Computed Tomographic Angiography for Localizing the Site of Plaque Disruption/Thrombus

Abstract

In the 1980s, our group published a series of articles using invasive angiography (ICA) to investigate the pathogenesis of unstable angina and acute myocardial infarction.1–5 In individuals in whom an angina-producing lesion could be assessed angiographically and the vessel was <100% occluded at the time of angiography, the qualitative morphology of these lesions was different from that of lesions associated with stable angina.1 Unstable angina was precisely defined as either the acute onset of rest pain or crescendo angina with an abrupt increase in duration and/or frequency in angina pectoris. Myocardial infarction was defined according to the terminology of the day as either subendocardial or transmural myocardial infarction. Article see p 105 Unstable angina or infarct lesions were severe (>70% diameter stenosis) and were usually eccentric with irregular borders, overhanging edges, ulcerations, and/or intra luminal filling defects. These lesions were found in more than two-thirds of the culprit vessels and were initially called type II eccentric lesions; later, they were called complex lesions.6 We proposed that these lesions represented plaque disruption and/or intracoronary thrombus formation, based on the postmortem angiographic/histological correlations of Levin and Fallon.7 These authors found that eccentric and irregular lesions on postmortem angiography in patients dying after myocardial infarction represented plaque disruption and or intracoronary thrombus formation in 79% on pathological examination. Other angiographic studies and other modalities including angioscopy and intravascular ultrasound have corroborated our initial observations in acute coronary syndromes (ACS).8,9 In patients with stable angina and a complex culprit lesion, it has also …