Q: What is Lp-PLA₂ ?
A: Lp-PLA₂ (lipoprotein-associated phospholipase A₂) is an enzyme that is implicated in the vascular inflammatory pathway that leads to plaque formation. It is responsible for generating potent pro-inflammatory mediators from oxidized LDL cholesterol. Additionally, Lp-PLA₂ has been shown to be independently associated with cardiovascular disease and stroke in multiple clinical trials.^1,2

Q: Who is an appropriate candidate for the PLAC® test?
A: An appropriate candidate is a patient whose preliminary stroke or CHD risk assessment does not provide a clear clinical direction. This may include patients with one major risk factor outside the desirable range or a positive family history.

Q: Do any currently available therapies affect Lp-PLA₂ levels?
A: Clinical research has shown that Lp-PLA₂ levels have been lowered by statins and fibrates.^3,4 More studies are forthcoming to further determine the effects of drug treatment and lifestyle changes on affecting Lp-PLA₂ levels. Regardless of specific treatment effects, an elevated Lp-PLA₂ level may indicate higher risk, which can be managed by a number of existing modalities.

Q: What can I do if I determine a patient is at high risk based on elevated Lp-PLA₂ levels?
A: Recent advances in clinical research have shown that patients at high risk for stroke or coronary heart disease can benefit from therapeutic intervention aimed at lowering the risk factors. However, there are currently no treatments specifically indicated to treat elevated Lp-PLA₂ levels.

Q: What are the levels of Lp-PLA₂ I should be concerned about?
A: Laboratories will report normal reference range data with all test results. However, in the ARIC Study, individuals with Lp-PLA₂ between 310-420 ng/mL had a 1.7-fold increase in risk; those with greater than 420 ng/mL had a 2.1-fold increase in risk.

Q: Are Lp-PLA₂ and C-Reactive Protein related?
A: C-Reactive Protein and Lp-PLA₂ are products of different biological processes. C-Reactive Protein is an acute phase reactant produced in response to systemic inflammation. Lp-PLA₂, an enzyme predominantly produced by macrophages, co-traffics with LDL and is responsible for generating pro-inflammatory mediators in the vasculature. In clinical evaluation, these two biomarkers have been shown to be independent of each other and, therefore, each provides unique information useful for assessing stroke and coronary heart disease risk.

Q: How do I perform the PLAC test on a patient?
A: The PLAC test is a simple blood test available through clinical reference labs nationwide.

Q: Do I have to do extra work to prepare the blood samples?
A: Please refer to the Ordering the PLAC Test overview for specimen collection requirements.

Q: Will the PLAC test be reimbursed?
A: The PLAC test is billed by clinical labs using codes that are usually covered in their contracts with payers and is reimbursed when medically necessary.

Q: How long does it take to get PLAC test results?
A: Turnaround times usually fall within 7 calendar days.

Q: How do cholesterol levels affect my CHD and stroke risk patients?
A: Predictive models used in cardiovascular disease, such as the Framingham Risk Score and Adult Treatment Panel III (ATP III), have determined all patient risk estimates and treatment recommendations entirely on coronary heart disease outcomes and do not include stroke. While increased cholesterol levels have been strongly associated with coronary heart disease event rates, lipids have not been shown to be a predictor for stroke events.

 

1. Ballantyne C, Hoogeveen R, Bang H, et al. Lipoprotein-Associated Phospholipase A2 , High-Sensitivity C-Reactive Protein, and Risk for Incident Coronary Heart Disease in Middle-Aged Men and Women in the Atherosclerosis Risk in Communities (ARIC) Study. Circulation. 2004;109:837-842.
2. Packard CJ, O'Reilly DS, Caslake MJ, et al. Lipoprotein-associated phospholipase A2 as an independent predictor of coronary heart disease. West of Scotland Coronary Prevention Study Group. N Engl J Med. 2000;343:1148-1155.
3. Tsimihodimos V, Kakafika A, Tambaki AP, et al. Fenofibrate induces HDL-associated PAF-AH but attenuates enzyme activity associated with apoB-containing lipoproteins. J Lipid Res. 2003;44:927-934.
4. Schaefer EJ, McNamara JR, Asztalos BF, et al. Effects of Atorvastatin Versus Other Statins on Fasting and Postprandial C-Reactive Protein and Lipoprotein-Associated Phospholipase A₂ in Patients With Coronary Heart Disease Versus Control Subjects. Am J Cardiol. 2005;95:1025-1032.

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You can find the latest information and education on Lp-PLA2 on the resource center.