BACKGROUND: Lower extremity ischaemia is often complicated by coronary artery disease (CAD). Patients with CAD often have impaired fibrinolytic capacity. Plasma plasminogen activator inhibitors (PAI) levels are known to be associated with levels of atherogenic lipids. Purified eicosapentaenoic acid reduces atherogenic lipid levels. OBJECTIVE: To examine the effect of purified eicosapentaenoic acid ethyl ester (EPA) on the fibrinolytic capacity in patients with stable CAD and arteriosclerosis obliterans (ASO). METHODS: Plasma levels of PAl activity and tissue-type plasminogen activator (t-PA) antigen were measured. We administered 1800 mg/day EPA for 8 weeks to 25 patients. RESULTS: Mean baseline plasma PAI activity (P < 0.01) and t-PA antigen (P < 0.01) levels were higher in the patient group than they were in the control group. At the conclusion of EPA administration, significant reductions in PAI activity (P < 0.01), t-PA antigen (P < 0.01) and serum levels of triglyceride (P < 0.01), total (P < 0.05) and low-density lipoprotein (P < 0.05) cholesterols were observed. Changes in PAI activity levels caused by EPA administration showed positive linear correlations with those in low-density lipoprotein cholesterol (r = 0.411, P < 0.05) and triglyceride (r = 0.652, P < 0.01). CONCLUSION: These findings indicate that the fibrinolytic capacity in patients with CAD and ASO is decreased by increased PAI activity, but that EPA may correct this fibrinolytic impairment by decreasing PAI activity via its inhibitory effect on atherogenic lipids.
BACKGROUND:Lower extremity ischaemia is often complicated by coronary artery disease (CAD). Patients with CAD often have impaired fibrinolytic capacity. Plasma plasminogen activator inhibitors (PAI) levels are known to be associated with levels of atherogenic lipids. Purified eicosapentaenoic acid reduces atherogenic lipid levels. OBJECTIVE: To examine the effect of purified eicosapentaenoic acid ethyl ester (EPA) on the fibrinolytic capacity in patients with stable CAD and arteriosclerosis obliterans (ASO). METHODS: Plasma levels of PAl activity and tissue-type plasminogen activator (t-PA) antigen were measured. We administered 1800 mg/day EPA for 8 weeks to 25 patients. RESULTS: Mean baseline plasma PAI activity (P < 0.01) and t-PA antigen (P < 0.01) levels were higher in the patient group than they were in the control group. At the conclusion of EPA administration, significant reductions in PAI activity (P < 0.01), t-PA antigen (P < 0.01) and serum levels of triglyceride (P < 0.01), total (P < 0.05) and low-density lipoprotein (P < 0.05) cholesterols were observed. Changes in PAI activity levels caused by EPA administration showed positive linear correlations with those in low-density lipoprotein cholesterol (r = 0.411, P < 0.05) and triglyceride (r = 0.652, P < 0.01). CONCLUSION: These findings indicate that the fibrinolytic capacity in patients with CAD and ASO is decreased by increased PAI activity, but that EPA may correct this fibrinolytic impairment by decreasing PAI activity via its inhibitory effect on atherogenic lipids.