In a forthcoming study, online-published in Circulation December 15, 2008, we learn more about the potential effects of the differing mechanisms of action between statins (with a liver mechanism of action) and Zetia, or ezetimibe (with a gut mechanism of action). What we learn would suggest that one's actual LDL/HDL numbers may matter less than the way in which the cholesterol-lowering agent works -- that is, it may have "other effects" which are, as yet, not well-understood. And those "other effects" may actually be providing the bulk of the benefit historically-associated with those lower cholesterol numbers.
A good friend, and an expert -- will be along shortly, to give you more, but here is a snippet from Circulation:
. . . .By inhibiting 3-hydroxy-3- ethylglutaryl coenzyme A reductase, statins not only reduce cholesterol biosynthesis but also decrease the formation of isoprenoids, which are important for mediating signaling through the Rho-associated coiled-coil containing protein kinase (ROCK) pathway. Increased ROCK activity has been implicated in endothelial dysfunction and vascular inflammation. We hypothesize that ezetimibe [Zetia], which inhibits intestinal cholesterol absorption, may not exert similar cholesterol-independent or pleiotropic effects of statins and, when used with a lower dose of statin, have less effect on ROCK activity than a higher dose of statin. . . .
[The study's] results indicate that high-dose statin monotherapy exerts greater effects on ROCK activity and endothelial function, but not on C-reactive protein, than low-dose statin plus ezetimibe. These findings provide additional evidence of statin benefits beyond cholesterol lowering. . . .
Look for a much better analysis, over at Gooznews, shortly.