Relation of Ruptured Plaque Culprit Lesion Phenotype and Outcomes in Patients With ST Elevation Acute Myocardial Infarction

Abstract

We used virtual histology intravascular ultrasound (VH-IVUS) to assess culprit plaque rupture in 172 patients with ST-segment elevation acute myocardial infarction. VH-IVUSdefined thin-capped fibroatheroma (VH-TCFA) had necrotic core (NC) >10% of plaque area, plaque burden >40%, and NC in contact with the lumen for >3 image slices. Ruptured plaques were present in 72 patients, 61% of which were located in the proximal 30 mm of a coronary artery. Thirty-five were classified as VH-TCFA and 37 as non-VHTCFA. Vessel size, lesion length, plaque burden, minimal lumen area, and frequency of positive remodeling were similar in VH-TCFA and non-VH-TCFA. However, the NC areas within the rupture sites of VH-TCFAs were larger compared to non-VH-TCFAs (p 0.002), while fibrofatty plaque areas were larger in non-VH-TCFAs (p <0.0001). Ruptured plaque cavity size was correlated with distal reference lumen area (r 0.521, p 0.00002), minimum lumen area (r 0.595, p <0.0001), and plaque area (r 0.267, p 0.033). Sensitivity and specificity curve analysis showed that a minimum lumen area of 3.5 mm2, a distal reference lumen area of 7.5 mm2, and a maximum NC area of 35% best predicted plaque rupture. Although VH-TCFA (35 of 72) was the most frequent phenotype of plaque rupture in ST-segment elevation myocardial infarction, plaque rupture also occurred in non-VH-TCFA: pathologic intimal thickening (8 of 72), thick-capped fibroatheroma (1 of 72), and fibrotic (14 of 72) and fibrocalcified (14 of 72) plaque. In conclusion, not all culprit plaque ruptures in patients with ST-segment elevation myocardial infarction occur as a result of TCFA rupture; a prominent fibrofatty plaque, especially in a proximal vessel, may be another form of vulnerable plaque. Further study should identify additional factors causing plaque rupture. © 2012 Elsevier Inc. All rights reserved. (Am J Cardiol 2012;109: 794–799)