瑞舒伐他汀和阿托伐他汀对氯吡格雷抗血小板活性的影响

目的观察瑞舒伐他汀和阿托伐他汀对氯吡格雷抗血小板活性的影响。方法选择60例冠心病患者接受阿司匹林100mg/d、氯吡格雷75 mg/d及低分子肝素5000 U/12 h治疗,5 d后随机分为阿托伐他汀20mg/d(阿托伐他汀组,30例)和瑞舒伐他汀10 mg/d(瑞舒伐他汀组,30例)。在服用氯吡格雷之前(基线值)、加用他汀类药物之前及服用他汀类药物3d后,用全血阻抗法分别测定不同浓度二磷酸腺苷(5、10、20μmol/L)诱导的血小板聚集率。结果与基线值比较,服用氯吡格雷5 d后和加服他汀类药物治疗3 d后,2组患者血小板聚集率明显降低,差异有统计学意义(P<0.05);与治疗前比较,阿托伐他汀组患者血小板聚集率有所升高,而瑞舒伐他汀组患者血小板聚集率有所下降,但差异无统计学意义(P>0.05)。结论经细胞色素3A4途径代谢的阿托伐他汀及不经细胞色素3A4代谢的瑞舒伐他汀,短期内对氯吡格雷抗血小板活性无影响。     

阿托伐他汀可以消弱氯吡格雷抗血小板聚集的能力

氯吡格雷 (Clopidogrel)是一种无活性的前体药物 ,需要在肝脏内转化成活性物质 ,并通过与血小板P2YacADP受体结合而发挥其抗血小板聚集的作用。而氯吡格雷在人体肝内活性转化的机制 ,目前仍不清楚。在用一种新型的床旁血小板聚集度计测定氯吡格雷对血小板的功能影响时 ,该文的作者发现当患者同时服用阿托伐他汀 (Atorvastatin)时 ,氯吡格雷的抗血小板聚集作用就会显著降低。由于阿托伐他汀通过肝内的CyP3 A4酶代谢 ,因此该文的作者推测 ,阿托伐他汀可能抑制氯吡格雷通过P45 0CyP3 A4酶进行活性转化这一过程 ,从而消弱氯吡格雷抗血小板…     

阿托伐他汀对大脑中动脉支架置入术不良事件的影响

目的 在大脑中动脉支架置入的患者中应用阿托伐他汀进行干预,探讨阿托伐他汀对不良事件及血脂和C-反应蛋白的影响.方法 将24例大脑中动脉狭窄（狭窄率≥70%）成功完成大脑中动脉支架置入术的患者随机分为两组,每组12例.治疗组：口服用阿托伐他汀40 mg＋氯吡格雷75 mg＋拜阿司匹林100nag,1 次/d;对照组：硫酸氢氯吡格雷75 mg＋拜阿司匹林100 mg,1次/d.支架置入术后1个月、3个月、6个月、12个月进行随访,记录两组的各阶段新发的不良事件（短暂性脑缺血发作、脑梗死、再狭窄、再次介入治疗）.并检测术前及术后不同时间点血脂及C-反应蛋白的水平.结果 与对照组比较,除1个月时的低密度脂蛋白胆固醇水平外,其余各时间点治疗组血脂及C-反应蛋白水平均低于对照组（P〈0.05或P〈0.01）;总不良事件的发生率,治疗组低于对照组,差异有统计学意义（P=O.000 17）;而C-反应蛋白术后较术前升高,至12个月时低于术前;治疗组术后血脂水平较术前明显降低.结论 大脑中动脉支架置入术后使用阿托伐他汀治疗可有效地预防支架置入术后不良事件的发生;阿托伐他汀可使患者术后的血脂和C-反应蛋白降低.     

氯吡格雷联合应用他汀类药物药效及副反应观察

目的观察氯吡格雷药效及副反应是否因为合用他汀药物而受到影响。方法124例临床诊断不稳定型心绞痛（UA）患者均给予氯吡格雷300 mg顿服,继75 mg/d,随机分为合用氟伐他汀80 mg/d组、合用阿托伐他汀10mg/d组和对照组,给药前及治疗2周后分别测定其血小板聚集率和血常规。结果患者血小板聚集率均明显降低,与治疗前比较,差异有显著性,3组血小板聚集率降低幅度无显著性差异,3组均未发现中性粒细胞及血小板计数减少患者。结论联合应用氟伐他汀或阿托伐他汀后,氯吡格雷药效及副反应未受影响。     

阿托伐他汀与氯吡格雷对ACS患者氯吡格雷羧酸衍生物血浓度与血小板聚集率的影响

目的:测定急性冠状动脉综合征(ACS)患者氯吡格雷羧酸衍生物血浓度和血小板聚集率,观察阿托伐他汀和氯吡格雷有无相互作用。方法:对照组为25例健康受试者,ACS组为66例ACS患者。均口服阿司匹林100mg/d、氯吡格雷75mg/d、阿托伐他汀20mg/d,5d后暂停阿托伐他汀,继续氯吡格雷和阿司匹林口服4d,分别于第5天、第9天采用液相色谱串联质谱法测量氯吡格雷羧酸衍生物血浓度,流式细胞仪测定血小板聚集率,比较两组差异。结果:对照组第5天和第9天氯吡格雷羧酸衍生物血浓度分别为(5.76±0.87)ng/dl和(5.67±0.88)ng/dl(P=0.351),血小板聚集率分别为(44.25±16.37)%与(47.61±16.67)%(P=0.083)。ACS组第5天和第9天氯吡格雷羧酸衍生物血浓度分别为(5.96±0.87)ng/dl和(5.86±0.97)ng/dl(P=0.115),血小板聚集率分别为(47.70±15.07)%与(47.02±15.45)%(P=0.622)。相关性分析显示,血氯吡格雷羧酸衍生物浓度和血小板聚集率呈正相关。结论:氯吡格雷羧酸衍生物血浓度和血小板聚集率相关性良好,氯吡格雷和阿托伐他汀未见相互作用。     

冠脉支架术后阿托伐他汀联用氯吡格雷两药相互作用的随访研究

目的研究在冠脉支架术后随访患者中不同剂量的阿托伐他汀与氯吡格雷长期联用产生的药物相互影响。方法105例冠心病患者,入院第2天随机服用阿托伐他汀和普伐他汀,66例行PC I术者入院当日加服氯吡格雷。共分为5组,A组23例,阿托伐他汀20 mg/d+氯吡格雷,B组20例,阿托伐他汀40 mg/d+氯吡格雷,C组23例,普伐他汀20 mg/d+氯吡格雷,D组20例,单用阿托伐他汀20 mg/d,E组19例,单用阿托伐他汀40 mg/d。分别在入院第1天及出院随访1、3月测定A、B、C组患者的血小板功能指标,并进行比较,测定各组的血脂等指标,分别比较A和D组、B和E组血脂等指标的差异。结果各组患者临床特征基线资料比较,差异无统计学意义;A、B、C组患者首次及随访1、3月测定的血小板功能指标CD62P、CD63、MPAR,组间差异无统计学意义,3组中各指标1、3月比基线均略有所下降（P<0.05）,但1月和3月比较差异无统计学意义,CD62P、CD63、MPAR互为正相关（P<0.05）;A和D组、B和E组在首次及治疗1、3月后相比较,血脂等在两对应组间差异均无统计学意义。结论冠脉支架术后40 mg/d以下的阿托伐他汀与常规剂量氯吡格雷较长时间联用,两药之间相互无明显影响,合用是安全的。     

强化降脂对老年不稳定型心绞痛患者血小板-单核细胞活化的影响

目的观察强化降脂对氯吡格雷抑制老年不稳定型心绞痛患者血小板-单核细胞表达CD42a+/CD14+短期内的影响。方法将50例老年不稳定型心绞痛患者随机分成实验组25例(阿托伐他汀40mg)及对照组25例(阿托伐他汀20mg),检测比较服药前及服药后6小时和服药10天后血小板-单核细胞表达CD42a+/CD14+的变化。结果服药前两组CD42a+/CD14+分别为(9.43±2.53,10.12±2.26)%,服药后6小时降至(7.69±1.86,8.39±2.19)%,与服药前比较差异无统计学意义(P>O.05),组间比较差异无统计学意义(P>0.05);服药10天后降至(6.18±1.90,7.26±2.10)%,较服药前明显降低,差异有统计学意义(P<0.05),但两组比较差异无统计学意义(P>0.05)。结论老年不稳定型心绞痛患者服用较大剂量阿托伐他汀强化降脂并不抑制氯吡格雷短期内抗血小板-单核细胞活化作用。     

阿托伐他汀可能抑制经皮冠脉介入治疗后氯吡格雷的抗血小板作用

加拿大蒙特利尔皇家维多利亚医院Brophy报道,经皮冠脉介入治疗（PCI）术后服用氯吡格雷的患者,如果同时接受阿托伐他汀治疗,可能导致心血管事件发生危险增加。氯吡格雷是一种抗血小板药物，为无活性的药物前体，在体内经细胞色素P4503A4酶（CYP3A4）的作用转化为活性成分。在PCI术后，氯吡格雷是常用的预防支架内血栓形成的抗血小板药物，阿托伐他汀可能与氯吡格雷的无活性药物前体竞争性结合CYP3A4，从而影响氯吡格雷的抗血小板作用。     

瑞舒伐他汀和阿托伐他汀对冠心病患者的调脂作用和安全性比较

目的探讨瑞舒伐他汀和阿托伐他汀对冠心病(CHD)患者的调脂作用和安全性。方法 2012年6月至2013年2月该院收治的CHD患者90例,按随机数字表法分为观察组和对照组,每组45例。对照组给予阿托伐他汀钙片20 mg/d,观察组给予瑞舒伐他汀钙片10 mg/d,均于晚饭后2 h服用,连续用药8 w。结果观察组治疗后总血清总胆固醇(TC)、低密度脂蛋白(LDL-C)水平下降幅度显著大于对照组(P<0.05),三酰甘油(TG)、高密度脂蛋白(HDL-C)水平两组比较无显著差异(P>0.05)。观察组LDL-C达标率、TC达标率〔66.67%(30/45)、71.11%(32/45)〕均显著高于对照组〔40.00%(18/45)、51.11%(23/45)〕(均P<0.05)。观察组不良反应3例,对照组5例,差异无统计学意义(P>0.05)。结论相比阿托伐他汀20 mg/d,瑞舒伐他汀10 mg/d降脂效果更强,安全性高。     

阿托伐他汀联合氯吡格雷对急性冠脉综合征血小板聚集率的影响

目的:探讨急性冠脉综合征(ACS)患者急性期负荷剂量氯吡格雷联合阿托伐他汀或普伐他汀对血小板聚集率和主要不良心血管事件发生率的影响。方法:102例ACS患者被随机分成两组:普伐他汀组(P组)和阿托伐他汀组(A组),两组均予氯吡格雷300mg顿服后,75mg/d维持。P组予普伐他汀。入院后24h内和第14天分别测定TC、HDL-C、LDL-C、血小板聚集率(PAR)、肝功能,并统计两组主要不良心血管事件的发生率。结果:(1)两组TC、HDL-C、LDL-C水平在基础状态和第14d,差异无显著性(P>0.05);(2)P组或A组PAR在治疗后和基线相比,差异有显著性(P<0.05);但P、A两组在治疗后相比,差异无显著性(P>0.05);(3)心血管死亡、再发心肌梗塞复合终点发生率在两组间差异无显著性(P>0.05)。结论:阿托伐他汀或普伐他汀与负荷剂量氯吡格雷联合治疗急性冠脉综合征安全有效,两组效果相似,无显著差异。     

早期服用氯吡格雷对急性冠状动脉综合征患者介入治疗近期临床预后的影响

目的探讨冠状动脉(冠脉)介入治疗(PCI)术前早期使用氯吡格雷能否较术前临时用药进一步改善非ST段抬高的急性冠脉综合征(NSTE-ACS)患者的近期预后。方法将拟行早期PCI治疗的NSTE-ACS患者随机分为早期用药组和对照组。早期用药组272名患者于入院临床诊断明确后立即开始服用氯吡格雷(首次给负荷量300mg,后以75mg/d维持)。对照组共入选265名患者,于冠脉造影后决定选择PCI治疗时开始用药,首次服用氯吡格雷300mg,术后以75mg/d维持。比较两组在PCI术后30d内死亡、支架血栓、心肌梗死、再发心绞痛和靶血管血运重建等心脏不良事件(MACE)的发生率。结果两组患者在临床病情、冠脉病变及支架置入治疗等方面比较,差异无统计学意义。PCI术后30d内早期用药组死亡、支架血栓、心肌梗死和靶血管血运重建等联合事件的发生率显著低于对照组。结论PCI术前早期使用氯吡格雷能够明显减少NSTE-ACS患者心血管不良事件的发生率,显著改善患者PCI术后的近期预后。     

高危急性冠状动脉综合征介入治疗早期或即刻应用替罗非班对主要不良心血管事件的影响

目的 观察高危非ST段抬高急性冠状动脉综合征(NSTE-ACS)经皮冠状动脉介入治疗(PCI)术前早期应用和术前即刻应用替罗非班对血小板功能和180 d主要不良心血管事件(MACE)的影响,探讨替罗非班的最佳应用时机.方法 2006年7月至2007年7月,160例备行PCI的高危NSTE-ACS患者随机分配到PCI前早期应用组(冠状动脉造影前4～6 h应用替罗非班)和PCI前即刻应用组(导丝通过冠状动脉病变后应用替罗非班).观察两组入院后、冠状动脉造影前和PCI后的血小板聚集率,随访术后24 h、3 d、7 d、30 d和180 d MACE.记录使用替罗非班治疗期间的出血并发症和血小板减少症的发生率.结果 应用替罗非班后,两组血小板聚集率均显著降低(P＜0.05).PCI前早期应用组冠状动脉造影前的血小板聚集率显著低于PCI前即刻应用组(8%比42%,P＜0.05).两组PCI后24 h和3 d内均未发生MACE,7 d MACE发生率均为1.3%.PCI前早期应用组术后30 d(3.8%比6.3%,P＞0.05)和180 d(13.0%比16.7%,P＞0.05)MACE发生率均低于PCI术前即刻应用组.两组180 d无MACE发生的生存率分别为87.0%和83.7%(P＞0.05).增龄(OR=1.164,P＜0.001)、高血压(OR=4.165,P=0.037)和2型糖尿病(OR=13.628,P＜0.001)是发生MACE的独立危险因素.替罗非班的应用时机对MACE发生率有一定程度的影响(OR=2.416,P=0.153).在使用替罗非班治疗期间,两组重度出血并发症发生率(2.5%比1.3%.P＞0.05)差异无统计学意义,中度出血并发症和轻度血小板减少症发生率均为1.25%.结论 在阿司匹林和氯吡格雷抗血小板治疗的基础上,高危NSTE-ACS患者PCI前早期应用替罗非班比PCI前即刻应用,能及早强化抗血小板治疗,有减少PCI后MACE发生率的趋势.增龄、高血压和2型糖尿病是高危NSTE-ACS患者PCI联合替罗非班治疗中发生MACE的独立危险因素.     

Effect of different loading doses of atorvastatin on percutaneous coronary intervention for acute coronary syndromes

BACKGROUND

Percutaneous coronary intervention (PCI)-induced myocardial damage is associated with late cardiovascular events. Treatment with atorvastatin before PCI can reduce myocardial damage during the peri-PCI period.

OBJECTIVES

To compare the safety and myocardial effects of different atorvastatin loading doses and dosing frequency before PCI in non-ST segment elevation acute coronary syndrome (NSTE-ACS) patients.

METHODS

Eighty NSTE-ACS patients were randomly divided into four groups (20 patients per group). The control group was given 40 mg atorvastatin each night. The three loading dose groups were treated the same as in the control group, but were given 80 mg atorvastatin 12 h before PCI (low-load group) in combination with 40 mg atorvastatin 2 h to 4 h before PCI (mid-load group) or 60 mg atorvastatin 2 h to 4 h before PCI (high-load group). All patients underwent PCI within 48 h to 72 h of admission, and received 40 mg atorvastatin for at least one month after PCI. Changes in myocardial markers and highly sensitive C-reactive protein were analyzed. Patients were followed up for 30 days to monitor the incidence of major adverse cardiac events (MACE).

RESULTS

No deaths or revascularizations were recorded. The incidences of MACE differed significantly between the four groups (40%, 25%, 10% and 0% for the control, low-load, mid-load and high-load groups, respectively; P<0.05). The incidence of MACE and cardiac troponin I level above the normal range, and post-PCI increases in creatine kinase-MB and highly sensitive C-reactive protein were significantly higher in the control group than in the high-load group (all P<0.007). The post-PCI alanine aminotransferase levels in all four groups were significantly higher than the pre-PCI levels, but were within normal ranges. No myalgia or myasthenia was observed.

CONCLUSION

The results of the present study show that short-term atorvastatin loading before PCI was well tolerated and had beneficial myocardial effects in patients with NSTE-ACS.     

Effects of rosuvastatin on platelet inhibition by clopidogrel in cardiovascular patients

Statin interference has been suggested among the mechanisms of reduction of the antiplatelet effect of clopidogrel. We thus sought to assess the influence of rosuvastatin on clopidogrel antiplatelet action in high-risk (HR) cardiovascular patients. To set the level of platelet inhibition by combined antithrombotic treatments we retrospectively studied two populations of HR patients, one under aspirin alone, the other under aspirin plus rosuvastatin, before and after addition of clopidogrel. The effects of rosuvastatin compared with atorvastatin were then prospectively investigated in patients who underwent percutaneous coronary intervention (PCI), under clopidogrel and aspirin treatment. Light transmission platelet aggregation (LTA) was studied in response to adenosine diphosphate (ADP) (5 μM) or arachidonic acid (0.5 mM). The inhibitory effect of clopidogrel in reducing ADP-induced LTA was similar in the two HR groups of patients. No difference in ADP-induced platelet aggregation was observed in the two PCI groups of patients with either atorvastatin or rosuvastatin. In conclusion, rosuvastatin does not interfere with the antiplatelet effect of clopidogrel in patients with cardiovascular disease.     

冠状动脉介入术后抗血小板治疗联合不同质子泵抑制剂对消化道出血的预防作用和心血管事件的影响

目的观察老年冠心病患者冠状动脉介入（PCI）术后氯吡格雷＋阿司匹林治疗与不同质子泵抑制剂联用在预防消化道出血及对血小板聚集率（PAR）和心血管事件发生情况的影响。方法选择符合入选条件的280例患者,在氯吡格雷十阿司匹林的基础上,随机分为5组,A组：对照组;B组：奥美拉唑20mg bid;C组：雷贝拉唑10mg bid;D组：兰索拉唑30mg qd;E组：埃索美拉唑20mg bid。治疗期间通过观察呕血、黑便、上腹不适或腹痛和反酸、烧心症状,行便隐血试验,胃镜检查,确定消化道损伤发生;同时观察心血管不良事件发生,并检测PAR。患者出院后门诊随访12个月。结果A、B、C、D、E组消化道损伤的发生率分别为28．85％、12．28％、10．53％、10．34％、8．93％;A组中出现3例消化道大出血,B、C、D、E组中均未出现;B、C、D、E四组与A组比较差异有统计学意义（P〈0．05）,B、C、D、E组之间无统计学差异。A、B、C、D、E组心血管事件发生率分别为5．77％、14．04％、7．02％、8．62％、8．93％;PAR分别为22％±7％、34％±11％、27％±6％、26％±7％、23％±6％,B组心血管事件发生率与PAR明显升高。结论PCI术后,氯吡格雷＋阿司匹林治疗与质子泵抑制剂联用可明显降低患者消化道出血的发生,奥美拉唑与其联用能明显提高血小板聚集率,降低抗血小板疗效,增加心脑血管事件的发生率,其他质子泵抑制剂对其抗血小板疗效无明显影响。     

Effects of high-dose statin administered prior to coronary angioplasty on the incidence of cardiac events in patients with acute coronary syndrome

INTRODUCTION: Statins given after acute coronary syndrome without ST elevation (NSTE-ACS) reduce the incidence of major adverse cardiac events (MACE) in long-term follow-up. AIM: To evaluate the effects of high-dose statin administered in patients with NSTE ACS and increased CRP level prior to percutaneous coronary intervention (PCI) on the incidence of MACE in long-term follow-up. METHODS: The study involved 140 consecutive patients with NSTE ACS and increased CRP level at baseline. Patients from group A (n=54) did not receive statin before PCI, whereas subjects in group B (n=86) were given 80 mg of atorvastatin. Patients in both groups received typical cardiological therapy including aspirin, thienopyridine and low molecular weight heparin. After PCI all patients received 40 mg of atorvastatin. Incidence of MACE (death, myocardial infarction (MI), re-PCI) during long-term followup was evaluated in both groups. RESULTS: Study groups did not differ with respect to demographic parameters and rate of ischaemic heart disease risk factors. Also, no differences occurred regarding CRP level (group A vs. B: hsCRP 10.8+/-1.8 mg/l vs. 8.2+/-2.8 mg/l; p=NS) and TIMI Risk Score (group A vs. B: 4.3+/-0.71 vs. 4.37+/-0.79; p=NS). During long-term follow-up the incidence of MI (9.25% vs. 1.2%, p=0.03), composite endpoint: death + MI (14.8% vs. 2.32%, p=0.013) and death + MI + re PCI (25.9% vs. 8.1%, p=0.006) was significantly higher in group A than group B. CONCLUSIONS: Administration of high-dose statin in NSTE ACS patients before PCI was associated with significant reduction of MACE in long-term follow-up. This effect was observed despite the same therapy given after PCI.     

Comparison of platelet P2Y(12) ADP receptor-mediated pathway inhibition in triple versus dual antiplatelet therapy as assessed by VASP-phosphorylation in Japanese patients undergoing coronary stenting

Despite wide interindividual variability in response to clopidogrel, platelet P2Y(12) ADP receptor inhibition in Japanese patients has not been fully studied using specific methodology. This study compared platelet P2Y(12) ADP receptor inhibition during treatment with clopidogrel versus clopidogrel plus cilostazol in patients undergoing coronary stenting. Forty-two patients in whom platelet function was measured within 2 months after coronary stenting were enrolled. All patients were treated with aspirin 100 or 200 mg/day, and were divided into a dual therapy group (aspirin plus clopidogrel 75 mg/day; n = 34) and a triple therapy group (aspirin plus clopidogrel 75 mg/day plus cilostazol 200 mg/day; n = 8). Vasodilator-stimulated phosphoprotein (VASP) phosphorylation analysis and 5 and 20 μmol/L-induced maximal platelet aggregation were assessed. No differences were found in baseline characteristics except for a higher incidence of diabetes mellitus (DM) in the triple therapy group. Although there were no differences in platelet aggregation between the 2 groups, VASP index was significantly lower in the triple therapy group than in the dual therapy group (23.1 ± 15.3% versus 51.2 ± 19.9%; P = 0.001). The rate of low responsiveness to clopidogrel, defined by VASP index > 50%, was lower in the triple therapy group than in the dual therapy group (12.5% versus 55.9%; P = 0.047). Similarly, in DM patients the triple therapy group had a lower VASP index compared with the dual therapy group (23.1 ± 15.3% versus 47.0 ± 23.5%; P = 0.015).Clopidogrel plus cilostazol is more effective in inhibiting the platelet P2Y(12) ADP receptor pathway than clopidogrel alone. This may be useful for reducing clopidogrel resistance in Japanese patients.     

Efficacy of Clopidogrel and Clinical Outcome When Clopidogrel Is Coadministered With Atorvastatin and Lansoprazole: A Prospective,Randomized, Controlled Trial

This prospective, randomized, nonblind, controlled trial evaluated the effects of clopidogrel on platelet function upon coadministration with atorvastatin and lansoprazole.One hundred four adult patients with non-ST-segment elevated acute coronary syndrome (NSTE-ACS) who underwent percutaneous coronary intervention (PCI) with drug-eluting stent implantation were included. All patients were treated with standard dual antiplatelet therapy (DAPT) plus rosuvastatin 10 mg daily after the operation. On the sixth day after PCI, patients were randomly divided into 4 groups, Group A: DAPT + atorvastatin 20 mg daily (a change from rosuvastatin to atorvastatin) + lansoprazole 30 mg daily, Group B: DAPT + atorvastatin 20 mg daily (a change from rosuvastatin to atorvastatin), Group C: DAPT + lansoprazole 30 mg daily (continuing to take rosuvastatin), Group D is the control group. Additional drugs were used according to the situation of patients. Platelet function and concentrations of platelet activation markers (granular membrane protein 140 (P-selectin), thromboxane B2 (TXB2), and human soluble cluster of differentiation 40 ligand (sCD40L)) were assessed before randomization and at 15- and 30-day follow-up visits. All patients were maintained on treatment for 6 months and observed for bleeding and ischemic events.A total of 104 patients were enrolled, 27 patients in group A, 26 patients in Group B/C, 25 patients in Group D separately, and all the patients were analyzed. There were no differences in platelet function and the levels of platelet activation markers (P-selectin, TXB₂, and sCD40L) among or within the 4 groups at the 3 time points of interest (P > 0.05). In the subsequent 6 months, no significant bleeding events occurred, and 12 patients experienced ischemic events, these results were also not significantly different among the groups (P > 0.05).In patients diagnosed with NSTE-ACS who have had drug-eluting stent implantation, simultaneously administering clopidogrel, atorvastatin, and lansoprazole did not decrease the antiplatelet efficacy of clopidogrel or increase adverse event frequency over 6 months.     

强化他汀治疗对择期PCI患者冠脉无复流及血浆APN与炎性因子的影响

目的:观察强化他汀治疗对择期经皮冠状动脉介入治疗（PCI）患者术中出现无复流风险及其血浆脂联素（APN）、血清高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、炎性因子高敏C反应蛋白(hs-CRP)的影响。方法:70例择期PCI患者随机分为强化他汀组（强化组,n=35）及常规他汀组（常规组,n=35）,强化组阿托伐他汀每日80 mg,2 d术前进行预处理,2 d后每日40 mg,服1月,常规组术前每日20 mg, 2 d,术后长期服用。分别检测术前及术后1月、3月hs-CRP、HDL-C、LDL-C、APN;观察术中无复流的发生率;主要终点是30 d内的主要不良心脏事件(MACE;死亡,心肌梗死或计划外的血管重建)。结果:两组均未出现MACE,均无明显不良反应。1月后两组APN、HDL-C均有上升,强化组APN:（8±4）mg/L,常规组:（6±3）mg/L;强化组上升明显（P<0.05）。两组hs-CRP、LDL-C均有下降,强化组hs-CRP:（3.2±2.1）mg/L,常规组:（4.5±2.3）mg/L;强化组显著性下降（P<0.05）;术前与术后比较差异有统计学意义(P<0.05)。强化组术中无复流3例,常规组5例,两组差异未达到统计学意义。结论:强化他汀治疗能够降低择期PCI患者血浆炎性因子水平,升高血浆APN水平。