自体骨骼肌卫星细胞移植对心肌梗死大鼠心功能的影响

目的 了解自体骨骼肌卫星细胞(satellite cell,SC)移植至心肌对心肌梗死(myocardial infarction,MI)大鼠心功能的影响及其可能机制.方法 45只Wistar大鼠采用随机抽签法分为假手术组、对照组及移植组,对照组及移植组大鼠经结扎冠状动脉前降支建立MI模型.将体外培养2周的大鼠自体SC以注射的方式移植到移植组大鼠梗死区周围,4周后测定各组大鼠血流动力学、心功能、血清血管内皮生长因子(vascular endothelial growth factor,VEGF)浓度及缺血心肌毛细血管密度的变化,同时观察移植细胞在梗死区的生长、增殖情况并探讨它们相互的关系.结果 SC在梗死区中可增殖分化为横纹肌纤维;与假手术组比较,尽管对照组及移植组大鼠之收缩压、舒张压、平均动脉压、左室收缩压及左室压力最大上升/下降速率均明显降低(P＜0.05,P＜0.01),左室舒张末压均明显增高(P＜0.01),但移植组左室压力最大上升速率、左室压力最大下降速率及左室舒张末压较之对照组则有明显改善(P＜0.05,P＜0.01);SC移植4周后,对照组大鼠毛细血管密度较之假手术组明显增高(P＜0.05);移植组大鼠缺血心肌中毛细血管密度及血清VEGF浓度较之假手术组、对照组亦明显升高(P＜0.05,P＜0.01).结论 SC在心肌梗死区中能增殖分化为横纹肌样细胞,并可分泌VEGF促使缺血心肌毛细血管增生,从而共同参与改善心功能.     

激活Notch信号的骨髓间充质干细胞移植促心肌梗死模型鼠血管新生研究

目的探讨干预Notch信号骨髓间充质干细胞（BMSCs）移植对心肌梗死（MI）大鼠心肌的治疗性血管新生作用及其机制。方法 60只Wistar大鼠经结扎冠状动脉前降支建立MI模型后,建模2周进行相应处理后,随机分为MI模型对照组（B组）、培养液移植对照组（C组）、激活Noth信号的BMSCs移植实验组（D组）、BMSCs移植对照组（E组）,每组15只;另选取10只为假手术对照组（A组）。4周后观察细胞生长及增殖情况,测定缺血心肌中血管内皮细胞生长因子（VEGF）蛋白的表达及缺血区心肌毛细血管密度的改变。结果 BMSCs在梗死区中可增殖分化为内皮细胞,与A、B、C组相比,D组、E组缺血心肌中VEGF蛋白的表达增多及毛细血管密度均明显增高（P〈0.01）,且D组较E组更明显（P〈0.05）。结论激活Notch信号有促进心肌梗死区BMSCs向内皮细胞分化,并通过自分泌和旁分泌的方式增加缺血心肌VEGF的表达,由此促进缺血心肌中毛细血管新生。     

延迟缺血预处理介导的心肌保护与血管再生的关系

目的:探讨延迟缺血预处理对急性心梗大鼠远期的心肌保护及其促进血管再生的作用.方法:分别制作4组大鼠模型.处理组:缺血预处理(IPC)后24h结扎冠脉建立急性心梗大鼠模型;对照组:开胸后只穿线未进行IPC,24h后结扎冠脉建立急性心梗大鼠模型;IPC组:只进行IPC不结扎冠脉;假手术组:既不进行IPC操作也不结扎冠脉.对前2组模型建立3d、7d和14d后免疫组化法检测梗死边缘区毛细血管新生、动脉再生.14d后评价心功能,测量心梗面积:对IPC组和假手术组采用免疫组化法检测缺血区心肌血管内皮生长因子(VEGF)表达.结果:处理组IPC后24h缺血区心肌可见到毛细血管新生,梗死3d、7d和14d后梗死边缘区心肌毛细血管密度和小动脉密度较对照组显著增加.处理组大鼠短轴缩短率较对照组显著升高,心梗面积减少.IPC组缺血区心肌VEGF表达较假手术组显著升高.结论:延迟缺血预处理改善心梗后远期心功能,减少心梗面积,增加梗死边缘区毛细血管新生和小动脉再生,至少部分与IPC后VEGF表达增加有关.     

三七总皂苷对大鼠缺血心肌血管新生及相关生长因子的影响

目的观察三七总皂苷促对大鼠缺血心肌血管新生及相关生长因子表达的影响。方法结扎左冠状动脉制备急性心肌梗死(AMI)模型大鼠,随机分为模型组和三七总皂苷低、高剂量组,另设假手术组。比较各组大鼠心肌微血管密度(MVD)和血管内皮生长因子(VEGF)、碱性成纤维细胞生长因子(b FGF)蛋白表达灰度值。结果模型组和三七总皂苷组大鼠MI边缘区MVD及VEGF、b FGF蛋白表达灰度值均明显高于假手术组(P<0.01);三七总皂苷组大鼠MI边缘区MVD及VEGF、b FGF蛋白表达灰度值明显高于模型组(P<0.05或P<0.01)。结论三七总皂苷可促进心肌梗死(MI)后大鼠缺血心肌血管新生而发挥缺血心肌保护作用,可能机制为增强心肌VEGF、b FGF蛋白表达。     

rAAV介导血管生长素基因转染改善心肌梗死大鼠左室重构

目的 观察腺相关病毒介导的血管生长素(ANG)基因转染对心肌梗死(MI)大鼠左室心肌组织ANG蛋白表达、毛细血管密度和左室重构的影响.方法 成年雄性Wistar大鼠,随机分为假手术组(sham-operation)、心肌梗死心肌内注射rAAV-lacZ组(MI-rAAV-lacZ)和心肌梗死心肌内注射rAAV-ANG组(MI-rAAV-ANG).直视下结扎冠状动脉左前降支建立MI模型,冠脉结扎后立即取rAAV-lacZ或rAAV-ANG梗死区周围四个点注射.四周后处死大鼠,左室称重,计算左室重量与体重比值.Western blot方法检测心肌组织ANG蛋白表达水平;免疫组化方法检测vWF表达以评价心肌组织毛细血管密度;组织学切片上测量非梗死区心肌细胞的横径和心肌间质纤维沉积指数.结果 与sham-operation组和MI-rAAV-lacZ组相比,MI-rAAV-ANG组大鼠左室心肌组织ANG水平显著升高;左室非梗死区毛细血管密度在MI-rAAV-lacZ组大鼠显著下降,而MI-rAAV-ANG组则与sham-operation组无显著差异;MI-rAAV-lacZ组大鼠表现出显著的左室非梗死区重构,包括左室重量增加、非梗死区心肌细胞横径增加、心肌间质纤维沉积增多,这些指标在MI-rAAV-ANG组与sham-operation组之间无显著差异.结论 用心肌内注射方式转染rAAV-ANG可显著上调MI大鼠左室心肌ANG蛋白表达,诱导新血管生成,改善MI后左室重构.     

人参皂苷Rg1对急性心肌梗死大鼠血管新生的作用

目的:研究人参皂苷Rg1对急性心肌梗死(AMI)大鼠血管新生的影响及其机制。方法:建立Wistar大鼠急性心肌梗死模型,分假手术组、急性心肌梗死对照组、人参皂苷Rg1低剂量治疗组(1mg/kg)和高剂量治疗组(5mg/kg),于术后3,7,10,14d测定血清心肌酶、心肌梗死面积、梗死区微血管密度,RT-PCR法检测梗死区心肌组织血管内皮生长因子(VEGF)mRNA的表达。结果:心肌梗死组织中各时段假手术组的微血管密度、VEGFmRNA表达均低于手术各组(P<0.01);治疗组心肌酶及心肌梗死面积明显降低(P<0.05),梗死区血管生成数量稳定持续增加,与对照组有显著差异(P<0.01);心肌梗死后VEGFmRNA表达随缺血时间的延长(3,7,10d组)有增高趋势,治疗组明显升高(P<0.01),14d时VEGFmRNA的增长出现停止或下降。结论:严重缺血急性期可刺激心肌组织产生大量的VEGF起自我保护作用,人参皂苷Rg1增加其表达,并可刺激心肌梗死区的血管生成。     

阿托伐他汀对大鼠心肌梗死后心肌纤维化及心肌肿瘤坏死因子-α的影响

目的 探讨阿托伐他汀对大鼠心肌梗死(MI)后心肌纤维化及心肌肿瘤坏死因子-α的影响及机制.方法 选取雌性Wistar大鼠结扎左冠状动脉,建立MI模型,术后将存活大鼠随机分为阿托伐他汀组(n=13)予阿托伐他汀10mg/(kg·d)灌胃,MI组(n=12)及假手术组(n=10)分别灌等量自来水,连续4周.心脏标本病理分析,分别测定左室截面直径;VG染色测定左室非梗死区(LVNIZ)和梗死区胶原容积分数(CVF);放免法测定NIZ血管紧张素Ⅱ(AngⅡ)和S-P法免疫组化检测NIZ肿瘤坏死因子-α(TNF-α)定位和表达.结果 ① MI组与阿托伐他汀组梗死范围和梗死区CVF均无统计学意义.②与假手术组相比,MI组左室截面直径,LVNIZ胶原容积分数、NIZ AngⅡ、TNF-α明显增加(P<0.01～0.001).TNF-α主要定位于心肌间质,梗死区表达最强,非梗死区心肌细胞中亦有表迭.③与MI组相比,阿托伐他汀组上述指标均显著降低(P<0.05～0.001).结论 阿托伐他汀不影响梗死愈合,并可能通过抑制心肌局部AngⅡ、TNF-α的表达而减轻心肌纤维化.     

辛伐他汀对大鼠心肌梗死后MMP-2,9 mRNA表达的影响

目的 :观察辛伐他汀对大鼠心肌梗死 (MI)后心肌基质金属蛋白酶 2 ,9(MMP 2 ,9)mRNA表达的影响。方法 :结扎大鼠左冠状动脉前降支 (LAD)制成急性心肌梗死模型 ,随机分为 3组 :分别为辛伐他汀干预组(MI S)、心肌梗死对照组 (MI C)和假手术组 (sham)。 4周后 ,RT PCR法检测左心室梗死区及非梗死区心肌MMP 2和MMP 9mRNA表达的情况。结果 :大鼠MI4周后左心室心肌MMP 2和MMP 9mRNA表达较假手术组明显升高 (P <0 .0 5 ) ,辛伐他汀组上述指标较梗死对照组显著降低 (P <0 .0 5 ) ,但仍高于假手术组 (P <0 0 5 ) ,三组血脂无显著性差异。结论 :辛伐他汀减少大鼠心肌梗死 4周后左心室心肌MMP 2和MMP 9mR NA表达 ,此改变不依赖其降脂作用。     

骨髓间充质干细胞移植对心肌梗死大鼠损伤心肌的修复效果

目的 探讨骨髓间充质干细胞(BMSCs)移植对心肌梗死大鼠损伤心肌的修复效果,为进一步提高BMSCs移植治疗心肌梗死的疗效提供实验依据.方法 将22只大鼠参照Olivette方法制作心肌梗死模型,共16只进入实验终点,随机分为2组:对照组(C组,n=8)梗死区注射P BS;骨髓间充质干细胞移植组(M组,n=8)梗死区注射BMSCs.术后喂养4周,行心脏彩超,取心脏组织,荧光显微镜观察BMSCs的分布、分化及梗死区毛细血管密度.结果 标记CM-Dil和cTnT免疫组织化学染色双重阳性的心肌样细胞在梗死区分布.与C组相比,M组大鼠左室收缩末期内径(LVEDd)、左室舒张末期内径(LVEDs)、射血分数(EF)、左室短轴缩短率(FS)均有明显改善(P＜0.05),毛细血管密度明显增加(P＜0.05).结论 BMSCs可在心肌梗死的大鼠心脏分化为心肌样细胞,提高梗死区毛细血管密度,改善心功能.     

瓜蒌皮注射液对急性心肌梗死大鼠缺血心肌损伤的保护作用

目的探讨瓜蒌皮注射液对急性心肌梗死大鼠缺血心肌的保护作用及其对血管内皮生长因子（VEGF）表达的影响。方法 60只SD大鼠随机分成正常对照组、单纯手术组、低剂量给药组、高剂量给药组、假手术组各12只。采用开胸结扎冠状动脉左前降支的方法建立心肌梗死模型,4周后处死动物。测定血清肌酸磷酸激酶同工酶MB（CK-MB）、一氧化氮（NO）,取梗死边缘区心肌组织行病理分析及分级。免疫组化技术及Western blot技术检测各组缺血心肌VEGF蛋白质水平表达变化;逆转录多聚酶链反应（RT-PCR）法检测缺血心肌VEGF mRNA表达变化。结果给药组心肌坏死病理积分较组单纯手术明显降低,手术组和给药组大鼠血清CK-MB明显高于对照组及假手术组,给药组血清CK-MB均较单纯手术组降低（P〈0.01）,且高剂量组低于低剂量组（P〈0.01）;单纯手术组大鼠血清NO明显低于给药组和对照组,给药组高于单纯手术组。单纯手术组VEGF及其mRNA表达较正常对照组和假手术组增加,给药组缺血心肌VEGF及其mRNA表达较单纯手术组增加（P〈0.01）,高剂量组缺血心肌VEGF及其mRNA表达高于低剂量给药组（P〈0.01）。结论瓜蒌皮注射液能够减轻心梗大鼠缺血心肌损伤,其作用机制可能增加心肌损伤大鼠心肌VEGF表达,与血清NO的含量有关,且作用与剂量相关。     

磁共振心肌灌注成像评价心肌梗死PTCA治疗前后心肌存活

目的 评价磁共振心肌灌注成像(MRMPI) 检测心肌梗死存活心肌的作用. 方法 选择心肌梗死患者51 例.采用1.5 T MR扫描仪,反转恢复快速小角度激励( IR-turbo FLASH) 序列,全部患者均在静脉注射钆喷替酸葡甲胺(Gd-DTPA) 0.1 mmol/kg、MRMPI 首过期及5~30 min 延迟期成像.21 例行静息、负荷99锝单光子发射计算机体层摄影术( single photon emission computed tomography, SPECT) 进行对照研究.首过期行短轴面成像,延迟期行短轴面及长轴面成像.结果 51例心肌梗死患者,42 例(82.3%) 首过期显示灌注减低;50 例(98%) 延迟增强.在21例168个心肌段SPECT诊断无活性心肌段48个,MRMPI 示梗死区均有延迟增强,SPECT诊断存活心肌段120 个,MRMPI 示97段无延迟增强.以静息、负荷99m锝SPECT 作为参考标准,MRMPI 的敏感度、特异度分别为100%、80.8%. 结论 MRMPI 可有效地检测心肌梗死的存活和非存活心肌,以及其程度和范围.     

Acute myocardial infarction due to myocardial bridge

Myocardial bridge (MB) is regarded as a common anatomic variant rather than a congenital condition anomaly,defined as the intramyocardial course of a portion of the coronary artery.It was first mentioned by Rayman in 1737 and first described by Grainicianu in the early 1920s.The current gold standard for diagnosing     

Intracoronary adenosine improves myocardial perfusion in late reperfused myocardial infarction

Background Myocardial perfusion associates with clinical syndromes and prognosis.Adenosine could improve myocardial perfusion of acute myocardial infarction within 6 hours,but few data are available on late perfusion of myocardial infarction (MI).This study aimed at quantitatively evaluating the value of intracoronary adenosine improving myocardial perfusion in late reperfused MI with myocardial contrast echocardiography(MCE).Methods Twenty-six patients with anterior wall infarcts were divided randomly into 2 groups:adenosine group(n=12) and normal saline group(n=14).Their history of myocardial infarction was about 3-12 weeks.Adenosine or normalsaline was given when the guiding wire crossed the lesion through percutaneous coronary intervention(PCI),then the balloon was dilated and stent(Cypher/Cypher select)was implanted at the lesion.Contrast pulse sequencing MCE with Sonovue contrast via the coronary route was done before PCI and 30 minutes after PCI.Video densitometry and contrast filled-blank area were calculated with the CUSQ off-line software.Heart function and cardiac events were followed up within 30 days.Results Perfusion in the segments of the criminal occlusive coronary artery in the adenosine group was better than that in the saline group(5.71±0.29 vs 4.95±1.22,P＜0.05).Ischemic myocardial segment was deminished significantly afterPCI,but the meliorated area was bigger in the adenosine group than in the saline group((1.56±0.60)cm2 vs(1.02±0.56) cm2,P＜0.05).The video densitometry in critical segments was also improved significantly in the adenosine group (5.53±0.36 vs 5.26±0.35,P＜0.05).Left ventricular ejection fraction(LVEF)was improved in all patients after PCI,but EF was not significant between the two groups((67±6)% vs(62±7)%,P＞0.05).There was no in-hospital or 30-day major adverse cardiac event(MACE)in the adenosine group but 3 MACE in the saline group in 30 days after PCI.Conclusions Adenosine could improve myocardial microvascular perfusion in the late reopening of an occluded infarct reIaled artery(3 to 12 weeks after AMI)and clinical outcome in the follow-up period,and myocardial microvascular perfusion is a powerful predictor of clinical events.     

Evaluation of Myocardial Viability after Myocardial Infarction with Intravenous Real-time Myocardial Contrast Echocardiography

The myocardial viability after myocardial infarction was evaluated by intravenous myocardial contrast echocardiography. Intravenous real-time myocardial contrast echocardiography was performed on 18 patients with myocardial infarction before coronary revascularization. Follow-up echocardiography was performed 3 months after coronary revascularization. Segmental wall motion was assessed using 18-segment LV model and classified as normal, hypokinesis, akinesis and dyskinesis. Viable myocardium was defined by evident improvement of segmental wall motion 3 months after coronary revascularization. Myocardial perfusion was assessed by visual interpretation and divided into 3 conditions： homogeneous opacification; partial or reduced opaciflcation or subendocardial contrast defect; contrast defect. The former two conditions were used as the standard to define the viable myocardium. The results showed that 109 abnormal wall motion segments were detected among 18 patients with myocardial infarction, including 47 segments of hypokinesis, 56 segments of akinesis and 6 segments of dyskinesis. The wall motion of 2 segments with hypokinesis before coronary revascularization which showed homogeneous opacification, 14 of 24 segments with hypokinese and 20 of 24 segments with akinese before coronary revascularization which showed partial or reduced opaciflcation or subendocardial contrast defect was improved 3 months after coronary revascularization. In our study, the sensitivity and specificity of evaluation of myocardial viability after myocardial infarction by intravenous real-time myocardial contrast echocardiography were 94.7% and 78.9%, respectively. It was concluded that intravenous real-time myocardial contrast echocardiography could accurately evaluate myocardial viability after myocardial infarction.     

Intracoronary adenosine improves myocardial perfusion

Background Myocardial perfusion associates with clinical syndromes and prognosis. Adenosine could improve myocardial perfusion of acute myocardial infarction within 6 hours, but few data are available on late perfusion of myocardial infarction （MI）. This study aimed at quantitatively evaluating the value of intracoronary adenosine improving myocardial perfusion in late reperfused MI with myocardial contrast echocardiography （MCE）.
Methods Twenty-six patients with anterior wall infarcts were divided randomly into 2 groups： adenosine group （n=12） and normal saline group （n=-14）. Their history of myocardial infarction was about 3-12 weeks. Adenosine or normal saline was given when the guiding wire crossed the lesion through percutaneous coronary intervention （PCI）, then the balloon was dilated and stent （Cypher/Cypher select） was implanted at the lesion. Contrast pulse sequencing MCE with Sonovue contrast via the coronary route was done before PCI and 30 minutes after PCI. Video densitometry and contrast filled-blank area were calculated with the CUSQ off-line software. Heart function and cardiac events were followed up within 30 days.
Results Perfusion in the segments of the criminal occlusive coronary artery in the adenosine group was better than that in the saline group （5.71：L-0.29 VS 4.95±1.22, P〈0.05）. Ischemic myocardial segment was deminished significantly after PCI, but the meliorated area was bigger in the adenosine group than in the saline group （（1.56±0.60） cm^2 vs （1.02±0.56） cm^2, P〈0.05）. The video densitometry in cntical segments was also improved significantly in the adenosine group （5.53±0.36 VS 5.26±0.35, P〈0.05）. Left ventricular ejection fraction （LVEF） was improved in all patients after PCI, but EF was not significant between the two groups （（67±6）% vs （62±7）%, P〉0.05）. There was no in-hospital or 30-day major adverse cardiac event （MACE） in the adenosine group but 3 MACE in the saline group in 30 days after     

四氢生物蝶呤对未成熟心肌保护作用及线粒体ATP酶活性的影响

目的:观察四氢生物蝾呤(BH4)对未成熟缺血再灌注心肌的保护作用及心肌线粒体ATP酶活性的影响.方法:建立幼鼠离体全心缺血再灌注模型,80只幼鼠随机分为实验组(BH4停搏液)和对照组(St.ThomasⅡ液),每组40只.测定缺血前、缺血再灌注30,60和120min时的冠状动脉流出量.分别测定两组之间不同时间点的心肌丙二醛(MDA)含量、心肌一氧化氮(NO)浓度以及心肌细胞线粒体Na ,K -ATP酶和Ca2 -ATP酶的活性.结果:BH4能显著提高冠脉流出量的恢复率,增加NO的产量,降低脂质过氧化物的产生并抑制心肌缺血再灌注后Na ,K -ATP酶和Ca2 -ATP酶活性的下降(P＜0.05).结论:BH4心脏停搏液通过增加NO的产量,保护心肌细胞线粒体ATP酶的功能,对未成熟心肌具有更好的保护效果.     

经静脉心肌声学造影术评价区域性心肌灌注的初步临床研究

目的 探讨经静脉心肌声学造影术（ＩＭＣＥ）的安全性,可行性及临床应用价值。方法 １４例住院病人行ＩＭＣＥ检查、心肌梗死６例,心绞痛６例,可疑冠心病２例。其中８例行冠脉造影术（ＣＡＧ）,７例行单光子发射计算机断层显像术（ＳＰＥＣＴ）检查。ＳＰＥＣＴ、ＩＭＣＥ均采用目测半定量方法（０￣３分）评价心肌灌注。冠脉根据其病变程度分为４组：正常（无狭窄）、中度狭窄（５０％￣７５％）,重度狭窄（７６％￣９９％）     

MRI心肌延迟增强扫描在心肌梗死诊断中的初步应用

目的 初步评价MRI心肌延迟强化在诊断心肌梗死中的价值.方法 2005～2006年对本院9例确诊为心肌梗死的患者,8例疑诊患者进行MRI多技术扫描.结果 9例确诊患者MRI延迟增强扫描心肌都有不同程度强化.8例疑诊患者中2例心内膜下心肌梗死,2例心肌缺血,1例肥厚型心肌病伴多灶性心肌坏死,1例广泛心肌损害,2例心肌显示正常.结论 MRI心肌延迟增强扫描对冠心病急慢性心肌梗死坏死心肌诊断是准确和可靠的.     

Relation of myocardial bridge to myocardial infarction: a meta-analysis

Background Small case series have suggested an association of coronary myocardial bridge （MB） with myocardial infarction （MI）.However,the relationship between MB and major adverse cardiac events （MACE） remains largely unknown.The aim of this study was to assess the relationship between MB and MACE involving MI.Methods We performed a systematic search of MEDLINE,PreMEDLINE,and all EMB Reviews as well as a reference list of relevant articles according to the SPICO （Study design,Patient,Intervention,Control-intervention,and Outcome） criteria using the following keywords：myocardial bridging,myocardial bridge,intramural coronary artery,mural coronary artery,tunneled coronary artery,coronary artery overbridging,etc.Bibliographies of the retrieved publications were additionally hand searched.Studies were included for the meta-analysis if they satisfied the following criteria：（1） they evaluate the association of MB with cardiovascular endpoint event; （2） they included individuals with MB and those without MB; 3） they excluded individuals with obstructive coronary artery disease （CAD）.Studies were reviewed by a predetermined protocol including quality assessment.Dates were pooled using a random effect model.Results Seven observational studies that followed 5 486 patients eligible for the enrolled criteria were included from 7 136 initially identified articles.The prevalence of MB was 24.8％ （1 363/5 486）.During 0.5-7.0 years of follow-up of this cohort of population,crude outcome rates were 8.0％ in the MB group and 7.7％ in the non-MB group.The odds ratio of overall MACE and MI were 1.34 （95％ confidence interval （CI）：0.57-3.17,P=0.51,n=7 studies） and 2.75 （95％ CI：1.08-7.02,P ＜0.03,n=5 studies） respectively for subjects of MB compared to non-MB.Conclusion Relationship between MB and MI appears to be a real one,although the study did not reveal a connection of MB to MACE,suggesting whether the necessity of antiplatelet therapy needs to be further studied in a larger cohort of patients with MB prospectively.     

99mTc-MIBI 心肌断层显像评价急性心肌梗塞后左心室重构

目的应用９９ｍＴｃ－ＭＩＢＩ静息心肌显像评价心肌梗塞后左心室重构。方法对７６例急性心肌梗塞患者的局部及整体左心室重构进行了９９ｍＴｃ－ＭＩＢＩ静息心肌显像评价,其中４２例为非门控静息心肌显像,３４例为门控静息心肌显像,９９ｍＴｃ－ＭＩＢＩ静息心肌断层显像于发病后平均１２ｈ、１～２周、１～３月分别进行。结果左心室重构的显像表现为梗塞膨展：室壁变薄（７２／７６）,室壁拉长（５８／７６）,局部扩张（５５／７６）及局部变形（５１／７６）;非梗塞心肌的重构：室壁变厚（３６／７６）及室壁拉长（４９／７６）;左心室整体变形（３５／７６）及左心室整体扩张（４２／７６）。将左心室重构分为３度：Ⅰ度（２５／７６）,无左心室整体变形及整体扩张;Ⅲ度（３１／７６）,有左心室整体变形及整体扩张;Ⅱ度（２０／７６）,介于Ⅰ度与Ⅲ度之间者,左心室重构的程度随病情的发展而改变,通过分析急性心肌梗塞后系列静息心肌显像,可对左心室重构程度的变化作出评价。结论左心室重构是评价急性心肌梗塞治疗效果和预后的重要依据;９９ｍＴｃ－ＭＩＢＩ心肌断层显像是评价急性心肌梗塞后左心室重构的有用技术。