Abstract 3532: Lipoprotein-Associated Phospholipase A2 and High Sensitivity C-Reactive Protein Levels and the Prediction of Cardiovascular Risk Among Coronary Artery Disease Patients With Differing Clinical Presentations
Background: Inflammation plays a role in the development and progression of coronary artery disease (CAD), with circulating markers of vascular inflammation being used in risk assessment including high sensitivity C-reactive protein (hsCRP) and lipoprotein-associated phospholipase A2 (LpPLA2). While hsCRP responds to the systemic inflammatory stimulus of acute myocardial infarction (AMI), LpPLA2 has been proposed to be more vascular-specific and to vary minimally based upon clinical presentation. To test this hypothesis, we evaluated both biomarkers among CAD patients presenting with stable angina (SA), unstable angina (USA) or acute myocardial infarction (AMI).
Methods: LpPLA2 (PLACTM test, diaDexus, Inc.) and hsCRP were measured from samples donated by consenting patients (N=1,010) enrolled in the registry of the Intermountain Heart Collaborative Study that underwent angiographic evaluation for CAD. Patients were categorized by presentation status (SA=637; USA=205; and AMI=168), stratified according to median levels of LpPLA2 (350.2 ng/mL) and hsCRP above and below 3 mgl/L and followed for 7.5 ± 2.4 years for CAD death.
Results: Age averaged 64 ± 12 years and 70% were male. While median hsCRP (mg/L) levels differed significantly by presentation [2.86, 2.80, and 13.7 for SA, USA, and AMI, respectively (p<0.0001)], median LpPLA2 (ng/mL) levels [350.2, 353.1, and 348.1 for SA, USA, and AMI, respectively (p=0.67)], did not. LpPLA2 was not only a better predictor of CAD death among the entire cohort (LpPLA2: adjusted Hazard Ratio [HR]= 1.47, p=0.04; hsCRP: adjusted HR=0.95, p=0.81), it was a better predictor among patients presenting with AMI (LpPLA2: adjusted HR3 1.80, p=0.30; hsCRP adjusted HR=0.76, p=0.63).
Conclusions: Among CAD patients, LpPLA2 varies minimally among differing presentations compared to hsCRP and is a better a predictor of CAD death among those presenting with AMI. This information supports the hypothesis that LpPLA2 is a vascular specific marker of inflammation and independent of transient systemic inflammatory effects.