title: Role of myocardial interstitial edema in conduction disturbances in acute myocarditis.
abstract: The presence of myocardial interstitial edema in acute myocarditis (AM) leads to thickening of the ventricular wall, and conduction disturbances, such as complete atrioventricular block (CAV), also frequently develop. This study was undertaken in order to clarify the relationship between conduction disturbances and myocardial interstitial edema in AM. The subjects comprised 50 patients with acute lymphocytic myocarditis. Based on the results of echocardiographic examinations during the acute stage, the patients were divided into a hypertrophy group (n = 29) in which the sum of the thickness of the interventricular septum and left ventricular (LV) posterior wall was >or=24 mm, and a non-hypertrophy group (n = 21) in which the sum of these parameters was <24 mm. Right ventricular endomyocardial biopsies were performed in the acute stage and the degree of interstitial edema was scored histologically. Left ventricular wall thickness and QRS duration in the acute stage were 27.7 +/- 3.6 mm and 124.1 +/- 29.6 ms, respectively, in the hypertrophy group, and 19.9 +/- 2.4 mm (P < 0.001) and 98.6 +/- 21.7 ms (P < 0.01) in the non-hypertrophy group. Complete atrioventricular block was found in 13 of 29 cases (45%) in the hypertrophy group and two of 21 cases (10%) in the non-hypertrophy group (P < 0.01). Myocardial interstitial edema was scored at 1.3 +/- 0.8 points in the hypertrophy group and 0.8 +/- 0.6 points in the non-hypertrophy group (P < 0.05). Left ventricular wall thickness and QRS duration in the convalescent stage decreased to 21.1 +/- 2.6 mm (P < 0.0001) and 97.1 +/- 17.4 ms (P < 0.01) in the hypertrophy group, respectively. Only one case (4%) in the hypertrophy group continued to show CAV during the convalescent stage (P < 0.05). The results of this study suggest that myocardial interstitial edema is implicated in the conduction disturbances that occur in AM.
authors.affiliation: Division of Cardiology, Department of Internal Medicine, Fujita Health University School of Medicine, Toyoake, Aichi 470-1192, Japan. morimoto@fujita-hu.ac.jp
authors.forename: Shin-ichiro
authors.initials: S
authors.lastname: Morimoto
authors.forename: Shigeru
authors.initials: S
authors.lastname: Kato
authors.forename: Shinya
authors.initials: S
authors.lastname: Hiramitsu
authors.forename: Akihisa
authors.initials: A
authors.lastname: Uemura
authors.forename: Masatsugu
authors.initials: M
authors.lastname: Ohtsuki
authors.forename: Yasuchika
authors.initials: Y
authors.lastname: Kato
authors.forename: Atsushi
authors.initials: A
authors.lastname: Sugiura
authors.forename: Kenji
authors.initials: K
authors.lastname: Miyagishima
authors.forename: Yukihiko
authors.initials: Y
authors.lastname: Yoshida
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Hishida
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D001706:Biopsy; D002312:Cardiomyopathy, Hypertrophic / Q000150:complications / Q000000981:diagnostic imaging / Q000503:physiopathology; D004487:Edema / Q000150:complications* / Q000503:physiopathology; D005260:Female; D006327:Heart Block / Q000209:etiology* / Q000503:physiopathology; D006329:Heart Conduction System / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009205:Myocarditis / Q000150:complications* / Q000000981:diagnostic imaging / Q000503:physiopathology; D009206:Myocardium / Q000473:pathology; D012307:Risk Factors; D014463:Ultrasonography