Mechanisms
Elevated Lp(a) does not thicken carotid arteries in healthy young adults, a study of 151 volunteers (Atherosclerosis 2007)
Original title: Elevated Lipoprotein(a) does not promote early atherosclerotic changes of the carotid arteries in young, healthy adults
This study measured carotid intima-media thickness (CCA-IMT) by high-resolution ultrasound in 151 healthy young volunteers without other cardiovascular risk factors, to test whether elevated Lp(a) contributes to early atherosclerotic vessel wall changes. CCA-IMT correlated negatively with HDL cholesterol and positively with age, BMI, total and LDL cholesterol, triglycerides, and homocysteine, but not with Lp(a). Dichotomising participants by Lp(a) below or at/above 300 mg/L revealed no significant difference in CCA-IMT between the groups. The findings suggest elevated Lp(a) alone does not promote early atherogenesis in healthy young adults, indicating its cardiovascular risk may operate through mechanisms other than early carotid wall thickening.
Original abstract
Background: Elevated levels of Lipoprotein(a) [Lp(a)] have been linked to an increased risk of ischemic cardiovascular events. Yet the mechanism by which Lp(a) might contribute to this increased risk is not clear.
Methods: To elucidate whether high plasma levels of Lp(a) contribute to the development of early atherosclerotic vessel wall changes, the intima-media thickness of the common carotid arteries [CCA-IMT] of 151 healthy young volunteers without additional relevant cardiovascular risk factors was measured by high-resolution ultrasound. Plasma concentrations of Lp(a) were quantified and other established risk factors, such as body mass index [BMI], plasma levels of cholesterol, triglycerides and homocysteine, were determined. Furthermore, the carotid arteries were examined for the presence of plaques and stenoses.
Results: Univariate analysis showed a significantly negative correlation of CCA-IMT with HDL cholesterol and positive correlations with age, BMI, total and LDL cholesterol, triglycerides and even with homocysteine, but not with Lp(a). When the study population was dichotomized according to Lp(a) levels, no statistically significant differences in CCA-IMT could be detected between persons with plasma Lp(a)<300mg/l or >or=300mg/l, respectively.
Conclusion: Our data suggest that elevated Lp(a) levels alone do not contribute to increased cardiovascular risk by promoting early atherogenesis in vivo.
Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.