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 P < or = 0.05). 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.
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 P < or = 0.05). 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.
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