冠心病患者的阿司匹林抵抗现象

目的　前瞻性评价冠心病患者发生阿司匹林抵抗 (AR)的流行病学概况 ,并探讨其预测因子。方法　 2 0 9例病情稳定的冠心病患者 ,每天服用 10 0mg阿司匹林 ,连服 7d ,服用最后 1剂后 2 4h内抽取的空腹静脉血为血样 ,分别用二磷酸腺苷 (ADP)和花生四烯酸 (AA)诱导血小板凝集试验 (PAgT) ,检测血小板聚集率。结果　患者中AR发生率为3 8% ,阿司匹林半敏感 (ASR)者占 2 5 8% ,且AR或ASR患者中的女性较阿司匹林敏感者 (AS)多 (3 5 2 %vs 18 2 % ,P<0 0 1) ,而AS者中吸烟者较AR或ASR者多 (0vs 9 5 % ,P <0 0 1)。结论　阿司匹林用于抗血小板治疗及预防动脉硬化事件的冠心病患者 ,若有AR存在可选择其他安全有效的抗血小板及抗凝制剂长期服用 ,预测AR及抗血栓治疗个体化 ,将是抗血栓治疗未来的方向。     

脑血管病患者发生阿司匹林抵抗的相关实验室研究

目的 探讨脑血管病患者发生阿司匹林抵抗(AR)概况及相关影响因素.方法 67例病情稳定的脑血管病患者,每日服用阿司匹林100mg,连服7天,第8天晨起采取空腹静脉血,分别以二磷酸腺苷(ADP)、花生四烯酸(AA)为诱导剂,检测血小板聚集功能.结果 用光学法测定血小板聚集功能,患者中AR发生率为10.4%(n=7),女性较多(72.3%∶41.5%,P=0.002),吸烟者亦较多(45.4%∶24.0%,P=0.01),与高血压同样存在相关性(37.5%∶24.8%,P=0.001)结论 脑血管患者服用阿司匹林用于抗血小板治疗及预防中,若有AR存在可选用其他安全有效的抗血小板制剂,预测AR及抗血小板治疗个体化,将是抗血小板治疗的发展方向.     

关于缺血性脑卒中的阿司匹林抵抗的临床分析

目的 证实阿司匹林抵抗的存在,观察多个因素和阿司匹林抵抗之间的关系.方法 103例急性缺血性脑卒中患者,入院2天内完成首次静脉血采集,之后除接受同等治疗外,所有患者服阿司匹林100 mg,连服10天,服用最后一剂后24 h内完成第2次采集.检测最大血小板聚集率.结果 阿司匹林抵抗(AR)存在,血小板聚集试验结果AR发生率为8.73％,阿司匹林半敏感(ASR)者为26.21％,阿司匹林敏感(AS)为64％.在AR或ASR患者中血小板聚集与糖尿病、高血压,高同型半胱氨酸血症、高脂血症等因素无关.结论 AR在脑梗死患者中确实存在.若有AR存在,应及时换用其它安全有效的抗血小板制剂长期服用,预测AR及抗血小板治疗个体化,将是未来抗血小板治疗的方向.     

脑梗死患者阿司匹林抵抗的临床分析

目的评价脑梗死患者阿司匹林抵抗（AR）发生的情况，分析其临床有关因素，探讨可能机制。方法255例急性脑梗死患者，每日服用阿司匹林（ASA）100mg，连服10d，服用最后1剂后24h内抽取静脉血为血样，分别用二磷酸腺苷（ADP）、花生四烯酸（AA）诱导做血小板聚集试验（PAgT），检测血小板聚集率（PA）。结果患者中AR发生率为8．24％，阿司匹林半敏感（ASR）者占30．59％，年长者及女性在AR或ASR患者中比在阿司匹林敏感（AS）中居多；而AS者中吸烟者较AR或ASR者多（11．53％vs5．05％）。结论AR在脑梗死患者中确实存在。ASA用于抗血小板治疗及预防动脉硬化事件的脑血管病患者，若有AR存在，应及时换用其他安全有效的抗血小板制剂长期服用，预测AR及抗血小板治疗个体化，将是抗血小板治疗未来的方向。     

脑梗死患者阿司匹林抵抗的临床分析

目的评价脑梗死患者阿司匹林抵抗(AR)发生的情况,分析其临床有关因素,探讨可能机制。方法255例急性脑梗死患者,每日服用阿司匹林(ASA)100mg,连服10d,服用最后1剂后24h内抽取静脉血为血样,分别用二磷酸腺苷(ADP)、花生四烯酸(AA)诱导做血小板聚集试验(PAgT),检测血小板聚集率(PA)。结果患者中AR发生率为8.24%,阿司匹林半敏感(ASR)者占30.59%,年长者及女性在AR或ASR患者中比在阿司匹林敏感(AS)中居多;而AS者中吸烟者较AR或ASR者多(11.53%vs5.05%)。结论AR在脑梗死患者中确实存在。ASA用于抗血小板治疗及预防动脉硬化事件的脑血管病患者,若有AR存在,应及时换用其他安全有效的抗血小板制剂长期服用,预测AR及抗血小板治疗个体化,将是抗血小板治疗未来的方向。     

冠心病患者阿司匹林抵抗现象及防治研究

目的:探讨小剂量阿司匹林对冠心病患者的阿司匹林抵抗(AR)现象及防治措施。方法:经冠脉造影确诊为冠心病患者130例,服用阿司匹林1天100mg,≥1周后,检测血小板聚集率(PAG)。130例随机分阿司匹林和氯吡格雷两组。两组均口服阿司匹林,氯吡格雷组同时加用氯吡格雷,1天75mg,7天后复查PAG。满足花生四烯酸(AA)诱导的PAG≥20%、ADP诱导的PAG≥70%两项者为AR;仅满足其中一项为阿司匹林半抵抗(ASR)。结果:130例患者中AR27例(20.77%),ASR25例(19.23%),AR ASR为40.00%。氯吡格雷组加用氯吡格雷后PAG显著降低,AR、AR ASR患者显著减少(P均<0.01),AR患者显著少于阿司匹林组(P<0.05);阿司匹林组PAG、AR、ASR、AR ASR无显著变化(P均>0.05)。结论:氯吡格雷能加强抗血小板疗效,可用于防治AR。     

糖尿病对小剂量阿司匹林治疗的阿司匹林抵抗的影响及相关因素分析

目的 探讨糖尿病对小剂量阿司匹林治疗的阿司匹林抵抗(AR)的影响及相关因素分析.方法 选择328例病情稳定的心脑血管病患者或有心脑血管病危险因素者,按照是否合并2型糖尿病将其分为合并糖尿病组(101例)和非糖尿病组(227例).两组均给予阿司匹林100 mg/d口服,连服14 d后分别以花生四烯酸(AA)、二磷酸腺苷(ADP)作诱导剂检测两组血小板聚集率.以同时满足AA诱导的血小板聚集率≥20%及ADP诱导的血小板聚集率≥70%者为AR;仅满足一项者为阿司匹林半抵抗(ASR),均不满足者为阿司匹林敏感(AS).分析两组AR、ASR、AS发生情况及影响AR/ASR的危险因素.结果 (1)合并糖尿病组ASR、AR+ASR发生率分别为35.6%和42.6%,非糖尿病组分别为23.8%和27.8%,两组ASR及ASR+AR发生率间差异有统计学意义(P＜0.05).(2)合并糖尿病组和非糖尿病组AR+ASR患者除血糖水平[分别为(7.1±2.6)mmol/L和(4.8±0.6)mmol/L]间差异有统计学意义(P＜0.01)外,其他临床相关指标间差异均无统计学意义(P＞0.05).(3)合并糖尿病组AR+ASR患者女性(60.5%)、吸烟者比例(11.6%)及TG水平[(1.7±0.7)mmol/L]与合并糖尿病组AS患者[分别为41.4%、29.3%和(2.2±1.7)mmol/L]比较,差异均有统计学意义(P＜0.05).(4)女性是合并糖尿病患者发生AR/ASR的独立危险因素[β=-1.185,χ2=7.738,P=0.005,OR=0.306,95%CI为(0.133,0.705)].结论 服用小剂量阿司匹林的心脑血管疾病合并糖尿病患者ASR及AR+ASR发生率高于心脑血管疾病非糖尿病患者.性别可能是糖尿病患者发生AR/ASR的相关危险因素之一.     

脑梗死患者中阿司匹林抵抗的临床研究

目的评价脑梗死患者阿司匹林抵抗（AR）发生的情况,分析其临床有关因素,探讨可能机制。方法 124例急性脑梗死患者,每日服用阿司匹林100mg,连服10d,服用最后1d后,24h内抽取空腹静脉血,分别用二磷酸腺苷（ADP）、花生四烯酸（AA）诱导做血小板聚集试验（PAgT）,检测最大血小板聚集率（MAR）。结果患者中AR发生率8.87%,阿司匹林半敏感（ASR）者占29.03%,年长者AR或ASR患者中女性敏感者居多;如有吸烟者较AR或ASR者居多（11.53%vs5.05%）。结论 AR在脑梗死患者中确实存在。ASA用于抗血小板治疗及预防动脉硬化事件的脑血管病患者,若有AR存在,应及时换用其他安全有效的抗血小板制剂,因阿司匹林需要长期应用,今后预测AR及抗血小板治疗个体化,将是未来抗血小板治疗的研究方向。     

动脉粥样硬化高危人群中阿司匹林抵抗调查分析

目的 调查社区动脉粥样硬化高危人群中阿司匹林抵抗(AR)或半抵抗(ASR)的发生率及其流行病学特征,并探讨其与危险因素的相关性.方法 筛选200例动脉粥样硬化高危患者服用阿司匹林(100 mg/d)至少7天以上,用二磷酸腺苷(ADP)和花生四烯酸(AA)作诱导剂测定其前后血小板聚集功能变化及血清血栓烷B2(TXB2)水平测定.结果 200例动脉粥样硬化高危人群中AR发生率为4.5%,ASR者占20.7%.血清TXB2,AA、ADP诱导的血小板聚集率与健康对照组相比有显著统计学差异(P＜0.01);血清TXB2与血小板聚集率有较好的相关性(r=0.871).结论 社区动脉粥样硬化高危人群服用阿司匹林后部分产生AR或ASR;AR或ASR人群发生冠心病事件的风险高于阿司匹林敏感(AS)人群;检测AA、ADP诱导的血小板聚集率,血清TXB2可作为动脉粥样硬化高危人群发生AR或ASR的评价指标.     

心脑血管病患者中阿司匹林抵抗与血脂水平相关性研究

目的 探讨心脑血管病患者中阿司匹林抵抗(AR)与血脂水平的相关性.方法 100倒病情稳定的心脑血管病志者,每天口服阿司匹林100mg,连服7d,服用最后一剂后24h内取空腹静脉血,分别用二磷酸腺苷(ADP)、花生四烯酸(AA)诱导血小板凝集试验(PAgT),检测血小板聚集率;在服用阿司匹林前采空腹静脉血检潮血脂.结果 100例患者中阿司匹林抵抗(AR)发生率为3%,阿司匹林半抵抗(ASR)发生率为13%:AR发生率与血脂水平无统计学意义.结论 在服用阿司匹林的心脑血管病患者中存在阿司匹林抵抗现象,其发生率与血脂水平无关.     

血栓弹力图在心脑血管病病人抗血小板治疗中的应用价值

目的:分析服用抗血小板药物心脑血管病病人血栓弹力图（TEG）结果,为临床治疗提供参考。方法:收集因心脑血管疾病住院病人249例,根据其服用抗血小板药物情况分为阿司匹林组（AA组,n=141）、氯吡格雷组（ADP组,n=20）、阿司匹林+氯吡格雷联合组（双联组,n=88）,用血栓弹力图仪检测病人血小板抑制率,分析3组抗血小板治疗的疗效差异。结果:双联组的AA途径和ADP受体途径血小板抑制率分别为（88.47±19.69）%和（68.08±28.12）%,均高于AA组的（77.71±29.7）%和ADP组的（52.57±26.97）%（P<0.01和P<0.05）。双联组的阿司匹林抵抗和氯吡格雷抵抗发生率分别为6.82%和11.36%,均低于AA组的21.99%和ADP组的30%（P<0.01和P>0.05）。结论:采用TEG仪检测心脑血管病病人的血小板聚集抑制率有利于指导临床制定个体化的抗血小板治疗方案。阿司匹林对心脑血管病人血小板聚集的抑制作用强于氯吡格雷。接受标准剂量抗血小板治疗的心脑血管病病人存在抗血小板抵抗;阿司匹林与氯吡格雷联用抗血小板有协同作用。     

Earlier application of loading doses of aspirin and clopidogrel decreases rate of recurrent cardiovascular ischemic events for patients undergoing percutaneous coronary intervention

Background  Aspirin and clopidogrel resistance plays a significant role in the development of cardiovascular ischemic events for ninety patients undergoing percutaneous coronary intervention. Recent studies have indicated that increasing the dose of antiplatelet drugs maybe a potent method to improve the inhibition of platelet aggregation.

Methods  Thrombelastograph (TEG) determinations were used to evaluate the effect of antiplatelet therapy. According to the results, 90 patients were divided into three groups and given different doses of aspirin and clopidogrel. Thirty patients with both an inhibition rate of aspirin >50% and an inhibition rate of clopidogrel >50% were defined as the control group. Sixty patients with an inhibition rate for aspirin <50% and an inhibition rate for clopidogrel <50% were defined as the resistance group. Patients in resistance group were randomly assigned to be given a routine dose (100 mg aspirin plus 75 mg clopidogrel per day, which we called a resistance plus routine dose group, R+R) and a loading dose (200 mg aspirin and 150 mg clopidogrel per day, which we called resistance plus loading dose group, R+L) of antiplatelet therapy. A 12-month follow-up was observed to examine the change of inhibition rate of antiplatelet therapy and to estimate the relationship between inhibition rate and the occurrence of cardiovascular ischemic events.

Results  After 6 months of antiplatelet therapy, the inhibition rate of aspirin in the R+L group increased from (31.4±3.7)% to (68.6±7.1)%, which was significantly higher than that in R+R group, (51.9±8.2)% (P <0.01). The inhibition rate of clopidogrel in the R+L group increased from (22.1±3.8)% to (60.2±7.4)%, which was significantly higher than in the R+R group, (45.9±4.3)% (P <0.01). The occurrence rates of cardiovascular ischemic events, stent thrombosis, recurrent unstable angina and myocardial infarction in the R+R group were 20%, 36% and 17%, respectively. Occurrence was significantly increased compared with that in the control group, 3%, 10% and 1%, respectively (P <0.01). In contrast, the occurrence rates in the R+L group (10%, 23% and 6%, respectively) were attenuated compared with those in the R+R group (P <0.01), although still higher than in the control group (P <0.01).

Conclusions  Almost all of the cardiovascular ischemic events occurred in the first six months after percutaneous coronary intervention. According to the result of TEG determinations, earlier application of a loading dose of aspirin and clopidogrel can decrease the rate of recurrent cardiovascular ischemic events.

     

西洛他唑联合氯吡格雷对冠状动脉药物涂层支架术后支架内再狭窄的影响

目的 探讨西洛他唑联合氯吡格雷抗血小板治疗对行冠状动脉(冠脉)药物涂层支架术患者支架内再狭窄(in-stent restenosis, ISR)的影响。方法 回顾性分析231例行冠脉药物涂层支架术且术后1年复查冠脉造影的冠心病患者的临床资料。根据不同的抗血小板治疗方案分为两组,其中214例术后1年内服用阿司匹林联合氯吡格雷(阿司匹林组),17例术后服用西洛他唑联合氯吡格雷(西洛他唑组),比较两组术后1年ISR的发生率及再次血运重建率。结果 两组患者的基线资料分析结果显示,西洛他唑组男性患者比例(88.2% vs 76.6%, P<0.001)及有消化道出血病史比例(35.3% vs 0.9%, P<0.001)明显高于阿司匹林组,其他临床资料差异无统计学意义(P>0.05)。支架术后1年,冠脉造影结果显示: 西洛他唑组与阿司匹林组ISR的发生率差异无统计学意义(29.4% vs 12.1%, P=0.06);西洛他唑组靶血管再次血运重建术与阿司匹林组无统计学差异(5.9% vs 6.1%, P=0.974);两组其他冠脉病变进展需行冠脉介入治疗(percutaneous coronary intervention, PCI)的患者比例亦无明显差异(17.6% vs 15.4%, P=0.734)。结论 对于行冠脉药物涂层支架术的患者,使用西洛他唑联合氯吡格雷抗血小板治疗与传统双联抗血小板治疗,预防ISR效果相当。对于消化道出血高风险或阿司匹林不耐受的人群,可考虑使用西洛他唑替代阿司匹林进行双联抗血小板治疗。     

阿司匹林和氯吡格雷双联抗血小板治疗心脏介入术后患者在社区随访的意义

目的研究阿司匹林和氯吡格雷双联抗血小板治疗在社区卫生服务中心就诊患者中的依从性、并发症及其在社区卫生服务中心应用的意义。方法选取2012年3月至2013年3月在上海市虹口区欧阳路街道社区卫生服务中心(社区中心)门诊就诊的服用阿司匹林和氯吡格雷双联抗血小板治疗的患者120例,社区中心给予口服拜阿司匹林每日1片(100 mg/片),同时加服氯吡格雷每日1片(75 mg/片),进行随访分析。结果 120例随访患者中男83例、女37例,年龄44⁹0(69.3±6.4)岁,在随访的人群中出血率和再入院率仅为3.33%,出血主要为消化道出血(3例)和脑出血(1例),120例随访患者社区中心随访1年用药费用显著低于本市三级医院一年用药费用[(1845.55±1064.89)元vs(3029.27±826.94)元],差异有统计学意义(t=8.749,P<0.001)。结论经过三级医院对心血管疾病患者的治疗后,转至社区中心继续进行阿司匹林联合氯吡格雷双联抗血小板治疗,依从性好、费用经济、并发症低,值得推广。     

外周动脉支架成形术后抗血小板药物预防再狭窄的临床观察

目的 研究抗血小板药物在外周动脉支架成形术后预防再狭窄的疗效.方法 将2003年1月至2006年7月在复旦大学附属华山医院血管外科行外周动脉支架植入术后且符合入组条件的动脉硬化闭塞症病人103例分为治疗组(56例)及对照组(47例).治疗组每日口服氯吡格雷(75 mg/d)+拜阿司匹林(100 mg/d);对照组术后每日皮下注射低分子肝素1周,并从术后第3天起口服华法令.主要终点事件为支架内闭塞、再狭窄以及临床出血率,次要终点事件为心血管事件、死亡以及药物不良反应等.结果 两组病人基线特征比较差异无统计学意义(P＞0.05).治疗组和对照组急性支架内血栓形成的发生率分别为1例(1.8%)和0例(0%),18个月的再闭塞率分别是3例(5.4%)和5例(10.6%),支架内再狭窄率分别是8例(14.3%)和12例(25.5%,P＞0.05).治疗组在出血并发症方面显著低于对照组(1.8%vs 19.1%,P＜0.01).两组的心血管事件发生率和病死率无统计学意义.结论 氯吡格雷联合阿司匹林可以预防外周动脉支架成形术后的再狭窄.     

缺血性脑卒中患者阿司匹林抵抗现象及处理策略

阿司匹林作为缺血性脑血管病的一级和二级预防用药，广受关注。然而长期服用阿司匹林的患者仍会发生动脉血栓形成事件，因此本文就阿司匹林抵抗的概念、发生机制、检测方法、预防措施及其在缺血性脑血管病中的临床意义加以综述。     

A prospective randomized antiplatelet trial of cilostazol versus clopidogrel in patients with bare metal stent

Background Cilostazol is a newly developed antiplatelet drug that has been widely applied for clinical use. Its antiplatelet action appears to be mainly related to inhibition of intracellular phosphodiesterase activity. Recently, cilostazol has been used for antiplatelet therapy after coronary bare metal stent implantation for thrombosis and restenosis prevention. This prospective randomized and double blind trial was designed to investigate the safety and efficacy of cilostazol for the prevention of late restenosis and acute or subacute stent thrombosis. Methods One hundred and twenty patients who underwent elective stent were randomly assigned to treatment group with cilostazol 200 mg/d (n = 60), clopidogrel 75 mg/d and aspirin 100 mg/d or to control group with clopidogrel treatment 75 mg/d (n = 60) and aspirin 100 mg/d. Follow-up coronary angiography was performed 6－9 months later.Results Nine months major adverse cardio-cerebral event (MACCE) were lower in treatment groups (P&lt;0.05). The quantitative coronary angiography (QCA) at 6 months follow-up showed that minimum lumen diameter (MLD) was higher in treatment group than that of control group [(2.14±0.52)mm vs (1.82±0.36)mm, P&lt;0.05]. Late lumen loss (LL) [(0.82±0.42)mm vs (1.31±0.58)mm; P&lt;0.01], restenosis rate (RR) (14% vs 32%; P&lt;0.05) and target lesion revascularizaion (TLR) rate (5% vs 17%; P&lt;0.05) were lower in treatment group than in control group.Conclusion Cilostazol therapy is an effective regimen for prevention not only stent thrombosis but also RR and TLR through reducing MLD without the risk of increasing bleeding.     

Antiplatelet effect of aspirin in patients with coronary artery disease

Cardiovascular disease is the number one cause of death globally, and atherothrombosis is the underlying cause of most cardiovascular events. Several studies have shown that antiplatelet therapy, including aspirin (acetylsalicylic acid), reduces the risk of cardiovascular events and death. However, it is well-known that many patients experience cardiovascular events despite treatment with aspirin, often termed "aspirin low-responsiveness". This fact has caused considerable debate: does biochemical aspirin low-responsiveness have prognostic value? Can low-responders be reliably identified? And if so, should antithrombotic treatment be changed? Is the whole discussion of antiplatelet drug response merely a result of low compliance? Compliance should be carefully optimised, before evaluating the pharmacological effect of a drug. It is well-known that cardiovascular disease is multifactorial, and, therefore, total risk reduction is not feasible. Aetiological factors to the variable platelet inhibition by aspirin seem to include genetic factors, pharmacological interactions, smoking, diabetes mellitus, and increased platelet turnover. It is a captivating thought that antiplatelet therapy may be improved by individually tailored therapy based on platelet function testing. Ongoing studies are challenging the current one-size-fits-all dosing strategy, but the preceding evaluation of platelet function assays has not been adequate. The overall objective of this thesis was to evaluate the reproducibility of and aggreement between a number of widely used platelet function tests and to explore the importance of platelet turnover for the antiplatelet effect of aspirin in patients with coronary artery disease. In the intervention studies (studies 1, 3, and 4), optimal compliance was confirmed by measurements of serum thromboxane, which is the most sensitive assay to confirm compliance with aspirin. In study 1, platelet function tests widely used to measure the antiplatelet effect of aspirin were evaluated in healthy individuals and patients with coronary artery disease. Pharmaco-specific metabolites were measured in urine and serum to investigate the pharmacodynamic effect of aspirin and to enable the comparison with the more global tests of platelet function. Based on repeated duplicate measurements, we evaluated the reproducibility of each test. We found that reproducibility of the classical reference method was not impressive and that the newer, so-called point-of-care tests differed markedly on reproducibility. With coefficients of variation of about 3%, the VerifyNow Aspirin test was clearly the most reproducible test - even after correction of the official scale, which begins at about 350 aspirin reaction units and, therefore, results in artificially low coefficients of variation. Among the platelet function tests investigated, Multiplate was most sensitive for aspirin treatment. In study 2 we performed the hitherto largest study of newly released, immature platelets as a marker of platelet turnover. The study population included healthy individuals, patients with stable coronary artery disease, and patients with acute coronary syndromes. The main finding was an increased fraction of immature platelets in patients with ST-segment myocardial infarction, indicating an increased platelet turnover. Smoking and type 2 diabetes were identified as independent determinants of platelet turnover. In study 3 we explored the relationship between platelet turnover and the antiplatelet effect of aspirin in patients with stable coronary artery disease. The study results support the hypothesis that an increased platelet turnover reduces the antiplatelet effect of aspirin. The main findings were: 1) platelet turnover correlated with platelet aggregation measured by Multiplate and with sP-selectin, a marker of platelet activation. 2) Patients with diabetes mellitus type 2 had reduced antiplatelet effect of aspirin compared with patients without diabetes. 3) Widely used platelet function tests differ with respect to dependence on platelet parameters, including platelet count. 4) Smoking, diabetes mellitus type 2, and thrombopoietin were identified as independent determinants of platelet turnover. 5) The relative fraction of immature platelets has been employed in most previous studies, but in stable patients the absolute immature platelet count does not seem dependent on the total platelet count, and it has a stronger correlation with both platelet activation measured by sP-selectin and with platelet aggregation during treatment with aspirin. In study 4 we investigated platelet turnover and the antiplatelet effect of aspirin in a nested case-control study on patients with previous definite stent thrombosis. Patients with stent thrombosis were compared with patients without stent thrombosis, with whom they were matched at a 1:2 ratio with respect to risk factors for stent thrombosis: age, sex, stent type, and indication for percutaneous coronary intervention. The study showed that patients with previous stent thrombosis have reduced antiplatelet effect of aspirin and a tendency towards increased platelet turnover. In conclusion, widely used platelet function tests markedly differ on reproducibility, and the agreement between tests is relatively poor. An increased platelet turnover as suggested by the presence of newly formed immature platelets is important for the antiplatelet effect of aspirin, and, perhaps also for the development of acute coronary thrombosis. In the future, individually tailored antiplatelet therapy may potentially improve the benefit-risk ratio of antiplatelet therapy.     

阿司匹林抵抗的研究现状

抗血小板治疗是心血管疾病治疗的基石之一,对冠状动脉疾病患者的治疗有重要影响,对减少不良心血管事件的发生,有积极的作用。近来阿司匹林抵抗受到了越来越多的关注,它被用来描述冠状动脉疾病患者在用阿司匹林抗血小板治疗后仍发生不良心血管事件。明确抵抗的原因和机制将使冠状动脉疾病患者受益匪浅。本文旨在对这一方面予以简要综述。