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(Circulation. 2009;120:376-383.)
© 2009 American Heart Association, Inc.
Coronary Heart Disease |
From the Tokyo Study Group on Myocardial Bridge, which consisted of the departments of pathology at Toho University School of Medicine (Y.I., Y.A., K.I., T.I.), Tokyo, Japan; St Lukes International Hospital (K. Suzuki, M.F., T.O.), Tokyo, Japan; Tokyo Saiseikai Central Hospital (K. Yamazaki), Tokyo, Japan; the National Hospital Organization Yokohama Medical Center (H.N.), Yokohama, Japan; Tokyo Metropolitan Hiroo Hospital (M.T.), Tokyo, Japan; Kyosai Tachikawa Hospital (K.O.), Tachikawa, Japan; Kitasato Institute Hospital (S.M.), Tokyo, Japan; Toda Chuo General Hospital (Y.E.), Toda, Japan; Tokyo Metropolitan Bokutoh Hospital (Y.K.), Tokyo, Japan; Kawasaki Municipal Kawasaki Hospital (H. Sugiura), Kawasaki, Japan; Kasukabe Municipal Hospital (T.T.), Kasukabe, Japan; Jiseikai Hospital (A.K.), Tokyo, Japan; Kawasaki Municipal Ida Hospital (T.S.), Kawasaki, Japan; Musashino Red Cross Hospital (K.T.), Musashino, Japan; Saiseikai Kawaguchi General Hospital (H. Satoh), Kawaguchi, Japan; National Disaster Medical Hospital (K. Yamada), Tachikawa, Japan; Yokosuka Municipal Uwamachi Hospital (M.Y.-I.), Yokosuka, Japan; and Saiseikai Yokohama East Hospital (R.S.), Yokohama, Japan; the Department of Gross Anatomy, Graduate School of Medical and Dental Science, Kagoshima University (K. Shimada), Kagoshima, Japan; and the Department of Medical Informatics, Toho University School of Medicine (C.N.), Tokyo, Japan.
Correspondence to Yukio Ishikawa, MD, Department of Pathology, Toho University School of Medicine, 5-21-16 Omori-nishi, Ota-ku, Tokyo 143-8540, Japan. E-mail yukio{at}med.toho-u.ac.jp
Received September 10, 2008; accepted May 20, 2009.
Background— A myocardial bridge (MB) that partially covers the course of the left anterior descending coronary artery (LAD) sometimes causes myocardial ischemia, primarily because of hemodynamic deterioration, but without atherosclerosis. However, the mechanism of occurrence of myocardial infarction (MI) as a result of an MB in patients with spontaneously developing atherosclerosis is unclear.
Methods and Results— One hundred consecutive autopsied MI hearts either with MBs [MI(+)MB(+) group; n=46] or without MBs (n=54) were obtained, as were 200 normal hearts, 100 with MBs [MI(–)MB(+) group] and 100 without MBs. By microscopy on LADs that were consecutively cross-sectioned at 5-mm intervals, the extent and distribution of LAD atherosclerosis were investigated histomorphometrically in conjunction with the anatomic properties of the MB, such as its thickness, length, and location and the MB muscle index (MB thickness multiplied by MB length), according to MI and MB status. In the MI(+)MB(+) group, the MB showed a significantly greater thickness and greater MB muscle index (P<0.05) than in the MI(–)MB(+) group. The intima-media ratio (intimal area/medial area) within 1.0 cm of the left coronary ostium was also greater (P<0.05) in the MI(+)MB(+) group than in the other groups. In addition, in the MI(+)MB(+) group, the location of the segment that exhibited the greatest intima-media ratio in the LAD proximal to the MB correlated significantly (P<0.001) with the location of the MB entrance, and furthermore, atherosclerosis progression in the LAD proximal to the MB was largest at 2.0 cm from the MB entrance.
Conclusions— In the proximal LAD with an MB, MB muscle index is associated with a shift of coronary disease more proximally, an effect that may increase the risk of MI.
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