Anwar Santoso*, Teuku Heriansyah and Mohammad S. Rohman Pages 3 - 10 ( 8 )
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.
Lipoprotein-associated phospholipase A2, LDL-C, cardiovascular disease, acute coronary syndromes, myocardial infarction, atherosclerosis.
Department of Cardiology and Vascular Medicine, National Cardiovascular Centre, Harapan Kita Hospital, Universitas Indonesia, Jakarta, Department of Cardiology and Vascular Medicine, Faculty of Medicine, Universitas Syiah Kuala, Zainoel Abidin General Hospital, Banda Aceh, Department of Cardiology and Vascular Medicine, Faculty of Medicine, Brawijaya University, Malang