 Stimulation of the angiotensin II type 1 AT1 receptors after arterial injury promotes vascular smooth muscle cell VSMC migration, proliferation, and extracellular matrix production, leading to the hope that blockade of this receptor by angiotensin-converting enzyme inhibitors ACEI or specific AT1 receptor antagonists ARBs might reduce intimal hyperplasia. However, despite confirmatory evidence in several animal models of restenosis, the large scale MERCATOR and MARCATOR trials of cilazapril with balloon angioplasty failed to show benefit. In 1999, Kondo reported the results of a randomized pilot trial of 100 patients who received Palmaz-Schatz stents and were randomized to receive the ACE inhibitor quinapril or placebo. The volume of neointimal hyperplasia assessed by IVUS was significantly less quinapril than the control group 18 0.6 mm3 vs. 25 0.6 mm3; p 0.05. The quinapril groups restenosis rate was 16, with the quinapril benefit being observed only in patients with the DD and ID genotypes. Also, other study reported on a consecutively treated cohort of 1,598 stented patients, noting that ACE inhibitor usage at the time and after stenting reduced the risk of subsequent revascularization dramatically adjusted odds ratio, 0.46; p 0.001. In the ValPREST trial which is a single-center randomized trial of patients receiving stents for type B2C lesions, comparing valsartan and ARV 80 mgs daily with open treatment, patients randomized to valsartan had a 19 incidence of restenosis compared with 39 in the open treatment arm p 0.005. 