http://www.medscape.com/viewarticle/504394_4 "
Plaque Stabilization and Decreased Plaque ThrombogenicityExperiments have demonstrated that cholesterol reduction is accompanied by favorable alterations in a number of mediators of plaque stability.[a title="Link: undefined">[39,40> Studies have shown that statins decrease macrophage number, reduce expression of tissue factor, adhesion molecules, and matrix metalloproteinases within plaque.[a title="Link: undefined">[39> The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors also reduce the oxidation of LDL, macrophage uptake of LDL,[a title="Link: undefined">[24,25> and reduce monocyte adhesion to endothelium.[a title="Link: undefined">[25> Lipid lowering with statins results in increased smooth-muscle cell content (a surrogate of plaque stability) and decreased collagen degradation (which may further enhance plaque stability).[a title="Link: undefined">[39> Clinical studies support these experimental observations and provide further evidence that statin therapy may be associated with plaque stabilization. Statins may also inhibit atherogenesis through the inhibition of vascular smooth-muscle cell proliferation and migration, and thus attenuate plaque growth and new lesion formation.[a title="Link: undefined">[41>
Another factor which may contribute toward decreased risk for stroke with statin therapy is the effect of statins on platelets and the endogenous balance of thrombosis/thrombolysis.[a title="Link: undefined">[40> Statin therapy decreases platelet activation and aggregation, and thereby may decrease the propensity toward thrombosis.[a title="Link: undefined">[10,23,42,43> Statin therapy inhibits tissue factor expression by macrophages, which plays an integral role in blood coagulation and is an important determinant of plaque thrombogenicity.[a title="Link: undefined">[23,25> There also may be a reduction in plasminogen activator inhibitor activity, which would facilitate fibrinolysis.[a title="Link: undefined">[23> All of these factors may contribute toward decreased risk for stroke seen in the statin studies. These statin effects may lead to decreased thrombus formation and thereby influence the development of clinical activity related to atherosclerotic plaque."
I think that the basic information comes from lab studies (animals?) Then in limited clinical studies they look for some of the same biological markers that they saw in the animals.
I am mostly speculating on this, because I don't want to have to run down all of the references.
http://content.onlinejacc.org/cgi/content/full/49/2/271 Atherosclerosis Regression, Vascular Remodeling, and Plaque Stabilization[a title="Link: undefined" name="RFN1">
* http://health.usnews.com/usnews/health/articles/040322/22healy.htm Meet the cholesterol busters