Study On Renin-angiotensin System And Fibrinolytic Function In Patients With Chronic Heart Failure

Objective To investigate the changes of renin-angiotensin system (RAS) and fibrinolytic function in patients with chronic heart failure (CHF), and to study the effect of RAS on fibrinolytic function in patients with CHF.Methods 75 patients with CHF were included in the CHF group, whereas 30 normal subjects were selected in the normal control (NC) group. The plasma levels of PRA, AngⅡ and ALD were measured in the CHF group and the NC group by radio immunoassay(RIA), and the concentrations of plasma t-PA and PAI-1 antigen were simultaneously measured by enzyme-linked immunosorbent assay(ELISA). Results ⑴ The mean levels of plasma PRA, AngⅡ, ALD, t-PA and PAI-1 in the CHF group were significantly higher than those in the NC group (all P<0.01). ⑵The mean levels of plasma PRA, AngⅡ, ALD, t-PA and PAI-1 in the CHF patients with rheumatic heart disease (RHD) (RHD subgroup) or dilated cardiomyopathy (DCM) (DCM subgroup) were markedly higher than those in the NC group (all P<0.01). There were no significant difference of plasma PRA, AngⅡ, ALD, t-PA and PAI-1 in the two CHF subgroups (all P>0.05). ⑶The mean levelsof plasma PRA, AngⅡ, ALD, t-PA and PAI-1 in the three cardiac function subgroups were significantly higher than those in the NC group (all P<0.01). There were no difference of plasma PRA, ALD and t-PA levels among the three cardiac function subgroups (all P>0.05). But the mean levels of plasma AngⅡ and PAI-1 in the NYHA class Ⅲ subgroup or the NYHA class Ⅳ subgroup were markedly higher than those in the NYHA class Ⅱ subgroup (all P<0.01). Compared with the NYHA class Ⅲ subgroup, the mean levels of plasma AngⅡ and PAI-1 in the NYHA class Ⅳ subgroup were significantly increased (all P<0.01). ⑷There was a positive correlation between plasma PAI-1 antigen concentrations and AngⅡ levels in the CHF group(r=0.9943, P<0.01). Conclusions There were overactivation of RAS and decreases in endogenous fibrinolytic function in the patients with CHF, and the more serious the heart failure was, the more significant the changes were. The more significant the RAS overactivation was, the more marked decreases in endogenous fibrinolytic function in patients with CHF. These findings indicated that during the development of the CHF state the RAS may contribute to regulating the endogenous fibrinolytic function.