Effects of metoprolol therapy on cardiac troponin-I levels after elective percutaneous coronary interventions.

AIMS: Beta-blockers (BBs) have been shown to improve survival and reduce the risk of re-infarction in patients following myocardial infarction. There are conflicting data about the effects of BB therapy on cardiac biomarkers after percutaneous coronary interventions (PCIs). The aim of the study was to investigate the effects of BB use on cardiac troponin-I (cTnI) levels in patients who had undergone elective PCI. METHODS AND RESULTS: In this prospective study, 287 patients with coronary artery disease were included. Patients were randomized either to BB or control groups prior to the intervention. Blood samples for cTnI were obtained before and at 6, 24, and 36 h after the procedure. Of the 287 patients included, 143 received metoprolol succinate 100 mg/day, and 144 received no BB and served as the control group. Baseline clinical characteristics of both groups, except for history of coronary artery bypass graft surgery, were similar. We observed no significant difference in the elevation of cTnI levels between the two groups after PCI (BB group, 17 patients, 11.9%; control group, 10 patients, 6.9%; P=0.2). CONCLUSION: Metoprolol succinate therapy seems to have no cardioprotective effect in limiting troponin-I rise after PCI.     

Effect of high dose statin therapy on platelet function; statins reduce aspirin resistant platelet aggregation in patients with coronary heart disease

Background Current evidence supports the preventive role of statins on platelet aggregation in patients with coronary heart disease. Aim Our aim was to determine the effects of aggressive statin therapy on platelet function in patients with coronary heart disease. Material and methods A total of 178 consecutive patients (37–68 years old, 35.9% women) with stable coronary artery disease (CAD) was enrolled in the study. Platelet function assays were realized by the Platelet Function Analyzer (PFA)-100 with collagen and epinephrine (Col/Epi) and collagen and ADP (Col/ADP) cartridges. Aspirin resistance was defined as having a closure time (CT) of <186 s with Col/Epi cartridges despite regular aspirin therapy. A statin therapy protocol applied to the patients with aspirin resistance for 3 months. Results We determined that 20 (11.2%) of patients had aspirin resistance by the PFA-100. Mean closure time measured with the Col/ADP cartridges was 83 ± 18 s (53–162 s). Of the patients 12 were not on a statin therapy and eight were taking 10 mg daily atorvastatin. After 3 months of 40 mg daily atorvastatin therapy 13 subjects with aspirin resistance became aspirin sensitive by PFA-100 (P < 0.0001). There was also a significant decrease in total and LDL cholesterol levels and an increase in HDL cholesterol at the third month of statin therapy (P < 0.0001 for all). Conclusion Statin therapy reduced the in vitro aspirin resistance in 65% of the patients after a therapy of 3 months. Further studies are needed to elucidate the mechanism of statins’ effects on platelet reactivity.     

Limited early antiplatelet effect of 300 mg clopidogrel in patients with aspirin therapy undergoing percutaneous coronary interventions

Aim Our aim was to evaluate the early efficacy and variabilityof the platelet inhibition exerted by 300 mg clopidogrel forthe purpose of acute percutaneous coronary interventions usingplatelet function tests. Methods and results Elective percutaneous coronary interventionwas used as a timely model in which clopidogrel was added toongoing acetylsalicylic acid (aspirin) (100 mg/day) at 2.5 hprior to procedure. Blood samples were collected before administrationof clopidogrel and immediately before the intervention from50 patients. Platelet functions were assessed with traditionalaggregation and PFA-100^®. At baseline, 14 (28%) patients were poor responders to aspirinaccording to PFA and 9 (18%) continued to show arachidonic acid-inducedaggregation. After clopidogrel ADP-triggered aggregation wasonly modestly inhibited in 40% of the patients. Eight percentof the study population was left without any measurable antiplateleteffect. The patients with modest response to clopidogrel hadhigher levels of c-peptide (1.5 nmol/L) than the ones respondingwell (0.9 nmol/L, ). Conclusion Neither ongoing aspirin treatment nor added clopidogreldid reach an expected extent of platelet inhibition. This studyshows that aspirin-treated patients undergoing PCI gain highlyvariable levels of platelet inhibition with short-term clopidogrel300 mg. At 2 h after adding clopidogrel it failed to enhance platelet inhibition in 40% of the patients.In future, targeted platelet function tests may be helpful toindividually select an effective antiplatelet medication forthese patients. This study suggests that for acute PTCA clopidogreldoes not reach the optimal antithrombotic efficacy in all patients.     

冠心病患者阿司匹林抵抗及其影响因素

目的探讨冠心病患者阿司匹林抵抗（Aspirin resistance,AR）现象及其影响因素。方法入选1 731例入院诊断为冠心病（急性冠状动脉综合征和稳定型心绞痛）的患者。采用血小板聚集仪分别测定花生四烯酸（AA）、腺苷二磷酸（二磷酸腺苷,ADP）诱导的血小板聚集率。AR定义为0.5 mmol/L花生四烯酸时血小板平均聚集率≥20%,用10μmol/L ADP时血小板平均聚集率≥70%。阿司匹林半抵抗（Aspirin semiresistance,ASR）即符合上述两个条件之一者。均不符合者为阿司匹林敏感（Aspirin sensitive,AS）。用统计学方法分析各组间各项临床特征差异及影响AR与ASR的危险因素。结果1 731例患者中AR的发生率3.58%（62/1 731）,ASR的发生率20.34%（352/1 731）。与AS相比,AR＋ASR中以女性、高龄、高脂血症患者较多,吸烟者较少。而且AS患者的血小板计数偏高,总胆固醇水平偏低。Logistic回归分析表明,女性[相对比值比（OR）=1.377,95%可信区间（CI）1.084～1.751,P=0.009〗、老年（OR=1.504,95%CI1.005～2.253,P=0.047）、总胆固醇（TCHO）（OR=1.249,95%CI1.114～1.401,P=0.000）升高是发生AR与ASR的危险因素。结论服用阿司匹林的冠心病患者中AR发生率为3.58%,ASR发生率为20.34%。发生AR与ASR危险因素有女性、高龄、高血脂。     

冠状动脉介入治疗后心肌钙蛋白T的动态变化及原因分析

目的：了解成功行经皮冠状动脉介入治疗（PCI）病人的心肌肌钙蛋白T（cTnT）水平的动态改变及临床意义。方法：选择成功行PCI术的68例患者，在术前、术后6h、24h分别检测肌酸激酶（CK）、肌酸激酶同功酶（CK-MB）及cTnT水平，并分析相关因素。结果：PCI术后CK—MB升高7例（10．3％）。cTnT术后升高32例（47．1％），C型病变：在cTnT升高组中17例（53．1％），与cTnT正常组10例（27．8％）比较有显著差异（P=0．0330）。三支血管病变：cTnT升高组中13例（40．6％），与cTnT正常组5例（13．9％）比较有显著差异（P=0．0126）。cTnT升高的原因和扩张压力总和、扩张次数及扩张时间有关（P=0．0072，P=0．0002，P=0．0213），支架长度和支架直径也和cTnT水平有关（P=0．0156，P=0．0012）。结论：PCI术后可引起CK-MB、cTnT水平轻度升高，在检测心肌损伤方面cTnT较CK、CK—MB更敏感。病变的复杂程度及手术操作的强度与cTnT水平升高有关。     

Residual platelet reactivity after aspirin and clopidogrel treatment predicts 2-year major cardiovascular events in patients undergoing percutaneous coronary intervention

Background

Studies on the prognostic significance of residual platelet reactivity despite the use of dual anti-platelet agents are limited and seldom extend beyond 1 year.

Methods

This study enrolled 144 patients treated with standard-dose aspirin and clopidogrel and undergoing percutaneous coronary intervention (PCI). Platelet reactivity was measured by the Platelet Function Analyzer-100 (PFA-100) just before PCI and presented as collagen/epinephrine closure time (CEPI-CT) and collagen/adenosine diphosphate closure time (CADP-CT). Primary endpoint included cardiovascular death, myocardial infarction, and stroke. Secondary endpoint was the primary endpoint plus hospitalization due to unstable angina or urgent target vessel revascularization.

Results

During the 24-month follow-up, 14 patients (9.7%) developed the primary endpoint events and 33 had the secondary endpoints. After controlling possible confounding factors, both CEPI-CT < 193 s and CADP-CT < 95 s were independently predictive of the primary endpoint (hazard ratio = 3.5; 95% confidence interval: 1.04–11.7; p = 0.044 and 5.3; 1.4–20.1; p = 0.015, respectively). Only CADP-CT < 95 s remained significantly predictive of secondary endpoints in the follow-up periods of 0–9 and 9–24 months, during which clopidogrel was mostly discontinued.

Conclusion

This study demonstrates that increased residual platelet reactivity measured by PFA-100 CADP-CT consistently predicts the occurrence of cardiovascular events following PCI throughout the 24-month follow-up period, irrespective of the changes in anti-platelet use.     

Reduced albumin-cobalt binding with transient myocardial ischemia after elective percutaneous transluminal coronary angioplasty: a preliminary comparison to creatine kinase-MB, myoglobin, and troponin I

BACKGROUND: Previous reports suggest that ischemic conditions rapidly reduce the capacity of human albumin to bind exogenous cobalt. A new assay based on human albumin-cobalt binding (ACB) may help detect early myocardial ischemia. We investigated altered ACB during the first 24 hours after transient ischemia induced during elective percutaneous transluminal coronary angioplasty (PTCA). We then compared ACB assay results with creatine kinase isoenzyme (CK-MB), myoglobin, and cardiac troponin I (cTn-I) values after PTCA. METHODS AND RESULTS: In 41 patients undergoing elective PTCA, plasma samples were tested for the ACB assay, CK-MB, myoglobin, and cTn-I before, immediately after, and 6 and 24 hours after PTCA. Thirteen additional patients served as a control group with albumin-cobalt assays performed before and after diagnostic coronary catheterization without angioplasty. ACB assay results demonstrated a significant mean percent difference (10.1%) immediately after PTCA compared with baseline (P < .000001) and returned to baseline by 6 hours after PTCA. ACB assay differences immediately after PTCA were significantly greater than in the control group (10.1% vs -0.9%, P < .001). Mean CK-MB, myoglobin, and cTn-I values were not elevated above baseline immediately after PTCA but were significantly elevated above baseline 6 and 24 hours after PTCA. CONCLUSIONS: These preliminary results suggest that human albumin undergoes a significant reduction in its capacity to bind exogenous cobalt soon after transient coronary occlusion during human PTCA and before significant elevations of CK-MB, myoglobin, or cTn-I. Further confirmatory investigations are warranted to determine if the ACB assay is a useful diagnostic test for early myocardial ischemia.     

冠状动脉病变介入治疗后血浆B型利钠肽和肌钙蛋白I的变化

目的观察不同类型冠状动脉病变介入治疗前后血液B型利钠肽(BNP)及心肌肌钙蛋白I(cTnI)的变化。方法选取接受冠状动脉介入治疗的患者52例,根据冠状动脉病变血管累及范围分为单支病变组、双支病变组,分别测定两组患者术前、术后6、24、48h BNP,cTnI水平,并记录术中球囊扩张时间、扩张次数、造影剂用量。结果单支病变组球囊扩张时间、扩张次数及造影剂用量均小于双支病变组(P<0.05);两组术后6h BNP水平均高于术前(P<0.05),术后24h达峰值;两组术后24h cTnI水平显著升高(P<0.05),但单支病变组BNP、cTnI峰值水平低于双支病变组(P<0.05)。结论多支病变或复杂病变患者介入治疗后BNP、cTnI水平升高明显,提示应进行术前危险评估,术后应给予适当药物辅助治疗改善预后。     

阿司匹林和氯吡格雷不同服药时间对急性冠状动脉综合征患者血小板聚集率昼夜节律变化的影响

目的 观察急性冠状动脉综合征患者日间、夜间不同时间服用阿司匹林和氯吡格雷对血小板聚集率昼夜变化的影响,确立冠心病患者更有效的服用抗血小板药物时间,提高临床治疗效果.方法 采用交叉试验设计,30例急性冠状动脉综合征患者分别设立为日间服药组(日间组)及夜间服药组(夜间组),于药物达稳态浓度后,用全血阻抗法以ADP及花生四烯酸为诱导剂检测24 h内5个时间点血小板聚集率.之后,两组交换,药物达稳态浓度后以相同方法再次测定24 h内5个时间点血小板聚集率.结果 花生四烯酸诱导的血小板聚集率,日间组10:00时最高[(7.96±3.64)欧姆],00:00时最低[(6.12±3.29)欧姆],两者比较差异无统计学意义(P＞0.05);夜间组20:00时最高[(7.86±4.28)欧姆],10:00时最低[(5.46±3.93)欧姆],两者比较差异有统计学意义(P＜0.05).ADP诱导的血小板聚集率,日间组10:00时最高[(9.93±5.73)欧姆],16:00时最低[(9.14±5.13)欧姆],两者比较差异无统计学意义(P＞0.05);夜间组20:00时最高[(9.40±5.39)欧姆],10:00时最低[(7.37±4.12)欧姆],差异无统计学意义(P＞0.05).同一时间点两组之间比较,2种诱导剂测定的血小板聚集率在10:00时日间组均明显高于夜间组(P＜0.05),其余4个时间点之间两组比较差异均无统计学意义.结论 日间服药与夜间服药血小板聚集率呈现不同的昼夜变化规律,夜间服用阿司匹林及氯吡格雷可抑制晨起血小板聚集高峰,夜间服药优于日间服药.     

Response to antiplatelet therapy and platelet reactivity to thrombin receptor activating peptide-6 in cardiovascular interventions: Differences between peripheral and coronary angioplasty

Background

The long-term prognosis of patients with peripheral arterial disease (PAD) is significantly worse than the prognosis of coronary artery disease (CAD) patients. Detrimental platelet activation could contribute to the increased rate of adverse cardiovascular events in PAD. We therefore investigated whether response to antiplatelet therapy and thrombin inducible platelet activation differ between patients with best medical therapy undergoing angioplasty and stenting for symptomatic PAD (n = 166) or CAD (n = 104).

Methods

Adenosine diphosphate (ADP), arachidonic acid (AA) and thrombin receptor activating peptide (TRAP)-6 inducible platelet reactivity was measured by multiple electrode aggregometry (MEA). Platelet surface expression of P-selectin and activated glycoprotein IIb/IIIa (GPIIb/IIIa) in response to ADP, AA, and TRAP-6, and the formation of monocyte-platelet aggregates (MPA) in response to ADP and TRAP-6 were assessed by flow cytometry.

Results

Patients with PAD had significantly higher platelet reactivity in response to ADP and AA by MEA compared to CAD patients. Likewise, the expression of P-selectin and GPIIb/IIIa following stimulation with ADP and AA, and MPA formation in response to ADP were significantly higher in PAD patients than in CAD patients. In response to TRAP-6, patients with PAD showed a significantly increased platelet aggregation by MEA, higher expression of activated GPIIb/IIIa, and more pronounced formation of MPA than CAD patients.

Conclusion

Following angioplasty and stenting, PAD patients exhibit a significantly diminished response to dual antiplatelet therapy and an increased susceptibility to TRAP-6 inducible platelet activation compared to CAD patients.     

Influence of platelet reactivity and inflammation on peri-procedural myonecrosis in East Asian patients undergoing elective percutaneous coronary intervention

Background and objectives

The contribution of multiple risk factors to peri-procedural myocardial infarction (PMI) in East Asians remains controversial. To assess the influence of clinical or laboratory covariates on PMI in these patients.

Methods

Stable patients (n = 341) undergoing elective percutaneous coronary intervention (PCI) were enrolled. Platelet reactivity was measured by conventional aggregometry and VerifyNow. Inflammation markers and lipid profile were determined by standard methods. PMI was defined according to Universal definition (troponin I or CK-MB ≥ 3 times the 99th percentile of the upper reference limit).

Results

PMI (defined by troponin I and CK-MB) occurred in 47 (13.8%) and 30 (8.8%) patients, respectively. There was no significant difference in ADP-induced platelet reactivity between patients with vs. without PMI. Patients with PMI (troponin I) had higher levels of 6 μg/mL collagen-induced platelet aggregation (PA) and VerifyNow ‘BASE’ compared with those without PMI. The combination of ‘6 μg/mL collagen-induced PA > 40%’ + ‘BASE > 318’ (odds ratio, 14.08; 95% confidence intervals, 1.68 to 111.11; p = 0.015) or ‘WBC > 6550/mm³’ + ‘C-reactive protein > 2.3 mg/L’ (odds ratio, 7.75; 95% confidence intervals, 2.49 to 24.39; p < 0.001) was associated with an increased risk of PMI (troponin I). The greatest likelihood ratio was observed when cholesterol, inflammation marker and platelet function were combined together.

Conclusion

This is the first study to demonstrate that heightened platelet responsiveness to collagen and thrombin may be a risk factor for myonecrosis in patients undergoing elective PCI. The utility of the combining measures of platelet function, inflammation and cholesterol to enhance risk stratification and thus facilitate personalized therapy deserves further study.     

强化抗血小板治疗对冠状动脉支架术后血小板高反应性的影响

目的 探讨强化抗血小板治疗对急性冠状动脉综合征患者冠状动脉支架术后血小板高反应性(HPR)的影响.方法 2009年3月至2011年2月在3家医院连续入选3316例置入药物洗脱支架的急性冠状动脉综合征患者,其中840例(25.3％)患者诊断为HPR.HPR定义为氯吡格雷300 mg和阿司匹林300 mg治疗24h后,20 μmol/L二磷酸腺苷诱导的血小板聚集率＞55％.HPR患者按1:2的比例随机接受标准抗血小板治疗(标准组,n=280)及强化抗血小板治疗(强化组,n=560).标准组患者服用阿司匹林300 mg/d和氯吡格雷75 mg/d.强化组患者服用阿司匹林300 mg/d和双倍剂量氯吡格雷(150 mg/d),3d后如 HPR 未改善则加用西洛他唑(50～100 mg,每天2次).观察患者的HPR改善率及发生的临床事件.结果 强化组患者治疗3d后HRP改善率为54.3％(304/560);256例HRP未改善的患者接受西洛他唑治疗3d后,强化组的HRP改善率为81.1％(454/560).术后30 d,强化组HPR改善率显著高于标准组(69.9％比55.7％,P=0.000).两组患者均未发生死亡及卒中事件.强化组发生亚急性支架血栓形成1例(0.2％),标准组未发生支架血栓形成事件(P =1.000).两组均未发生死亡和主要及次要出血事件,轻度出血发生率两组之间差异无统计学意义(强化组为4.3％,标准组为2.1％,P=0.166).结论强化抗血小板治疗可显著改善急性冠状动脉综合征患者冠状动脉支架术后的HPR,且不增加出血风险,但其临床获益还需更长时间随访研究的证实.     

老年患者在冠脉支架术后长期联合运用阿司匹林和氯吡格雷的安全性及有效性的临床观察

目的观察老年患者在冠脉支架植入术后联合运用阿司匹林和氯吡格雷的疗效及安全性。方法将行冠脉支架植入术的105例非ST段抬高的ACS患者按年龄分为两组：年龄≥70岁为古稀组（45例）,年龄〈70岁为非古稀对照组（60例）,两组均在冠脉支架植入术后联合运用阿司匹林和氯吡格雷（9～12个月,平均9个月）。观察两组患者主要心血管事件（心血管性死亡,心肌梗死,进行靶血管再通治疗）及严重出血、轻度上消化道出血、皮疹及瘀斑、轻度白细胞减少等副反应的发生率。结果古稀组发生5例心血管事件（心肌梗死2例,靶血管再通3例）;非古稀对照组发生6例心血管事件（心肌梗死3例,靶血管再通3例）,两组间差异无统计学意义（P〉0.05）;两组均无严重出血,其他副反应包括轻度上消化道出血、皮疹及瘀斑、轻度白细胞减少两组间差异无统计学意义（P〉0.05）。结论老年患者在冠脉支架术后长期联合运用阿司匹林和氯吡格雷是安全有效的,和对照组相比在减少冠脉支架术后心血管事件的发生同样有效,且出血等副反应无明显增加。     

服用阿司匹林后血小板聚集功能对介入治疗后心肌坏死指标的影响

目的研究阿司匹林抵抗（aspirin resistance,AR）现象在冠心病患者中的发生情况,以及对非急诊PCI手术后心肌坏死情况的影响。方法入选了256例13服阿司匹林100mg≥7天的患者。所有患者入院后检测血小板聚集功能、心肌坏死标志物：肌酸激酶同工酶（CK-MB）和肌钙蛋白Ⅰ（TnⅠ）。根据血小板聚集功能检测结果分为AR和阿司匹林敏感两组。PCI术前至少12h前给予氯吡格雷300mg负荷量和75mg／d维持量,术后24h内再次测定心肌坏死标志物。比较两组心肌坏死标志物升高的例数。结果入选256例患者中67例（26．2％）存在AR。女性在AR组中的比例明显比敏感组高（52．2％比20．6％,P=0．0065）。PCI术后,CK—MB升高情况：AR组38例（56．7％）,阿司匹林敏感组42例（22．2％）,P=0．012,TnI升高情况：AR组41例（61．2％）,阿司匹林敏感组67例（35．4％）,P=0．006,两组间差异有统计学意义。AR组中PCI术后CK-MB升高患者所占比例是阿司匹林敏感组的2．5倍。同样AR组中PCI术后TnI升高患者所占比例是阿司匹林敏感组的近2倍（1．73倍）。经多元逐步回归检验患者是否存在对阿司匹林的抵抗现象是PCI术后CK—MB升高的独立预测指标（OR=2．5;95％可信区间为1．5～6．5;P=0．018）。结论AR现象在冠心病患者中确实存在,而且能显著增加非急诊PCI治疗患者术后心肌坏死危险性。     

阿司匹林和西洛他唑对冠心病合并糖尿病患者血小板聚集活性的影响

目的:探讨阿司匹林对冠心病合并糖尿病患者血小板聚集活性的影响;西洛他唑对血小板聚集活性作用是否有类似改变。方法:入选的冠心病患者中合并与合并2型糖尿病患者各45例。根据其口服药物又分为阿司匹林组、西洛他唑组和联合用药组,每组各15例。记录患者基本情况并测定血小板聚集活性、血浆血栓素(TX)B2、6-K-前列腺素(PG)F1a和髓过氧化物酶(MPO)水平,并进行统计分析。结果:(1)多元逐步回归分析显示血糖是影响血小板聚集的独立因素(R=0.914,P<0.01);(2)方差分析显示糖尿病患者血小板聚集活性、血浆TXB2、MPO水平较非糖尿病患者明显增高,6-K-PGF1a水平降低(P<0.001);(3)非糖尿病患者阿司匹林组和西洛他唑组血小板聚集活性和TXB2没有明显差异,西洛他唑组血浆6-K-PGF1a水平高于阿司匹林组,而MPO水平低于阿司匹林组(P<0.001);糖尿病患者西洛他唑组血小板聚集活性、TXB2和MPO水平低于阿司匹林组,而6-K-PGF1a水平高于阿司匹林组(P<0.05~0.001)。结论:对冠心病合并糖尿病患者西洛他唑较阿司匹林可以更有效地抑制血小板聚集。     

经皮冠状动脉介入治疗后血小板聚集率高的患者强化抗血小板治疗的研究

目的研究经皮冠状动脉介入治疗（PCI）后血小板聚集率仍然高的患者强化抗血小板治疗与主要心脏事件的关系。方法选择2004年1月至2006年6月我院住院进行择期PCI的冠心病患者1556例,服药前、术后24小时、28天检测二磷酸腺苷（ADP）诱导的血小板聚集率。其中有402例患者[男178例,女224例,平均年龄（57．34±6．47）岁]术后血小板聚集率仍然高,其24小时的血小板聚集度与基线（服药前）的绝对值〈30％。把这部分患者随机分为两组,对照组（n=201）继续服用阿司匹林100mg、氯吡格雷75mg;治疗组（n=201）除继续服用阿司匹林100mg、氯吡格雷75mg,每天加西洛他唑200mg,分两次服用。连续应用6个月,观察两组患者6个月主要心脏不良事件（包括死亡、非致死性急性心肌梗死、急性或亚急性血栓、靶血管重建、脑卒中）以及出血等不良事件的发生率。结果28天血小板聚集的抑制〈30％患者对照组有89．6％（180／201）,治疗组有9．4％（19／201）,两组相比,差异有统计学意义（P〈0．05）。两组均无急性血栓发生;亚急性血栓对照组有3．0％（6／201）,治疗组有0．5％（1／201）,两组相比,差异无统计学意义（P〉0．05）;对照组有2例死亡,治疗组无死亡;两组均未发生脑卒中;非致死性急性心肌梗死对照组1．5％（3／201）,治疗组0．5％（1／201）;两组相比,差异无统计学意义（P〉0．05）;靶血管重建对照组有15．9％（32／201）,治疗组6．5％（13／201）,两组相比,差异有统计学意义（P〈0．01）;出血的发生率对照组4．0％（8／201）,治疗组6．0％（12／201）,两组相比,差异无统计学意义（P〉0．05）。主要心脏事件的累计危险率治疗组低于对照组,差异有统计学意义（P〈0．05）。结论PCI后应用抗血小板药物,血小板聚集率经治疗后仍然高（即血小板聚集抑制〈30％）的患者,强化抗血小板治疗可以减少主要心脏事件的累计危险率,而没有增加出血并发症。     

冠状动脉支架术后血浆肌钙蛋白I对预后的影响

目的探讨不稳定性心绞痛患者经皮冠状动脉介入术(PCI)后血浆肌钙蛋白I(cTnI)对预后的预测价值。方法选择172例单支病变接受PCI术的不稳定性心绞痛患者,术后24h抽取静脉血化验cTnI,观察12～25个月的严重心脏不良事件。结果术后cTnI升高组(n=51)的严重心脏不良事件明显高于术后cTnI正常组(17.65%vs7.44%,P<0.05),cTnI升高组的血脂水平、他汀类药物、植入支架枚数、球囊预扩张时间、术前hsCRP水平与cTnI正常组比较,差异有统计学意义。结论cTnI的升高对PCI术后患者的预后有着重要的影响,尽早、足量的他汀类药物以及关注炎症的相关指标可使病人获益更大。     

Effect of additional temporary glycoprotein IIb/IIIa receptor inhibition on troponin release in elective percutaneous coronary interventions after pretreatment with aspirin and clopidogrel (TOPSTAR trial)

OBJECTIVES: The Troponin in Planned PTCA/Stent Implantation With or Without Administration of the Glycoprotein IIb/IIIa Receptor Antagonist Tirofiban (TOPSTAR) trial investigated: 1) the amount of troponin T (TnT) release after nonacute, elective percutaneous coronary intervention (PCI) in patients pretreated with aspirin and clopidogrel; and 2) the effect of additional glycoprotein (GP) IIb/IIIa receptor inhibiton on postinterventional TnT release. BACKGROUND: No data are available yet as to whether additional administration of a GP IIb/IIIa receptor antagonist might be beneficial in patients undergoing elective PCI already pretreated with aspirin and clopidogrel. METHODS: After bolus application of the study medication (tirofiban [T] or placebo [P]), PCI was performed followed by an 18-h continuous infusion of T/P. Primary end point of the study was incidence and amount of TnT release after elective PCI after 24 h. RESULTS: A total of 12 h after PCI troponin release was detected in 63% of the patients receiving P and in 40% of the patients receiving T (p < 0.05), after 24 h in 69% (P) and 48% (T) (p < 0.05) and after 48 h in 74% (P) versus 58% (T) (p < 0.08) of the patients. No differences were observed regarding major bleeding, intracranial bleeding or nonhemorrhagic strokes. After nine months a reduction of combined death/myocardial infarction/target vessel revascularization could be observed in the tirofiban group ([T] 2.3% vs. [P] 13.04%, p < 0.05). CONCLUSIONS: Troponin T release occurs after successful intervention in 74% of the patients undergoing elective PCI after 48 h even after pretreatment with aspirin and clopidogrel. The GP IIb/IIIa receptor antagonist tirofiban is able to decrease the incidence of troponin release significantly in this patient population.