lipoprotein-associated phospholipase A2 (Lp-PLA2) is an inflammatory biomarker that offers several advantages relative to other markers, including specificity for vascular inflammation, minimal biovariability, and stability in states of myocardial ischemia
Lp-PLA2
is a secreted calcium-independent member of the phospholipase A2 superfamily produced mainly, if not exclusively, by monocytes, macrophages, T-lymphocytes and mast cells
Lp-PLA2 activity has been shown to be upregulated in atherosclerotic lesions - this association is particularly in more complex plaques with co-localising with macrophages
however the positive association of plasma Lp-PLA2 with CHD is not fully explained by this enhanced expression
for example, unlike Lp-PLA2, elevated CRP levels that reflect ongoing inflammation were not identified in WOSCOPS as a strong independent risk factor of future cardiovascular disease
also Lp-PLA2 does play an active role during the oxidation of LDL
Lp-PLA2 levels are not solely a reflection of atherosclerotic burden - thus Lp-PLA2 is differentiated from other inflammatory components of atherosclerosis
about two-thirds of Lp-PLA2 in plasma resides on LDL, with the remainder distributed across high-density lipoprotein and very low-density lipoprotein (1)
Lp-PLA2 and oxidised LDL
one of the consequences of LDL oxidation is the rapid degradation of oxidised phosphatidylcholines generating substantial quantities of lysophosphatidylcholine (lyso-PC) and free oxidised fatty acids - the cleavage of oxidised phosphatidylcholines within modified LDL-particles is carried out solely by Lp-PLA2
Lp-PLA2 remains latent until LDL undergoes oxidative damage
lyso-PC and free oxidised fatty acids highly effective inflammatory mediators capable of attracting monocytes and exacerbating the atherogenic process
observational studies carried out in primary prevention settings have shown a relationship between Lp-PLA2 and cardiovascular risk, although the magnitude of the association has varied
with respect to secondary prevention setting
among community subjects presenting with MI, increased Lp-PLA2 levels measured early after MI are strongly and independently associated with mortality and provide incremental value in risk discrimination over traditional predictors (2)
increased concentrations of Lp-PLA2 predict future cardiovascular events in patients with manifest CHD independent of a variety of potential risk factors including markers of inflammation, renal function, and hemodynamic stress (3)
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