Mechanisms contributing to the progression of left ventricular dysfunction to end-stage heart failure

被引：7

作者：

Böhm, M ^{[1
]}

Kilter, H ^{[1
]}

Kindermann, M ^{[1
]}

机构：

[1] Univ Saarlandes Kliniken, Innere Med Klin 3, D-66421 Homburg, Germany

来源：

EUROPEAN HEART JOURNAL SUPPLEMENTS | 2003年 / 5卷 / 0I期

关键词：

heart failure; cardiac hypertrophy; RAAS; angiotensin II; sympathetic nervous system; beta-adrenergic receptors; apoptosis;

D O I：

10.1016/S1520-765X(03)80003-2

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Chronic heart failure is a progressive syndrome that starts with impaired left ventricular function and progresses to end-stage heart failure, with associated high mortality and morbidity. Initial events produce direct effects on myocardial gene expression and neuroendocrine signal transduction. Neuroendocrine activation, which includes stimulation of the renin-angiotensin and sympathetic nervous systems, as well as the release of cytokines, has important structural and functional effects on the heart. Identification of the mechanisms that underlie chronic heart failure has enabled the development of therapeutic strategies for early intervention in left ventricular dysfunction, with the aim of inhibiting progression to advanced heart failure. (C) 2003 The European Society of Cardiology. Published by Elsevier Science Ltd. Alt rights reserved.

引用

页码：14 / 21

页数：8

共 61 条

[1] Selective downregulation of VEGF-A165, VEGF-R1, and decreased capillary density in patients with dilative but not ischemic cardiomyopathy [J].

Abraham, D ;

Hofbauer, R ;

Schäfer, R ;

Blumer, R ;

Paulus, P ;

Miksovsky, A ;

Traxler, H ;

Kocher, A ;

Aharinejad, S .

CIRCULATION RESEARCH, 2000, 87 (08) :644-647

[2] How to RECOVER from RENAISSANCE? The significance of the results of RECOVER, RENAISSANCE, RENEWAL and ATTACH [J].

Anker, SD ;

Coats, AJS .

INTERNATIONAL JOURNAL OF CARDIOLOGY, 2002, 86 (2-3) :123-130

[3]

ANVERSA P, 1993, CIRCULATION, V87, P22

[4] Primitive cells and tissue regeneration [J].

Anversa, P ;

Kajstura, J ;

Nadal-Ginard, B ;

Leri, A .

CIRCULATION RESEARCH, 2003, 92 (06) :579-582

[5] β-Adrenergic receptor blockade arrests myocyte damage and preserves cardiac function in the transgenic Gsα mouse [J].

Asai, K ;

Yang, GP ;

Geng, YJ ;

Takagi, G ;

Bishop, S ;

Ishikawa, Y ;

Shannon, RP ;

Wagner, TE ;

Vatner, DE ;

Homcy, CJ ;

Vatner, SF .

JOURNAL OF CLINICAL INVESTIGATION, 1999, 104 (05) :551-558

[6] Apoptosis and post-infarction left ventricular remodeling [J].

Baldi, A ;

Abbate, A ;

Bussani, R ;

Patti, G ;

Melfi, R ;

Angelini, A ;

Dobrina, A ;

Rossiello, R ;

Silvestri, F ;

Baldi, F ;

Di Sciascio, G .

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2002, 34 (02) :165-174

[7] Myocardial-directed overexpression of the human β1-adrenergic receptor in transgenic mice [J].

Bisognano, JD ;

Weinberger, HD ;

Bohlmeyer, TJ ;

Pende, A ;

Raynolds, MV ;

Sastravaha, A ;

Roden, R ;

Asano, K ;

Blaxall, BC ;

Wu, SC ;

Communal, C ;

Singh, K ;

Colucci, W ;

Bristow, MR ;

Port, JD .

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2000, 32 (05) :817-830

[8] INCREASE OF GI-ALPHA IN HUMAN HEARTS WITH DILATED BUT NOT ISCHEMIC CARDIOMYOPATHY [J].

BOHM, M ;

GIERSCHIK, P ;

JAKOBS, KH ;

PIESKE, B ;

SCHNABEL, P ;

UNGERER, M ;

ERDMANN, E .

CIRCULATION, 1990, 82 (04) :1249-1265

[9] EVIDENCE FOR REDUCTION OF NOREPINEPHRINE UPTAKE SITES IN THE FAILING HUMAN HEART [J].

BOHM, M ;

LAROSEE, K ;

SCHWINGER, RHG ;

ERDMANN, E .

JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1995, 25 (01) :146-153

[10]

BOHM M, 1988, EUR HEART J, V9, P844

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