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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:2517.)
© 2006 American Heart Association, Inc.

Atherosclerosis and Lipoproteins

Lipoprotein-Associated Phospholipase A₂ and Prognosis After Myocardial Infarction in the Community

Yariv Gerber; Joseph P. McConnell; Allan S. Jaffe; Susan A. Weston; Jill M. Killian; Véronique L. Roger

From the Division of Cardiovascular Diseases (Y.G., A.S.J., V.L.R.) and Departments of Health Sciences Research (Y.G., S.A.W., J.M.K., V.L.R.) and Laboratory Medicine and Pathology (J.P.M., A.S.J.), Mayo Clinic College of Medicine, Rochester, Minn.

Correspondence to Dr Véronique L. Roger, Division of Cardiovascular Diseases, Mayo Clinic, 200 First St SW, Rochester, MN 55905. E-mail roger.veronique{at}mayo.edu

Objective— We evaluated the role of lipoprotein-associated phospholipase A₂ (Lp-PLA₂), an inflammatory biomarker, in defining risk after myocardial infarction (MI).

Methods and Results— Olmsted County, Minn, residents who experienced an MI meeting standardized criteria between 2003 and 2005 (n=271) were prospectively identified and followed. Lp-PLA₂ levels were measured at baseline and evaluated along with traditional risk indicators. Lp-PLA₂ was modestly associated with total and low-density lipoprotein cholesterol, smoking, and age (inversely) but not with MI characteristics or severity, comorbidities, C-reactive protein, or the time from symptom onset to blood sampling. During the first year of follow-up, 42 deaths occurred. The survival estimates (95% confidence intervals [CI]) at 1 year were 92% (86% to 98%), 85% (78% to 93%), and 74% (65% to 84%) in the lowest, middle, and upper Lp-PLA₂ tertiles, respectively (P=0.007). After adjustment for age and sex, the hazard ratios for death in the middle and upper Lp-PLA₂ tertiles were 2.20 (95% CI: 0.88 to 5.54) and 4.93 (95% CI: 2.10 to 11.60), compared with the lowest tertile, respectively (P_trend<0.001). Further adjustment for other risk indicators resulted in even stronger associations. Lp-PLA₂ also contributed to risk discrimination as indicated by the increases in the area under the receiver operating characteristic curves obtained in each of the models examined (all P0.05).

Conclusions— Among community subjects presenting with MI, increased Lp-PLA₂ levels measured early after MI are strongly and independently associated with mortality and provide incremental value in risk discrimination over traditional predictors.

We evaluated the role of lipoprotein-associated phospholipase A₂ (Lp-PLA₂), an inflammatory biomarker, in defining risk after myocardial infarction (MI). Among community subjects presenting with MI, increased Lp-PLA₂ levels measured early after MI are strongly and independently associated with mortality and provide incremental value in risk discrimination over traditional predictors.

Key Words: lipoprotein-associated phospholipase A₂ • inflammation • risk stratification • secondary prevention • myocardial infarction

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