertional angina but did not show a significant circadian variation in both groups. We conclude that 1) plasma levels of FPA, BTG, and PF4 were increased in patients with variant angina as compared with those with stable exertional angina; 2) there was a significant circadian variation in the plasma levels of FPA in parallel with that of the frequency of the attacks with the peak level occurring from midnight to early morning in patients with variant angina; and 3) elevated levels of plasma FPA are the result and not the cause of coronary spasm.

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)