Do statins have a role in reduction/prevention of post-PCI restenosis?

The pathophysiology of post-PCI restenosis involves neointimal formation that consists of three phases: thrombosis (within 24 h), recruitment (3-8 days), and proliferation, which starts on day 8 of PCI. Various factors suggested to be predictors/risks for restenosis include C-reactive protein (CRP), inflammatory mediators (cytokines and adhesion molecules), oxygen radicals, advanced glycation end products (AGEs) and their receptors (RAGE), and soluble RAGE (sRAGE). The earlier noted factors produce thrombogenesis, vascular smooth muscle cell proliferation, and extracellular matrix formation. Statins have pleiotropic effects. Besides lowering serum cholesterol, they have various other biological effects including antiinflammatory, antithrombotic, CRP-lowering, antioxidant, antimitotic, and inhibition of smooth muscle cell proliferation. They inhibit matrix metalloproteinase and cyclooxygenase-2, lower AGEs, decrease expression of RAGE and increase levels of serum sRAGE. They also increase the synthesis of nitric oxide (NO) by increasing endothelial NO synthase expression and activity. Preprocedural statin therapy is known to reduce peri- and post-PCI myonecrosis and reduce the need for repeat revascularization. There is evidence that statin-eluting stents inhibit in-stent restenosis in animal models. It is concluded that because of the above attributes of statins, they are suitable candidates for reduction of post-PCI restenosis and post-PCI myonecrosis. The future directions for the use of statins in reduction of post-PCI restenosis and myonecrosis have been discussed.