Association of matrix metalloproteinase expression and left ventricular function in idiopathic dilated cardiomyopathy

Citation
O. Yokoseki et al., Association of matrix metalloproteinase expression and left ventricular function in idiopathic dilated cardiomyopathy, JPN CIRC J, 64(5), 2000, pp. 352-357
Citations number
35
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JAPANESE CIRCULATION JOURNAL-ENGLISH EDITION
ISSN journal
00471828 → ACNP
Volume
64
Issue
5
Year of publication
2000
Pages
352 - 357
Database
ISI
SICI code
0047-1828(200005)64:5<352:AOMMEA>2.0.ZU;2-X
Abstract
Myocardial remodeling is an important predictor for the development of dila ted cardiomyopathy (DCM). Matrix metalloproteinases (MMPs) are the family o f proteins responsible for extracellular remodeling, and tissue inhibitors of metalloproteinases (TIMPs) tightly control their activity. In the presen t study, the expression of MMP-2, MMP-9, TIMP-1 and TIMP-2 was determined b y immunohistochemistry in right ventricular endomyocardial biopsy samples f rom 16 patients with idiopathic DCM, and its clinical significance was eval uated by comparison with parameters of cardiac function. To obtain a semi-q uantitative assessment of MMP and TIMP expression, the average number of po sitive cells per high power field was counted. The left ventricular ejectio n fraction (LVEF) significantly correlated with the expression of both MMP- 2 (r=- 0.68) and TIMP-2 (r=-0.58). Patients were classified into 2 groups a ccording to the degree of MMP-3 expression: strongly positive and weakly po sitive. LVEF, left ventricular (LV) end-diastolic pressure, right ventricul ar end-diastolic pressure, pulmonary capillary wedge pressure and the plasm a norepinephrine level were significantly greater in the strongly positive group (p<0.05). In conclusion, the expression of MMPs and TIMPs in the card iac matrix of patients with idiopathic DCM is closely associated with myoca rdial remodeling and subsequent deterioration of LV performance. These find ings suggest new therapeutic targets for patients with idiopathic DCM.