January 2012 FMU Clip

Let's now then go back and review because we're going pretty quickly for probably the listener who's trying to keep track of this. So we have the F2 isoprostane, we have the HSCRP, we've got the myeloperoxidase, and we've got the LP PLA2, the plaques type analysis. How do they fit together then in a schematic representation?

Yeah. So what we would suggest is that F2 isoprostane is really defining patient who has a lifestyle risk. They're deconditioned, they smoke, they have a bad diet that leads to increased oxidative state, increased risk long term of not only cardiovascular disease, but also cancer. If we're now looking for presence of marker of disease, we're really looking at hscrp, which based on our studies would really be a measure of atheroma burden, and then albumin creatinine ratio, which is really a measure of endothelial dysfunction. Working our way from lifestyle to presence of disease to activity of disease. Now we're looking at the myeloperoxidase and the LPPLE2 or the plaque test, which are really looking at vulnerable plaque formation from really two different points of view. The LPPLA2 or the plaque test, really looking at it from the vessel wall point of view, or inside the house, if you will, looking at the activity in the necrotic core, macrophage activation, things of that nature. And the myeloproxidase test, really looking at it from the lumen side, what the white cells are seeing outside the house, if you will, fissures, erosions, hot atheroma, that's starting to come through a collagen cap. And together, this really not only helps us define whether a given patient has risk, but where they are on a risk spectrum. Are we really focusing on lifestyle? Are we trying to modulate disease, or are we really trying to quiesce the function that's going on in the vessel wall that's risking a clinical event.