The estimated effects of fibrate therapy on plasma concentration and activity of PAI-1 were independent of treatment duration and changes in plasma triglyceride levels in the meta-regression analysis .
This meta- analysis of RCTs suggested that fibrate therapy does not reduce plasma concentration or activity of PAI-I. The putative benefits of fibrate therapy in patients with cardiovascular disease appear to be exerted via mechanisms independent of effects on PAI-1
OBJECTIVE The aim of this systematic review was to perform a meta- analysis of r and omized controlled trials ( RCTs ) examining the efficacy of fibrate therapy in reducing plasma concentration or activity of plasminogen activator inhibitor 1 ( PAI-1 ) .
Gemfibrozil treatment of combined hyperlipoproteinemia. No improvement of fibrinolysis despite marked reduction of plasma triglyceride levels.
Hypertriglyceridemia is linked to impaired fibrinolytic function , and lipid-lowering treatment with fibric acid derivatives could hypothetically improve fibrinolysis in this condition . We therefore conducted a double-blind , placebo-controlled , crossover study of gemfibrozil treatment on fibrinolytic function in 21 men with combined hyperlipoproteinemia . Measurements were performed at rest and during mental stress and after venous occlusion . The patients had clearly disturbed fibrinolytic function , with elevated plasminogen activator inhibitor-1 ( PAI-1 ) activity at rest ( approximately 25 U/mL ; reference , < 15 U/mL ) . Gemfibrozil reduced plasma total and VLDL cholesterol as well as all triglyceride fractions , whereas HDL cholesterol increased ( P < .001 for all ) . Total triglyceride levels were reduced by 57 + /- 4 % ( from 5.3 to 2.1 mmol/L ) . Fasting serum insulin levels were not altered by gemfibrozil treatment . Plasma levels of PAI-1 activity and tissue-type plasminogen activator ( TPA ) activity or antigen were unaffected by gemfibrozil treatment both at rest and during the provocations . The levels of D-dimer , plasmin/antiplasmin complex , and fibrinogen were also uninfluenced by gemfibrozil treatment . Mental stress elevated plasma TPA ( P=.0036 ) and lowered PAI-1 ( P=.0012 ) activity during placebo but not gemfibrozil treatment ( P=.28 and P=.17 , respectively ) , but treatment effects did not differ by ANOVA on delta values ( ie , stress minus rest ) . Venous occlusion reduced PAI-1 activity , whereas TPA and plasmin/antiplasmin complex increased during both treatments . Thus , gemfibrozil treatment did not improve fibrinolysis or lower fibrinogen levels in men with combined hyperlipoproteinemia despite marked reduction of plasma triglyceride levels . It seems unlikely that improved fibrinolysis explains the primary preventive effect of gemfibrozil
The estimated effects of fibrate therapy on plasma concentration and activity of PAI-1 were independent of treatment duration and changes in plasma triglyceride levels in the meta-regression analysis .
This meta- analysis of RCTs suggested that fibrate therapy does not reduce plasma concentration or activity of PAI-I. The putative benefits of fibrate therapy in patients with cardiovascular disease appear to be exerted via mechanisms independent of effects on PAI-1
OBJECTIVE The aim of this systematic review was to perform a meta- analysis of r and omized controlled trials ( RCTs ) examining the efficacy of fibrate therapy in reducing plasma concentration or activity of plasminogen activator inhibitor 1 ( PAI-1 ) .