Lipoprotein (a) (Lp(a)) is an independent risk factor for myocardial infarction (MI). It may also inhibit the fibrinolysis system, and Lp (a) affects the natural course of MI and the results of thrombolytic therapy. The purpose of this study was to investigate the influence of Lp (a) on the residual lesion stenosis of the infarction-related arteries (residual stenosis) in acute MI patients in whom reperfusion therapy was not performed. We studied 129 MI patients not given reperfusion therapy who underwent coronary angiography in the chronic stage. Morning fasting blood was collected and Lp (a), blood sugar, total cholesterol (TC), triglycerides (TG), and hemoglobin A1c (HbA1c) were measured. Residual stenosis was compared between the low Lp(a) group (< 30 mg/dL) and the high Lp(a) group (> or = 30 mg/dL). It was severe in the high Lp(a) group (85.0 +/- 24.9% vs 94.5 +/- 15.5%, P = 0.0044). We also compared residual stenosis and TIMI classification between younger and older, non-DM and DM, non-HT and HT, low-TC (< 220 mg/dL) and high-TC (> or = 220 mg/dL), low-TG (< 150 mg/dL) and high-TG (> or = 150 mg/dL), and low-Lp (a) and high-Lp (a) patients. Only the serum Lp (a) level affected the residual stenosis and TIMI classification (P < 0.05).
Conclusion: These findings suggest that elevated Lp (a) levels inhibit fibrinolysis.