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Multicenter Study Comparative Study
Relation of ruptured plaque culprit lesion phenotype and outcomes in patients with ST elevation acute myocardial infarction.
- Sang Wook Kim, Young Joon Hong, Gary S Mintz, Sung Yun Lee, Jun Hyung Doh, Seong Hoon Lim, Hyun Jae Kang, Seung Woon Rha, Jung Sun Kim, Wang-Soo Lee, Seong Jin Oh, Sahng Lee, Joo Yong Hahn, Jin Bae Lee, Jang Ho Bae, Seung Ho Hur, Seung Hwan Han, Myung Ho Jeong, and Young Jo Kim.
- Chung-Ang University Hospital, Seoul, Korea. swivus@gmail.com
- Am. J. Cardiol. 2012 Mar 15; 109 (6): 794-9.
AbstractWe used virtual histology intravascular ultrasound (VH-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 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.Copyright © 2012 Elsevier Inc. All rights reserved.
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