American Journal of Cardiology
Volume 101, Issue 12, Supplement , Pages S34-S40, 16 June 2008

Lipoprotein-Associated Phospholipase A2 and Risk of Stroke

  • Philip B. Gorelick, MD, MPH

      Affiliations

    • Corresponding Author InformationAddress for reprints: Philip Gorelick, MD, MPH, Department of Neurology and Rehabilitation, University of Illinois at Chicago College of Medicine, 912 South Wood Street, 855N NPI, M/C 796, Chicago, Illinois 60612-7330.

Stroke is the second-leading cause of death worldwide and is a disabling disease of both older and younger adults. Stroke is also among the most highly preventable disorders because there are well-defined risk factors and preventatives. The establishment of new risk markers or factors for stroke risk assessment provides a new avenue for stroke prevention. Lipoprotein-associated phospholipase A2 (Lp-PLA2) is an enzyme that hydrolyzes oxidized phospholipids, releasing lysophosphatidylcholine, which has proinflammatory properties thought to be involved in the development of atherosclerosis and plaque rupture. In 2005, the Lp-PLA2 blood test was approved by the US Food and Drug Administration (FDA) for assessing the risk of ischemic stroke and coronary artery disease. In epidemiologic studies, low-density lipoprotein cholesterol and other lipid factors have not been shown to be consistent predictors of stroke risk. Lp-PLA2 measures, on the other hand, have shown a consistent association with stroke risk, conferring about a 2-fold increase in stroke occurrence. This relation has been studied in both first and recurrent stroke and is reviewed in this article. Importantly, a recent study has now shown that Lp-PLA2 may increase the area under the curve beyond that of traditional cardiovascular risk factors and C-reactive protein. Therefore, Lp-PLA2 determination may provide a pivotal opportunity to appropriately classify previously misclassified persons who are actually at high risk of stroke and in need of aggressive stroke intervention.

 

 Statement of author disclosure: Please see the Author Disclosures section at the end of this article.

PII: S0002-9149(08)00714-5

doi:10.1016/j.amjcard.2008.04.017

American Journal of Cardiology
Volume 101, Issue 12, Supplement , Pages S34-S40, 16 June 2008