EARLY ANGIOGRAPHY DURING INFARCTION: A SEARCH FOR SPASM

Abstract

ABSTRACTThe predominant cause of continuing injury during transmural myocardial infarction is intracoronary thrombosis linked to plaque rupture or plaque hemorrhage. The initiating events, however, remain unknown primarily because angiography is performed late. Postmortem analysis of patients dying suddenly may not be relevant since it is not known whether a transmural myocardial infarction would have followed. Therefore, we must make conclusions from early therapeutic responses and from angiography performed always with some delay.Sixty patients were studied. Twenty‐five showed anterior transmural infarction and were evaluated by systemic nitroglycerin response, followed by coronary angiography after six hours to seven days. Only three of twenty‐five showed greater than 50 % reduction in precordial ST segment elevation during the thirty‐minute postnitroglycerin observation period. Angiography showed left anterior descending occlusion in thirteen and high grade stenosis in twelve. Nitroglycerin response was seen only in patients with left anterior descending stenosis. The mechanism of nitroglycerin response, however, was not observed.Thirty‐five patients with either anterior or inferior transmural infarction received sublingual and intravenous nitroglycerin on admission and coronary angiography within six hours, during which intracoronary nitroglycerin was infused into the obstructed coronary artery. Only two patients responded to systemic nitroglycerin with a greater than 50 % fall in ST segment elevation. At angiography the offending vessel was stenotic and not further dilatable with intracoronary nitroglycerin. Thirty‐two patients receiving intracoronary nitroglycerin showed no reduction in coronary stenosis and no reversal of obstruction. Three patients with coronary occlusion (two with inferior infarction, one with anterior infarction) responded to intracoronary nitroglycerin with slow antegrade flow. This restored flow was adequate to outline intracoronary filling defects but inadequate to reduce injury or to induce ventricular irritability. In these patients streptokinase infusions cleared the defects and augmented antegrade flow.In conclusion, neither responsivity to nitroglycerin nor early coronary angiography demonstrate that coronary spasm is pronounced after onset of transmural myocardial infarction.