| Background: The patients who had serious heart valve disease symptoms, the case fatality rate is high, result in decreased quality of life in patients. Valve replacement is the only effective way to alleviate symptoms of the patients, the postoperative hemodynamics can be corrected, but the recovery of cardiac function and long-term survival is different. According to the European and American guidelines, the indicators to evaluate the severity and prognosis of heart valve disease include: aortic area, left ventricular ejection fraction, across the disc pressure and so on. Clinical observation found that these indicators sometimes were not significant collection with the patient’s symptoms, postoperative recovery of cardiac function and long-term survival rate. Recently research shows that: the degree of myocardial fibrosis of cardiac function in patients take a decisive role in the patients’ s long-term survival rate who had serious heart valve disease and had valvular replacement surgery. Nine months postoperatively in patients with high degree of fibrosis of cardiac function improvement is bad and 10 years of survival rate is much lower than the patients who had low degree of fibrosis.C1q/TNF-Related Protein-3 is a kind of fat acid factor that can promote the release of adiponectin and leptin. CTRP-3 is a potent anti-inflammatory factor, it can inhibit fatty acid, Lipopolysaccharide(Lipopolysaccharide, LPS)and TLR(Toll-like receptor) mediated inflammatory pathways. CTRP-3 independently, lowering blood sugar, in vitro experiments show that it can promote the proliferation and migration of endothelial cells.Our previous studies have shown that CTRP-3 could prevent ischemic myocardial cells in mice death, promote the regeneration of the myocardial cells, reduce the range of fibrosis after myocardial infarction, myocardial cells secrete factors that promote angiogenesis, increase after infarction myocardial contraction force. But weather CTRP-3 and myocardial fibrosis degree have correlation did not clear in reports.Object:To explore the correlation between myocardial fibrosis and C1q/TNF-Related Protein-3 via compare the leve of myocardial fibrosis between Valvular heart disease patients and No Valvular heart disease patients, and detect the level of C1q/TNF-Related Protein-3 of the the two groups. We also explore the effect of C1q/TNF-Related Protein-3 in myocardial fibrosis, predict the prognosis of heart disease patients after valve replacement, and find a new prospective factor and treatment target for myocardial fibrosis of heart disease patients.Experiment: 1. The experiment is divided into three groups: Control group: 20 ventricular septal defect or artrial septal defect patients deal with surgery in our hospital during the period of 2013.6 ~ 2014.6.Valvular heart disease group: 20 mitral valve malformation or aorta valve malformation patients deal with valve replacement in our hospital replacement during the period of 2013.6~2014.6.Rheumatic heart disease group: 30 rheumatic heart disease patients deal with valve replacement in our hospital replacement during the period of 2013.6~2014.6.4.Inclusion criteria: Control group: 20~40 years old ventricular septal defect or artrial septal defect patients have no surgical contraindication. Lactate ventricular developed pressure>55%, pulmonary arterial pressure<28mm Hg.Valvular heart disease group: 20~40 years old mitral valve malformation or aorta valve malformation patients measured up the The American heart valvular disease treatment guideline, and have no surgical contraindication. Rheumatic heart disease group: 20~40 years old rheumatic heart disease patients measured up the The American heart valvular disease treatment guideline, and have no surgical contraindication.5.Exclusion criteria: Exclude the patients who had hypertension, hyperlipidemia, myocardial infarction, coronary heart disease, cardiac surgery, diabetes or malignant tumor before. Exclude the patients who had fever, arthritis, annular erythema, subcutaneous nodules, chorea in hospital.Exclude the patients who’s BMI<19.6.Method:(1) Collect the auricula dextra tissue, pericardiac fat, valve tissue and blood samples of patients after anesthesia on the surgery day.(2)We collect blood plasma from blood samples after centrifuged and saved in-70℃.(3) Myocardium dyeing used Masson(Operated according to the Masson trichromatic dyeing kit instructions). Calculated volume ratio.(4) Detect the concentration of C1q/TNF-Related Protein-3 the used enzyme-linked immuno sorbent assay(Operated according to the kit instruction).(5) Dyeing myocardium used HE method.(6) Observed slide used light microscope.(7)Statistic.Result: 1.Compared with control group, the age and gender in valve disease patients was not significantly different(P>0.05).2.The result of myocardium masson dye reveal: Compared with control group, the aortic stenosis patients’ s right auricle organization, pericardial fat and ale tissue extracellular collagen fiber obviously hyperplasia, vascular lumen significantly narrow and the blood vessel walls obvious thick. After was Use the image analysis software calculated the photographic myocardial collagen fiber volume ratio, the control group is(5..66±2.31)%, the aortic stenosis group is(18.92±4.01)%(P<0.05).3.The result of myocardium HE dye reveal: Compared with the control group, the left ventricular myocyte of the aortic stenosis group was hypertrophy obviously, the nucleus increased obviously and the cell cytoplasm staining owe evenly obviously.4.Compared with the control group, the level of C1q/TNF-Related Protein-3 was significantly higher in aortic stenosis patients(P<0.01). There was a significantly positive correlation between CVF and C1q/TNF-Related Protein-3. Significant cardiac hypertrophy can be observed in HE staining slices of valve heart disease group.6.Compared with the control group, the myocardialof aortic valve stenosis group hypertrophy obviously(P<0.05).Conclusion: The result of this experiment shows: compared with the control group, the myocyte of aortic stenosis patients hypertrophy obviously, myocardial fibrosis was significantly elevated and plasma and the myocardial cell CTRP-3 levels were significantly elevated. Aortic stenosis patients plasma and the myocardial CTRP3 content and the degree of myocardial fibrosis were positively correlated. Combined with our previous study that CTRP-3 could prevention and treatment of ischemic myocardial cells in mice death, promote the regeneration of the myocardial cells, reduce the range of fibrosis after myocardial infarction, promote the myocardial cells secrete to stimulate angiogenesis. the phenomenon that the level of CTRP-3 increased maybe result from the pressure overload myocardial remodeling and myocardial fibrosis during the cardiac decompensation period induce compensatory increase CTRP-3 to paly a role of protection effect. |
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