Abstract
To test the hypothesis that angiotensin converting enzyme inhibitors (ACEi) affect soluble tumor-necrosis-factor-related apoptosis-inducing ligand (sTRAIL) and this interaction is associated with less in-drug-eluting-stent (DES) neointimal hyperplasia following percutaneous coronary intervention (PCI). From our database of patients with elective PCI and baseline intravascular ultrasound (IVUS) evaluation of the implanted DES, we randomly selected 60 patients who were prescribed an ACEi and 60 matched controls, who did not receive an ACEi following PCI. All patients underwent coronary angiography and IVUS. sTRAIL was measured in samples from the stented coronary artery and a peripheral vein. sTRAIL concentration was higher in the ACEi group, both in coronary and peripheral samples: 104 [78-139] pg/ml versus 63 [45-100] pg/ml (P < 0.001) and 99 [73-135] pg/ml versus 69 [49-103] pg/ml (P = 0.002), respectively. There was an inverse association (standardized beta -0.760; P < 0.001) between sTRAIL and lumen area loss in both treatment groups. In the multivariable analysis, log(sTRAIL) was an independent negative predictor of lumen area loss (standardized beta -0.660, adjusted 95% confidence interval -0.722 to -0.466). Treatment with ACEi was associated with higher sTRAIL levels and lower lumen area loss in the IVUS evaluation of implanted DES. sTRAIL levels were negatively associated with in-stent neointima hyperplasia in these post-PCI patients.
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