Lp(a) predicts carotid stenosis and occlusion but not total plaque area, suggesting a thrombotic mechanism, a study of 876 patients (Arterioscler Thromb Vasc Biol 2008)

Original title: Lipoprotein(a) is associated differentially with carotid stenosis, occlusion, and total plaque area

Arterioscler Thromb Vasc Biol · 3 July 2008 · 7

Klein JH, Hegele RA, Hackam DG, Koschinsky ML, Huff MW, Spence JD

This study examined Lp(a) relationship with carotid stenosis, occlusion, and total plaque area, distinct atherosclerosis phenotypes, in 876 consecutive patients from an atherosclerosis prevention clinic, of whom 22 (2.5%) had internal carotid artery occlusion. Lp(a) was a significant independent predictor of carotid stenosis (P<0.0001) and, in logistic regression, of occlusion (P=0.001), but not of total plaque area (P=0.13). Patients with occlusion had significantly higher Lp(a) than those without (0.27 vs 0.17 g/L, P=0.007). The findings show Lp(a) predicts carotid stenosis and occlusion but not plaque area, supporting the hypothesis that Lp(a) cardiovascular risk relates primarily to thrombosis and impaired fibrinolysis rather than plaque progression, a relationship that may extend to other arterial beds.

Original abstract

Background: Lipoprotein(a) [Lp(a)] is a putative risk factor for myocardial infarction and stroke and is related to thrombosis and impaired fibrinolysis. We studied relationships of Lp(a) with carotid stenosis, occlusion, and total plaque area, distinct phenotypes of atherosclerosis that may be differentially affected by cardiovascular risk factors.

Methods And Results: Multivariable linear regression analysis was used to study relationships of Lp(a) to phenotypes of carotid atherosclerosis among 876 consecutive patients from an atherosclerosis prevention clinic with complete data for all variables used in the model. Occlusion of an internal carotid artery was present in 22 (2.5%) patients (one with bilateral occlusions). Risk factors predicted carotid plaque area, stenosis, and occlusion differently. Lp(a) was a significant independent predictor of baseline stenosis (P<0.0001) but not of plaque area (P=0.13); in logistic regression, Lp(a) significantly predicted occlusion (P=0.001). Patients with occlusion had significantly higher levels of Lp(a): 0.27+/-0.25 g/L versus 0.17+/-0.18 g/L without occlusion; P=0.007.

Conclusions: Lp(a) was a significant independent predictor of carotid stenosis and occlusion, but not of carotid plaque area, supporting the hypothesis that the effect of Lp(a) on atherogenesis and cardiovascular risk is largely related to thrombosis and impaired fibrinolysis. Stenosis and occlusion may not be attributable to plaque progression, but to plaque rupture and thrombosis; this relationship may also apply to other arterial beds.

Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.