Acetylcholine causes endothelium-dependent dilation of normal arteries in most animal species. The effect of acetylcholine on normal human coronary arteries is controversial. Pathologic studies and epicardial echocardiography have shown that diffuse atherosclerosis is often present despite angiographic evidence of discrete coronary artery disease (CAD). Therefore, we postulated that acetylcholine would cause vasoconstriction of coronary arteries that are angiographically normal in patients with CAD. Coronary artery diameter, measured by automated quantification of digitized cineangiograms, was determined before and after the intracoronary infusion of 0.2 mM acetylcholine at 0.8-1.6 ml/min. The diameter of stenotic or irregular segments of six atherosclerotic coronary arteries decreased from 1.80±0.42 mm before acetylcholine to 1.26±0.46 mm after acetylcholine (p=0.0025). Acetylcholine had a significantly diYferent effect on the diameter of two groups of coronary arteries that are angiographically normal. Acetylcholine caused a 0.16±0.09-mm increase in the diameter of 14 normal coronary arteries in patients without CAD, whereas it caused a 0.26+0.12-mm decrease in the diameter of 14 normal coronary arteries in patients with CAD (p <0.01). Thus, the normal response to intracoronary acetylcholine is vasodilation, suggesting that endotheliumderived relaxing factor is released from normal human coronary endothelium. The vasoconstrictive effect of acetylcholine in the angiographically normal coronary arteries of patients with CAD suggests the presence of a diffuse abnormality of endothelial function. (Circulation 1989;79:287-291) T here is growing evidence that acetylcholine and a number of other substances induce vasodilation by stimulating the release of an endothelium-derived relaxing factor (EDRF) from endothelial cells, whereas nitroglycerin and other endothelium-independent vasodilators induce vasodilation through the direct stimulation ofvascular smooth muscle."2,3 Thus, acetylcholine or aggregating platelets cause relaxation of arteries with an intact endothelium but cause contraction of arteries denuded of endothelium.1"2'3 An impairment of endotheliumdependent vasodilation has been observed in rabbits4 and monkeys5'6 that were fed an atherogenic diet. atherosclerosis and restored endothelium-dependent relaxation to normal.6 Conflicting data exist, however, regarding the existence of endothelium-mediated vasodilation in human coronary arteries. Several in vitro studies conclude that acetylcholine and carbachol, both muscarinic agonists, constrict human coronary arteries,7-10 whereas other studies suggest that acetylcholine dilates normal human coronary arteries.1" Similarly, a discrepancy exists regarding the effect of acetylcholine on human coronary arteries in vivo. After the intracoronary infusion of acetylcholine, Horio et al12 observed at least a 25% decrease in the diameter of normal or almost normal coronary arteries in 27 of 70 arteries, whereas Ludmer et al13 reported an 11% increase in the diame...

We randomly assigned 56 patients who presented within 12 hours of their first symptoms of acute myocardial infarction to treatment with either intracoronary streptokinase or coronary angioplasty. The mean (+/- SD) duration of symptoms (3.0 +/- 1.2 hours in the group treated with angioplasty vs. 3.6 +/- 1.8 in the group treated with streptokinase; P not significant) and time to recanalization (4.1 +/- 1.4 hours vs. 4.8 +/- 1.7 hours; P not significant) were similar in both groups. Coronary recanalization was achieved in 83 percent of the patients treated with angioplasty and in 85 percent of those treated with streptokinase (P not significant). Residual luminal stenosis in the coronary artery was significantly decreased after angioplasty, as compared with streptokinase therapy (43 +/- 31 percent of patients vs. 83 +/- 17; P less than 0.001). Residual stenosis of 70 percent or more was present in 4 percent of the angioplasty-treated patients and in 83 percent of the streptokinase-treated patients (P less than 0.01). Ventricular function after therapy was assessed by serial contrast ventriculograms. Increases in both global ejection fraction (8 +/- 7 percent vs. 1 +/- 6; P less than 0.001) and regional wall motion (+1.32 +/- 1.32 SD vs. +0.59 +/- 0.79 SD; P less than 0.05) were greater for the angioplasty group. We conclude that angioplasty and streptokinase produce similar rates of early coronary reperfusion during evolving transmural myocardial infarction. However, angioplasty is significantly more effective in alleviating the underlying coronary stenoses, and this may result in more effective preservation of ventricular function after therapy.

Modest survival benefits have been reported in patients with acute myocardial infarction complicated by cardiogenic shock who were treated with early surgical revascularization or thrombolytic therapy. To determine whether coronary angioplasty improves survival, 87 patients with cardiogenic shock complicating acute myocardial infarction at the University of Michigan, Ann Arbor, Michigan, from 1975 to 1985 were retrospectively analyzed. Patients in group 1 (n= 59) were treated with conventional therapy; patients in group 2 (n=24) were treated with conventional therapy and angioplasty. Extent of coronary artery disease, infarct location, and incidence of multivessel disease were similar between groups. Hemodynamic variables including cardiac index, mean arterial pressure, and pulmonary capillary wedge pressure were also similar. The 30-day survival was significantly improved for group 2 patients (50% vs. 17%, p=0.006). Survival in group 2 patients with successful angioplasty was 77% (10 of 13 patients) versus 18% (two of 11 patients) in patients with unsuccessful angioplasty, (p=0.006). The findings suggest that angioplasty improves survival in cardiogenic shock compared with conventional therapy with survival contingent upon successful reperfusion of the infarct-related artery. (Circulation 1988;78:1345-1351 C ardiogenic shock remains a lethal complication of acute myocardial infarction.

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To determine whether coronary patency could be detected early during thrombolytic therapy, commonly used markers of perfusion were recorded in 386 patients with acute myocardial infarction treated with tissue plasminogen activator. Infarct artery angiography 90 minutes after initiation of therapy was used to determine perfusion status. Of patients with complete resolution of ST segment elevation before the angiogram, 96% (95% confidence interval, 79% to 100%) showed perfusion on the angiogram, and among those with partial improvement, 84% (95% confidence interval, 76% to 90%) showed perfusion, but these findings occurred in only 6% and 38% of patients respectively. When complete resolution of chest pain occurred before the angiogram, 84% of patients (95% confidence interval, 75% to 90%) showed perfusion, but this finding occurred in only 29% of patients. Although arrhythmias occurred frequently in the first 90 minutes of therapy, none were associated with a higher patency rate. No other factors predicted coronary patency. A logistic regression model showed 25% of patients with 90% or greater probability of patency, but 56% of patients with no ST segment or symptom resolution had patent arteries.