diaDexus
Home About diaDexus Products & Technology Investors & Media Careers Contact us
Investors & Media
News Room
- 2006 Archive
- 2005 Archive
- 2004 Archive
- 2003 Archive
- 2002-1997 Archive
PLAC Test Media Materials

Contacts: Barbara Sullivan
Sullivan& Associates
(714) 374-6174
bsullivan@sullivanpr.com
Christina Andrian
diaDexus, Inc.
(650) 246-6476
candrian@diadexus.com

STUDY SUGGESTED LP-PLA2 PLAYS A CAUSAL ROLE IN PLAQUE INSTABILITY AND SUBSEQUENT SUDDEN CORONARY DEATH

Data support link between Lp-PLA2 and major cardiovascular events

South San Francisco, CA - November 1, 2006 - diaDexus, Inc., today announced the publication of a study showing a significant association between increased levels of lipoprotein-associated phospholipase A2 (Lp-PLA2), a novel marker of cardiac inflammation, and the likelihood for cardiovascular plaque rupture. The report was published in the November 2006 issue of Arteriosclerosis, Thrombosis, and Vascular Biology.

The expression of Lp-PLA2 was measured in coronary lesions using the same antibody to Lp-PLA2 that is used in diaDexus' PLAC® test for cardiovascular risk. The PLAC test, a simple blood test that measures Lp-PLA2, has been cleared for marketing by the U.S. Food and Drug Administration as an aid in predicting risk for coronary heart disease and ischemic stroke associated with atherosclerosis.

The study, conducted by researchers at Georgetown University's Department of Pathology and CVPath, International Registry of Pathology, in Gaithersburg, Md., and led by Renu Virmani, M.D., examined 30 samples from the coronary arteries of 25 sudden coronary death patients for the presence of Lp-PLA2. "Our data clearly connect unstable plaque and increased expression of Lp-PLA2 and add to the published reports confirming circulating levels of Lp-PLA2 as an independent cardiovascular risk factor," Virmani said.

Results showed that Lp-PLA2 was strongly expressed within the core and surrounding cells of samples demonstrating the most advanced levels of heart disease (vulnerable and ruptured plaque). The expression of Lp-PLA2 was higher in ruptured plaque samples, compared with low or nearly absent levels in early, less severe lesions, suggesting a causal role of Lp-PLA2 in the progression of atherosclerosis leading to coronary events due to plaque rupture.

Richard B. Lanman, M.D., chief medical officer of diaDexus, said a key finding of the study is that minimal Lp-PLA2 staining was found in early atherosclerotic plaques, while only advanced, rupture-prone plaques had intense staining for the enzyme. "This study suggests that Lp-PLA2 may provide additional information beyond its role as a risk factor for coronary and stroke events," Lanman said. "As a marker of unstable plaque, elevated Lp-PLA2 may indicate that aggressive intervention with lifestyle changes and lipid modifying medicines is warranted without delay."

Lp-PLA2 is an enzyme that associates in the blood primarily with low-density lipoprotein (LDL, the "bad" cholesterol). Lp-PLA2 is carried to the walls of coronary arteries by LDL, where the enzyme can activate an inflammatory response, promoting atherosclerosis. As a result, Lp-PLA2 serves as a specific indicator of vascular inflammation.

About diaDexus
diaDexus, Inc., a privately held biotechnology company based in South San Francisco, Calif., is focused on the discovery, development, and commercialization of clinically valuable, patent-protected diagnostic products. In addition to the PLAC test, diaDexus is developing a pipeline of novel cancer diagnostic tests.

For more information, visit www.plactest.com or www.diaDexus.com

Printer-Friendly Version
Subscribe

Sign up for automatic diaDexus news notification


name


email