COMPARATIVE STUDY
JOURNAL ARTICLE
MULTICENTER 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, Young Jo Kim
American Journal of Cardiology 2012 March 15, 109 (6): 794-9
22196783
We 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.

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