High-Sensitivity C-Reactive Protein and Lipoprotein-Associated Phospholipase A 2 Stability Before and After Stroke and Myocardial Infarction

Abstract

Background and Purpose— High-sensitivity C-reactive protein (hsCRP) and lipoprotein-associated phospholipase A 2 (Lp-PLA 2 ) are hypothesized to be biomarkers of systemic inflammation and risk of myocardial infarction (MI) and stroke. Little is known, however, about the stability of these markers over time, and in particular, about the effects of acute vascular events on these marker levels. Methods— Serum samples were collected at 4 annual intervals in 52 stroke-free participants from the Northern Manhattan Study (NOMAS) and assayed for hsCRP and Lp-PLA 2 mass and activity levels using standard techniques. Log transformation of levels was performed as needed to stabilize the variance. Stability of marker levels over time was assessed using random effects models unadjusted and adjusted for demographics and other risk factors. In addition, samples from 37 initially stroke-free participants with stroke (n=17) or MI (n=20) were available for measurement before and after the vascular event (median 5 days, range 2 to 40 days). Levels before and after events were compared using nonparametric tests. Results— HsCRP and Lp-PLA 2 activity levels were stable over time, whereas Lp-PLA 2 mass levels decreased on average 5% per year ( P =0.0015). Using accepted thresholds to define risk categories of Lp-PLA 2 mass, there was no significant change over time. HsCRP increased after stroke (from median 2.2 mg/L prestroke to 6.5 mg/L poststroke; P =0.0067) and MI (from median 2.5 mg/L pre-MI to 13.5 mg/L post-MI; P <0.0001). Lp-PLA 2 mass and activity levels both decreased significantly after stroke and MI (for Lp-PLA 2 mass, from median 210.0 ng/mL to 169.4 ng/mL poststroke, P =0.0348, and from median 233.0 ng/mL to 153.9 post-MI, P <0.0001). Conclusion— Lp-PLA 2 mass levels decrease modestly, whereas hsCRP and Lp-PLA 2 activity appear stable over time. Acutely after stroke and MI, hsCRP increases whereas Lp-PLA 2 mass and activity levels decrease. These changes imply that measurements made soon after stroke and MI are not reflective of prestroke levels and may be less reliable for long-term risk stratification.