The role of lipoprotein(a) in the formation of arterial plaques, stenoses and occlusions

Abstract

A brief review is presented, discussing the relationships between lipoprotein(a) (Lp[a]) and carotid plaque, stenosis and occlusion. Because of compensatory enlargement, stenosis probably results not from plaque growth, but from plaque rupture and thrombosis. Lp(a) is a complex molecule that links thrombosis, thrombolysis and atherosclerosis. The study of Lp(a) as a risk factor for cardiovascular events has probably been complicated by functional difference in isoform size of the apolipoprotein(a) component, which is related to plasminogen. In multivariable regression models with traditional risk factors, plasma Lp(a) independently predicts carotid stenosis (P<0.0001), but not plaque area (P=0.13). In logistic regression models, plasma Lp(a) significantly predicts occlusion (P<0.001). Lp(a) probably causes stenosis, occlusion and cardiovascular events by increasing thrombosis and impairing fibrinolysis at sites of plaque rupture. Future imaging studies of therapy to lower Lp(a) should not use intermediate end points such as intima-media thickness or plaque volume, but should assess development of stenosis and occlusion.