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.