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Originally Posted by butterflytrans
The thing is, zip2play, is that the plaque doesn't form inside the artery's lumen...instead, it forms between the innermost layer of the artery wall and the middle layer of the wall (the tunica intima and media respectively)....also, a piece of the plaque doesn't necessary break off, but the inside wall of the artery becomes weak, it kinda tears and the underlying plaque is exposed. This sets off the clotting cascade and you get the clot formed. The only reason I know this is 'cause I got nailed on an exam once asking where the plaque is actually located.
Don't want to step on anyone's toes, just wanted to bring this little tidbit of info up 
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Butterfly,
I agree completely with the mechanism, but I still assert that the slow process of plaque formation and arterial weakening is climaxed suddenly, most often at a moment of high blood pressure, high blood flow, high heart rate....the basketball game. There is always a proximate cause....often shovelling now, or god forbid, SEX!

And I also think that the clot doesn't necessarily always form in place but often on the floating detritus moving downstream from the rupture. I don't have a solid foundation on the latter opinion though (never stopped me before

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Truth be told, when I've read that Lipitor has been showing some evidence of long time plaque reductions, I can't say I haven't worried just a bit that maybe leaving them in peace might be safer. (I'm thinking about the analogy of ripping apart a spent nuclear reactor...

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Never worry about stepping on these Size 12's....they're tough as, well, shoeleather?
Butterfly,
Can you help me picture the mechanism whereby angioplasty COMPRESSES the plaques to a smaller size. I think of plaque as mostly fat which like all liquids, gels, what have you, is incompressible. Where does it go....or is it a spongelike structure where pressure can force a liquid component out (into the bloodstream?). Or is it just squooshed out into a longer thinner plaque within the artery wall?