Acute coronary syndromes (ACS), i.e. unstable angina and myocardial infarction, are the leading causes of death in developed countries and developing countries alike. Lipid lowering intervention studies have demonstrated a 30% risk reduction in recurrent cardiovascular events and death, despite only modest improvement in angiographic stenosis. This discrepancy suggested that cholesterol lowering by statins may lead to stabilization of vulnerable plaques rather than reducing stenosis per se. The predominant effect of statins is to lower lipid levels by inhibiting cholesterol biosynthesis. 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.