title: Evolution of nonculprit coronary atherosclerotic plaques assessed by serial virtual histology intravascular ultrasound in patients with ST-segment elevation myocardial infarction and chronic total occlusion.
abstract: OBJECTIVE
  The pathophysiology and natural course of coronary nonculprit plaques remain unclear. We investigated whether the short-term natural course of nonculprit plaques differs between ST-segment elevation myocardial infarction (STEMI) and chronic total occlusion (CTO) patients.
  
  
  METHODS
  We performed serial virtual histology intravascular ultrasound on nonculprit plaques in 26 STEMI and 11 CTO lesions at baseline and the 6-month follow-up.
  
  
  RESULTS
  At baseline, more lesions in the STEMI group were virtual histology intravascular ultrasound-derived thin-cap fibroatheromas (TCFA; 76.9 vs. 18.1%, P=0.002). During the follow-up period, the plaque composition changed dynamically in the STEMI group (fibrofatty: 9.8±1.9 to 17.3±2.9%, P=0.030; dense calcium: 12.7±1.8 to 8.1±1.7%, P=0.026; necrotic core: 21.1±1.8 to 15.4±2.2%, P=0.052), with a consistent plaque size. In the CTO group, the plaque composition and plaque size remained consistent without a significant change. Also, more lesions in the STEMI group remained as or progressed to TCFA, compared with the CTO group (67 vs. 11%, P=0.089). Factors associated with a persistent TCFA or with a new development of TCFA were a large necrotic core volume index and the diagnosis of STEMI, whereas new statin usage was a protective factor.
  
  
  CONCLUSIONS
  Nonculprit lesions in STEMI patients were more unstable at the baseline compared with those in CTO patients. During follow-up, nonculprit lesions in STEMI and CTO patients showed a distinct pattern of change; the former were stabilized in plaque composition, whereas the latter remained consistent. The diagnosis of STEMI and a large necrotic core volume were predictors of evolution to a TCFA, and new statin usage was a protective factor.
authors: aDepartment of Internal Medicine, Seoul National University Bundang Hospital, Seongnam bDepartment of Internal Medicine, Seoul National University Hospital, Seoul, South Korea.
authors: Jeehoon
authors: J
authors: Kang
authors: Ki-Hyun
authors: KH
authors: Jeon
authors: Seong-Wook
authors: SW
authors: Kim
authors: Jin Joo
authors: JJ
authors: Park
authors: Chang-Hwan
authors: CH
authors: Yoon
authors: Jung-Won
authors: JW
authors: Suh
authors: Young-Seok
authors: YS
authors: Cho
authors: Tae-Jin
authors: TJ
authors: Youn
authors: In-Ho
authors: IH
authors: Chae
authors: Dong-Ju
authors: DJ
authors: Choi
mesh_terms: D000368:Aged; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging* / Q000473:pathology / Q000628:therapy; D054059:Coronary Occlusion / Q000000981:diagnostic imaging* / Q000473:pathology / Q000628:therapy; D003331:Coronary Vessels / Q000000981:diagnostic imaging* / Q000187:drug effects / Q000473:pathology; D005260:Female; D005355:Fibrosis; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D008297:Male; D008499:Medical Records; D008875:Middle Aged; D009336:Necrosis; D062645:Percutaneous Coronary Intervention; D058226:Plaque, Atherosclerotic; D011237:Predictive Value of Tests; D012189:Retrospective Studies; D012422:Rupture, Spontaneous; D000072657:ST Elevation Myocardial Infarction / Q000000981:diagnostic imaging* / Q000473:pathology / Q000628:therapy; D013997:Time Factors; D016896:Treatment Outcome; D018084:Ultrasonography, Interventional
chemical_list: D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors