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This Article Full Text Full Text (PDF) All Versions of this Article: clinchem.2007.086298v1 53/8/1440    most recent Submit an electronic Letter to the Editor about this paper Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Winkler, K. Articles by März, W. Search for Related Content PubMed PubMed Citation Articles by Winkler, K. Articles by März, W. Related Collections Lipids, Lipoproteins, and Cardiovascular Risk Factors

Lipoprotein-Associated Phospholipase A₂ Predicts 5-Year Cardiac Mortality Independently of Established Risk Factors and Adds Prognostic Information in Patients with Low and Medium High-Sensitivity C-Reactive Protein (The Ludwigshafen Risk and Cardiovascular Health Study)

¹ Department of Clinical Chemistry, University Medical Center Freiburg, Germany.
² Cardiology Group, Frankfurt-Sachsenhausen, Germany.
³ LURIC Study Nonprofit LLC, Freiburg, Germany.
⁴ Division of Endocrinology, Department of Medicine, University Hospital, Ulm, Germany.
⁵ Synlab Center of Laboratory Diagnostics, Heidelberg, Germany.

^aAddress correspondence to this author at: Department of Medicine, Hugstetter Straße 55, D-79106 Freiburg, Germany. Fax 49-761-270-3444; e-mail kwinkler{at}ukl.uni-freiburg.de.

Background: Lipoprotein-associated phospholipase A₂ (LpPLA₂), also denoted as platelet-activating factor acetylhydrolase, is a lipoprotein-bound enzyme involved in inflammation and atherosclerosis. In this cohort study we investigated LpPLA₂ activity to predict cardiac mortality in patients scheduled for coronary angiography.

Methods: LpPLA₂ activity was determined in 2513 patients with and in 719 patients without angiographically confirmed coronary artery disease (CAD).

Results: During the median observation period of 5.5 years, 501 patients died. In patients with tertiles of LpPLA₂ activity of 420–509 U/L or 510 U/L, unadjusted hazard ratios (HRs) for cardiac death were 1.7 (95% CI 1.3–2.4; P = 0.001), and 1.9 (95% CI 1.4–2.5; P <0.001), respectively, compared with patients with LpPLA₂ activity 419 U/L. After we accounted for established risk factors and included angiographic CAD status, high-sensitivity C-reactive protein (hsCRP), and N-terminal pro-B-type natriuretic peptide, the 3rd tertile of LpPLA₂ activity predicted cardiac 5-year mortality with an HR of 2.0 (95% CI 1.4–3.1; P = 0.001). LpPLA₂ activity increased the adjusted risk for cardiac death by 2-fold in patients with hsCRP <3 mg/L in the 2nd (HR 2.4, 95% CI 1.4–4.2; P = 0.002) and 3rd (HR 2.1, 95% CI 1.1–4.0; P = 0.02) tertiles of LpPLA₂ activity and in patients with hsCRP of 3–10 mg/L in the 3rd tertile (HR 1.9, 95% CI 1.0–3.6; P = 0.03) of LpPLA₂ activity.

Conclusions: LpPLA₂ activity predicts risk for 5-year cardiac mortality independently from established risk factors and indicates risk for cardiac death in patients with low and medium-high hsCRP concentrations. Therefore, LpPLA₂ activity may provide information for the identification and management of patients at risk beyond established risk stratification strategies.