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Updated: May 2, 2026

Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein
Published on: October 12, 2017
[Lipoprotein(a) is associated to atherosclerosis in primary hypercholesterolemia]
Ana M Bea1, Rocío Mateo-Gallego1, Estíbaliz Jarauta1
1Unidad de Lípidos y Laboratorio de Investigación Molecular, Hospital Universitario Miguel Servet, IIS Aragón, Universidad de Zaragoza, Zaragoza, España.
Insights
Lipoprotein(a) [Lp(a)] is linked to atherosclerosis in individuals with familial hypercholesterolemia without specific gene mutations (FH-). High Lp(a) levels (>50mg/dL) significantly correlate with increased cardiovascular disease risk in this group.
Area of Science:
- Cardiovascular Medicine
- Clinical Biochemistry
- Genetics
Context:
- Elevated Lipoprotein(a) [Lp(a)] is a suspected risk factor in hypercholesterolemia.
- Familial hypercholesterolemia (FH) encompasses genetic conditions affecting cholesterol metabolism.
- Understanding Lp(a)'s role in different FH phenotypes is crucial for risk stratification.
Purpose:
- To investigate the association between Lipoprotein(a) [Lp(a)] levels and atherosclerosis.
- To evaluate Lp(a)'s impact on carotid intima-media thickness (IMT) and cardiovascular disease (CVD) prevalence across distinct hyperlipidemic groups.
- To differentiate the role of Lp(a) in FH patients with and without identified pathogenic mutations (FH+ vs. FH-).
Summary:
- A study of 909 individuals (FH+, FCH, FH-) measured plasma lipids, Lp(a), and carotid IMT.
- Regression analysis revealed Lp(a) was significantly associated with carotid IMT in FH- subjects.
- Cardiovascular disease was more prevalent in FH- individuals with Lp(a) >50mg/dL.
Impact:
- Identifies Lipoprotein(a) [Lp(a)] as a significant contributor to atherosclerosis burden in familial hypercholesterolemia patients lacking specific gene mutations (FH-).
- Highlights elevated Lp(a) levels (>50mg/dL) as a marker for increased cardiovascular disease risk in the FH- population.
- Provides evidence for targeted risk assessment and potential therapeutic strategies focusing on Lp(a) in specific hypercholesterolemic subgroups.
Introduction:
Several studies have suggested that Lp(a) could be a risk factor mainly in hypercholesterolemic patients.
Methods:
A total of 909 individuals were selected for this study. 307 were diagnosed of familiar hypercholesterolemia with a pathogenic mutation in LDLR or APOB genes (FH+), 291 of familiar combined hyperlipidemia (FCH) and 311 of familial hypercholesterolemia without a pathogenic mutation in LDLR nor APOB genes (FH-). Main risk factor were studied, included statin treatment. Plasma lipids, Lp(a), HbA1c and C-reactive protein. Intima-media thickness (IMT) of common and bulb carotid in both sides were measured in all subjects.
Results:
Lp(a) values (median, interquartile range) were 21.9mg/dL (9.24-50.5) in FH+, 22.4mg/dL (6.56-51.6) in FCH and 32.7 (14.6-71.5) in FH- (P<.001). Regression analysis including age, gender, HDL cholesterol, LDL cholesterol corrected for Lp(a), Lp(a), C-reactive protein, packs of cigarettes/day per year, systolic blood pressure and glucose as independent variables, demonstrate that Lp(a) was associated with carotid IMT in FH- subjects. Cardiovascular disease was more frequent in subjects with Lp(a) >50mg/dL (17.9%) than in subjects with Lp(a) <15mg/dL (9.6%), and between 15-50mg/dL (10.1%), and it was concentrated mostly in FH-group (6.7, 11.3, and 23.4% for the groups of Lp(a) <15mg/dL 15-50mg/dL, and >50mg/dL, respectively).
Conclusions:
Our results indicate that Lp(a) is associated with atherosclerosis burden especially in subjects with FH- and concentrations of Lp(a)>50mg/dL.
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