Apoptosis as a possible cause of wall thinning in end-stage hypertrophic cardiomyopathy

被引：38

作者：

Ino, T ^{[1
]}

Nishimoto, K ^{[1
]}

Okubo, M ^{[1
]}

Akimoto, K ^{[1
]}

Yabuta, K ^{[1
]}

Kawai, S ^{[1
]}

Okada, R ^{[1
]}

Sueyoshi, N ^{[1
]}

机构：

[1] JUNTENDO UNIV,SCH MED,CARDIOVASC PATHOL RES LAB,DEPT INTERNAL MED,BUNKYO KU,TOKYO 113,JAPAN

来源：

AMERICAN JOURNAL OF CARDIOLOGY | 1997年 / 79卷 / 08期

关键词：

DILATED CARDIOMYOPATHY; DISEASE;

D O I：

10.1016/S0002-9149(97)00066-0

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

A 15-year-old boy with hypertrophic cardiomyopathy died of congestive heart failure with progressive left ventricular wall thinning with poor systolic function. Microscopic examination revealed patchy fibrosis in the ventricular myocardium with wall thinning, and immunohistochemical evaluation of apoptosis showed apoptotic cells and bodies in the destroyed myocytes along the border between the fibrotic area and myofibril.

引用

页码：1137 / &

页数：6

共 10 条

[1] PROGRESSION FROM HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY TO TYPICAL DILATED CARDIOMYOPATHY-LIKE FEATURES IN THE END STAGE [J].

FUJIWARA, H ;

ONODERA, T ;

TANAKA, M ;

SHIRANE, H ;

KATO, H ;

YOSHIKAWA, J ;

OSAKADA, G ;

SASAYAMA, S ;

KAWAI, C .

JAPANESE CIRCULATION JOURNAL-ENGLISH EDITION, 1984, 48 (11) :1210-1214

[2]

FUNAKOSHI M, 1984, JPN HEART J, V25, P805

[3] Coexistence of Sudden Cardiac Death and End-Stage Heart Failure in Familial Hypertrophic Cardiomyopathy [J].

Hecht, Gabriela M. ;

Klijes, Heinrich G. ;

Roberts, William C. ;

Maron, Barry J. .

JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1993, 22 (02) :489-497

[4] Apoptosis as a possible cause of gradual development of complete heart block and fatal arrhythmias associated with absence of the AV node, sinus node, and internodal pathways [J].

James, TN ;

Martin, ES ;

Willis, PW ;

Lohr, TO .

CIRCULATION, 1996, 93 (07) :1424-1438

[5] SUDDEN-DEATH IN HYPERTROPHIC CARDIOMYOPATHY - A PROFILE OF 78 PATIENTS [J].

MARON, BJ ;

ROBERTS, WC ;

EPSTEIN, SE .

CIRCULATION, 1982, 65 (07) :1388-1394

[6] HYPERTROPHIC CARDIOMYOPATHY AND TRANSMURAL MYOCARDIAL-INFARCTION WITHOUT SIGNIFICANT ATHEROSCLEROSIS OF THE EXTRAMURAL CORONARY-ARTERIES [J].

MARON, BJ ;

EPSTEIN, SE ;

ROBERTS, WC .

AMERICAN JOURNAL OF CARDIOLOGY, 1979, 43 (06) :1086-1102

[7] FAMILIAL HYPERTROPHIC CARDIOMYOPATHY IS A GENETICALLY HETEROGENEOUS DISEASE [J].

SOLOMON, SD ;

JARCHO, JA ;

MCKENNA, W ;

GEISTERFERLOWRANCE, A ;

GERMAIN, R ;

SALERNI, R ;

SEIDMAN, JG ;

SEIDMAN, CE .

JOURNAL OF CLINICAL INVESTIGATION, 1990, 86 (03) :993-999

[8] OCCURRENCE AND SIGNIFICANCE OF PROGRESSIVE LEFT-VENTRICULAR WALL THINNING AND RELATIVE CAVITY DILATATION IN HYPERTROPHIC CARDIOMYOPATHY [J].

SPIRITO, P ;

MARON, BJ ;

BONOW, RO ;

EPSTEIN, SE .

AMERICAN JOURNAL OF CARDIOLOGY, 1987, 60 (01) :123-129

[9] CLINICAL COURSE AND PROGNOSIS OF HYPERTROPHIC CARDIOMYOPATHY IN AN OUTPATIENT POPULATION [J].

SPIRITO, P ;

CHIARELLA, F ;

CARRATINO, L ;

BERISSO, MZ ;

BELLOTTI, P ;

VECCHIO, C .

NEW ENGLAND JOURNAL OF MEDICINE, 1989, 320 (12) :749-755

[10] ALPHA-TROPOMYOSIN AND CARDIAC TROPONIN-T MUTATIONS CAUSE FAMILIAL HYPERTROPHIC CARDIOMYOPATHY - A DISEASE OF THE SARCOMERE [J].

THIERFELDER, L ;

WATKINS, H ;

MACRAE, C ;

LAMAS, R ;

MCKENNA, W ;

VOSBERG, HP ;

SEIDMAN, JG ;

SEIDMAN, CE .

CELL, 1994, 77 (05) :701-712

← 1 →