| Congestive Heart Failure (CHF) is a common and severity clinical syndrome. Framingham investigation found that mortality in the patients who have suffered from CHF for 6 years was to reach 70%. So the pathogenesis and therapy of CHF are a focal point of cardiovascular diseases. The basic mechanism of occurrence and develop to lead to CHF was myocardium remodeling. The stimulation-to conduct agents of myocardium remodeling include norepinephrine, angiotensin II, mechanical irritation, endothelin, cytokine, oxidative stress and so on. Blood vessel endothelium dysfunction also plays an important role in the process of CHF. It has been known that a third β -blockade Carvedilol can inhibit myocardium remodeling related with the stimulation-to conduct agents and reduce mortality rate in chronic heart failure. Therefore, the purpose in this study is to observe the change of blood vessel endothelium function and cytokine (tumor necroses factor- α TNF- α , interleukin-6 IL-6) and to investigate the mechanism of Carvedilol improve cardiac function in the patients with CHF. METHODS:Fifty-two patients with CHF (Cardiac function II-IV and LVEF<45%) were divided randomly into CHF treatment group or Carvedilol treatment group for 12 weeks. In group 1 (n=25), routine CHF treatment includes cardiac glycoside, diuretic and ACEI or ARB, and in group 2 (Carvedilol treatment group, n=27), the Carvedilol was added. In addition, 26 sex- and age-matched healthy individuals served as controls. All objects were detected nitrogen monoxide (NO), endothelin ET-1, TNF-α , IL-6, echocardiography, change of brachial artery blood tube bore and blood flow (in accordance with Celermajaer's method). After 12 weeks all patients withCHF were detected above-mentioned markers again. Data are expressed as X±S, ANOVA and paried Student's t test were performed for statistical analysis. Department data were analyzed bi-metavariable correlation analysis. Enumeration data were analyzed by Chi square test. Value of P<0.05 were considered statistically significant.RESULTS:The change of endothelium dependent vasodilation (D%) and blood flow (Q%) under reactive hyperemia, LVEF, LVDd, LVDs did not significantly different (P>0.05) between CHF treatment group or Carvedilol treatment group before treatment. The change of endothelium dependence vasodilatation dilatation (D%) in CHF treatment group was (4.05 ±4.25% ) vs. (11.5 ±3.98%) in control group (P<0.01), and (D%) in Carvedilol treatment group was (4.06±4.18%) vs. (11.5± 3.98%) in control group (P<0.01). The change of blood flow (Q%) in CHF treatment group was (99.79 ± 61.23%) vs, (243.67 ± 78.65%) in control group (P<0.01), and (Q%) in Carvedilol treatment group was (103.54 ± 58.98%) vs. (243.67 ± 78.65%) in control group (P<0.01). After 12 weeks the change of endothelium dependent blood tube bore dilatation (D%) under reactive hyperemia in Carvedilol treatment group was (8.76 ± 6.53%) vs. (5.75±4.38%) in CHF treatment group (P<0.01), and the change of blood flow (Q%) under reactive hyperemia in Carvedilol treatment group was (201.35 ± 117.68%) vs. (136.27 ± 86.54%) in CHF treatment group (P<0.01).The tite of ET-1 in CHF treatment group and Carvedilol treatment group were (90.2 ± 22.9pg/ml) and (90.6 ± 22.75pg/ml) vs. (41.86±10.5 pg/ml) in control group (P<0.01 and P<0.01 ) before treatment. The tite of NO in CHF treatment group and Carvedilol treatment group were (121.44±30.82umol/L ) and (121.52 ± 30.48 umol/L) vs. (83.85±20.91umol/L) in control group (P<0.01 and P<0.01 ) before treatment. The NO/ET-1 ratio in CHF treatment group and Carvedilol treatment group were( 1.35 ± 0.13)and (1.34±0.12) vs.(2.00±0.15) in control group (P<0.01 and P,0.01 ) before treatment. After 12 weeks the tite of ET-1 in Carvedilol group was (66.14±18.99pg/ml) vs. (82.89 ±19.64pg/ml) in CHF treatment group (P<0.01) and the NO/ET-1 ratio in Carvedilol treatment group was (1.65 ± 0.14) vs. (1.34±0.14) in CHF treatment group (P<0.01).The tite of TNF- a in CHF treatment group and...
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