Vascular-specific inflammation — more specific to arterial wall biology than hs-CRP.
Lp-PLA2 is an enzyme produced by macrophages and bound to LDL particles inside arterial walls. Unlike hs-CRP (general systemic inflammation), Lp-PLA2 is relatively specific to vascular inflammation and plaque instability. Elevation correlates with plaque rupture risk independent of LDL-C.
The FDA-cleared PLAC Test is the standard assay. It adds incremental risk information over the standard lipid panel, particularly in patients with unexplained CV events or strong family history.
Lp-PLA2 is influenced by: active vascular inflammation, plaque burden, smoking, LDL levels (substrate availability), and statins (reduce it). Unlike hs-CRP, it is relatively unaffected by infection, arthritis, or acute inflammation — making it cleaner for cardiovascular risk assessment.
Order when hs-CRP is chronically elevated for non-cardiac reasons, or when refining risk stratification in family history of early events. Not commonly repeated more than annually unless tracking response to a targeted anti-inflammatory or lipid intervention.
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Start tracking →Informational only — not medical advice. Reference ranges vary by lab and individual context. Work with a licensed provider to interpret your specific results.