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Lipoprotein(a) as a risk factor for ischemic heart disease: metaanalysis of prospective studies
W Y Craig1, L M Neveux, G E Palomaki
1Foundation for Blood Research, Scarborough, ME 04070-0190, USA. wcraig@fbr.org
Insights
Lipoprotein(a) [Lp(a)] is linked to atherosclerosis. A meta-analysis of prospective studies confirms higher Lp(a) levels in individuals who develop ischemic heart disease, supporting its causal role.
Area of Science:
- Cardiovascular Science
- Biochemistry
- Epidemiology
Background:
- In vitro and retrospective studies suggest lipoprotein(a) [Lp(a)] plays a role in atherosclerosis.
- Prospective studies have yielded inconsistent conclusions regarding the association between Lp(a) and ischemic heart disease (IHD).
Purpose of the Study:
- To conduct a meta-analysis of prospective studies to clarify the relationship between Lp(a) and IHD.
- To evaluate the evidence for a causal role of Lp(a) in atherosclerosis development.
Main Methods:
- Meta-analysis of data from multiple prospective studies investigating Lp(a) levels and IHD incidence.
- Analysis of Lp(a) concentrations in cases (individuals who developed IHD) versus controls (those who did not).
Main Results:
- Lp(a) concentrations were significantly higher in cases compared to controls across the analyzed studies.
- The observed effect size was consistent between men and women.
- Variability in Lp(a) measurements was noted, potentially due to assay standardization and sample storage conditions.
Conclusions:
- The findings provide robust evidence supporting a causal role for lipoprotein(a) in the pathogenesis of atherosclerosis.
- Measuring Lp(a) may aid in managing individuals with a family history or existing ischemic heart disease.
- Current Lp(a) measurement variability and effect size preclude its use as a general population screening test for IHD.
Abstract:
Although in vitro studies support a pathophysiologic role for lipoprotein(a) [Lp(a)] in the development of atherosclerosis, and retrospective studies consistently report that there is a relationship between Lp(a) and ischemic heart disease (IHD), the conclusions drawn from prospective studies about this relationship have been inconsistent. To address this issue, we have performed a metaanalysis of data available from prospective studies. Lp(a) concentrations expressed as mass units vary markedly between studies, reflecting the need for assay standardization. In 12 of 14 prospective studies, Lp(a) concentrations are higher in subjects who later develop IHD (cases) than in those who do not (controls), although there is variation in the size of the effect. Sample storage temperature may contribute to this variability. When the studies are analyzed collectively, Lp(a) concentrations are significantly higher in cases than in controls, and the extent of the effect is similar in men and women. These findings provide evidence in support of a causal role for Lp(a) in the development of atherosclerosis. Measurement of Lp(a) may be useful to guide management of individuals with a family history of IHD or with existing disease. The separation in values between cases and controls is not, however, sufficient to allow the use of Lp(a) as a screening test in the general population.