was the most significant independent risk factor in stroke group (OR: 13.
These same patients who thought they had a clean bill of health actually have raised levels of other cardiovascular risk factors such as small particle pattern LDL as well as less than favorable Lp-PLA2
levels and an imbalance in apolipoprotein B (ApoB) and lipoprotein(a), to name a few.
Impact of the LDL subfraction phenotype on Lp-PLA2
distribution, LDL modification and HDL composition in type 2 diabetes.
Accordingly, in a recent study of stable IHD patients treated with atorvastatin, plasma concentrations of NT-proBNP, neopterin, lipoprotein(a) [Lp(a)], and soluble receptor for advanced glycation end-products (sRAGE) were predictive of major cardiovascular events, whereas LDL-cholesterol, HDL-cholesterol, triglycerides, hs-CRP, adiponectin, cystatin C, Lp-PLA2
, monocyte chemotactic protein-1, matrix metalloproteinase-9, myeloperoxidase, osteopontin, soluble CD-40 ligand, sICAM-1, and soluble vascular cell adhesion molecule 1 (sVCAM-1) were not (55).
The higher the level of Lp-PLA2
in the blood, the greater the risk of stroke, first or recurrent heart attack or poor outcome after a heart attack.
The FDA reviewed data from the Lp-PLA2
Activity study, a sub-study from the National Institute of Health-sponsored Reasons for Geographic and Racial Differences in Stroke (REGARDS) project, which used the test in about 4,600 adults aged 45-92 years; 42% were men, 58% were women, 41.
The PLAC Test for Lp-PLA2
Activitymeasures the activity of lipoprotein-associated phospholipase A2 (Lp-PLA2
) in a patient s blood.
DiaDexus will be also able to improve sales and marketing activities related to the planned introduction in the USA of the PLAC Test for Lp-PLA2
Activity, as well as assess additional collaboration and licence opportunities.
M2 EQUITYBITES-July 18, 2014-diaDexus' PLAC Test for Lp-PLA2
Activity accepted for US FDA's review
Darapladib is designed to prevent heart attacks and strokes in a completely different way from cholesterol-lowering drugs by targeting an enzyme called Lp-PLA2
that is linked to artery-clogging plaques.
The main physiological action of Lp-PLA2
is the hydrolysis of strongly inflammatory phospholipids, such as platelet-activating factor which may increase risk of CVD.
In case further risk stratification is required, inflammatory markers such as hsCRP and Lp-PLA2
may be checked.