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Lipoprotein-associated phospholipase A2 — a marker for vulnerable plaque
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Traditional risk factors such as lipids, blood pressure, smoking and diabetes are accepted targets for therapy. Modifying these has been shown to reduce cardiovascular and cerebrovascular events. Future risk may be predicted using tools such as the Framingham point score. The degree of a patient’s risk assists clinicians in choosing how aggressive therapy should be. However, even despite reaching currently accepted targets, many patients go on to experience an event. This is known as residual risk, which I have commented upon in a previous post.
Framingham point scoring classifies patients into low-, intermediate- and high-risk groups. The low-risk and high-risk groups are not the problem. Low-risk groups may not require pharmacotherapy but they still should be encouraged to initiate and continue healthy lifestyle behavior, including participating in regular physical activity, encouraging weight loss or maintenance, avoiding tobacco and so on. We all know that the high-risk groups should be managed as aggressively as possible. The intermediate-risk group, however, is more problematic. It is estimated that with closer investigation, about 50% of patients in the intermediate-risk group will be reassigned to either the lower-risk or higher-risk category.
Several nontraditional markers for future cardiovascular risk have been suggested to further evaluate selected patients. All other factors being equal, elevated highly-sensitive CRP has been shown to be associated with increased risk, but it does have issues with specificity and reproducibility. Imaging biomarkers such as carotid intima-media thickness, may be used to identify subclinical atherosclerosis and to guide as well as monitor therapy. However, carotid intima-media thickness is often not covered by insurance which continues to prevent its widespread use.
Recently, a new marker for cardiovascular risk has become clinically available: lipoprotein-associated phospholipase A2 (Lp-PLA2). Lp-PLA2 plays a direct role in plaque formation, endothelial dysfunction and vascular inflammation. It is more specific and has less variability than highly sensitive CRP. Lp-PLA2 has also been shown to be an independent risk factor for cardiovascular events. It is expressed in much greater amounts in vulnerable plaque compared with more stable plaque.
An excellent review was published as a supplement to the American Journal of Cardiology in June. The authors suggested that Lp-PLA2 be used as an adjunct beyond traditional factors in cardiovascular risk assessment. Individuals in the intermediate-risk group should be reclassified into the high-risk group if their Lp-PLA2 is higher than 200 mg/dL with a new LDL target of <100 mg/dL. Individuals in the high-risk group should be placed into the very high-risk category if their Lp-PLA2 is higher than 200 mg/dL with an new LDL target of <70 mg/dL. It was suggested that Lp-PLA2 be retested annually for risk monitoring.
I strongly believe in the merits of proven risk factors and only pursue nontraditional testing in selected patients. However, in certain situations, Lp-PLA2 and other emerging biomarkers have allowed me to better individualize therapy.
Am J Cardiol. 2008;101:3F-57F.