Coronary heart disease (CHD) is caused by a narrowing of coronary artery’s lumen as a result of atherosclerosis process on the vessel wall that cause diminished blood flow and oxygen supply to myocardium. On its course, CHD can be progressive and sudden changes from stable to acute condition known as acute coronary syndrome (ACS) often occurred. The sudden changes were associated with acute thrombosis on the eroded, cracked or ruptured atherosclerotic plaque. Plaque rupture is associated with the change a stable plaque to labile and vulnerable plaque. Current laboratory studies also aimed for an early detection of plaque changes before the rupture of atherosclerotic plaque. Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a novel plaque destabilization marker that can be detected before the rupture of plaque, ischemia, infarct or necrosis myocardium. Lp-PLA2 also reported as an endothelial dysfunction marker which is the early phase of atherosclerosis and used in risk stratification of ACS. Lp-PLA2 is produced by macrophages, lymphocytes and mast cells. The enzyme hydrolyzes oxLDL and produces lysophosphatidylcholine (lysoPC) and oxidized fatty acid (oxFA). LysoPC and oxFA cause endothelial dysfunction and induce white muscle cells and macrophages apoptosis which in turn lead to necrotic core broadening in the atherosclerotic plaque, thinning of fibrous cap, and plaque destabilization which then can cause plaque rupture. Laboratory tests for Lp-PLA2 can be performed by means of mass or enzyme activity measurement i.e. ELISA for Lp-PLA2 mass measurement as well as photometric or radioimmunoassay for activity measurement. Lp-PLA2 mass measurement reported to be more precise and accurate as a marker of CHD risk compared to the enzyme activity measurement.
|Journal||Journal of the Indonesian Medical Association : Majalah Kedokteran Indonesia|
|Publication status||Published - 2010|