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Simvastatin does not inhibit intimal hyperplasia and restenosis but promotes plaque regression in normocholesterolemic patients undergoing coronary stenting: A randomized study with intravascular ultrasound

2005; Elsevier BV; Volume: 149; Issue: 3 Linguagem: Inglês

10.1016/j.ahj.2004.10.032

1097-6744

Anna Sonia Petronio, Giovanni Amoroso, Ugo Limbruno, Barbara Papini, Marco De Carlo, Andrea Micheli, Nicola Ciabatti, Mario Mariani,

Cardiac Imaging and Diagnostics

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, peristent 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.