Lipoprotein-associated phospholipase A2 (Lp-PLA2) is an enzyme family of phospholipase
A2 produced by the inflammatory cell in atherosclerotic plaque. It is transported in the circulation,
attached mainly to low-density lipoprotein-cholesterol (LDL-C). It hydrolyzes glycerophospholipids
particularly fatty acids at the sn-2 position and produces numerous bioactive lipids; and
leads to endothelial dysfunction, atherosclerotic plaque inflammation, and development of the necrotic
core in plaques.
There are two kinds of phospholipase A2, namely: secretory phospholipase A2 (sPLA2) and Lp-
PLA2. They are deemed as evolving predictors of cardiovascular disease (CVD) risk in hospitaland
population-based studies, including healthy subjects, acute coronary syndromes (ACS) and patients
with CVD. Unfortunately, Lp-PLA2 inhibitor (darapladib) and s-PLA2 inhibitor (varespladib
methyl) failed to prove to lower the risk of composite CVD mortality, myocardial infarction and
stroke in those with stable CVD and ACS.
Herein, we describe the explanation based on the existing data why there is still a discrepancy
among them. So, it highlights the opinion that phospholipase A2 is merely the inflammatory biomarkers
of CVD and playing an important role in atherosclerosis. Further, there is more spacious
room to prove the causation.