Lipoprotein(a) Is Associated With the Progression and Vulnerability of New-Onset Carotid Atherosclerotic Plaque

Background:Although important progress has been made in understanding Lp(a) (lipoprotein[a])-mediated stroke risk, the contribution of Lp(a) to the progression of vulnerable plaque features associated with stroke risk remains unclear. This study aims to evaluate whether Lp(a) is associated with carotid plaque progression, new-onset plaque features, and plaque vulnerability in a prospective community-based cohort study. Methods:Baseline Lp(a) levels were measured using latex-enhanced turbidimetric immunoassay among 804 participants aged 45 to 74 years and free of cardiovascular disease in the Chinese Multi-provincial Cohort Study-Beijing project. Carotid atherosclerosis was measured twice by B-mode ultrasonography over a 10-year interval during the 2002 and 2012 surveys to assess the progression of total, vulnerable and stable plaques, and plaque vulnerability. The total plaque area and plaque vulnerability score were calculated. Results:The median baseline Lp(a) level was 10.20 mg/dL (interquartile range, 6.20 to 17.18 mg/dL). Modified Poisson regression analysis showed that Lp(a) & GE;50 mg/dL was significantly associated with 10-year progression of total carotid plaque (relative risk [RR], 1.41 [95% CI, 1.21-1.64]; E-value=2.17), vulnerable plaque (RR, 1.93 [95% CI, 1.54-2.41]), and stable plaque (RR, 1.51 [95% CI, 1.11-2.07]) compared with Lp(a) <50 mg/dL. Moreover, among participants without plaque at baseline, Lp(a) & GE;50 mg/dL was related to an increased total plaque area (& beta;=0.36 [95% CI, 0.06-0.65]; P=0.018) and increased plaque vulnerability score (& beta;=0.30 [95% CI, 0.01-0.60]; P=0.045) in multivariable linear regression. Conclusions:Elevated Lp(a) levels were associated with 10-year carotid plaque progression and plaque vulnerability, providing a basis for Lp(a) as a treatment target for stroke prevention.

Automated summary

This study found that Lp(a) is closely associated with carotid plaque progression and the formation of vulnerable plaques, suggesting that Lp(a) may be a treatment target for stroke prevention.