Objective   To approach the expressions and the roles of connective tissue growth factor (CTGF) and membrane type 1 matrix metalloproteinases (MT1-MMP) in valve disease with pressure overload which induces extracellular matrix remodeling of left ventricle.    Methods   Of 32 patients

16 cases were pressure overload group (PO)

who had the multiple valve disease with predominately aortic valve stenosis

having a ring diameter of aorta valve less than 1.3 cm

cross valve pressure gradient equal or more than 40 mmHg

and valvular regurgitation less than 4.0 cm; The other 16 cases

as mitral stenosis group (MS)

were simple mitral stenosis patients with single valve replacement. Meanwhile

5 normal individuals served as control

who died from accident. Echocardiography was used to analyze the left ventricular function and detect the hypertrophic level of the left ventricle. Left ventricle muscle samples were obtained during operation. Histological features were studied by Masson staining

and collagenous contents were quantitated with a computer-assisted imaging analysis system. The mRNA expressions of CTGF and MT1-MMP were detected with RT-PCR.    Results   Concentric hypertrophy was observed significant in PO group

but myocardial hypertrophy was not found in MS group. Compare to the MS group and control

PO group had significantly more collagenous contents in left ventricle

thickened vessel wall

and narrow lumen of blood vessel (P0.05). The mean mRNA levels of CTGF and MT1-MMP were significantly increased in PO group than in MS group and control (P0.01). The mRNA levels of CTGF and MT1-MMP expressions in MS and control group were both lower. There was no statistically difference of MT1-MMP mRNA expression between MS group and control group (P0.05)

but CTGF mRNA expression was increased in MS group compare to control (P0.01).    Conclusion   CTGF and MT1-MMP expressions are significantly increased at mRNA level in pressure overload induced by valve disease. It may be one of the important factors which is involved in the progress of concentric hypertrophy and the process of extracellular matrix remodeling of left ventricle.