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Gauging cardiovascular risk with the PLAC test



USED TO GAUGE a patient's risk of coronory heart disease (CHD) and stroke, the PLAC test measures lipoprotein-associated phospholipase A2 (Lp-PLA2) levels in the blood. A cardiovascular-specific inflammatory enzyme, Lp-PLA2 resides mainly on low-density lipoprotein (LDL) cholesterol and contributes to the formation of atherosclerotic plaque that's vulnerable to rupture.

According to the Atherosclerosis Risk in Communities study, elevated blood Lp-PLA2 levels can provide early evidence of risk even when blood LDL levels are normal (less than 130 mg/dL). This study found an elevation of Lp-PLA2 to be independently associated with CHD, even after adjustment for traditional risk factors and C-reactive protein (CRP).

Arterial plaque is thought to result largely from an inflammatory process. At areas of disruption to the intima, LDL and Lp-PLA2 enter the intima, where LDL is oxidized and Lp-PLA2 triggers proinflammatory and proatherogenic activities. Monocytes then enter the intima, mature into macrophages, engulf the LDL, and develop into foam cells that form plaque with a fibrous cap. Over time, the macrophages secrete substances that cause the cap to thin, threatening rupture and clot formation.

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Who gets the test

The PLAC test is most commonly used in conjunction with the patient's history and clinical evaluation to predict his risk of a cardiovascular event or to establish individualized prevention guidelines. It may be appropriate when the following factors are present:

  • family history of stroke or CHD
  • borderline LDL level (100 to 129 mg/dL)
  • optimal LDL level (less than 100 mg/dL) and major risk factor for CHD or stroke
  • unreliable CRP level because of known or suspected inflammation.
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Performing the test

No special patient preparation is necessary. Following facility protocol, draw blood into the appropriate tube, label the tube, and send it to the lab right away. The lab may send the specimen to an off-site lab for analysis.

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What do the results mean?

Each lab reports normal reference range data with the test results. (Quest Diagnostics uses 135 to 330 ng/mL for men; 100 to 265 ng/mL for women.) A high Lp-PLA2 level indicates an increased risk of a cardiovascular event independent of other risk factors. (See Measuring risk for details.)

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How to help your patient

Currently, no treatments are specifically indicated to treat elevated Lp-PLA2 levels, but drug companies are working to develop Lp-PLA2 inhibitors. Research has shown, however, that statins and fibrates reduce both Lp-PLA2 levels and the incidence of CHD. Additional studies are needed to target desired Lp-PLA2 levels and to determine how drug therapy and lifestyle affect them.

Teach all your patients about heart-healthy living with proper diet, exercise, and medical follow-up if necessary. If the health care practitioner prescribes a treatment plan, educate your patient about his medications and how to control risk factors such as obesity, smoking, a sedentary lifestyle, and hypertension. Refer him to a dietitian or other health care professional if he needs more help.

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Measuring risk

The Atherosclerosis Risk in Communities study reported that men and women with a lipoprotein-associated phospholipase A2 (Lp-PLA2) level greater than 420 ng/mL had a twofold increase in risk of coronary heart disease after adjusting for other cardiovascular risk factors. The following data indicate risk level.



Raymonde A. Brown is professor in charge of undergraduate nursing at the school of nursing at The Pennsylvania State University in University Park.

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Ballantyne CM, 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. 109(7):837–842, February 24, 2004.
Brilakis ES, et al. Association of lipoprotein-associated phospholipase A2 levels with coronary artery disease risk factors, angiographic coronary artery disease, and major adverse events at follow-up. European Heart Journal. 26(2):137–144, January 2005.
Koenig W, et al. Lipoprotein-associated phospholipase A2 adds to risk prediction of incident coronary events by C-reactive protein in apparently healthy middle-aged men from the general population: Results from the 14-year follow-up of a large cohort from Southern Germany. Circulation. 110(14):1903–1908, October 5, 2004.
Schaefer EJ, 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. American Journal of Cardiology. 95(9):1025–1032, May 2005.
Tsimihodimos V, et al. Fenofibrate induces HDL-associated PAF-AH but attenuates enzyme activity associated with apoB-containing lipoproteins. Journal of Lipid Research. 44(5):927–934, May 1, 2003.
© 2006 Lippincott Williams & Wilkins, Inc.