Abstract: Objective To investigate the involvement of mitogen-activated protein kinase（MAPK）and PI3K(phosphatidylinositol 3 kinase)/ Protein kinase B (Akt) signal transduction pathways in the mechanism of myocardium remodeling in patients with congestive heart failure(CHF) Methods Thirty nine patients of mitral valve disease with CHF were randomly selected and 30 cases of healthy persons were included as controls. Cardiac function parameters were measured by echocardiography. Concentrations of AngⅡ in plasma and myocardial tissues were determined by radio immunoassay. Activity of PKC was determined by using competive prote in binding method, activity of MAPK was detected by the methods of immunoprecitipation. Immunoprecitipation was used to assay the protein expression and phosphorylation of PI3K and Akt(Protein kinase B), protein expression of c-fos and α－skeletal-actin in myocardial tissues. Results Pathological changes of myocardial tissues in CHF with valvular heart disease showed typical myocardial remodeling. The hypertrophy was dominant at early stagy of CHF, while at end stage the characteristics include disordered alignament of the myocytes, the discontinuity and dissolving of cardiomyofibrills, destroyed subcellular organs, and the hyperplasia of interstitial tissue. AngⅡconcentrations in plasm and myocardial tissues in patients with CHF were higher than those in the control group(P<0.01), their levels were positively correlated to the levels of CHF; the activities of PKC and MAPK in myocardial tissues in patients with CHF were higher than those in control group(P<0.01), their levels were positively correlated to the levels of CHF (P<0.01). Compared to control group, phosphorylation of PI3K , Akt were higer in heart function class Ⅱgroup than that of heart function classⅢ and heart function class Ⅳgroups(P<0.01),there were no difference between heart function class Ⅲand Ⅳgroups; protein expression of c-fos was obvious in heart function Ⅱgroup (P<0.01) , but it is higer in heart function class Ⅲ and Ⅳ groups compared with heart function Ⅱgroup(P<0.01). The protein expression of α－skeletal-actin also increased in myocardial tissues in CHF groups, but positively correlated to cardiac function, there were big differences from control group(P<0.01). Conclusion Both PKC/MAPK and PI3K/Akt signal pathways involve in the pathogenesis of myocardial remodeling in CHF patients with valvular heart disease