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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:5.)
© 2006 American Heart Association, Inc.

Editorials

Lipoprotein-Associated Phospholipase A₂ and Cardiovascular Risk

State of the Evidence and Future Directions

Carlos Iribarren

From the Division of Research, Northern California Kaiser Permanente, Oakland.

Correspondence to Carlos Iribarren, Senior Research Scientist, Division of Research, Northern California Kaiser Permanente. E-mail carlos.iribarren@kp.org

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Lipoprotein-associated phospholipase A₂ (Lp-PLA₂) is an enzyme that circulates in blood, bound mainly to LDL particles (80%) but also to HDL particles (20%). It has been shown to be a risk factor for cardiovascular disease, and it is believed to form bioactive lipid mediators resulting in vascular inflammation. At the same time, Lp-PLA₂ is implicated in the degradation of the platelet-activating factor (PAF), a potent mediator of inflammation (this is why this enzyme is also known as platelet-activating factor acetylhydrolase [PAF-AH]), a function that would lead to cardioprotection.

See page 106

In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Yang and colleagues provide new evidence that Lp-PLA₂ is an independent correlate of coronary endothelial-dependent dysfunction in a sample of 172 patients with no significant coronary artery disease (<30% stenosis) undergoing diagnostic coronary angiography.¹ Microvascular and epicardial endothelial-dependent dysfunction were assessed as change in coronary blood flow and change in coronary artery diameter in response to intracoronary acetylcholine, respectively. After adjustment for relevant covariables, the odds ratio for either type of endothelial-dependent dysfunction in the highest tertile of Lp-PLA₂, compared with the lowest tertile, was 3.3 (95% CI, 1.6 to 6.6), making the association unlikely to be attributable to confounding factors. Moreover, the association remained strong in subgroup analysis among patients not taking lipid lowering medication. This additional analytical step is important because statin therapy has been shown to reduce Lp-PLA₂ levels.^2,3 On the other hand, no relation was found between Lp-PLA₂ levels and endothelial-independent dysfunction measured . . . [Full Text of this Article]

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