糖尿病患者经皮冠状动脉介入术后氯吡格雷抵抗的临床观察

目的:探讨Ⅱ型糖尿病患者经皮冠状动脉介入术后氯吡格雷抵抗现象。方法:入院急性冠脉综合征(ACS)患者46例,其中糖尿病患者11例,非糖尿病患者35例,予氯吡格雷负荷量300 mg,继予75 mg/d维持,在服用氯吡格雷前,服药后2、4、6、24、48与30 d取血,测定5μmol/L二磷酸腺苷(ADP)诱导的血小板聚集率,分析两组间临床特征、血小板抑制率的差异。结果:糖尿病患者11例中氯吡格雷抵抗的发生率为55%,高于非糖尿病患者26%(P0.05)。结论:在经PCI治疗的ACS并发Ⅱ型糖尿病患者中氯吡格雷抵抗的发生率高于非糖尿病患者。     

非ST段抬高型急性冠状动脉综合征患者经皮冠状动脉介入治疗术后强化抗血小板治疗临床效果

目的 观察非ST段抬高型急性冠状动脉综合征患者经皮冠状动脉介入治疗(PCI)术后应用不同剂量的氯吡格雷疗效和安全性.方法 共入选急性非ST段抬高型冠状动脉综合征行PCI术的患者506例,计算机简单随机法分为标准组、强化组.标准组入院后给予氯吡格雷300 mg顿服,后予75 mg/d维持;强化组入院后给予300 mg顿服,后予150 mg/d口服至PCI术后5d,后75 mg/d维持.所有患者均于入院、顿服氯吡格雷300 mg后24 h、术前及术后5d行ADP诱导的血小板聚集率(PA)检查.于入院及术后5d行血常规检查,观察血小板变化,并随访术后30 d主要心血管事件和出血事件的发生情况.结果 强化组术前及术后5d的PA明显下降,强化组术前及术后5d的PA(％)较标准组明显减低,差异具有统计学意义(t=18.3929,P＜0.05;t=13.1384,P＜0.005).强化组与标准组比较30 d主要心血管事件有减低趋势,但未见有统计学意义.两组TIMI出血事件未见有明显差异.结论 强化抗血小板治疗可以明显抑制血小板聚集率,同时出血风险未见明显增加,是安全可行的.     

经皮冠状动脉介入术后氯吡格雷抵抗的临床观察

目的观察因急性冠脉综合征（ACS）行冠状动脉介入治疗（PCI）患者应用氯吡格雷后血小板聚集率的变化及氯吡格雷抵抗的发生情况。方法ACS患者37例,予氯吡格雷负荷量300mg,继予75mg/d维持,在服用氯吡格雷前,服药后2、4、6、24、48h以及服药后30d取血,测定ADP诱导的血小板聚集率,观察血小板聚集率变化并根据抑制程度判断氯吡格雷抵抗发生率。结果给药后2、4、6、24、48h及30d时,氯吡格雷抵抗的发生率分别为62%、46%、32%、38%、49%和43%,氯吡格雷抵抗者用药后血小板抑制率明显低于反应者,其中1例抵抗者出现亚急性支架内血栓形成。结论PCI治疗的部分患者中存在氯吡格雷抵抗。     

急性冠状动脉综合征高龄患者介入治疗后双联抗血小板长期治疗的安全性研究

目的:观察急性冠状动脉综合征(ACS)高龄患者经皮冠状动脉介入治疗(PCI)后长期联合应用阿司匹林和氯吡格雷的安全性。方法:将接受PCI的416例ACS患者分为非高龄组(A组,年龄0.05)。2组出血发生率分别为3.2%和4.0%(P>0.05),血小板及白细胞减少发生率组间差异无统计学意义(P>0.05)。多元Logistic回归分析结果提示阿司匹林长期维持治疗、氯吡格雷维持治疗时间超过12个月、合并使用质子泵抑制剂是ACS患者PCI后长期使用双联抗血小板药并发出血的独立危险因素[比值比(OR)分别为0.048、5.396、0.181,均P0.05)。结论:75岁以上的高龄ACS患者PCI后长期双联抗血小板治疗的出血发生率与75岁以下人群相比并未明显增加,但长期双联抗血小板治疗仍需注意防止出血并发症的发生。     

经皮冠状动脉介入术后双联抗血小板治疗2a临床评价

目的评价经皮冠状动脉介入治疗（P-PCI）术后应用阿司匹林和氯吡格雷双联抗血小板治疗2 a的临床疗效及安全性。方法将128例行P-PCI的急性ST段抬高心肌梗死患者分为两组。A组术后应用阿司匹林和氯吡格雷2 a;B组应用阿司匹林和氯吡格雷1 a,以后均长期应用阿司匹林。评估两组间主要心脏不良事件及安全性指标。结果 A组2例（3.1%）发生主要心脏不良事件与B组6例（9.5%）比较差异有统计学意义（P〈0.05）;两组安全性指标比较差异无统计学意义。结论急性ST段抬高心肌梗死患者P-PCI术后应用双联抗血小板治疗2 a可获得更好的临床效果。     

急性冠状动脉综合征合并糖尿病患者经皮冠状动脉介入术后替格瑞洛与氯吡格雷抗血小板疗效及预后研究

目的应用血栓弹力图评价替格瑞洛与氯吡格雷在急性冠状动脉综合征(ACS)合并糖尿病(DM)患者经皮冠状动脉介入(PCI)术后抗血小板治疗的疗效和预后。方法入选2016年6月至2017年1月期间在陕西省第四人民医院心血管内科住院治疗的ACS合并DM患者100例。采用前瞻性、随机对照的研究方法,按随机数字表分为两组:氯吡格雷组和替格瑞洛组,每组50例。PCI术后24~48 h行血栓弹力图检测,比较两组花生四烯酸(AA)诱导的血小板抑制率和二磷酸腺苷(ADP)诱导的血小板抑制率以及最大血凝块幅度(MAADP)。术后随访6个月,比较两组主要不良心血管事件(MACE)、出血事件和呼吸困难的发生率。采用SPSS 19.0软件进行数据处理。根据数据类型,分别采用t检验或x~2检验进行组间比较。结果与氯吡格雷组相比,替格瑞洛组AA抑制率[(72.3±26.6)%vs(54.0±31.4)%,P=0.041]和ADP抑制率[(76.5±22.1)%vs(43.4±28.7)%,P=0.016]均显著增高,MAADP幅度显著降低[(33.2±10.5)vs(48.2±13.6)mm,P=0.024]。替格瑞洛组AA抑制率50%(14.0%vs38.0%,P=0.006)和ADP抑制率30%(6.0%vs28.0%,P=0.003)的患者数量显著低于氯吡格雷组。术后6个月替格瑞洛组MACE发生率较氯吡格雷组显著降低(8.2%vs 22.9%,P=0.045);两组出血事件和呼吸困难发生率间差异无统计学意义。结论对于ACS合并DM患者,PCI术后服用替格瑞洛的抗血小板疗效明显优于氯吡格雷。     

高强度他汀对急性冠状动脉综合征患者血小板聚集率的影响

目的比较不同剂量阿托伐他汀对急性冠状动脉综合征(acute coronary syndrome,ACS)患者血小板功能的影响。方法 50例ACS患者随机分为观察组(阿托伐他汀40mg/d,n=25)、对照组(阿托伐他汀20mg/d,n=25)。两组分别在给药前,负荷300mg氯吡格雷后2小时,服药后10天取一次静脉血行血小板聚集实验,最大聚集率(Maximum aggregation rate of platelet,MARP)用%表示。结果服药前观察组和对照组1μmol/L和2μmol/L的二磷酸腺苷(adenosine diphosphate,ADP)诱导的MARP分别为(61.67±9.65)%vs(65.55±5.54)%;(70.50±7.01)%vs(61.33±7.89)%。口服他汀治疗2小时后,观察组、对照组1μmol/L和2μmol/L的ADP诱导的MARP明显下降至(39.00±11.45)%vs(31.00±10.16)%;(47.00±8.67)%vs(44.50±10.09)%(P0.05)。口服他汀治疗10天后,1μmol/L和2μmol/L的ADP诱导的MARP进一步下降至(35.67±7.12)%vs(21.67±6.68)%;(38.33±9.16)%vs(32.83±5.34)%,与基线及口服2小时后相比差异有统计学意义(P0.05)。与对照组比较,观察组口服2小时后与10天后1μmol/LADP诱导的MARP差异有统计学意义(P0.05);与对照组比较,观察组基线值与10天后2μmol/LADP诱导的MARP差异有统计学意义(P0.05);但两组患者1μmol/L和2μmol/L ADP诱导的MARP均50%。结论与20mg阿托伐他汀比较,ACS患者服用40mg阿托伐他汀后,短期内可减弱氯吡格雷对血小板聚集的抑制作用,但未发生残余血小板高反应。     

急性冠脉综合征患者氯吡格雷抵抗的相关影响因素分析

目的 分析氯吡格雷抵抗的相关影响因素,观察氯吡格雷抵抗和心血管事件之间的相关性.方法 选取欲行冠状动脉造影检查的119例急性冠脉综合征（ACS）患者,于术前24 h内未使用及使用氯吡格雷治疗7 d后采集肘静脉血,进行血小板聚集率（PA）检测.根据测算的PA值分为氯吡格雷抵抗（CR）组和非氯吡格雷抵抗（NCR）组,分析CR的影响因素.随访3个月,观察心血管事件和CR之间的相关性.结果 119例ACS患者中,氯吡格雷抵抗（CR）组32例（26.9%）,非氯吡格雷抵抗（NCR）组87例（73.1%）,氯吡格雷抵抗发生率为26.9%.合并糖尿病的ACS患者组CR的发生率较高,为59.4%,非糖尿病ACS患者CR的发生率较低,为32.2%（P＜0.01）,置入2枚以上支架组CR的发生率较NCR组高（43.8%比8.0%,P＜0.05）.CR组服药前基础的血小板聚集率为38.22±8.22,与NCR组血小板聚集率53.95±9.42比较差异有统计学意义（P＜0.05）.3个月后随访主要心血管事件可以看出,CR组心血管事件的发生率较NCR组高（12.5%比1.1%）,两者比较差异有统计学意义（P＜0.05）.结论 ACS患者氯吡格雷抵抗的发生率较高,同时影响临床抗血小板治疗的效果.糖尿病人群更易发生氯吡格雷抵抗.另外,置入支架数的增多使患氯吡格雷抵抗的危险性增加.氯吡格雷抵抗影响患者的预后,与心血管事件的发生有很大的相关性.     

急性冠状动脉综合征合并慢性肾病患者介入术后双联抗血小板治疗的研究进展

阿司匹林联合P2Y12受体抑制剂是预防急性冠状动脉综合征（ACS）经皮冠状动脉介入治疗后支架内血栓形成及全身动脉粥样硬化血栓事件的标准双联抗血小板治疗方案。ACS合并慢性肾病（CKD）患者血栓风险和出血发生率更高,因此,确定这一人群的最佳抗血小板药物治疗策略至关重要。既往大多数临床试验将晚期CKD患者排除在外,因而临床医师对这部分患者的抗血小板治疗策略缺乏循证医学证据。现综述ACS合并CKD患者抗血小板治疗研究进展,以期为临床医师面临此类患者时选择合适的抗血小板治疗策略提供借鉴。     

不同质子泵抑制剂对非ST段抬高型急性冠状动脉综合征患者氯吡格雷抗血小板疗效的影响

目的探讨质子泵抑制剂对接受氯吡格雷抗血小板治疗的非ST段抬高型急性冠状动脉综合征(NSTE-ACS)患者疗效的影响。方法采用前瞻性研究,共纳入2012年1月至2013年6月接受冠状动脉内药物洗脱支架置入的NSTE-ACS患者145例,采取密封信封抽样形式分为A和B两组,在标准药物治疗(氯吡格雷、阿司匹林、低分子肝素、硝酸酯类、调脂药以及其他常规治疗)基础上,A组合用泮托拉唑(72例)而B组合用奥美拉唑(73例)。观察1年内患者的消化道出血事件以及主要不良心血管事件,包括全因死亡、心原性死亡、卒中、因心绞痛或心力衰竭再住院、血运重建。结果 A和B两组心血管事件发生率差异无统计学意义(均为P>0.05),其中全因死亡(6.9%比5.5%)、心原性死亡(4.2%比5.5%)、因心绞痛或心力衰竭再住院(16.6%比15.0%)和血运重建(11.1%比12.3%),消化道出血发生率差异亦无统计学意义(5.6%比5.5%,P>0.05)。结论本研究入选的NSTE-ACS患者中,两类质子泵抑制剂对氯吡格雷抗血小板疗效的影响无显著差异。     

对接受介入治疗的急性冠状动脉综合征患者的慢性肾脏病调查

目的探讨中国急性冠脉征接受介入治疗患者中慢性肾脏病的患病率及危险因素。方法对于全国20个中心的1854例在2007年2月1日以前接受介入治疗的急性冠脉综合征患者进行病史采集、肾脏损伤指标及相关危险因素的检测。结果在1793例资料完整的患者中,白蛋白尿的患病率为10.6%,肾功能下降的患病率为10.0%,血尿或非感染性白细胞尿的患病率为7.1%。在急性冠脉综合征接受介入治疗的患者中慢性肾脏病的患病率为22.8%,知晓率为11.3%。多因素logistic回归提示,性别、既往慢性肾脏病病史、高血压、糖尿病、贫血、高尿酸血症、尿蛋白阳性以及年龄每增加10岁均是肾小球滤过率(eGFR)低于60ml.min-1.1.73m-2的危险因素。结论慢性肾脏病在急性冠脉综合征接受介入治疗的患者中患病率高,但临床中自我知晓率明显偏低,对所有因急性冠脉综合征而住院的患者尤其那些合并相关危险因素的患者应进行eGFR估算。     

Association of contrast-induced acute kidney injury with long-term cardiovascular events in acute coronary syndrome patients with chronic kidney disease undergoing emergent percutaneous coronary intervention

Background

The association between contrast-induced acute kidney injury (CI-AKI) and chronic kidney disease (CKD) in patients with acute coronary syndrome (ACS) treated with percutaneous coronary intervention (PCI) has not been fully reported. We evaluated the association of CI-AKI on cardiovascular events in ACS patients with CKD.

Methods

A total of 1059 ACS patients who underwent emergent PCI in our multicenter registry were enrolled (69 ± 12 years, 804 men, 604 STEMI patients). CKD was defined as at least stage 3 CKD, and CI-AKI was defined as an increase of at least 0.5 mg/dL and/or an increase of at least 25% of pre-PCI to post-PCI serum creatinine levels within 1 week after the procedure. Primary endpoints included cardiovascular death, myocardial infarction, and cerebrovascular disorder (stroke or transient ischemic attack).

Results

In our study, 368 (34.7%) patients had CKD. During follow-up periods (435 ± 330 days), CI-AKI and primary endpoints occurred in 164 (15.5%) patients and 106 (10.0%) patients, respectively. Multivariate Cox proportional hazards model revealed that age, female gender, peak creatinine kinase > 4000, IABP use, CI-AKI (hazard ratio [HR], 2.17; 95% confidential interval [CI], 1.52 to 4.00; P < 0.001), and CKD (HR, 1.66; 95% CI, 1.01 to 2.72; P = 0.046) were independent predictors of primary endpoints. Kaplan–Meier analysis showed that occurrence of primary endpoints increased significantly with an increase in CKD stage, and CI-AKI yielded worse long-term prognosis at every stage of CKD (P < 0.001).

Conclusions

CI-AKI was revealed to be a significant incremental predictor of cardiovascular events at each stage of CKD in ACS patients.     

Contrast-induced nephropathy after a second percutaneous coronary intervention in patients with chronic kidney disease

Background Data are limited regarding the risk of contrast-induced nephropathy (CIN) for patients after the second contrast exposure. Objective To examine the risk of CIN after the second contrast exposure in patients of acute coronary syndrome (ACS) with chronic kidney disease (CKD). Methods Patients of ACS scheduled for a second elective PCI. Patients were required to have an estimated creatinine clearance (CrCl) between 15 and 60 ml/min. The value of serum creatinin (sCr) prior to the second contrast exp...     

Prognostic implications of chronic kidney disease and anemia after percutaneous coronary intervention in acute myocardial infarction patients

Anemia is a common complication of chronic kidney disease (CKD), and a few studies suggest that both CKD and anemia have a marked impact on the prognosis of patients with cardiovascular disease. We retrospectively analyzed the prevalence of CKD and anemia in 312 patients with acute myocardial infarction (AMI). The patients were divided into four groups according to the presence of CKD and anemia. Chronic kidney disease was defined as estimated glomerular filtration rate <60 ml/min/1.73 m², and anemia was defined according to the World Health Organization definition. Of 312 AMI patients, 166 (53.2%) had CKD and 87 (27.8%) had anemia. A powerful relationship was observed between both CKD and anemia and major adverse cardiac and cerebrovascular events (MACCE) or death by any cause. After adjustment for comorbidities, the hazard ratio (HR) for MACCE was significantly higher in the anemia-only group (HR 5.42, 95% confidence interval (CI) 1.38–21.27, P = 0.015), the CKD-only group (HR 6.4, 95% CI 2.09–19.58, P = 0.001), and the CKD and anemia group (HR 11.61, 95% CI 3.65–36.89, P < 0.001). With respect to death by any cause, the HR was significantly higher in the CKD-only group (HR 2.68, 95% CI 1.02–7.02, P = 0.045) and the CKD and anemia group (HR 4.40, 95% CI 1.56–12.43, P = 0.005). One-half of the patients with AMI had CKD as well. Furthermore, when anemia coexisted with CKD, these conditions had a multiplicative amplification effect on the risk of MACCE and death by any cause in patients with AMI.     

Platelet reactivity in patients with chronic kidney disease undergoing percutaneous coronary intervention

This study aimed to evaluate the platelet reactivity in real-world patients with different chronic kidney disease (CKD) stages after percutaneous coronary intervention (PCI), and to examine whether high residual platelet reactivity (HRPR) is associated with higher incidence of adverse cardiovascular events in a 2-year follow up. A total of 10 724 consecutive patients receiving DAPT with aspirin and clopidogrel after PCI throughout 2013 were enrolled. We applied modified thromboelastography (mTEG) in 6745 patients. Kaplan–Meier analysis and Cox proportional regression analysis were applied to illustrate end points for patients. The prevalence of HRPR for adenosine diphosphate (ADP) was higher in patients with CKD3-5 than patients with CKD1-2 (47.0% vs. 37.3%, p = 0.002), but not for arachidonic acid (AA). No significant difference was observed for MACCE between patients with or without HRPR for ADP (HR 1.004, 95%CI: 0.864–1.167, p = 0.954). Patients with HRPR for ADP was associated with less bleeding events than patients without HRPR for ADP (HR 0.795, 95%CI: 0.643–0.982, p = 0.034). In this large cohort of real-world patients after PCI, the deterioration of renal function was linked to HRPR for ADP. HRPR was not associated with MACCE in patients with CKD in a 2-year follow up. Bleeding risks were significantly lower in PCI patients with versus without HRPR for ADP.     

Outcomes after percutaneous coronary interventions in patients with chronic kidney disease

Introduction Chronic kidney disease (CKD) is a significant contributor to cardiovascular morbidity and mortality. Patients with CKD are known to have a greater prevalence of cardiovascular disease than the general population, and patients with concurrent CKD and coronary artery disease (CAD) have greater mortality than patients without CKD.The rate of cardiovascular mortality is approximately 50%, five to 10 times higher than the general population.     

急性冠脉综合征合并恶性肿瘤患者冠脉介入术后的预后分析

目的 探讨急性冠脉综合征(ACS)合并恶性肿瘤患者经皮冠状动脉介入(PCI)后的临床特点及其预后.方法 回顾性分析2011年2月至2018年7月于解放军总医院第一医学中心心内科住院治疗的67例急性冠脉综合征合并恶性肿瘤患者的临床资料,患者行PCI后根据其结局将其分为生存组(n=54)和死亡组(n=13),采用多因素Lo...     

急性冠状动脉综合征冠状动脉支架术后氯吡格雷联用胃黏膜保护剂的临床观察

目的探讨急性冠状动脉综合征(ACS)患者冠状动脉支架术后不同质子泵抑制剂(PPI)或H2受体拮抗剂(H2RA)与氯吡格雷联用的安全性。方法选取150例成功行冠状动脉支架术的ACS患者,给予双重抗血小板治疗,将受试对象随机分为5组,A1组:埃索美拉唑组(30例);A2组:雷贝拉唑组(30例);B1组:雷尼替丁组(30例);B2组:法莫替丁组(30例)和C组:对照组(30例)。其中A1和A2组统称为PPI组,B1和B2组为H2RA组,至术后30 d继续给予双重抗血小板治疗,所有患者均随访1年,主要终点是不良心血管事件(MACE,包括心原性死亡、非致死性急性心肌梗死、紧急靶血管血运重建、亚急性支架内血栓、脑卒中),次要终点是出血事件。结果 5组的临床基本资料差异无统计学意义;与对照组(6.9%)比较,PPI组、H2RA组1年内累积MACE发生率分别为5.36%、3.45%,3组间MACE发生率相近(HR:0.91,95%CI:0.17～4.88;HR:2.17,95%CI:0.27～17.42,P=0.915、0.467);与A1组(3.7%)比较,A2组MACE发生率为6.9%(HR:0.60,95%CI:0.08～4.70,P=0.629),与B1组(6.7%)比较,B2组为0(HR:0.14,95%CI:0.01～2.32,P=0.172)。所有患者均未发生严重出血;与对照组(10.34%)比较,PPI组、H2RA组1年内累积轻微出血发生率分别为12.5%、10.34%(HR:0.80,95%CI:0.22～2.96;HR:0.97,95%CI:0.24～3.86,P=0.734、0.964);与A1组(11.11%)比较,A2组轻微出血发生率为13.79%(HR:0.81,95%CI:0.18～3.59,P=0.769),与B1组(6.67%)比较,B2组为14.29%(HR:0.46,95%CI:0.09～2.27,P=0.366)。结论冠状动脉支架术后不同PPI或H2RA与氯吡格雷联用不增加1年内MACE与出血发生率。     

Chronic inflammation in patients with acute coronary syndrome and chronic kidney disease

Chronic kidney disease is a worldwide growing problem in public health. It is a risk factor for complications in patients with acute coronary syndrome (ACS). Diabetes, hypertension (hypertrophy and left ventricular failure), impaired fibrinolysis and coagulation processes, as well as the rapid development of atherosclerosis (partly associated with chronic inflammation) are responsible for higher prevalence of cardiovascular diseases in patients with chronic kidney disease. Inflammatory process of unknown aetiology belongs to the so-called non-traditional risk factors in development of cardiovascular system diseases. It is thought that this process is responsible for adverse remodelling of atherosclerosis plaque and its instability which causes plaque rupture and as a result a coronary syndrome occurrence. Important inflammatory mediators, which take part in pathogenesis of ACS, are acute phase proteins such as: C-reactive protein, adhesion molecules VCAM-1, ICAM-1, selectins, plasma amyloid A, metalloproteinases, interleukins-1 and -6, tumour necrosis factor-a and vascular endothelial growth factor.