title: Plaque erosion in the culprit lesion is prone to develop a smaller myocardial infarction size compared with plaque rupture.
abstract: BACKGROUND
  Acute myocardial infarction (MI) stems from a disruption of the plaque in the coronary artery. Based on postmortem examinations, such plaque disruption has been classified as either a rupture or an erosion. Unfortunately, it has been difficult to clinically identify plaque ruptures and plaque erosions during the development of acute MI. To elucidate the relationships between clinical features and the morphological characteristics of the infarct-related lesions, we observed the culprit lesions in patients with acute MI by coronary angioscopy and intravascular ultrasound.
  
  
  METHODS
  We examined culprit lesions in 107 patients with acute MI using coronary angioscopy and intravascular ultrasound immediately before performing percutaneous coronary intervention. The lesions were then classified as plaque ruptures or nonruptured erosions, and their clinical features were compared.
  
  
  RESULTS
  Among the lesions studied, 44 were classified as plaque ruptures, 28 were classified as plaque erosions, and 35 were unclassified. Patients with nonruptured eroded plaques had more preinfarction angina before the onset of MI than those with ruptured plaques (53.6% vs 22.7%, P = .0074). They also had less ST-segment elevation MI (71.4% vs 93.2%, P = .0185), lower peak creatine kinase levels (2029 +/- 1517 vs 4033 +/- 2699 IU/L, P = .0009), less distal embolization after percutaneous coronary intervention (3.6% vs 36.4%, P = .0014), and less Q-wave MI 1 month after onset (40.7% vs 88.4%, P < .0001).
  
  
  CONCLUSIONS
  Patients with eroded plaque lesions have smaller infarctions than those with ruptured plaque lesions, suggesting that an eroded plaque is less potently thrombogenic than a ruptured plaque.
authors.affiliation: Department of Cardiology, Kinki University School of Medicine, Osakasayama, Osaka, Japan. hayashi@med.kindai.ac.jp
authors.forename: Takahiro
authors.initials: T
authors.lastname: Hayashi
authors.forename: Takashi
authors.initials: T
authors.lastname: Kiyoshima
authors.forename: Masayoshi
authors.initials: M
authors.lastname: Matsuura
authors.forename: Masafumi
authors.initials: M
authors.lastname: Ueno
authors.forename: Naoya
authors.initials: N
authors.lastname: Kobayashi
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Yabushita
authors.forename: Atsuhiro
authors.initials: A
authors.lastname: Kurooka
authors.forename: Mitsugu
authors.initials: M
authors.lastname: Taniguchi
authors.forename: Masaru
authors.initials: M
authors.lastname: Miyataka
authors.forename: Akio
authors.initials: A
authors.lastname: Kimura
authors.forename: Kinji
authors.initials: K
authors.lastname: Ishikawa
mesh_terms: D000368:Aged; D000787:Angina Pectoris / Q000150:complications / Q000473:pathology; D017546:Angioscopy; D003324:Coronary Artery Disease / Q000150:complications / Q000000981:diagnostic imaging / Q000473:pathology*; D003331:Coronary Vessels / Q000000981:diagnostic imaging / Q000473:pathology; D003937:Diagnosis, Differential; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000209:etiology / Q000473:pathology*; D012422:Rupture, Spontaneous / Q000175:diagnosis; D018084:Ultrasonography, Interventional