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• W2059249988 abstract "Restenosis after coronary stenting is mainly caused by intimal hyperplasia. Both experimental and clinical studies suggest that statins may be able to inhibit intimal hyperplasia and, therefore, in-stent restenosis (ISR), by mechanisms beyond lipid lowering.In a 12-month study, we randomized 71 normocholesterolemic patients to 20 mg simvastatin or no treatment, 2 weeks before elective coronary stenting. Patients were evaluated by quantitative coronary angiography and intravascular ultrasound, immediately after the index procedure and at the 12-month catheterization.Binary ISR was present in 15% and in 18% of simvastatin-treated patients and controls, respectively (P = NS). Intimal hyperplasia did not differ significantly between the 2 groups (3.6 +/- 1.8 vs 3.8 +/- 2.3 mm3/mm, 34% +/- 15% vs 35% +/- 23% for simvastatin vs controls, P = NS). However, persistent plaque decreased with simvastatin but increased in controls (-4.0 +/- 4.0 vs +1.6 +/- 3.8 mm3/mm, -14% +/- 10% vs +6% +/- 12%, P < .05). The same behavior was shown by intermediate plaques at nonstented sites (-2.5 +/- 3.0 vs +1.0 +/- 3.0 mm3/mm, -10% +/- 8% vs +9% +/- 9%, P < .05). Major adverse events at 12 months were present in 11% and 24% of simvastatin-treated patients and controls, respectively (P = .20).In normocholesterolemic patients undergoing coronary stenting, simvastatin does not prevent intimal hyperplasia or ISR, but it promotes atherosclerotic regression both at stented and at nonstented sites." @default.
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• W2059249988 date "2005-03-01" @default.
• W2059249988 modified "2023-09-27" @default.
• W2059249988 title "Simvastatin does not inhibit intimal hyperplasia and restenosis but promotes plaque regression in normocholesterolemic patients undergoing coronary stenting: A randomized study with intravascular ultrasound" @default.
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• W2059249988 doi "https://doi.org/10.1016/j.ahj.2004.10.032" @default.
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