title: Histopathologic profiles of coronary atherosclerosis by myocardial bridge underlying myocardial infarction.
abstract: OBJECTIVE
  Anatomic properties of myocardial bridge (MB) are sometimes responsible for myocardial infarction (MI) through the changes in the atherosclerosis distribution in the left ascending coronary artery (LAD). The purpose of this study was to investigate histopathologic profiles of atherosclerotic lesions resulting from the MB presence in the LAD in the MI cases.
  
  
  METHODS
  In 150 consecutive autopsied MI hearts either with MBs [MI(+)MB(+); n = 67] or without MBs [MI(+)MB(-); n = 83] and 100 normal hearts with MBs [MI(-)MB(+)], LADs were consecutively cross-sectioned at 5-mm intervals. The most advanced intimal lesion and unstable plaque-related lesion characteristics (UPLCs) in each section were histopathologically evaluated in conjunction with the anatomic properties of the MB, such as its thickness, length, location, and MB muscle volume burden (MMV: the total volume of MB thickness multiplied by MB length).
  
  
  RESULTS
  The MB showed a significantly greater thickness (P = 0.0090), length (P = 0.0300), and MMV (P = 0.0019) in MI(+)MB(+) than in MI(-)MB(+). Mean age of acute MI cases was significantly younger (P = 0.0227) in MI(+)MB(+) than in MI(+)MB(-). Frequency of plaque fissure/rupture in the proximal LAD was significantly higher in acute MI cases of MI(+)MB(+) than in MI(+)MB(-). UPLCs tended to be located proximally in MI(+)MB(+) and frequent 2.0 cm or more proximal to the MB entrance in MI(+)MB(+).
  
  
  CONCLUSIONS
  In MI(+)MB(+), UPLCs tend to be located more proximally, and a plaque in the LAD proximal to the MB is prone to rupture, resulting in MI at younger age.
authors.affiliation: Department of Pathology, Toho University School of Medicine, 5-21-16 Omori-nishi, Ota-ku, Tokyo 143-8540, Japan. yukio@med.toho-u.ac.jp
authors.forename: Yukio
authors.initials: Y
authors.lastname: Ishikawa
authors.forename: Yoshikiyo
authors.initials: Y
authors.lastname: Akasaka
authors.forename: Yuri
authors.initials: Y
authors.lastname: Akishima-Fukasawa
authors.forename: Ami
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authors.lastname: Iuchi
authors.forename: Koyu
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authors.lastname: Suzuki
authors.forename: Mieko
authors.initials: M
authors.lastname: Uno
authors.forename: Eriko
authors.initials: E
authors.lastname: Abe
authors.forename: Yang
authors.initials: Y
authors.lastname: Yang
authors.forename: Chin-Ping
authors.initials: CP
authors.lastname: Li
authors.forename: Kiyoshi
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authors.lastname: Mukai
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Niino
authors.forename: Michio
authors.initials: M
authors.lastname: Tanaka
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Kawahara
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Sugiura
authors.forename: Toshihito
authors.initials: T
authors.lastname: Shinagawa
authors.forename: Shojiroh
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authors.lastname: Morinaga
authors.forename: Kentaro
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authors.lastname: Ogata
authors.forename: Junko
authors.initials: J
authors.lastname: Onuma
authors.forename: Maki
authors.initials: M
authors.lastname: Yanagida-Iida
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Taki
authors.forename: Akio
authors.initials: A
authors.lastname: Komatsu
authors.forename: Hideaki
authors.initials: H
authors.lastname: Satoh
authors.forename: Kazuaki
authors.initials: K
authors.lastname: Yamada
authors.forename: Reiko
authors.initials: R
authors.lastname: Shimokawa
authors.forename: Kazutoshi
authors.initials: K
authors.lastname: Shibuya
authors.forename: Kei
authors.initials: K
authors.lastname: Takahashi
authors.forename: Toshiharu
authors.initials: T
authors.lastname: Ishii
mesh_terms: D000368:Aged; D003324:Coronary Artery Disease / Q000473:pathology*; D005260:Female; D006801:Humans; D008297:Male; D009203:Myocardial Infarction / Q000473:pathology*; D009206:Myocardium / Q000473:pathology