http://circ.ahajournals.org/content/109/23_suppl_1/III-39.full Pleiotropic effects of a drug are actions other than those for which the agent was specifically developed. These effects may be related or unrelated to the primary mechanism of action of the drug, and they are usually unanticipated. Pleiotropic effects may be undesirable (such as side effects or toxicity), neutral, or, as is especially the case with HMG-CoA reductase inhibitors (statins), beneficial. Pleiotropic effects of statins include improvement of endothelial dysfunction, increased nitric oxide bioavailability, antioxidant properties, inhibition of inflammatory responses, and stabilization of atherosclerotic plaques. These and several other emergent properties could act in concert with the potent low-density lipoprotein cholesterol-lowering effects of statins to exert early as well as lasting cardiovascular protective effects. Understanding the pleiotropic effects of statins is important to optimize their use in treatment and prevention of cardiovascular disease.
http://www.ncbi.nlm.nih.gov/pubmed/17430164 Besides the lipid lowering effects, statins have also been shown to modulate the inflammatory status and improve endothelial function amongst others, commonly referred to as "pleiotropic effects". In the present review we will discuss different determinants which lead to plaque vulnerability and subsequently we will expand on the plaque stabilizing or "pleiotropic" effects of statin treatment.
http://eurheartj.oxfordjournals.org/content/23/21/1664.abstract Aims Heat released from atherosclerotic plaques as a result of the local inflammatory process, may be measured in vivo by a thermography catheter. Statins seem to have an antiinflammatory effect which results in plaque stabilization. The aim of this study was to investigate the effect of statins on plaque temperature.
Conclusions Patients on statin treatment produce less heat from the culprit coronary lesion than those not treated. Thus, statins seem to have a favourable effect on heat release from atherosclerotic plaques, and whether this effect has an impact on plaque stabilization needs to be investigated in future studies.
http://www.ncbi.nlm.nih.gov/pubmed/12615292 The traditional view of cardiovascular disease held that the degree of stenosis defined high-risk lesions and that removal of cholesterol shrank these lesions and thereby enlarged the lumen. Advances in understanding of the pathophysiology of the acute coronary syndromes refute this view. We now appreciate that vascular biology determines plaque stability and that statins stabilize plaque by favorably altering this biology. They do so chiefly (but probably not exclusively) by cholesterol lowering. In addition to reducing the cholesterol content of plaque, lipid lowering inhibits inflammation, and decreases collagenolytic activity and thrombotic potential. The role of lipid-independent effects remains unclear because many studies used statin concentrations too high to have any clinical relevance. However, data suggest that statin-induced alterations in the function of small G proteins may contribute to the anti-inflammatory and antithrombotic actions of statins in clinical practice.