Apolipoprotein(a) (Lp[a]) genetic variants are linked with atherosclerotic burden but not with primary thrombotic phenotypes, according to a study published on Aug. 13 in the Journal of the American College of Cardiology.

 

Previous studies have shown an association between Lp(a) variants and coronary artery disease (CAD), but the pathophysiologic mechanism of the relationship has not been established. This new study confirmed these previous findings and showed a correlation between the Lp(a) variants and the number of obstructed coronary arteries. Additionally, the risk variants were associated with an earlier diagnosis of CAD. "These findings imply that the risk conferred by Lp(a) levels is mediated through the atherosclerotic, rather than the thrombotic, aspects of vascular disease," the authors note.

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While two variants in the Lp(a) gene were found to be associated with three atherosclerosis-related diseases, large artery atherosclerosis, peripheral arterial disease and abdominal aortic aneurysm, there was no association between Lp(a) variants and venous thromboembolism or cardioembolism and small vessel disease ischemic stroke subtypes. The study also did not find an association between the variants and carotid intimamedia thickness.

In an analysis of the findings the authors write, "evaluating Lp(a) risk alleles may therefore contribute to more effective primary and secondary prevention of atherosclerotic disease."

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