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Updated: Aug 14, 2026

Isolation and Analysis of Plasma Lipoproteins by Ultracentrifugation
Published on: January 28, 2021
Serum lipoprotein lipase concentration and risk for future coronary artery disease: the EPIC-Norfolk prospective
Jaap Rip1, Melchior C Nierman, Nicholas J Wareham
1Department of Vascular Medicine, Academic Medical Center, Amsterdam, The Netherlands.
Insights
Lower serum lipoprotein lipase (LPL) levels are linked to higher coronary artery disease (CAD) risk. High LPL concentrations may protect against CAD by improving triglyceride and HDL-C levels.
Area of Science:
- Cardiovascular Science
- Lipid Metabolism
Background:
- Lipoprotein lipase (LPL) is implicated in coronary artery disease (CAD) risk.
- Prospective population data on LPL and CAD have been limited due to measurement challenges.
- Recent advancements allow reliable LPL measurement in serum, enabling new prospective studies.
Purpose of the Study:
- To investigate the prospective association between serum LPL concentration and future CAD risk.
- To evaluate the potential atheroprotective role of LPL.
Main Methods:
- Serum LPL concentration was measured in the EPIC-Norfolk population cohort.
- 1006 cases of fatal or nonfatal CAD were identified over 7 years.
- Cases were matched with 2 controls each, considering age, sex, and enrollment time.
Main Results:
- Serum LPL concentration was significantly lower in CAD cases compared to controls (P<0.0001).
- Individuals in the highest LPL quartile had a 34% lower risk of future CAD (OR 0.66).
- This association remained significant after adjusting for traditional CAD risk factors (OR 0.77, P=0.02).
Conclusions:
- Reduced serum LPL levels are associated with an increased risk of future CAD.
- High LPL concentrations may be atheroprotective, potentially by reducing triglycerides and increasing HDL-C.
- Serum LPL concentration correlates positively with HDL and LDL size.
Background:
Lipoprotein lipase (LPL) is associated with coronary artery disease (CAD) risk, but prospective population data are lacking. This is mainly because of the need for cumbersome heparin injections, which are necessary for LPL measurements. Recent retrospective studies, however, indicate that LPL concentration can be reliably measured in serum that enabled evaluation of the prospective association between LPL and future CAD.
Methods And Results:
LPL concentration was determined in serum samples of men and women in the EPIC-Norfolk population cohort who developed fatal or nonfatal CAD during 7 years of follow-up. For each case (n=1006), 2 controls, matched for age, sex, and enrollment time, were identified. Serum LPL concentration was lower in cases compared with controls (median and interquartile range: 61 [43-85] versus 66 [46-92] ng/mL; P<0.0001). Those in the highest LPL concentration quartile had a 34% lower risk for future CAD compared with those in the lowest quartile (odds ratio [OR] 0.66; confidence interval [CI], 0.53 to 0.83; P<0.0001). This effect remained significant after adjustment for blood pressure, diabetes, smoking, body mass index, and low-density lipoprotein (LDL) cholesterol (OR, 0.77; CI, 0.60-0.99; P=0.02). As expected from LPL biology, additional adjustments for either high-density lipoprotein cholesterol (HDL-C) or triglyceride (TG) levels rendered loss of statistical significance. Of interest, serum LPL concentration was positively linear correlated with HDL and LDL size.
Conclusions:
Reduced levels of serum LPL are associated with an increased risk for future CAD. The data suggest that high LPL concentrations may be atheroprotective through decreasing TG levels and increasing HDL-C levels.
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