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PLAC-Test

Uncover your hidden risk for heart attack and stroke with PLAC®-Test

Heart attack and stroke are the leading causes of death in industrialized countries. 50% of heart attacks occur in patients with normal cholesterol — most cardiovascular (CV) events are due to plaque rupture1,2,3

The PLAC®-Test is a CE certified test to determine the individual risk of stroke and heart attack.

PLAC®-Test is a simple blood test that measures the amount of an enzyme in your blood called Lp-PLA2 (Lipoprotein associated phospholipase A2). Lp-PLA2 is a vascular-specific inflammatory marker critical in the formation of rupture-prone plaque4. When your arteries are inflamed, a fatty deposit called plaque builds up in the walls of the artery. If the amount of Lp-PLA2 in your blood is high, it may indicate that the plaque might rupture through the inside wall of the artery into your bloodstream, where it may cause a clot that could result in a heart attack or stroke. The higher the level of Lp-PLA2, the higher the risk of a CV event.5

An early diagnosis and an adapted therapy can help to prevent cardiovascular events.

Add the PLAC®-Test to your CVD risk assessment strategy. Knowing your risk is the first step toward preventing heart attack and stroke.

When should the test be requested?

The PLAC®-Test is recommended for patients with established CVD or patients at moderate to intermediate risk for CVD, such as patients with, including but not limited to, two or more of the following risk factors:

·      Family history of cardiovascular diseases
·      Diabetes
·      Obesity
·      Smoker
·      Physical inactivity
·     Men older than 45 or women older than 55 years
·      High cholesterol
·      High blood pressure

Interpretation of the results:

The PLAC®-Test determines the individual risk of patients for coronary heart disease and stroke associated with atherosclerosis; preventive measures and an efficient patient management can be initiated accordingly. Through the early identification of people at high risk who will benefit from a more intensive treatment, cardiovascular events can be prevented.

Additional information:

The PLAC®-Test can be carried out at any time at Laboratoires Réunis. Blood withdrawal is possible in all our centers. Fasting is not required. Please note that the test is currently not reimbursed by the luxbg. CNS (Caisse Nationale de Santé).

If you have any further questions or need additional information, please contact us: +352 780290-1 or (contact(at)labo.lu).

Lp-PLA2 testing is recognized in the guidelines of the European Society of Cardiology, American Association of Clinical Endocrinologists, American Heart Association and American Stroke Association. More than 125,000 published patient results confirm that the PLAC®-Test for Lp-PLA2 is an evidence-based assay by measuring the new modifiable risk factor, lipoprotein-associated phospholipase A2, for CVD events.

 

REFERENCES:

1. Jang Y, Waterworth D, Lee J-E, et al. Carriage of the V279F null allele within the gene encoding Lp-PLA2 is protective from coronary artery disease in South Korean males. PLoS ONE. 2011;6(4):e18208. doi:10.1371/journal.pone.0018208. 2. The Lp-PLA2 Studies Collaboration. Lipoprotein-associated phospholipase A2 and risk of coronary disease, stroke, and mortality: collaborative analysis of 32 prospective studies. Lancet. 2010;375:1536-1544. 3. White HD, Simes J, Stewart RAH, et al. Changes in lipoprotein-associated phospholipase A2 activity predict coronary events and partly account for the treatment effect of pravastatin: results from the long-term intervention with pravastatin in ischemic disease study. J Am Heart Assoc. 2013;2:e000360. doi:10.1161/JAHA.113.000360. 4. Dohi T, Miyauchi K, OkazakiS, et al. Decreased circulating lipoprotein-associated phospholipase A2 levels are associated with coronary plaque regression in patients with acute coronary syndrome. Atherosclerosis. 2011. doi:10.1016/j.atherosclerosis.2011.09.019. 5. Kolodgie FD, Burke AP, Skorija KS,et al. Lipoprotein-associated phospholipase A2 protein expression in the natural progression of human coronary atherosclerosis. Arterioscler Thromb Vasc Biol. 2006;26(11):2523-2529.

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