Association of Lipoprotein(a) With Atherosclerotic Plaque Progression

Yannick Kaiser, Marwa Daghem, Evangelos Tzolos, Mohammed N Meah, Mhairi Doris, Alastair J Moss, Jacek Kwiecinski, Jeffrey Kroon, Nick S. Nurmohamed, Pim van der Harst, Philip D Adamson, Michelle C Williams, Damini Dey, David E Newby, Erik S.g. Stroes, Kang H Zheng, Marc R Dweck

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

Background: Lipoprotein(a) [Lp(a)] is associated with increased risk of myocardial infarction, although the mechanism for this observation remains uncertain.
Objectives: To investigate whether Lp(a) is associated with adverse plaque progression.
Methods: Lp(a) was measured in patients with advanced stable coronary artery disease undergoing coronary CT angiography (CCTA) at baseline and 12 months to assess progression of total, calcific, non-calcific and in particular low-attenuation plaque (necrotic core). High Lp(a) was defined as Lp(a) ≥70 mg/dL. The relationship of Lp(a) with plaque progression was assessed using linear regression analysis, adjusting for body mass index, segment involvement score, and ASSIGN score.
Results: 191 patients (65.9±8.3 years, 152 (80%) men) were included in the analysis, with median Lp(a) values of 100 [82-115] and 10 [5-24] mg/dL in the high and low Lp(a) groups respectively. At baseline, there was no difference in coronary artery disease severity or plaque burden. Patients with high Lp(a) showed accelerated progression of low-attenuation plaque compared with low Lp(a) patients (26.2±88.4 mm3 vs -0.7±50.1 mm3, p=0.020). Multivariable linear regression analysis confirmed the relation between Lp(a) and low-attenuation plaque volume progression (β=10.5% increase for each 50 mg/dL Lp(a), 95% confidence interval 0.7-20.3%). There was no difference in total, calcific, and non-calcific plaque volume progression.
Conclusion: Among patients with advanced stable coronary artery disease, Lp(a) is associated with accelerated progression of coronary low-attenuation plaque (necrotic core). This may explain the association between Lp(a) and the high residual risk of myocardial infarction, providing support for Lp(a) as a treatment target in atherosclerosis.
Original languageEnglish
JournalJournal of the American College of Cardiology
Publication statusPublished - 25 Jan 2022


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