Biomarkers of pathophysiology in hypertrophic cardiomyopathy: implications for clinical management and prognosis

被引：74

作者：

Cambronero, Francisco ^{[2
]}

Marin, Francisco ^{[2
]}

Roldan, Vanessa ^{[3
]}

Hernandez-Romero, Diana ^{[2
]}

Valdes, Mariano ^{[2
]}

Lip, Gregory Y. H. ^{[1
]}

机构：

[1] City Hosp, Univ Dept Med, Haemostasis Thrombosis & Vasc Biol Unit, Birmingham B18 7QH, W Midlands, England

[2] Hosp Univ Virgen Arrixaca, Dept Cardiol, Murcia, Spain

[3] Univ Murcia, Ctr Reg Hemodonac, E-30001 Murcia, Spain

来源：

EUROPEAN HEART JOURNAL | 2009年 / 30卷 / 02期

关键词：

TUMOR-NECROSIS-FACTOR; BRAIN NATRIURETIC PEPTIDE; ACUTE CORONARY SYNDROMES; CARDIAC TROPONIN-T; ALPHA-MHC403/+ MOUSE MODEL; VON-WILLEBRAND-FACTOR; GROWTH-FACTOR-I; FACTOR-ALPHA; HEART-FAILURE; OBSTRUCTIVE CARDIOMYOPATHY;

D O I：

10.1093/eurheartj/ehn538

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

The study of biomarkers and their signalling pathways has allowed the development of new therapeutic strategies in a range of disorders. The aim of the present systematic review is to provide an overview of different biomarkers in patients with hypertrophic cardiomyopathy that could give some insight into the pathophysiologic mechanism(s) underlying the typical clinical and histological manifestations of the disease. Several pathophysiological models are presented and discussed, including studies that have investigated these biomarkers for diagnostic and prognostic reasons, in relation to disease progression and/or mortality.

引用

页码：139 / 151

页数：13

共 135 条

[11] Altered crossbridge kinetics in the αMHC403/+ mouse model of familial hypertrophic cardiomyopathy [J].

Blanchard, E ;

Seidman, C ;

Seidman, JG ;

LeWinter, M ;

Maughan, D .

CIRCULATION RESEARCH, 1999, 84 (04) :475-483

[12] Familial hypertrophic cardiomyopathy from mutations to functional defects [J].

Bonne, G ;

Carrier, L ;

Richard, P ;

Hainque, B ;

Schwartz, K .

CIRCULATION RESEARCH, 1998, 83 (06) :580-593

[13]

Brito Dulce, 2004, Rev Port Cardiol, V23, P1557

[14] Cardiac failure in transgenic mice with myocardial expression of tumor necrosis factor-α [J].

Bryant, D ;

Becker, L ;

Richardson, J ;

Shelton, J ;

Franco, F ;

Peshock, R ;

Thompson, M ;

Giroir, B .

CIRCULATION, 1998, 97 (14) :1375-1381

[15] Cardiac fibrosis as a cause of diastolic dysfunction [J].

Burlew, BS ;

Weber, KT .

HERZ, 2002, 27 (02) :92-98

[16]

Buzás K, 2004, EUR CYTOKINE NETW, V15, P53

[17] Medical progress - Coronary microvascular dysfunction [J].

Camici, Paolo G. ;

Crea, Filippo .

NEW ENGLAND JOURNAL OF MEDICINE, 2007, 356 (08) :830-840

[18] PROTECTION FROM FAS-MEDIATED APOPTOSIS BY A SOLUBLE FORM OF THE FAS MOLECULE [J].

CHENG, JH ;

ZHOU, T ;

LIU, CD ;

SHAPIRO, JP ;

BRAUER, MJ ;

KIEFER, MC ;

BARR, PJ ;

MOUNTZ, JD .

SCIENCE, 1994, 263 (5154) :1759-1762

[19] Genetic screening of calcium regulation genes in familial hypertrophic cardiomyopathy [J].

Chiu, Christine ;

Tebo, Molly ;

Ingles, Jodie ;

Yeates, Laura ;

Arthur, Jonathan W. ;

Lind, Joanne M. ;

Semsarian, Christopher .

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2007, 43 (03) :337-343

[20] Hypertrophic cardiomyopathy due to sarcomeric gene mutations is characterized by impaired energy metabolism irrespective of the degree of hypertrophy [J].

Crilley, JG ;

Boehm, EA ;

Blair, E ;

Rajagopalan, B ;

Blamire, AM ;

Styles, P ;

McKenna, WJ ;

Östman-Smith, I ;

Clarke, K ;

Watkins, H .

JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 2003, 41 (10) :1776-1782

← 1 2 3 4 5 6 7 8 9 10 →