Background Progression of coronary atherosclerosis (ATS) has clinical implications. Serum levels of gamma-glutamyltransferase (GGT), a marker of oxidative stress, predict the risk of cardiovascular events. However, the role of GGT levels in the progression of coronary ATS has never been established. Materials and methods Consecutive patients undergoing two coronary angiographies (CAs) separated by at least 6 months were prospectively enrolled between May 2008 and June 2010. All patients were discharged on statins after the first CA. The severity and extent of coronary ATS were graded according to Bogaty's score, and the variation (Delta) in stenosis score and extent index between follow-up (S-2 and E-2) and basal values (S-1 and E-1) were calculated. Predictors of Delta S2-1 and Delta E2-1 were assessed among clinical and laboratory data, including GGT levels, analyzed as Delta between follow-up and basal values (Delta GGT(2-1)). Results We enrolled 100 consecutive patients (age 64 +/- 11 years, 68% men). Compliance with statin therapy was 100%. At multiple regression analysis, Delta GGT(2-1) was the only independent predictor of Delta S2-1 (B = 0.18, SE = 0.07, P = 0.05), with Delta low-density lipoprotein-cholesterol(2-1) levels being of borderline statistical significance (P = 0.07). On multiple regression analysis, Delta GGT(2-1) was the only independent predictor of Delta E2-1 (B = 0.32; SE = 0.11; P = 0.04), with active smoking habit and Delta fibrinogen(2-1) levels being of borderline statistical significance (P = 0.08 and 0.06, respectively). Conclusion Delta GGT(2-1) is associated with angiographic coronary ATS progression in patients with ischemic heart disease on statin treatment, suggesting that oxidative stress may be another therapeutic target for preventing ATS progression beyond that of lipid-lowering therapies. Coron Artery Dis 24:40-47 (C) 2012 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins. Coronary Artery Disease 2013, 24:40-47

Serum levels of gamma-glutamyltransferase and progression of coronary atherosclerosis

D'Amario D;
2013-01-01

Abstract

Background Progression of coronary atherosclerosis (ATS) has clinical implications. Serum levels of gamma-glutamyltransferase (GGT), a marker of oxidative stress, predict the risk of cardiovascular events. However, the role of GGT levels in the progression of coronary ATS has never been established. Materials and methods Consecutive patients undergoing two coronary angiographies (CAs) separated by at least 6 months were prospectively enrolled between May 2008 and June 2010. All patients were discharged on statins after the first CA. The severity and extent of coronary ATS were graded according to Bogaty's score, and the variation (Delta) in stenosis score and extent index between follow-up (S-2 and E-2) and basal values (S-1 and E-1) were calculated. Predictors of Delta S2-1 and Delta E2-1 were assessed among clinical and laboratory data, including GGT levels, analyzed as Delta between follow-up and basal values (Delta GGT(2-1)). Results We enrolled 100 consecutive patients (age 64 +/- 11 years, 68% men). Compliance with statin therapy was 100%. At multiple regression analysis, Delta GGT(2-1) was the only independent predictor of Delta S2-1 (B = 0.18, SE = 0.07, P = 0.05), with Delta low-density lipoprotein-cholesterol(2-1) levels being of borderline statistical significance (P = 0.07). On multiple regression analysis, Delta GGT(2-1) was the only independent predictor of Delta E2-1 (B = 0.32; SE = 0.11; P = 0.04), with active smoking habit and Delta fibrinogen(2-1) levels being of borderline statistical significance (P = 0.08 and 0.06, respectively). Conclusion Delta GGT(2-1) is associated with angiographic coronary ATS progression in patients with ischemic heart disease on statin treatment, suggesting that oxidative stress may be another therapeutic target for preventing ATS progression beyond that of lipid-lowering therapies. Coron Artery Dis 24:40-47 (C) 2012 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins. Coronary Artery Disease 2013, 24:40-47
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11579/147210
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