抗血小板治疗对急性心肌梗死合并慢性肾病患者血小板功能的影响

Effects of chronic kidney disease on platelet response to antiplatelet therapy in acute myocardial infarction patients

目的探讨双联抗血小板治疗对急性心肌梗死合并慢性肾病患者血小板聚集功能的影响。方法回顾分析2011年9月至2012年6月，195例植入药物洗脱支架的急性心肌梗死住院患者。其中非慢性肾病组133例，慢性肾病组62例，所有患者在服用氯吡格雷300mg和阿司匹林300mg治疗24h后，测定二磷酸腺苷诱导的血小板聚集率，比较其差异。血小板聚集率〉55％定义为血小板高反应性。结果与非慢性肾病组相比，慢性肾病组糖尿病发生率[24．8％（33／133）比43．5％（27／62），P=0．01]，贫血发生率[5．3％（7／133）比16．1％（10／62），P=0．03）及血小板高反应性比例增高（28．6％（38／133）比45．2％（28／62），P=0．03]。多因素Logistic分析提示慢性肾病，糖尿病是血小板高反应发生的独立预测因素。慢性肾病组血小板聚集率较非慢性肾病组明显高（65．1％±10．2％比45．3％±7．8％，P〈0．01）。慢性肾病组及非慢性肾病组在使用双联血小板治疗前血小板聚集率无差异（79．2％±7．6％比78．4％±8．2％，P=0．51），而抗血小板治疗后，慢性肾病组血小板聚集率较非慢性肾病组明显高（63．2％±8．6％比43．2％±．2％，P〈0．01）。结论慢性肾病是急性心肌梗死患者血小板高反应性的影响因素，但其临床意义还需进一步研究证实。

Objective To elucidate the effects of dual antiplatelet therapy on platelet response in acute myocardial infarction patients with chronic kidney disease. Methods From September 2011 to June 2012, a total of 195 acute myocardial infarction patients with drug eluting stent implanting were enrolled. Among them, 133 cases had normal renal function and 62 cases suffered chronic kidney disease （CKD）. Platelet reactivity was examined after clopidogrel 300 mg and aspirin 300 mg treatment for 24 h. High on treatment platelet reactivity （HPR） was defined as 〉 55% for light transmission aggreometry. Results The CKD patients had a higher incidence of diabetes mellitus （43.5% （27/62） vs 24. 8% （33/133）, P = 0.01 ）, anemia （ 16. 1% （10/62） vs 5.3 % （7/133）, P = 0. 03） and high on treatment platelet reactivity （45.2% （28/62） vs 28. 6% （ 38/133 ）, P = 0. 03 ） than those with normal kidney function. Logistic regression analyses showed that CKD and diabetes mellitus were independent predictors of HPR. Prevalence of HPR was higher in CKD patients than normal kidney function patients（65.1% ± 10. 2% vs 45.3% ± 7.8%, P 〈 0. 01 ）. In subgroup analysis, testing was done before and after antiplatelet treatment. At baseline, no differences existed in platelet aggregation. However, absolute decrease in reactivity after antiplatelet treatment was significantly less in CKD patients than those with normal kidney function（63. 2% ± 8. 6% vs 43.2% ± 5.2%, P 〈 0.01 ）. Conclusion CKD is an important contributor to apparent HPR.