Lp-PLA2
Lipoprotein-associated phospholipase A2 — an enzyme specific to vascular inflammation.
Optimal Range
< 200 ng/mL (optimal)
Risk-Stratified Targets
| Population / Context | Target |
|---|---|
| Optimal | < 200 ng/mL (mass) |
| Elevated riskAlso measured as activity: < 150 nmol/min/mL is optimal | ≥ 200 ng/mL (mass) |
Why It Matters
Unlike hsCRP (which reflects general inflammation), Lp-PLA2 is specific to inflammation within arterial walls. Elevated levels indicate active plaque vulnerability and near-term cardiovascular risk.
Understanding Lp-PLA2
Lipoprotein-associated phospholipase A2 (Lp-PLA2) is an enzyme that circulates bound to LDL particles and is released when these particles become trapped and oxidized within arterial walls. Unlike hsCRP, which reflects general systemic inflammation from any source, Lp-PLA2 is highly specific to vascular inflammation — making it a more targeted marker of active atherosclerotic disease.
Lp-PLA2 plays a direct role in plaque destabilization. When LDL particles infiltrate the arterial wall and become oxidized, Lp-PLA2 cleaves the oxidized phospholipids, producing inflammatory mediators that recruit macrophages and promote the formation of the necrotic core within plaques. This process is what makes plaques vulnerable to rupture — the event that triggers most heart attacks and strokes.
Elevated Lp-PLA2 is particularly concerning when found alongside elevated hsCRP, as the combination indicates both systemic and vascular inflammation — a high-risk phenotype. The PLAC test for Lp-PLA2 is FDA-cleared for cardiovascular risk assessment. When elevated, it should prompt aggressive management of modifiable cardiovascular risk factors and consideration of advanced imaging to assess plaque burden directly.
Key Research
Lipoprotein-associated phospholipase A2 and risk of coronary disease, stroke, and mortality: collaborative analysis of 32 prospective studies
Thompson A et al. · Lancet (2010)
Key finding: Lp-PLA2 is independently associated with risk of coronary heart disease and ischemic stroke after adjusting for conventional risk factors.