Morphological changes in atrial appendages removed during the maze procedure: a comparison with autopsy controls

被引:17
作者
Connelly, JH [1 ]
Clubb, FJ
Vaughn, W
Duncan, M
机构
[1] St Lukes Episcopal Hosp, Dept Pathol, Houston, TX 77030 USA
[2] Texas Heart Inst, Dept Biostat, Houston, TX 77030 USA
[3] Texas Heart Inst, Dept Cardiovasc Surg, Houston, TX 77030 USA
关键词
atrial appendages; maze;
D O I
10.1016/S1054-8807(01)00057-6
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Atrial fibrillation (AF) is commonly encountered in clinical practice and typically it is treated with pharmacological agents. Some patients whose arrhythmias are resistant to pharmacological therapy undergo the maze procedure. which is a surgical treatment. The atrial appendages are removed as part of the surgical procedure. These appendages often demonstrate mycocyte hypertrophy, vacuolar degeneration and other changes that may be seen in cardiomyopathies. We examined 19 of these appendages and compared them with 17 autopsy controls, 12 of whom had documented coronary atherosclerotic disease and 5 of whom did not. We semiquantitatively measured the amount of vacuolar degeneration, interstitial fibrosis, myocyte hypertrophy and intramyocardial adipose tissue. Univariate and multivariate analysis was performed and revealed that vacuolar degeneration were significantly more common in appendages of patients with arrhythmias than the autopsy controls (P < .0004). The other three histological features studied were not significantly different in the three groups. Ultrastructural studies on atrial tissue excised during the maze procedure, retrieved from the paraffin blocks, revealed degenerative changes similar to cardiomyopathic myocardial tissue. Vacuolar degeneration is commonly seen in atrial appendages removed in patients with chronic AF. Myocyte hypertrophy is a nonspecific finding and may occur in patients with arrhthymias and coronary artery disease. (C) 2001 Elsevier Science Inc. All rights reserved.
引用
收藏
页码:39 / 42
页数:4
相关论文
共 10 条
[1]   Myocardial cell death in fibrillating and dilated human right atria [J].
Aimé-Sempé, C ;
Folliguet, T ;
Rücker-Martin, C ;
Krajewska, M ;
Krajewski, S ;
Heimburger, M ;
Aubier, M ;
Mercadier, JJ ;
Reed, JC ;
Hatem, SN .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1999, 34 (05) :1577-1586
[2]   Structural changes of atrial myocardium due to sustained atrial fibrillation in the goat [J].
Ausma, J ;
Wijffels, M ;
Thone, F ;
Wouters, L ;
Allessie, M ;
Borgers, M .
CIRCULATION, 1997, 96 (09) :3157-3163
[3]  
BHARATI S, 1992, ATRIAL FIBRILLATION, P15
[4]   THE SURGICAL-TREATMENT OF ATRIAL-FIBRILLATION .3. DEVELOPMENT OF A DEFINITIVE SURGICAL-PROCEDURE [J].
COX, JL ;
SCHUESSLER, RB ;
DAGOSTINO, HJ ;
STONE, CM ;
CHANG, BC ;
CAIN, ME ;
CORR, PB ;
BOINEAU, JP .
JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY, 1991, 101 (04) :569-583
[5]   Histological substrate of atrial biopsies in patients with lone atrial fibrillation [J].
Frustaci, A ;
Chimenti, C ;
Bellocci, F ;
Morgante, E ;
Russo, MA ;
Maseri, A .
CIRCULATION, 1997, 96 (04) :1180-1184
[6]   EPIDEMIOLOGIC FEATURES OF CHRONIC ATRIAL-FIBRILLATION - THE FRAMINGHAM-STUDY [J].
KANNEL, WB ;
ABBOTT, RD ;
SAVAGE, DD ;
MCNAMARA, PM .
NEW ENGLAND JOURNAL OF MEDICINE, 1982, 306 (17) :1018-1022
[7]   Promotion of atrial fibrillation by heart failure in dogs - Atrial remodeling of a different sort [J].
Li, DS ;
Fareh, S ;
Leung, TK ;
Nattel, S .
CIRCULATION, 1999, 100 (01) :87-95
[8]   THE RELATIONSHIP OF HUMAN ATRIAL CELLULAR ELECTROPHYSIOLOGY TO CLINICAL FUNCTION AND ULTRASTRUCTURE [J].
MARYRABINE, L ;
ALBERT, A ;
PHAM, TD ;
HORDOF, A ;
FENOGLIO, JJ ;
MALM, JR ;
ROSEN, MR .
CIRCULATION RESEARCH, 1983, 52 (02) :188-199
[9]   CHRONIC RAPID ATRIAL-PACING - STRUCTURAL, FUNCTIONAL, AND ELECTROPHYSIOLOGICAL CHARACTERISTICS OF A NEW MODEL OF SUSTAINED ATRIAL-FIBRILLATION [J].
MORILLO, CA ;
KLEIN, GJ ;
JONES, DL ;
GUIRAUDON, CM .
CIRCULATION, 1995, 91 (05) :1588-1595
[10]   ELECTROCARDIOGRAPHIC FINDINGS AMONG ADULT POPULATION OF A TOTAL NATURAL COMMUNITY TECUMSEH MICHIGAN [J].
OSTRANDER, LD ;
BRANDT, RL ;
KJELSBERG, MO ;
EPSTEIN, FH .
CIRCULATION, 1965, 31 (06) :888-+