Valsartan for prevention of restenosis after stenting of type B2/C lesions: the VAL-PREST trial

The following study was performed to evaluate the effects of chronic 6-month administration of the angiotensin I receptor antagonist valsartan on restenosis rate after stenting of type B2/C lesions in comparison to placebo. Despite encouraging results of the BENESTENT and STRESS trials, stenting of complex coronary lesions leads to an in-stent restenosis rate of up to 40%. Several attempts at systematic medical therapy (e.g., ACE inhibitors) have not improved these results. Because of the important role of angiotensin in endothelial function, the hypothesis that angiotensin I receptor antagonists after stent implantation lead to a reduction of the in-stent restenosis rate should be tested in a single-center trial. Two hundred and fifty patients with type B2/C coronary lesions were randomized in an open-label study with respect to age, gender, lesion type and indication of percutaneous coronary intervention to a chronic administration of 80 mg valsartan or placebo (beta-blocking agents and/or ACE inhibitors). In-stent restenosis rate according to quantitative coronary angiography (QCA) and need for reintervention as primary and secondary endpoints were analyzed after a repeat angiogram at 6 months in 99 patients with 80 mg valsartan and 101 patients with placebo. Chronic administration of 80 mg valsartan reduced the in-stent restenosis rate to 19.2% (n = 19/99) in comparison to placebo with an in-stent restenosis rate of 38.6% (n = 39/101) (p < 0.005). Reintervention rate was 28.7% (n = 29/101) in the placebo group and only 12.1% (n = 12) in the valsartan group (p < 0.005). QCA analysis of stented coronary segments disclosed no differences in reference vessel diameter (2.68 +/- 0.26 mm in the valsartan group versus 2.71 +/- 0.24 mm in the placebo group) but significant differences in stented vessel diameter (2.17 +/- 0.27 mm in the valsartan group and 1.60 +/- 0.20 mm in the placebo group) (p < 0.000001).