Review of the evidence for the clinical utility of lipoprotein-associated phospholipase A2 as a cardiovascular risk marker.
A substantial body of peer-reviewed studies has been published validating the role of inflammation in atherogenesis and supporting lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) as a cardiovascular risk marker independent of and additive to traditional risk factors. As with elevated high-sensitivity C-reactive protein, an elevated Lp-PLA(2) level approximately doubles the risk for primary and secondary cardiovascular events. Interestingly, when both inflammatory markers are increased together, they provide an even greater predictive capability to help identify very-high-risk individuals who would benefit most from aggressive lipid-lowering therapy. High levels of Lp-PLA(2) are present in inflamed, rupture-prone plaques, and it appears that Lp-PLA(2) is released from these plaques into the circulation. Over 25 prospective epidemiologic studies have demonstrated the association of elevated Lp-PLA(2) levels with future coronary events and stroke-11 of 12 prospective studies have shown a statistically significant association between elevated Lp-PLA(2) and primary coronary or cardiovascular events, 12 of 13 have shown a statistically significant association with recurrent coronary or cardiovascular events, and 6 studies have shown a positive association with stroke. Lp-PLA(2) should be viewed today as an important cardiovascular risk marker whose utility is as an adjunct to the major risk factors to adjust absolute risk status and thereby modify low-density lipoprotein cholesterol goals. The low biologic fluctuation and high vascular specificity of Lp-PLA(2) makes it possible to use a single measurement in clinical decision making, and it also permits clinicians to follow the Lp-PLA(2) marker serially. Ultimately, Lp-PLA(2) may also be classified as a risk factor, but this should not detract from its utility today as a risk marker.
Division of Cardiology, Department of Medicine, University of Washington, 325 9th Avenue, Seattle, WA 98104, USA. mcorson@u.washington.edu
Marshall A
MA
Corson
Peter H
PH
Jones
Michael H
MH
Davidson
D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase / Q000097:blood*; D050197:Atherosclerosis / Q000097:blood* / Q000201:enzymology; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis; D002318:Cardiovascular Diseases / Q000097:blood* / Q000201:enzymology; D006801:Humans; D007249:Inflammation / Q000097:blood* / Q000201:enzymology; D011237:Predictive Value of Tests; D018570:Risk Assessment; D012307:Risk Factors; D012680:Sensitivity and Specificity
D015415:Biomarkers; D002097:C-Reactive Protein; D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase