Lipoprotein(a): A Genetic Risk Factor for Coronary and Peripheral atherothrombosis

pp 361-370

Abstract

Lp (a) has been considered a risk factor for atherosclerotic cardiovascular disease from more than twenty years ago and that idea is now reinforced by the knowledge of its structure. This plasma particle presents a composition similar to LDL where its apo B-100 is linked by a disulphide bridge to apo (a),a glycoprotein with an evident homology to plasminogen but without its fibrinolytic activity. Like the well known atherogenic action of LDL, Lp(a) could undergo chemical modifications at the arterial intima, be entraped by macrophages and originate foam cells. On the other hand, Lp(a) competes in vitro with the binding of plasminogen to fibrinogen or fibrin at the endothelial cell surface, inhibiting t-Pa effect and reducing plasmin formation. So, it represents a bridge between the fields of atherosclerosis and thrombosis. Apo (a) is a protein with are markable size polymorphism which is considered a genetic trait. The apo (a) gene controls plasma Lp (a) levels, although some ambiental and pathophysiologic variations have been described. According with epidemiological and clinical studies, plasma Lp(a) levels higher than 30 mg/dl determine an atherothrombotic risk factor. Elevated plasma Lp(a) concentrations were found in myocardial and cerebral infarction, carotid atherosclerosis, abdominal aortic aneurism, intermittent claudication and were associated with vein graft stenosis and restenosis after coronary artery bypass surgery and coronary angioplasty, respectively. Up to now, the treatments to reduce Lp(a) plasma levels did not arrive to satisfactory results, and to get this goal is an obligatory challenge, specially in patients with other risk factors and/or cardiovascular disease.