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Published on: September 26, 2018
Association of Lipoprotein(a) With Atherosclerotic Plaque Progression
Yannick Kaiser1, Marwa Daghem2, Evangelos Tzolos2
1Department of Vascular Medicine, Amsterdam Cardiovascular Sciences, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.
Insights
High lipoprotein(a) levels are linked to faster progression of dangerous low-attenuation plaque in coronary arteries. This finding may explain the increased heart attack risk associated with lipoprotein(a) and suggests it as a treatment target.
Area of Science:
- Cardiovascular Medicine
- Biochemistry
- Medical Imaging
Background:
- Lipoprotein(a) [Lp(a)] is a known risk factor for myocardial infarction.
- The precise mechanism linking Lp(a) to cardiovascular events remains unclear.
- Understanding Lp(a)'s role in atherosclerosis progression is crucial for risk stratification.
Purpose of the Study:
- To investigate the association between Lp(a) levels and the progression of coronary artery plaque.
- To specifically examine the impact of Lp(a) on different plaque components, including low-attenuation plaque (necrotic core).
Main Methods:
- Lp(a) levels were measured in patients with advanced stable coronary artery disease.
- Coronary computed tomography angiography was used for baseline and 12-month plaque assessment.
- Linear regression analysis was employed to evaluate the relationship between Lp(a) and plaque progression, with adjustments for relevant covariates.
Main Results:
- Patients with high Lp(a) (≥ 70 mg/dL) exhibited accelerated progression of low-attenuation plaque compared to those with low Lp(a).
- Multivariable analysis confirmed a significant association between higher Lp(a) levels and increased low-attenuation plaque volume.
- No significant differences in the progression of total, calcific, or noncalcific plaque were observed between high and low Lp(a) groups.
Conclusions:
- Elevated Lp(a) is associated with accelerated progression of coronary low-attenuation plaque, a marker of vulnerable plaque.
- This finding provides a potential mechanism for the observed association between Lp(a) and myocardial infarction risk.
- Lp(a) emerges as a potential therapeutic target for managing atherosclerosis and reducing residual cardiovascular risk.
Background:
Lipoprotein(a) [Lp(a)] is associated with increased risk of myocardial infarction, although the mechanism for this observation remains uncertain.
Objectives:
This study aims 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 computed tomography angiography at baseline and 12 months to assess progression of total, calcific, noncalcific, and low-attenuation plaque (necrotic core) in particular. 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 (a Scottish cardiovascular risk score comprised of age, sex, smoking, blood pressure, total and high-density lipoprotein [HDL]-cholesterol, diabetes, rheumatoid arthritis, and deprivation index).
Results:
A total of 191 patients (65.9 ± 8.3 years of age; 152 [80%] male) were included in the analysis, with median Lp(a) values of 100 (range: 82 to 115) mg/dL and 10 (range: 5 to 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% CI: 0.7%-20.3%). There was no difference in total, calcific, and noncalcific plaque volume progression.
Conclusions:
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.
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