BACKGROUND: Antiplatelet therapy with clopidogrel decreases ischemic complication especially in patients with acute coronary syndromes or after percutaneous coronary interventions. Our study was designed to test the effects of clopidogrel on soluble CD40 ligand (sCD40l) and on high-sensitivity C-reactive protein (hs-CRP) in patients with stable coronary artery disease (CAD). METHODS: This is a randomized, double-blind, placebo-controlled study. A total of 73 patients with stable CAD for > 6 months were randomized to receive either clopidogrel (loading dose 300 mg followed by 75 mg/d) for 8 weeks or placebo. Soluble CD40 ligand and hs-CRP were measured at baseline and at completion of the study. RESULTS: All patients were on aspirin therapy, and 74% were on statins. Median and interquartile ranges (IQR) of sCD40l decreased from 64 pg/mL (43-99) at baseline to 53 pg/mL (35-77) at 8 weeks (P = .03) in the clopidogrel group and remained unchanged in the placebo group (59 pg/mL, IQR 35-77 vs 55 pg/mL, IQR 35-78) (P = non significant). Levels of hs-CRP were not affected by therapy and remained unchanged in both groups. CONCLUSIONS: In patients with stable CAD, clopidogrel inhibits the release of sCD40l by platelets, which may contribute to the clinical benefit provided by this drug. This, however, does not translate in a reduction of subclinical inflammation, as measured by hs-CRP.
RCT Entities:
BACKGROUND: Antiplatelet therapy with clopidogreldecreases ischemic complication especially in patients with acute coronary syndromes or after percutaneous coronary interventions. Our study was designed to test the effects of clopidogrel on soluble CD40 ligand (sCD40l) and on high-sensitivity C-reactive protein (hs-CRP) in patients with stable coronary artery disease (CAD). METHODS: This is a randomized, double-blind, placebo-controlled study. A total of 73 patients with stable CAD for > 6 months were randomized to receive either clopidogrel (loading dose 300 mg followed by 75 mg/d) for 8 weeks or placebo. Soluble CD40 ligand and hs-CRP were measured at baseline and at completion of the study. RESULTS: All patients were on aspirin therapy, and 74% were on statins. Median and interquartile ranges (IQR) of sCD40l decreased from 64 pg/mL (43-99) at baseline to 53 pg/mL (35-77) at 8 weeks (P = .03) in the clopidogrel group and remained unchanged in the placebo group (59 pg/mL, IQR 35-77 vs 55 pg/mL, IQR 35-78) (P = non significant). Levels of hs-CRP were not affected by therapy and remained unchanged in both groups. CONCLUSIONS: In patients with stable CAD, clopidogrel inhibits the release of sCD40l by platelets, which may contribute to the clinical benefit provided by this drug. This, however, does not translate in a reduction of subclinical inflammation, as measured by hs-CRP.
Authors: Mir Abolfazl Ostad; Eva Nick; Vitor Paixao-Gatinho; Boris Schnorbus; Robert Schiewe; Peter Tschentscher; Thomas Munzel; Ascan Warnholtz Journal: Clin Res Cardiol Date: 2010-07-21 Impact factor: 5.460
Authors: Steven Haller; Satjit Adlakha; Grant Reed; Pamela Brewster; David Kennedy; Mark W Burket; William Colyer; Haifeng Yu; Dong Zhang; Joseph I Shapiro; Christopher J Cooper Journal: Clin J Am Soc Nephrol Date: 2011-08-04 Impact factor: 8.237
Authors: Joanna J Wykrzykowska; Ascan Warnholtz; Peter de Jaeger; Nick Curzen; Keith G Oldroyd; Jean Philippe Collet; Jurrien M Ten Berg; Tessa Rademaker; Dick Goedhart; Jurgen Lissens; Peter-Paul Kint; Patrick W Serruys Journal: J Thromb Thrombolysis Date: 2009-11 Impact factor: 2.300