Guido Schnyder1, Gilles Rouvinez. 1. Division of Cardiology, UCSD Medical Center, University of California, San Diego, California 92103-8784, USA. g.schnyder@lycos.com
Abstract
BACKGROUND: Restenosis after percutaneous coronary angioplasty (PTCA) remains an important limitation of this procedure. AIM: To assess the relationship between homocysteine levels and restenosis after PTCA, and discuss the potential benefit of homocysteine-lowering therapy. METHOD: MEDLINE-based literature review. RESULTS: The conflicting literature on the association between homocysteine levels and restenosis after PTCA can partially be explained by differences in methodology. Depending on the type of studies considered, a pooling of data resulted in a 22%-36% risk reduction of restenosis in lesions exposed to low homocysteine levels. The strongest reduction was found in balloon-only treated lesions (42%), while only a trend (14%) was seen in stented lesions. Based on the only available trial, homocysteine-lowering therapy yielded a 54% restenosis rate reduction, 76% in balloon-only treated lesions and 31% in stented lesions. Furthermore, homocysteine-lowering therapy provided a significant clinical benefit with a 40% relative reduction in major adverse events at 6 months' follow-up. CONCLUSIONS: This review suggests that plasma homocysteine is a modifiable risk factor for restenosis, which when lowered improves outcome after PTCA. This inexpensive treatment with virtually no side-effects could therefore be considered as adjunctive therapy for patients undergoing PTCA, while awaiting results from further studies.
BACKGROUND:Restenosis after percutaneous coronary angioplasty (PTCA) remains an important limitation of this procedure. AIM: To assess the relationship between homocysteine levels and restenosis after PTCA, and discuss the potential benefit of homocysteine-lowering therapy. METHOD: MEDLINE-based literature review. RESULTS: The conflicting literature on the association between homocysteine levels and restenosis after PTCA can partially be explained by differences in methodology. Depending on the type of studies considered, a pooling of data resulted in a 22%-36% risk reduction of restenosis in lesions exposed to low homocysteine levels. The strongest reduction was found in balloon-only treated lesions (42%), while only a trend (14%) was seen in stented lesions. Based on the only available trial, homocysteine-lowering therapy yielded a 54% restenosis rate reduction, 76% in balloon-only treated lesions and 31% in stented lesions. Furthermore, homocysteine-lowering therapy provided a significant clinical benefit with a 40% relative reduction in major adverse events at 6 months' follow-up. CONCLUSIONS: This review suggests that plasma homocysteine is a modifiable risk factor for restenosis, which when lowered improves outcome after PTCA. This inexpensive treatment with virtually no side-effects could therefore be considered as adjunctive therapy for patients undergoing PTCA, while awaiting results from further studies.