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

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• 作者：Sang Wook Kim ; MD^a ; ^{swivus@gmail.com} ; Young Joon Hong ; MD^b ; Gary S. Mintz ; MD^c ; Sung Yun Lee ; MD^d ; Jun Hyung Doh ; MD^d ; Seong Hoon Lim ; MD^e ; Hyun Jae Kang ; MD^f ; Seung Woon Rha ; MD^g ; Jung Sun Kim ; MD^h ; Wang-Soo Lee ; MD^a ; Seong Jin Oh ; MDⁱ ; Sahng Lee ; MD^j ; Joo Yong Hahn ; MD^k ; Jin Bae Lee ; MD^l ; Jang Ho Bae ; MD^m ; Seung Ho Hur ; MDⁿ ; Seung Hwan Han ; MD^o ; Myung Ho Jeong ; MD^b ; Young Jo Kim ; MD^p
• 刊名：The American Journal of Cardiology
• 出版年：2012
• 期刊代码：5_00029149
• 类别：med
• 出版时间：15 March, 2012
• 卷：109
• 期：6
• 页码：794-799
• 文件大小：1633 K

摘要

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 鈮? 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.