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 mgsimvastatin 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. 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 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). 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.
RCT Entities:
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 12-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 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). 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.
Authors: Jung Sun Cho; Myung Ho Jeong; Doo Sun Sim; Young Joon Hong; Kyung Seob Lim; Jung Ha Kim; Hyoung Doo Kim; Ju Yeal Baek; Hee Jeoung Yoon; Sung-Ho Her; Seung Won Jin; Ju Han Kim; Youngkeun Ahn; Jeong Gwan Cho; Jong Chun Park; Jung Chaee Kang Journal: J Korean Med Sci Date: 2010-04-16 Impact factor: 2.153
Authors: Young Joon Hong; Myung Ho Jeong; Yun Ha Choi; Eun Hye Ma; Jum Suk Ko; Min Goo Lee; Keun Ho Park; Doo Sun Sim; Nam Sik Yoon; Hyun Ju Youn; Kye Hun Kim; Hyung Wook Park; Ju Han Kim; Youngkeun Ahn; Jeong Gwan Cho; Jong Chun Park; Jung Chaee Kang Journal: Korean J Intern Med Date: 2010-11-27 Impact factor: 3.165