title: [Cyclic alteration in atheroma plaque morphology observed by intracoronary ultrasound: initiation mechanism of acute myocardial infarction].
abstract: Rupture of plaque is an important factor in the initiation of acute myocardial infarction. Plaque rupture is related to stress distribution in atheroma, but morphological alteration in coronary atheroma plaque in vivo is little understood. Atheroma plaque was observed during the cardiac cycle using 3.5 or 2.8 F, 30 MHz intracoronary ultrasound (ICUS) in seven patients with coronary artery disease. Coronary ostial pressure (P) measurements were simultaneously performed. Seven of the eccentric stenotic sites were analyzed. Intima-medial thickness (Th) and regional radius of curvature (R) at the middle and lateral portions of the atheroma were measured. Delta Th and % delta Th were calculated from change in thickness from end-diastole to peak systole. These parameters of the middle portion were compared with those of the lateral portion. The lateral % delta Th was 20.1 +/- 13.6% (delta Th 0.13 +/- 0.08 mm; 0.69 to 0.56 mm), and was significantly greater than the middle % delta Th [5.8 +/- 6.6% (delta Th 0.06 +/- 0.08 mm; 1.24 to 1.18 mm), p < 0.05]. Regional radius of curvature did not significantly differ. Wall stress calculated as P x R/Th was greater at the lateral portion (peak systole 3.7 x 10(5) dynes/cm2, end-diastole 1.9 x 10(5) dynes/cm2) than at the middle portion (peak systole 1.4 x 10(5) dynes/cm2, end-diastole 0.9 x 10(5) dynes/cm2). The change in stress from end-diastole to peak systole at the lateral portion was significantly greater (1.8 x 10(5) dynes/cm2) than that at the middle portion (0.5 x 10(5) dynes/cm2). The change in stress during the cardiac cycle, caused by the increase in intracoronary pressure, was greater at the lateral than at the middle of the plaque. This imbalanced distribution of stress may result in greater thinning of plaque at the lateral portion. Therefore, the distortion of plaque may be a mechanism for atheroma rupture at the lateral portion.
authors.affiliation: Second Department of Internal Medicine, Kagawa Medical School.
authors.forename: K
authors.initials: K
authors.lastname: Yoshikawa
authors.forename: K
authors.initials: K
authors.lastname: Mizushige
authors.forename: K
authors.initials: K
authors.lastname: Ohmori
authors.forename: T
authors.initials: T
authors.lastname: Ueda
authors.forename: Y
authors.initials: Y
authors.lastname: Takano
authors.forename: H
authors.initials: H
authors.lastname: Morita
authors.forename: H
authors.initials: H
authors.lastname: Matsuo
mesh_terms: D000368:Aged; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging* / Q000473:pathology / Q000503:physiopathology; D003331:Coronary Vessels / Q000000981:diagnostic imaging* / Q000473:pathology*; D003971:Diastole; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000209:etiology*; D013312:Stress, Physiological / Q000150:complications; D018084:Ultrasonography, Interventional