New Orleans, LA, November 9, 2004 High levels of an enzyme lipoprotein-associated phospholipase A2 (Lp-PLA2) believed to trigger a cascade of inflammatory events in atherosclerosis can independently predict increased risk of stroke, even after accounting for both traditional and novel cardiovascular risk factors, according to a new analysis by investigators from the ongoing Atherosclerosis Risk in Communities (ARIC) study presented at the American Heart Association's Scientific Sessions 2004.

Middle-aged participants with the highest levels of Lp-PLA2 had a statistically significant doubling of risk of suffering an ischemic stroke over a period of about six years compared to those with the lowest levels of the enzyme after taking age, gender and race into consideration (p <0.001). Even when traditional cardiovascular risk factors such as systolic blood pressure, smoking status and diabetes, and the novel risk marker of systemic inflammation C-reactive protein (CRP) are accounted for, elevated levels of Lp-PLA2 remained associated with a significantly increased stroke risk of almost twofold.

"These ARIC findings illustrate that Lp-PLA2 can be an independent and significant warning -- above and beyond standard risk factors -- identifying individuals with an increased risk of stroke. Lp-PLA2 may prove to be a useful independent diagnostic measure, and ongoing research is evaluating whether Lp-PLA2 is an important therapeutic target to reduce stroke," said Christie M. Ballantyne, M.D., director of the Center for Cardiovascular Disease Prevention at Baylor College of Medicine and the Methodist DeBakey Heart Center, Houston, and a lead investigator of ARIC.

GlaxoSmithKline (GSK) is actively investigating Lp-PLA2 inhibitors and the role they may play in further reducing the risk of stroke and coronary heart disease. Lp-PLA2 is an enzyme that helps process a form of low-density lipoprotein, or "bad," cholesterol (LDL-C) into products w
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Contact: Marybeth Farrell, GlaxoSmithKline
marybeth.m.farrell@gsk.com
610-787-3095
Porter Novelli
9-Nov-2004

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