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Serum Concentrations Of Matrix Metalloproteinase-1 And Tissue Inhibitor Of Metalloproteinase-1 In Congestive Heart Failure

Posted on:2005-10-01Degree:MasterType:Thesis
Country:ChinaCandidate:Y Y WangFull Text:PDF
GTID:2144360125957691Subject:Cardiovascular medicine
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Background and Objective: Chronic congestive heart failure (CHF) is the deteriorating stage in all kinds of underlying heart diseases. The morbidity of heart failure is very high and the 5 years survival rate is similar to malignant tumor. It threatens the healthy of people and the quality of life greatly. In the last decades, great progress has been made in the research of CHF. It's well known that left ventricular remodeling is a very important mechanism of CHF. The structure foundation of ventricular remodeling is the alteration of myocardial cells and extracellular matrix (ECM), whidh is primarily made up of type I collagen and type III collagen. Remodeling of ECM is considered to contribte to progression of left ventricular remodeling and heart failure. The matrix metalloproteinases (MMPs) are a family of functionally related zinc-containing enzymes that denature and degrade fibrillar collagens and other components of ECM. ECM remodelling and fibrosis regulated by MMPs are believed to be important contributors to the progression of heart failure. MMP-1 can denature and degrade fibrillar collagens, especially type I collagen and type III collagen in the certain site of them. Tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) is an endogenous biological regulator ,which plays an important role in regulating the activity Of MMPs. MMP-1 and TIMP-1 have beendemonstrated to play a significant role in ventricular remodeling and heart failure. The objective of this research is to investigate.the relationship between the changes of concentration of serum MMP-1, TIMP-1 and heart function, etiology of heart failure, medical imagine, and evaluate the value of the change of serum MMP-1 and serum TIMP-1 in clinic practice.Methods: 70 hospitalized CHF patients were enrolled. All these patients were divided into 4 groups according to the NYHA heart function. There were 18 patients in the class I group, 16 patients in the class II group, 18 patients in the class III and 20 patients in the class IV group. Also these patients were divided into different groups based on the underlying diseases causing cardiac dysfunction. They were the hypertension group, 23 patients; the coronary heart disease group, 24 patients and the dilated cardiomyopathy group, 23 patients. At the same time 18 healthy subjects were served as control. All patients were examined to exclude inflammation, cancer, hepatic dysfunction, renal failure, hyperthyroidism or hypothyroidism, bones and joints diseases, diabetes and other metabolism diseases. They were treated irregularly with or without angiotensin converting enzyme inhibitor (ACEI) or/and P -bloker before hospitalization. All patients received the general examination including the hepatic and renal function before accepted. The serum concentrations of MMP-1 and TIMP-1 were measured by enzyme-linked immunosorbent assay (ELISA). Two-dimensional M-mode and Doppler ultrasound recording were obtained to determine the left ventricular ejection fraction (LVEF), fraction shortening (FS ), left ventricular end-diastolic diameter(LVEDd), and cardiac thoracis ratio was obtained by chest film.Results:1. Compared with the control group, the hepatic and renal functions were not abnormal in the heart failure groups.2. The concentrations of serum MMP -1 in heart failure groups were as follows: the class I group 4.0 0.22 ng/ml, the class II group 4.6 0.24 ng/ml, the class III 5.1 0.24ng/ml and class IV group 5.7+0.41 ng/ml. The concentrations of serum MMP -1 were significantly higher in chronic heart failure patients compared with the controlgroup, 3.3 0.34 ng/ml (P<0.01). And there was a remarkable difference among the heart failure groups, too. The concentrations of serum TIMP-1 in heart failure patients were: the class I group 178.3 8.61 ng/ml, the class II group 189.9 17.39 ng/ml,the class III group 202.5 18.24 ng/ml, and the class IV group 126.4 15.12 ng/ml. It was significantly increased in the patients of class I, II and III as compared with that of the control group, which was 159.8 10.
Keywords/Search Tags:heart failure, ventricular remodeling, matrix metalloproteinase, tissue inhibitor of matrix metalloproteinase, collagen, cardiac fibrosis
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