Relation of Ruptured Plaque Culprit Lesion Phenotype and Outcomes in Patients With ST Elevation Acute Myocardial Infarction
- Authors
- Kim, Sang Wook; Hong, Young Joon; Mintz, Gary S.; Lee, Sung Yun; Doh, Jun Hyung; Lim, Seong Hoon; Kang, Hyun Jae; Rha, Seung Woon; Kim, Jung Sun; Lee, Wang-Soo; Oh, Seong Jin; Lee, Sahng; Hahn, Joo Yong; Lee, Jin Bae; Bae, Jang Ho; Hur, Seung Ho; Han, Seung Hwan; Jeong, Myung Ho; Kim, Young Jo
- Issue Date
- 15-Mar-2012
- Publisher
- EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC
- Citation
- AMERICAN JOURNAL OF CARDIOLOGY, v.109, no.6, pp.794 - 799
- Journal Title
- AMERICAN JOURNAL OF CARDIOLOGY
- Volume
- 109
- Number
- 6
- Start Page
- 794
- End Page
- 799
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/16519
- DOI
- 10.1016/j.amjcard.2011.10.042
- ISSN
- 0002-9149
- Abstract
- We used virtual histology intravascular ultrasound (VU-IVUS) to assess culprit plaque rupture in 172 patients with ST-segment elevation acute myocardial infarction. VH-IVUS-defined 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-VH-TCFA. 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 mm(2), a distal reference lumen area of 7.5 mm(2), 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. (C) 2012 Elsevier Inc. All rights reserved. (Am J Cardiol 2012;109: 794-799)
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