Journal
AMERICAN HEART JOURNAL
Volume 149, Issue 3, Pages 520-526Publisher
MOSBY-ELSEVIER
DOI: 10.1016/j.ahj.2004.10.032
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Background 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. Methods 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 1 2-month catheterization. Results 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 mm(3)/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 mm(3)/mm, - 14% +/- 10% vs +6% +/- 12%, P <.05). The some behavior was shown by intermediate plaques at nonstented sites (-2.5 +/- 3.0 vs +1.0 +/- 3.0 mm(3)/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). Conclusions 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.
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