Restenosis rate reduction after coronary angioplasty with simvastatin and probucol

Citation
Am. Herrera et al., Restenosis rate reduction after coronary angioplasty with simvastatin and probucol, REV ESP CAR, 52(10), 1999, pp. 778-784
Citations number
47
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
REVISTA ESPANOLA DE CARDIOLOGIA
ISSN journal
03008932 → ACNP
Volume
52
Issue
10
Year of publication
1999
Pages
778 - 784
Database
ISI
SICI code
0300-8932(199910)52:10<778:RRRACA>2.0.ZU;2-6
Abstract
Introduction and objectives. The restenosis rates after coronary angioplast y persist as an important problem even though multiple drug therapies and d ifferent devices have been tried. The reduction of the cholesterol and low density lipoproteins levels (and their oxidation) have proved to have a ben eficial effect on atherosclerosis evolution. Both the lipid lowering and an tioxidant agents have caused a reduction in the neointimal formation genera ted with the angioplasty balloon in animals, and their combination to impro ve endothelial dysfunction in humans. The aim of the present study is to pr ove whether the whole administration of two potent agents such as simvastat in and probucol, which reduce the lipid levels and their oxidation, are abl e to lessen the restenosis related process. Patients and methods. Thirty five consecutive patients with coronary angiop lasty with no stent to whom 20 mg simvastatin and 500 mg probucol bid were given (group-A) were studied in a prospective non-randomized study. They we re compared to a historic group of 40 patients under the standard treatment (group-B). Both groups were angiographically evaluated to determine the re stenosis percentage. A lipid profile mas performed on group-A patients. Results. The restenosis occurred in 4 (11.4%) in group-A and in 17 (42.5%) in group-B patients and in 4 (10.0%) and 18 (39.1%) lesions respectively (p < 0.01). A new PTCA was performed on 2 (5.7%) group-A patients vs 13 (32.5 %) in group-B (p < 0.01). There was a reduction in residual stenosis (34.2 +/- 19.7%, vs 48.8 +/- 23.5%, p < 0.01) and a greater minimum luminal diame ter (1.76 +/- 0.59 vs 1.46 +/- 0.70 mm, p < 0.05) in group-A than in group- B patients. Conclusions. Although studies with more patients are required, a combined L ipid lowering and antioxidant therapy could achieve a reduction in angiopla sty coronary restenosis.