增强型体外反搏改善经皮冠状动脉介入治疗术后心肌无再流现象

目的 探讨增强型体外反搏(EECP)能否改善急性心肌梗死(AMI)靶血管重建后心肌无再流现象.方法 靶血管重建后心肌无再流的AMI病人162例随机分为常规药物治疗组(n=81).体外反搏治疗36 h后.心肌声学造影(MCE)评估危险区心肌灌注.同时测量两组病人治疗前后血浆内皮素(ET)、一氧化氮(NO)和丙二醛(MDA)水平.结果 反搏治疗组病人危险区心肌灌注明显改善,标化A×β值(毛细血管灌注=毛细血管容积×充盈速率)从0.11±0.07升高到0.92±0.08(P<0.05);药物治疗组病人危险区心肌灌注无显著变化,标化A×β值为0.10±0.09 vs 0.12±0.05(P>0.05).反搏治疗组病人血浆ET水平从(113.6±44.1)ng/L下降到(79.3±31.7)ng/L(P<0.05),MDA水平从(5.8±0.6)ng/L下降到(3.9±0.7)ng/L(P<0.05),NO水平从(38.7±6.0)μmol/L上升到(99.5±15.7)μmol/L(P<0.05);药物治疗组病人血浆ET水平从(119.3±43.1)ng/L上升到(146.0±38.6)ng/L(P<0.05),MDA水平为(5.5±0.8)vs(5.4±0.4)ng/L(P>0.05),NO水平为(41.4±8.3)vs(52.1±10.2)μmol/L(P<0.05);试验结束时反搏治疗组病人血浆ET和MDA水平明显低于药物治疗组,而血浆NO水平明显高于药物治疗组.结论 增强型体外反搏可明显改善靶血管重建后心肌无再流的AMI病人心肌灌注,这一作用可能是通过改善血管内皮功能和降低氧化应激实现的.     

急性心肌梗死的心肌再灌注血流与脑钠肽的关系

目的探讨急性心肌梗死(AMI)心肌血流再灌注水平与血浆脑钠肽(BNP)水平的关系及其临床意义。方法对67名AMI成功行急诊介入治疗(PCI)的患者分别进行TIMI心肌灌注分级(TMPG)、心肌灌注显影分级(MBG)和校正的TIMI血流帧数计数(CTFC),采用荧光免疫抗原抗体结合方法测定发病24h即刻血浆脑钠肽(BNP)水平并评价其相互关系。结果TMPG方法评定的心肌灌注水平中,TMPG0/1级组12例,TMPG2级组29例,TMPG3级组26例,其对应血浆BNP平均水平分别为(1026±1119)ng/L,(346±192)ng/L和(219±95)ng/L。各组间血浆BNP水平差异有统计学意义(P=0·001)。其中TMPG0/1级组血浆BNP水平分别高于TMPG2级组和TMPG3级组(P<0·01,P<0·001);TMPG2级组高于TMPG3级组(P<0·01)。MBG方法评定的心肌灌注水平中,MBG0/1级组22例,MBG2级组25例,MGG3级组20例,其对应血浆BNP平均水平分别为(735±886)ng/L,(343±137)ng/L和(148±65)ng/L。各组间血浆BNP水平差异有统计学意义(P<0·001)。其中MBG0/1级组血浆BNP水平分别高于MBG2级组和MBG3级组(P<0·05,P<0·001);MBG2级组高于MBG3级组(P<0·001)。CTFC方法评定的冠脉血流中CTFC>40帧组20例,CTFC≤40帧组47例,血浆BNP平均水平分别为(453±265)ng/L和(397±650)ng/L,CTFC>40帧组血浆BNP水平高于CTFC≤40帧组(P=0·0036)。结论AMI患者心肌血流再灌注水平与血浆BNP水平负相关,再灌注水平越低组血浆BNP水平越高。心肌缺血损伤是BNP释放的重要刺激因素。     

冠心病患者心肌脂肪酸结合蛋白水平的变化及其临床意义

目的探讨冠心病患者血浆心肌脂肪酸结合蛋白(H-FABP)的水平变化及其临床意义。方法选择78例胸痛发作6小时内的冠心病患者,其中急性心肌梗死(AMI)32例、不稳定性心绞痛(UAP)24例、稳定性心绞痛(SAP)22例,并选69例健康体检者为对照组。采用夹心ELISA法检测H-FABP含量。结果AMI组的H-FABP水平(78.58ng/ml±52.2ng/ml)明显高于UAP组(12.57ng/ml±5.80ng/ml),P<0.01、SAP组(3.52ng/ml±2.29ng/ml)和对照组(3.30ng/ml±1.56ng/ml),P<0.01;UAP组的H-FABP水平明显高于SAP组和对照组,P<0.01;SAP组和对照组的H-FABP水平比较无差异(P>0.05)。结论血浆H-FABP水平可作为心肌坏死或损伤的早期判断指标,可为冠心病患者的危险分层及治疗提供依据。     

刺五加注射液对急性脑梗死病人血管紧张素Ⅱ和内皮素的影响

目的观察刺五加注射液对急性脑梗死病人血管紧张素Ⅱ(AngⅡ)和内皮素(ET)的影响,以探讨其对疗效的作用机制。方法将60例急性脑梗死病人随机分为治疗组和对照组,对照组采用常规西医药物救治,治疗组加用刺五加注射液静脉输注。用放射免疫分析法(RIA)测定两组治疗前后AngⅡ和ET含量变化,并进行比较分析。结果总有效率治疗组为93.3%,与对照组80.0%比较有统计学意义(P<0.05)愈显率治疗组为76.6%,对照组为56.6%(P<0.05);治疗组AngⅡ水平由治疗前287.9ng/L±79.35ng/L降至169.5ng/L±49.83ng/L,ET水平由治疗前94.19ng/L±28.72ng/L降至63.39ng/L±13.71ng/L;治疗后两组间比较,AngⅡ水平治疗组为169.5ng/L±49.83ng/L,对照组248.5ng/L±64.71ng/L,ET水平治疗组63.39ng/L±13.71ng/L,对照组84.56ng/L±21.64ng/L)。结论刺五加注射液对急性脑梗死的作用机制与其能调整AngⅡ和ET水平失衡、促进脑循环及脑保护有关。     

组织因子和组织因子途径抑制物1对无复流作用的实验研究

目的 观察缺血再灌注时兔心肌组织和血浆中组织因子(TF)和组织因子途径抑制物1(TFPI-1)水平的变化,研究外源性TFPI-1对无复流严重程度的影响,探讨TF激活的外源性凝血系统及TFPI-1抑制途径在无复流发病过程中的作用.方法 40只新西兰大白兔随机分为4组(每组10只):缺血再灌注组(IR组,结扎回旋支120 min,再灌注60 min)、缺血再灌注TFPI-1组(TFPI-1组,再灌注时rTFPI-1 100 ng/kg静脉注射,1ng·kg~(-1)·min~(-1)静脉滴注)、缺血组(结扎回旋支180 min)和假手术组,每组10只.用硫磺素S和Evan's蓝活体染色区分无复流区和缺血区.无复流严重程度用无复流面积/缺血面积表示.用逆转录-聚合酶链反应方法测定无复流区、缺血区及正常区心肌组织TF和TFPI-1 mRNA表达水平,ELISA方法测定开胸前、冠状动脉结扎前即刻及结扎120 min、再灌注10和60 min血浆TF和TFPI-1水平.结果 开胸前、冠状动脉结扎前即刻及结扎120 min,各组血浆TF、TFPI-1水平差异无统计学意义(P>0.05);再灌注10和60 min时,IR组血浆TF水平均显著高于缺血组和假手术组[10min:(20.7±4.1)pg/ml比(13.9±2.2)pg/ml(P<0.001),(20.7±4.1)pg/ml比(13.2±2.6)pg/ml(P<0.001);60 min:(15.8±2.6)pg/ml比(13.5±1.6)pg/ml(P<0.05),(15.8±2.6)pg/ml比(12.1±0.7)Pg/ml(P<0.001)].再灌注10 min时,IR组血浆TFPI-1水平较缺血组及假手术组无明显变化(P>0.05);60 min时,血浆TFPI-1水平[(9.7±1.6)ng/ml]反而显著低于缺血组[(11.6±1.6)ng/ml,P<0.05]及假手术组[(10.1±1.3)ng/ml,P<0.01].IR组无复流区心肌组织TF mRNA表达高于缺血组及假手术组(P<0.05或P<0.001);TFPI-1 mRNA表达较缺血组无明显变化(P>0.05).TFPI-1组无复流严重程度明显低于IR组(0.39±0.11比0.54±0.06,P<0.01).结论 无复流区心肌组织TF转录水平及再灌注过程中TF血浆蛋白水平表达明显上调;而无复流区心肌组织TFPI-1转录水平无明显变化,再灌注过程中血浆蛋白水平反而相对降低;外源性rTFPI-1可以减轻无复流严重程度.TF激活的外源凝血途径在无复流发病过程中起到重要作用.     

急性心肌梗死合并糖尿病患者血浆B型钠尿肽水平预测主要心脏不良事件的价值

目的探讨合并糖尿病的急性心肌梗死(AMI)患者的血浆N末端前体B型钠尿肽(NT-proBNP)水平对主要心脏不良事件(MACE)的预测价值。方法选择冠心病(AMI)患者139例,根据诊断分为AMI合并糖尿病组(合并组)73例,AMI组66例,另选择同期住院的非冠心病患者64例作为对照组,采用化学发光法检测血浆NT-proBNP水平,分析NT-proBNP判断6个月后MACE的发生率。结果合并组血浆NT-proBNP水平显著高于AMI组和对照组[(796.7±256.4)ng/L vs(642.5±231.5)ng/L和(89.6±103.3)ng/L,P<0.05,P<0.01],血浆NT-proBNP水平与冠状动脉造影Gensini评分呈正相关(r=0.726,P<0.01),合并组NT-proBNP>920ng/L的患者6个月MACE发生率较≤920ng/L者明显增高(60.0%vs 15.2%,P<0.01)。结论血浆NT-proBNP水平与AMI合并糖尿病患者的病情严重程度有一定的相关性。     

急性心肌梗死介入治疗后细胞因子变化与心肌灌注的关系

目的 探讨急性心肌梗死(AMI)患者急诊经皮冠状动脉介入治疗(PCI)后白细胞介素8(IL-8)、可溶性细胞间黏附分子1(sICAM-1)变化与心肌灌注的关系. 方法急性ST段抬高型心肌梗死患者98例,接受急诊PCI治疗,于术前5 min,术后6 h、12 h、24 h分别抽取动脉血标本,采用酶联免疫双抗体夹心法(ELISA)检测ICAM-1及IL-8.PCI术后1个月做双核素心肌灌注显像(DISA SPECT)检查,根据心肌灌注程度分为心肌灌注不良组、心肌灌注良好组. 结果 IL-8在PCI术前5 min两组均已呈现升高趋势(P＞0.05),术后6 h心肌灌注不良组进一步升高达峰值(P＜0.01),术后12 h、24 h心肌灌注不良组[分别为(94.3±169.9)和(44.1±27.8)ng/L]仍高于心肌灌注良好组[分别为(27.4±26.8)和(21.5±12.2)ng/L,P＜0.01和P＜0.05].两组sICAM-1在PCI术前5 min比较,差异无统计学意义(P＞0.05);术后6 h、12 h、24 h均持续高于心肌灌注良好组(P＜0.05). 结论 急性心肌梗死PCI术后心肌灌注不良患者血浆IL-8、sICAM-1水平明显高于心肌灌注良好者,提示细胞因子IL-8、sICAM-1参与血运重建后心肌灌注障碍的发生、发展.     

替罗非班对急性心肌梗死后白介素-17的表达及其与室性心律失常的相关性分析

目的研究替罗非班对急性心肌梗死(AMI)后白介素-17(IL-17)的表达及其与室性心律失常的相关性。方法选取2014年3月—2015年4月辽宁省大连市友谊医院治疗的AMI病人62例,所有研究对象均根据投硬币法被分为观察组和对照组,每组31例。对照组行经皮冠状动脉介入(PCI)术及常规的溶栓治疗,观察组在对照组基础上辅以替罗非班治疗。观察病人在治疗后白介素-10(IL-10)、IL-17、巨噬细胞移动抑制因子(MIF)及心肌血流灌注指标变化情况,比较两组病人的临床疗效。结果治疗后,观察组病人的IL-10水平高于对照组[(2.87±0.45)pg/m L比(2.15±0.42)pg/m L],IL-17、MIF水平明显低于对照组[(26.23±1.32)ng/L、(11.32±2.04)ng/L比(54.32±2.36)ng/L、(14.21±2.45)ng/L],组间比较差异有统计学意义(P0.05)。观察组病人的每搏量(SV)、心排血量(CO)、心排血指数(CI)、左室射血分数(LVEF)明显高于对照组,LVEDD、LVESD明显低于照组,组间比较差异有统计学意义(P0.05)。观察组总有效率为90.32%(28/31),高于对照组的67.74%(21/31),差异有统计学意义(P0.05)。结论 AMI后心肌白介素-17的表达和室性心律失常存在正相关性,采取替罗非班治疗AMI后,对抗炎反应的平衡起着调节性作用,可改善病人的心功能。     

急性心肌梗死患者PCI后BNP、hsCRP、cTnI的预后意义

目的:观察急性心肌梗死(AMI)患者经皮冠状动脉成形术(PCI)后脑钠肽(BNP)、高敏C反应蛋白(hsCRP)、心肌肌钙蛋白I(cTnI)水平的预后意义。方法:入选90例行PCI的AMI患者,于PCI后1d、7d测定血浆中BNP、hsCRP、cTnI水平,随访6个月内的主要心脏不良事件(MACE),并与AMI药物治疗患者(45例,药物治疗组),健康体检者(30例,健康对照组)进行对比分析。结果:术后1d,与健康对照组比较,AMI两组患者hsCRP、BNP、cTnI水平均明显升高(P均<0.01),但PCI组和药物治疗组比较无显著差异(P>0.05)。术后7d,与药物治疗组比较,PCI组hsCRP[(13.5±3.3)mg/L比(7.5±0.3)mg/L]、BNP[(2036±135)ng/L比(336±27)ng/L]、cTnI[(7.3±0.3)ng/L比(2.3±0.3)ng/L]水平明显降低(P<0.01),PCI组MACE发生率明显低于药物治疗组(27.8%比46.7%),P<0.01。结论:急诊PCI治疗优于药物治疗,联合检测脑钠肽、高敏C反应蛋白和心肌肌钙蛋白I水平有助于判断急性心肌梗死行PCI患者的预后。     

主动脉内球囊反搏治疗对晚期扩张型心肌病患者血浆脑钠尿肽的影响

目的:观察主动脉球囊反搏(intra-aortic balloon pump,IABP)治疗在晚期扩张型心肌病（dilated cardiomyopathy,DCM）患者对血浆脑钠尿肽(brain natriuretic peptide,BNP)值变化的影响。方法: 晚期DCM患者41例,在最优药物治疗基础上按是否应用IABP分为IABP植入组（植入组,21例）,非植入组（对照组,20例）。免疫化学发光法测患者人院后第1、2、7天血浆BNP浓度。结果: 入院第1天两组BNP值差异无统计学意义。入院后第2、7天,植入组BNP值明显低于对照组 ［(1778±289) ng/L vs. (2553±346) ng/L,P<0．05;(835±190) ng/L vs.(1376±301) ng/L,P<0.05］。结论: 在最优药物治疗基础上,IABP能进一步降低晚期DCM患者BNP值。     

Absence of preinfarction angina is associated with a risk of no-reflow phenomenon after primary coronary angioplasty for a first anterior wall acute myocardial infarction

BACKGROUND: No-reflow phenomenon after primary coronary angioplasty is associated with poorer left ventricular (LV) function and prognosis after acute myocardial infarction (AMI). The purpose of this study was to determine the clinical significance of preinfarction angina in the no-reflow phenomenon. METHODS AND RESULTS: A total of 40 patients with first anterior AMI were examined. All patients underwent primary balloon angioplasty or stenting within 12 h of the onset of AMI. No-reflow, defined as TIMI grade 2 flow or less without residual stenosis after angioplasty, was observed in 15 patients. Patients with no-reflow were older (67+/-9 vs. 58+/-10 years, P=0.006) and had a lower incidence of preinfarction angina (7% vs. 48%, P=0.01) than those without no-reflow. Patients with no-reflow had poorer LV function at predischarge and a higher incidence of pump failure, LV aneurysm, malignant ventricular arrhythmias or cardiac death during the hospital course in association with higher peak serum C-reactive protein levels (12.7+/-8.0 vs. 7.1+/-5.5 mg/dl, P=0.02). Multivariate analysis showed that the absence of preinfarction angina was a major independent determinant of no-reflow (RR=17.1, P=0.02). CONCLUSIONS: The absence of preinfarction angina is more frequently observed in patients with no-reflow. The beneficial effect of preinfarction angina on LV function may be explained, at least in part, by prevention of no-reflow after reperfusion.     

急性心肌梗死再灌注心律失常不增加心肌损伤

目的探讨急性心肌梗死（AMI）患者PCI再灌注心律失常的临床意义。方法回顾性分析近年在我院接受直接PCI且成功开通梗死相关血管（IRA）的AMI患者228例。将其中开通IRA后数分钟内发生心肌缺血再灌注损伤（MIRI）的119例患者（MIRI组）分为3个亚组,即严重心动过缓和低血压（缓慢性心律失常组）、需电复律的严重室性心律失常（快速性心律失常组）和IRA前向血流≤TIMI2级且除外急性闭塞（无复流组）。结果（1）临床和造影资料：与无MIRI组相比,MIRI组缺血时间短,梗死前心绞痛所占比例低,多支血管病变、下壁梗死、右冠状动脉IRA、PCI前IRA血流TIM10级和肾功能不全所占比例高,住院病死率较高（13．4％比4．6％,P=0．021）。（2）血清心肌酶水平：缓慢性心律失常组肌酸激酶（OK）峰值中位数显著低于无MIRI组（20LOIU／L比2521IU／L,P=0．039）,肌酸激酶同工酶（CK．MB）峰值中位数有低于无MIRI组的趋势（98IU／L比142IU／L,P=0．091）;快速性心律失常组CK峰值中位数（2317IU／L）和CK-MB峰值中位数（134IU／L）与无MIRI组相比差异无统计学意义（P=0．627,0．500）;无复流组CK峰值中位数（4573IU／L）和CK-MB峰值中位数（338IU／L）均显著高于无MIRI组（P均=0．000）。（3）超声心功能：无复流组左心室射血分数显著低于无MIRI组（38．7％±8．3％比51．2％±8．1％,P=0．000）,左心室舒张末期容积显著大于快速性心律失常组[（135±32）ml比（105±19）ml,P=0．029],左心室收缩末期容积显著大于无MIRI组[（82±33）ml比（54±24）ml,P=0．008]和缓慢性心律失常组[（56±19）ml,P=0．025]。结论再灌注心律失常可能提示梗死区存活心肌多,而且不增加心肌损伤;无复流增加心肌损伤,导致永久的心功能障碍。     

Angiographic no-reflow phenomenon as a predictor of adverse long-term outcome in patients treated with percutaneous transluminal coronary angioplasty for first acute myocardial infarction

OBJECTIVES: We sought to elucidate the long-term prognostic importance of angiographic no-reflow phenomenon after percutaneous transluminal coronary angioplasty (PTCA) for acute myocardial infarction (AMI). BACKGROUND: Angiographic no-reflow phenomenon, a reduced coronary antegrade flow (Thrombolysis in Myocardial Infarction [TIMI] flow grade < or =2) without mechanical obstruction after recanalization, predicts poor left ventricular (LV) functional recovery and survival in the early phase of AMI. We hypothesized that angiographic no-reflow phenomenon also predicts long-term clinical outcome. METHODS: We studied 120 consecutive patients with their first AMI treated by PTCA without flow-restricting lesions. The patients were classified as either no-reflow (n = 30) or reflow (TIMI-3) (n = 90) based on post-PTCA cineangiograms to follow up (5.8 +/- 1.2 years) for cardiac death and nonfatal events. RESULTS: Patients with no-reflow had congestive heart failure (p < 0.0001), malignant arrhythmia (p = 0.038), and cardiac death (p = 0.002) more often than did those with reflow. Kaplan-Meier curves showed lower cardiac survival and cardiac event-free survival (p < 0.0001) in patients with no-reflow than in those with reflow. Multivariate analyses disclosed that no-reflow phenomenon was an independent predictor of long-term cardiac death (relative risk [RR] 5.25, 95% confidence interval [CI] 1.85 to 14.9, p = 0.002) and cardiac events (RR 3.71, 95% CI 1.79 to 7.69, p = 0.0004). At follow-up, survivors with no-reflow had higher end-diastolic and end-systolic LV volume indices and plasma brain natriuretic peptide levels, and lower LV ejection fractions (p = 0.0002, p < 0.0001, p = 0.002, p < 0.0001, respectively) than did those with reflow, indicating that no-reflow may be involved in LV remodeling. CONCLUSIONS: Angiographic no-reflow phenomenon strongly predicts long-term cardiac complications after AMI; these complications are possibly associated with LV remodeling.     

Endothelin-1 and acute myocardial infarction: a no-reflow mediator after successful percutaneous myocardial revascularization.

AIMS: No-reflow after a primary percutaneous coronary intervention (PCI) is associated with a high incidence of left ventricular (LV) failure and a poor prognosis. Endothelin-1 (ET-1) is a potent endothelium-derived vasoconstrictor peptide and an important modulator of neutrophil function. Elevated systemic ET-1 levels have recently been reported to predict a poor prognosis in patients with acute myocardial infarction (AMI) treated by primary PCI. We aimed to investigate the relationship between systemic ET-1 plasma levels and no-reflow in a group of AMI patients treated by primary PCI. METHODS AND RESULTS: A group of 51 patients (age 59+/-9.9 years, 44 males) with a first AMI, undergoing successful primary or rescue PCI, were included in the study. Angiographic no-reflow was defined as coronary TIMI flow grade < or =2 or TIMI flow 3 with a final myocardial blush grade < or =2. Blood samples were obtained from all patients on admission for ET-1 levels measurement. No reflow was observed in 31 patients (61%). Variables associated with no-reflow at univariate analysis included culprit lesion of the left anterior coronary descending artery (LAD) (67 vs. 29%, P=0.006) and ET-1 plasma levels (3.95+/-0.7 vs. 3.3+/-0.8 pg/mL, P=0.004). At multivariable logistic regression analysis, ET-1 was the only significant predictor of no-reflow (P=0.03) together with LAD as the culprit vessel (P=0.04). CONCLUSION: ET-1 plasma levels predict angiographic no-reflow after successful primary or rescue PCI. These findings suggest that ET-1 antagonists might be beneficial in the management of no-reflow.     

Predictive factors for development of the no-reflow phenomenon in patients with reperfused anterior wall acute myocardial infarction

OBJECTIVES: We sought to elucidate the clinical factors related to the development of no-reflow phenomenon after successful coronary reperfusion in patients with an acute myocardial infarction (AMI). BACKGROUND: Myocardial contrast echocardiography revealed that the no-reflow phenomenon is observed in some patients with a reperfused AMI, and those patients usually have poor functional and clinical outcomes. It is still unknown what clinical factors are related to the development of the no-reflow phenomenon. METHODS: Myocardial contrast echocardiography was performed 15 min after successful coronary reperfusion therapy in 199 patients with an anterior wall AMI who underwent successful coronary reperfusion with primary coronary angioplasty within 24 h after the onset of AMI. Multiple logistic regression analysis was used to identify independent predictors of the no-reflow phenomenon. RESULTS: Seventy-nine patients showed the no-reflow phenomenon. Univariate analysis indicated that pre-infarction angina within 48 h before symptom onset, Killip class, Thrombolysis in Myocardial Infarction flow grade 0 on the initial coronary angiogram, the number of abnormal Q-waves and the wall motion score (WMS) on the echocardiogram obtained at hospital admission are related to the no-reflow phenomenon. Multivariate logistic regression analysis revealed that all of these factors, except for Killip class, are independent predictive factors of the no-reflow phenomenon. CONCLUSIONS: Development of the no-reflow phenomenon is related to the severity of myocardial damage (number of Q-waves), the size of the risk area (WMS) and the occlusion status of infarct-related artery. In addition, ischemic preconditioning (pre-infarction angina) seems to be the factor that attenuates the no-reflow phenomenon.     

Pressure-derived collateral flow index as a parameter of microvascular dysfunction in acute myocardial infarction.

OBJECTIVES: The goal of this study was to examine the implications of the pressure-derived collateral flow index (CFIp) in acute myocardial infarction (AMI). BACKGROUND: Higher CFIp is associated with less severe myocardial ischemia during angioplasty in the non-infarcted heart. It remains unknown whether CFIp also identifies collateral function in AMI patients with and without no-reflow phenomenon. METHODS: The study population included 48 patients with a first AMI. After successful percutaneous transluminal coronary angioplasty (PTCA) stent, we measured mean aortic pressure (Pa), central venous pressure (Pv) and coronary wedge pressure (Pcw) of the infarct-related artery to calculate: CFIp = (Pcw - Pv)/(Pa - Pv). Myocardial contrast echocardiography (MCE) was performed with the intracoronary injection of microbubbles to assess myocardial perfusion. Left ventriculograms at days 1 and 28 were provided for the measurement of the regional wall motion (RWM, SD/chord). RESULTS: There was no difference in CFIp among subsets based on angiographic collateral grades (grade 0, 1, 2, 3; 0.28 +/- 0.07, 0.27 +/- 0.09, 0.27 +/- 0.08, 0.23 +/- 0.08, p = NS). The CFIp was significantly higher in patients with MCE no-reflow (n = 16) than in those with MCE reflow (n = 32) (0.34 +/- 0.07 vs. 0.23 +/- 0.06, p < 0.01). There was a significant inverse correlation between the extent of functional improvement (DeltaRWM[28 d-1 d]) and CFIp (r = 0.56, p < 0.01), implying that higher CFIp is associated with worse functional improvement. CONCLUSIONS: In AMI, CFIp is unlikely to reflect collateral function but seems to increase with the severity of microvascular dysfunction. Because higher CFIp was associated with poorer functional recovery, it provides a simple and useful estimate of clinical outcomes in AMI.     

急性心肌梗死患者直接介入治疗后无再流与血浆组织因子及其途径抑制物的关系

目的 通过测定急性心肌梗死(AMI)患者直接经皮冠状动脉介入治疗(PCI)前后血浆组织因子(TF)、组织因子途径抑制物(TFPI)水平的变化,探讨TF、TFPI与无再流的关系.方法 选择2006年5月至2007年5月于我院急诊行PCI的AMI患者53例,用ELISA法检测患者PCI术前、术后即刻、术后24 h外周静脉血 TF、TFPI水平.比较其中无再流者与再灌流者不同时点TF、TFPI水平的变化.结果 PCI术前、术后即刻、术后24 h无再流组血浆TF、TFPI水平均明显高于再灌流组[TF(275.3±46.2)ng/L比(236.8±44.3)ng/L、(332.7±41.3) ng/L 比(282.3±38.7) ng/L、(315.5±47.8) ng/L 比(248.1±46.9) ng/L;TFPI(165.2±38.4) μg/L 比(128.5±18.7) μg/L、(176.3±36.8)μg/L 比(135.6±20.3) μg/L、(149.8±31.7) μg/L 比(118.7±19.2) μg/L;均P＜0.01];PCI术后即刻,丽组TF水平均较术前明显升高(P＜0.01);PCI术后24 h,无再流组TF水平仍高于术前水平(P＜0.05),再灌流组与术前比较无差异(P＞0.05);PCI前后两组TFPI水平均无明显变化(P＞0.05).结论 AMI患者直接PCI后无再流的发生与血浆,TF水平呈正相关,TF可激活外源性凝血途径,形成微血栓而导致无再流,而TFPI可阻止血栓形成而防治无再流的发生.     

急性心肌梗死介入术后无复流患者血清补体4a水平和血小板聚集率的变化

目的 探讨急性心肌梗死(AMI)经皮冠状动脉介入治疗(PCI)术后无复流患者血清补体4a(C4a)水平和血小板聚集率的变化.方法 入选行PCI的AMI患者119例,其中介入术后冠状动脉无复流患者(无复流组)28例,冠状动脉恢复血流患者(复流组)91例和疑似冠心病而行冠状动脉造影检查结果正常者(对照组)30例.检测对照组冠状动脉造影前和无复流组、复流组介入术前30 min,术后即刻、30 min、1 h、2 h、半年的C4a水平和血小板聚集率,并观察其变化.结果 无复流组、复流组和对照组术前30 min C4a水平差异无统计学意义.无复流组和复流组术前30 min血小板聚集率均高于对照组(P均＜0.05).无复流组术后即刻、30min和1 h C4a水平和血小板聚集率均高于术前和术后2 h、半年,同时也均高于复流组术后即刻、30 min和1 h(P均＜0.05).复流组不同时间的C4a水平和血小板聚集率差异无统计学意义.无复流组术后即刻、30 min和1 h,C4a水平与血小板聚集率呈正相关(r值分别为0.91、0.79和0.60,P均＜0.01).结论 C4a水平和血小板聚集率在AMI患者PCI术后早期短暂升高.

Abstract：

Objective To observe serum C4a and platelet aggregation rates changes in acute myocardial infarction (AMI) patients before and after percutaneous coronary intervention (PCI)and association with the development of no-reflow phenomenon. Methods From June 2006 to August 2009, 119 AMI patients underwent PCI (28 cases of no-reflow group, 91 cases of reflow group)and 30 subjects with suspected coronary heart diseases and normal coronary angiography results (control group) were enrolled in this study. C4a and platelet aggregation rate were measured at 30 minutes before PCI, immediately after PCI,30 minutes,l hour,2 hour, and 6 months post PCI in AMI patients and at before coronary angiography in control subjects. Results The levels of serum C4a at 30 minutes prior to PCI in control, no-reflow, and reflow groups were similar(P ＞0. 05). Platelet aggregation rate at 30 minutes prior to PCI was significantly higher in no-reflow group and reflow group than in control group ( all P ＜ 0. 05 ). Serum C4a and platelet aggregation rates were significantly higher in no-reflow group at immediate, 30 minutes and 1 hour after PCI than at 30 minutes prior to PCI, two hours and 6 months after PCI ( all P ＜ 0. 05), and were significantly higher than in reflow group at immediate, 30 minutes and 1 hour after PCI ( all P ＜ 0. 05 ). Serum C4a and platelet aggregation rates were similar at different time points in reflow group ( all P ＞ 0. 05 ). The levels of C4a in no-reflow group at immediate, 30 minutes and 1 hour after PCI were positively correlated with platelet aggregation rates (r=0. 91,0. 79 ,0. 60 ,respectively ,all P＜0.01). Conclusion The transient increase on levels of C4a and platelet aggregation rate early post PCI are verified in no-reflow patients with AMI undergoing PCI.     

急性前壁心肌梗死患者相关血管再通后血液中成熟型肾上腺髓质素变化研究

目的探讨急性心肌梗死(AMI)再灌注后,有活性的成熟型肾上腺髓质素(AM)在冠状窦-主动脉差值是否有变化。方法对146例首次发生急性前壁心肌梗死患者和51例冠状动脉造影阴性作对照。入选的心肌梗死患者症状出现后24 h内完成冠状动脉腔内成形术(PICA)的再灌注治疗。再灌注后取主动脉和冠状窦血,测定血浆AM的两种分子形态(AM-m和AM-Gly)。结果AMI患者主动脉和冠状窦血浆AM-m,AM-Gly水平明显高于对照组[(1．7±1．4)pmol／L比(0．4±0．3)pmoL／L,P<0．01]。AMI患者血浆AM-m水平的冠状窦-主动脉差值明显高于对照组,而AM- Gly在两组之间差异无统计学意义(P=0．30)。AM-m的冠状窦-主动脉差值,在伴有左心室功能障碍的AMI患者(n=49)明显高于不伴有左心室功能障碍的AMI患者(n=97)。主动脉和冠状窦的血浆AM-m水平与左室射血分数呈负相关(r=-0．50,r=-0．48,P<0．01)。结论AMI再灌注后,尤其伴有严重左心室功能障碍的患者冠状动脉循环血液中AM的有活性的成熟型(AM-m)合成加速,提示AMI再通后AM经自分泌和(或)旁分泌可能对心血管起保护作用。     

梗死前心绞痛对急性心肌梗死患者经皮冠状动脉介入治疗术后无再流现象的影响

目的探讨梗死前心绞痛(PIA)对急性心肌梗死(AMI)患者经皮冠状动脉介入治疗(PCI)后无再流现象的影响。方法100例首次AMI患者均在发病12h内行PCI术。所有患者按照有无无再流现象分为2组:无再流组(15例)和再流组(85例)。监测心肌酶谱和C反应蛋白(CRP)变化;放射性核素测定心功能;观察室壁瘤、心力衰竭发生率和住院病死率。结果无再流组PIA发生率显著低于再流组(P<0.01);而前壁梗死的发生率高于再流组(P<0.05);肌酸激酶同工酶峰值和CRP水平均显著高于再流组(P<0.01)。无再流组放射性缺损面积显著大于再流组(P<0.01);左室射血分数显著低于再流组(P<0.01);心力衰竭、室壁瘤发生率和死亡率均高于再流组(P<0.05)。多元Logistic回归分析结果显示,缺乏PIA是发生无再流现象的独立预测因素(OR=6.12,P=0.01)。结论缺乏PIA是发生无再流现象的独立预测因素,而无再流现象与心力衰竭和死亡率增高密切相关。