Objectives To investigate the inhibitory effect of clopidogrel on release of soluble CD40 ligand （sCD40L） by ADP-activated platelet in patients with non-ST-segment elevation acute coronary syndromes（NSTEACS）. Meth...Objectives To investigate the inhibitory effect of clopidogrel on release of soluble CD40 ligand （sCD40L） by ADP-activated platelet in patients with non-ST-segment elevation acute coronary syndromes（NSTEACS）. Methods Forty-two patients with NSTEACS were treated with clopidogrel for 6 - 8 days. In order to obtain platelet rich plasma （PRP） samples, the venous blood was drawn before and after treatment, respectively. The platelets were activated by adenosine diphosphate （ADP） , thus releasing sCD40L, sCD40L levels were determined by en- zyme-linked immunosorbent assay （ELISA） at different time of the reaction. Results Plasma sCD40L concentration before treatment was （0. 199 ± 0. 155 ） ng/mL, and （0. 190 ± 0. 176） ng/mL after treatment （ P 〉 0.05 ）. Before treatment the PRP sCD40L level at 20-minute of platelet activation was （4.34 ± 2.51 ） ng/mL, and decreased to （2.79 ±1.93 ） ng/mL after treatment （ P 〈 0. 001 ）. The corresponding level at 40 - minute of platelet activation was （5.29 ± 3. 13 ） ng/mL before treatment and （ 2.87 ± 1.59 ） ng/mL after treatment（ P 〈 0. 001 ）. Conclusions Short-term clopidogrel administration might inhibit the release of sCD40L by ADP-activated platelet in patients with NSTEACS, suggesting that, in addition to its antiplatelet potency, clopidogrel may still have an anti-inflammatory effect.展开更多
Background Recently,studies have disclosed soluble CD40 ligand （sCD40L） during atherosclerosis development and plaque destabilization.The objective of the present study was to test the hypothesis that sCD40L levels ...Background Recently,studies have disclosed soluble CD40 ligand （sCD40L） during atherosclerosis development and plaque destabilization.The objective of the present study was to test the hypothesis that sCD40L levels are higher in acute coronary syndrome （ACS） patients with a greater extent of angiographic coronary involvement.Methods This cross-sectional study examined ACS patients who underwent coronary angiography by measuring their sCD40L levels.In order to estimate the serum levels of sCD40L,10 ml of peripheral venous blood was drawn within 24 hours of admission.sCD40L levels were measured using an enzyme-linked immunosorbent assay （ELISA,RapidBio,West Hills,CA,USA）.Demographic data,presence of concomitant diseases,ACS characteristics,and angiographic findings were evaluated.A review of medical records and patient interviews were conducted to assess coronary risk factors.And the severity of coronary artery disease was evaluated using the Gensini score index.Results Two hundred and eighty-nine patients were included in the study,of whom 186 were male,with an average age of 64.1±10.0 years.Median sCD40L levels were 1.7 ng/ml （0.3-7.3 ng/ml） and Gensini scores were 50 （0-228）.After adjusting for demographic variables and cardiovascular risk factors,the Gensini score was associated with the natural logarithm of the sCD40L level （Coefficient b=0.002,95％ CI 0.000-0.003,P=0.029）.Conclusion sCD40L levels were independently associated with angiographic severity of coronary artery disease in patients with ACS.展开更多
文摘Objectives To investigate the inhibitory effect of clopidogrel on release of soluble CD40 ligand （sCD40L） by ADP-activated platelet in patients with non-ST-segment elevation acute coronary syndromes（NSTEACS）. Methods Forty-two patients with NSTEACS were treated with clopidogrel for 6 - 8 days. In order to obtain platelet rich plasma （PRP） samples, the venous blood was drawn before and after treatment, respectively. The platelets were activated by adenosine diphosphate （ADP） , thus releasing sCD40L, sCD40L levels were determined by en- zyme-linked immunosorbent assay （ELISA） at different time of the reaction. Results Plasma sCD40L concentration before treatment was （0. 199 ± 0. 155 ） ng/mL, and （0. 190 ± 0. 176） ng/mL after treatment （ P 〉 0.05 ）. Before treatment the PRP sCD40L level at 20-minute of platelet activation was （4.34 ± 2.51 ） ng/mL, and decreased to （2.79 ±1.93 ） ng/mL after treatment （ P 〈 0. 001 ）. The corresponding level at 40 - minute of platelet activation was （5.29 ± 3. 13 ） ng/mL before treatment and （ 2.87 ± 1.59 ） ng/mL after treatment（ P 〈 0. 001 ）. Conclusions Short-term clopidogrel administration might inhibit the release of sCD40L by ADP-activated platelet in patients with NSTEACS, suggesting that, in addition to its antiplatelet potency, clopidogrel may still have an anti-inflammatory effect.
文摘Background Recently,studies have disclosed soluble CD40 ligand （sCD40L） during atherosclerosis development and plaque destabilization.The objective of the present study was to test the hypothesis that sCD40L levels are higher in acute coronary syndrome （ACS） patients with a greater extent of angiographic coronary involvement.Methods This cross-sectional study examined ACS patients who underwent coronary angiography by measuring their sCD40L levels.In order to estimate the serum levels of sCD40L,10 ml of peripheral venous blood was drawn within 24 hours of admission.sCD40L levels were measured using an enzyme-linked immunosorbent assay （ELISA,RapidBio,West Hills,CA,USA）.Demographic data,presence of concomitant diseases,ACS characteristics,and angiographic findings were evaluated.A review of medical records and patient interviews were conducted to assess coronary risk factors.And the severity of coronary artery disease was evaluated using the Gensini score index.Results Two hundred and eighty-nine patients were included in the study,of whom 186 were male,with an average age of 64.1±10.0 years.Median sCD40L levels were 1.7 ng/ml （0.3-7.3 ng/ml） and Gensini scores were 50 （0-228）.After adjusting for demographic variables and cardiovascular risk factors,the Gensini score was associated with the natural logarithm of the sCD40L level （Coefficient b=0.002,95％ CI 0.000-0.003,P=0.029）.Conclusion sCD40L levels were independently associated with angiographic severity of coronary artery disease in patients with ACS.
