Relation Between Serum Lipoprotein (a) and Residual Lesion Stenosis of Coronary Artery After Myocardial Infarction Without Reperfusion Therapy

Abstract

SUMMARYLipoprotein (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 A 1 c (HbA 1 c) were measured.Residual stenosis was compared between the low Lp(a) group (< 30 mg/dL) and the high Lp(a) group (≥ 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 (≥ 220 mg/dL), low-TG (< 150 mg/dL) and high-TG (≥ 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. (Jpn Heart J 2004; 45: 397-407) Key words: Lipoprotein (a), Acute myocardial infarction LIPOPROTEIN (a) (Lp(a)), discovered by Berg, K. 1) in 1963, is a lipoprotein resembling low density lipoprotein that consists of apolipoprotein (a) (apo(a)) bound to apo B-100 by a disulphide linkage. Lp (a) is thought to be an independent risk factor in atherosclerotic disorders such as myocardial infarction, arteriosclerosis obliterans, and cerebral infarction.2-5) Plasminogen and apo (a) have structural homology 6) and apo (a) and Lp (a) competitively affect the action of From the

Very low lipoprotein(a) and increased mortality risk after myocardial infarction

“…This suggests that Lp(a) may influence intraconary thrombus formation and resolution during MI. This finding is in line with several historical studies coming from thrombolytic era of myocardial infarction treatment, which have shown a higher proportion of spontaneous recanalization of the infarct-related artery in patients with low Lp(a) levels [14][15][16]. However, in another study increased Lp(a) was associated with intermittent occlusion of the infarct-related artery, as compared to the persistent occlusion [17].…”

Lipoprotein (a): truly a direct prothrombotic factor in cardiovascular disease?

“…Notably, typical predictors of fibrinolytic potential were not significant predictors, including levels of plasminogen activator inhibitor type 1 (PAI-1) (108). Similar findings were reported by two other studies in the ensuing years (109,110). However, one very small study (32 subjects) found that Lp(a) levels were higher in MI patients exhibiting intermittent occlusion of the infarct-related artery than patients with persistent occlusion, a result seemingly at odds with an anti-fibrinolytic role for Lp(a) (111).…”

South Asian Cardiovascular Disease & Cancer Risk: Genetics & Pathophysiology

“…Mechanistic, epidemiological, and recent genetic findings suggest Lp(a) is a causal risk factor for premature atherosclerotic cardiovascular disease (CVD) demonstrating atherogenic and thrombogenic properties, including enhanced uptake by macrophages, interference with fibrinolysis, and increased expression of adhesion molecules [58–60]. Lp(a) powerfully inhibits the fibrinolysis system, leading to atherothrombosis and MI [61].…”