不同治疗方法对急性心肌梗死心室重构及心脏功能的影响

目的评价服用药物、溶栓治疗和冠状动脉介入治疗术对急性心肌梗死心室重构及心功能的影响。方法以院内1997年1月~2004年10月急性心肌梗死患者168例为研究对象,根据治疗方法不同将其分为三组,分别于急性期和6个月之后进行超声心动图检查,测定左心室射血分数、左心室舒张末期容积、左心室收缩末期容积,并计算左心室室壁运动指数。结果三种方法治疗急性心肌梗死疗效均具有统计学意义。结论急诊冠状动脉介入治疗急性心肌梗死心室重构及心脏功能优于药物和溶栓治疗。     

PPARγ配体对急性心肌梗死心室重构炎症因子的影响

现在对当前急性心肌梗死后心室重构的发病机理认识基础之上,综述了PPARγ的配体在心室重构的发生过程中,对炎症反应的影响的研究进展.     

G-CSF对急性心肌梗死大鼠心室重构的影响

通过结扎冠状动脉前降支建立大鼠急性心肌梗死(AMI)模型,将大鼠随机分成四组:AMI后1周模型组、AMI后人重组粒细胞集落刺激因子(rhG-CSF)治疗1周组、AMI后2周模型组、AMI后rhG-CSF治疗2周组.另设1、2周假手术组各8只.治疗组皮下注射rhG-CSF 5 μg/(kg·d),连续7 d;AMI模型组和假手术组皮下注射等量生理盐水.测量各组心室重构参数.结果 与假手术组比较,AMI后1周,心室腔明显扩大(P<0.05);AMI后2周时,心室腔内径扩大更明显(P<0.01),且心室质量指数(VWI)比假手术组明显增加(P<0.05);rhG-CSF治疗2周组VWI低于AMI后2周模型组,心室腔扩大程度小于模型组(P<0.05).认为注射rhG-CSF可动员自体骨髓干细胞,缩小梗死面积,改善大鼠AMI后心室重构,促进梗死处血管再生及细胞增殖.     

氯沙坦对急性心肌梗死后心室重构的影响

目的:研究氯沙坦对急性心肌梗死后心室重构的影响。方法:符合入选标准的120例急性心肌梗死患者被随机均分为三组:氯沙坦组(A组)。卡托普利组(B组),常规治疗组(C组),分别于治疗前,治疗后6个月进行超声心动图检查。结果:对照组常规治疗后.左室舒张末容积(LVEDV)、左室射血分数(LVEF)、每搏量(SV)均进一步恶化(P<0.05),A、B组的LVEDV、LVEF、SV较C组则无显著恶化(P<0.05～<0.01).A组又好于B组(P<0.05)。结论:氯沙坦能明显改善急性心肌梗死后心室重构。     

去肾交感神经术对猪急性心肌梗死后心功能及心室重构的影响

目的:探讨去肾交感神经术(renal sympathetic denervation,RDN)对急性心肌梗死(AMI)后心功能及心室重构的影响。方法:微球栓塞前降支中远端构建AMI猪模型。实验分组为:对照组,建模后未接受RDN(n=10);RDN组,建模后1周接受RDN(n=10)。建模后1周(RDN前)及建模后4周对两组猪利用超声心动图检测左心功能和左心室大小,并检测相关血清学指标。结果:建模后4周,与对照组相比,RDN组的左室射血分数(EF)明显升高[(55.34±7.12)%对(50.52±2.23)%,P=0.035],左室收缩末期内径(LVESD)明显减小[(24.43±2.23)mm对(29.33±3.53)mm,P=0.020];与自身RDN治疗前比较,RDN组EF[(55.34±7.12)%对(49.23±4.58)%,P=0.034]和E/A(0.93±0.24对0.85±0.10,P=0.048)明显升高,LVESD明显减小[(24.43±2.23)mm对(26.55±2.11)mm,P=0.048];RDN组的去甲肾上腺素[(247.31±103.13)ng/L对(337.90±60.33)ng/L,P0.05]和肾素[(414.92±202.40)ng/L对(587.54±235.62)ng/L,P0.05)]水平显著低于对照组。结论:RDN可以提高猪AMI后的左心收缩功能,改善心室重构。     

急性心肌梗死病人左心室重构及心功能的影响因素

目的观察冠心病各种危险因素对急性心肌梗死病人左室重构和心功能的影响.方法 124例急性心肌梗死病人应用超声测定心脏各项指标,分析血压、血脂、吸烟、血尿酸等冠心病危险因素对急性心肌梗死病人左室射血分数(LVEF)的影响,以及高血压对左室重构和功能的影响.结果急性心肌梗死时的收缩压与LVEF值呈明显负相关,收缩压越高,LVEF值越低(P<0.05).其他冠心病危险因素舒张压、血脂、吸烟、血尿酸与LVEF值变化无明显相关性.有高血压病的心肌梗死病人LVEF值明显降低,左室舒张末期内径和左室质量显著高于无高血压病组病人(P<0.001).结论高血压病对急性心肌梗死病人左室重构和心脏功能有明显的影响.     

阿托伐他汀对急性心肌梗死患者心室重构及心功能的影响

目的 探讨阿托伐他汀对急性心肌梗死(AMI)后心室重构、心功能的影响.方法 血脂正常的AMI患者63例,随机分为阿托伐他汀治疗组(A组)33例和常规治疗组(B组)30例.B组仅给予常规治疗,A组于常规治疗基础上给予阿托伐他汀20 mg/d.患者于治疗后7、180 d查肝功能、高密度脂蛋白(HDL)、C反应蛋白(CRP)、脑钠素(BNP)水平,超声心动图检查测定左心室射血分数(LVEF)、舒张末期容积指数(EDVI)和收缩末期容积指数(ESVI).结果 治疗180 d时,A组CRP、BNP降低,HDL明显升高(P<0.05),LVEF、EDVI、ESVI明显改善(P<0.05);B组无明显变化.180 d与7 d比较,A组EDVI、ESVI、LVEF改善,CRP、HDL升高,BNP降低,差异有统计学意义(P<0.05).结论 阿托伐他汀治疗可以延缓动脉粥样硬化的进程,防止心室重构,改善患者心功能和远期预后.     

心脏肥大细胞与心肌梗死后心室重构

在心脏组织内,肥大细胞存在于心肌之间和靠近血管的位置.近年来对于心脏肥大细胞(CMC)在急性心肌缺血中作用的研究有升温之势.心肌梗死时,CMC数量增多功能处于活跃状态,并释放介质.随着心肌梗死后心肌的坏死,开始了大规模心室重构的调节过程.CMC释放的介质可以激活基质金属蛋白酶,后者参与了心肌梗死后的心室重构过程.目前有...     

还原型谷胱甘肽对急性心肌梗死患者氧化应激和心室重构的影响

目的 观察还原型谷胱甘肽对急性心肌梗死患者氧化应激和心功能的影响.方法 选择急性心肌梗死患者92例,随机分成治疗组(48例)和对照组(44例).对照组给予常规治疗,治疗组在常规治疗的基础上给予还原型谷胱甘肽治疗.两组疗程均为14 d.所有患者测定不同时间血浆中超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)的水平;测定治疗前和治疗4 w后的心功能.结果SOD和GSH-Px水平方面,治疗组较治疗前明显增高(P＜0.01),对照组则明显下降(P＜0.01),两组间比较差异更加明显(P＜0.01).与对照组比较,治疗组左心室舒张末期内径(LVEDd)和左心室射血分数(LVEF)均有明显改善(P＜0.01),治疗组比对照组改善更明显(P＜0.01);对照组仅LVEDd较治疗前有明显改善(P＜0.01),而LVEF无明显改善(P＞0.05).结论 还原型谷胱甘肽能有效改善急性心肌梗死患者的氧化应激状态和心功能,抑制左心室重构.     

脂质体携载前列腺素E对急性心肌梗死冠状动脉介入治疗后心室重构及血清炎症因子水平的影响

目的:探讨脂质体携载前列腺素E对急性心肌梗死冠状动脉介入(PCI)治疗后心室重构及血清TNF-α、IL-6水平的影响。方法:选取2017年1月至2018年1月,我院收治的急性心肌梗死患者94例,患者均行PCI治疗,随机分为对照组和观察组,每组各47例,对照组采用培哚普利进行治疗,观察组在对照组基础上采用脂质体携载前列腺素E进行治疗,对两组患者治疗1 d和2周后的心室重构变化水平、治疗前后炎性因子水平、血管内皮功能、6 min内患者步行距离以及临床治疗进行比较。结果:两组患者治疗1 d后心室重构变化水平均无明显差异(P0. 05),治疗2周后对照组LVEF水平低于观察组但LVESV、LVEDV两项指标水平高于对照组(P0. 05);治疗2周后对照组患者的炎症因子水平显著高于观察组(P0. 05);观察组治疗2周后血管内皮功能明显优于对照组(P0. 05);治疗2周后对照组患者临床治疗有效率低于观察组(P0. 05);治疗2周后对照组患者6 min的步行距离短于观察组(P0. 05)。结论:对急性心肌梗死PCI治疗后患者采用脂质体携载前列腺素E,可显著降低患者血清内的炎性因子水平,提高临床治疗效果。     

急性心肌梗死经皮冠状动脉介入治疗患者心肌胶原与左心室重构的关系

目的探讨急性心肌梗死经皮冠状动脉介入(percutaneous coronary intervention,PCI)治疗患者心肌胶原变化与左心室重构关系。方法选择2011年12月至2012年9月入住宝安区人民医院的急性心肌梗死患者共70例为研究对象。按照入院后患者是否行直接PCI治疗分为直接PCI治疗组(n=30)和择期PCI治疗组(n=30),其中10例(其中直接PCI治疗组5例,择期PCI治疗组5例)患者出院后不愿意随访。所有入选患者术前、术后3 d及术后30 d均分别以酶联免疫吸附法测定血清Ⅰ型C端胶原前肽(carboxy-terminal propeptide of type I procollagen,PICP)、Ⅲ型N端胶原前肽(amino-terminal propeptide of type III procollagen,PⅢNP)和Ⅰ型C端胶原末肽(carboxy-terminal telopeptide of collagen type I,CITP)浓度;术后3 d、术后30 d均行心脏超声检查;术后30 d行单光子发射计算机断层显像测量心肌梗死面积。结果术后30 d直接PCI治疗组血清PICP、PⅢNP、CITP浓度较择期PCI治疗组明显降低,差异有统计学意义[PICP:(7.76±1.47)ng/mL vs.(10.73±1.67)ng/mL,P﹤0.05;PⅢNP:(11.17±4.72)ng/mL vs.(37.80±6.83)ng/mL,P﹤0.05;CITP:(31.18±6.78)ng/mL vs.(45.10±9.70)ng/mL,P﹤0.05]。术后30 d直接PCI治疗的左心室舒张末期内径、左心室收缩末期内径、心肌梗死面积明显低于择期PCI治疗组[(46.57±6.10)mm vs.(52.63±6.50)mm,P﹤0.05;(34.25±4.86)mm vs.(37.33±3.56)mm,P﹤0.05;22.8%±3.4%vs.28.2%±6.8%,P﹤0.05]。结论直接PCI治疗可有效地挽救濒死的心肌,减轻心室重构,保护心功能,改善患者远期预后。检测血清心肌胶原浓度能作为预测心室重构的指标。     

易化经皮冠状动脉介入治疗对急性心肌梗死后心室重构的阻抑作用

目的:通过平衡法核素心室造影(ERNA)方法,对比评价溶栓、经桡动脉入径直接经皮冠状动脉介入治疗(PCI)和易化PCI对老年急性心肌梗死(AMI)患者心室重构的阻抑作用。方法:选择发病10h内的首次急性前壁ST段抬高型心肌梗死患者143例,随机分为直接PCI组71例和易化PCI组72例,另选择同期入院且一般临床资料匹配,但仅行溶栓治疗的70例患者为溶栓组。3组患者分别于AMI后1周、28周行ERNA,测定左室收缩功能参数及反常容积指数(PVI),随访28周内主要恶性心脏事件(MACE)的发生率。结果:①直接PCI组在PCI前梗死相关动脉(IRA)开通率明显低于溶栓组和易化PCI组(8.45%:31.43%,χ2=11.69;8.45%:30.56%,χ2=11.09;均P<0.01)。易化PCI组术后IRA血流TIMI-3级率高于直接PCI组(98.61%:88.73%,χ2=4.35,P<0.05)。②AMI后28周随访时,易化PCI组左室射血分数(LVEF)、左室峰射血率(PER)较溶栓组增高(t=2.21、2.29,均P<0.05),同时左室峰射血率时间(TPER)、PVI降低(t=2.41、2.37,均P<0.05);易化PCI组LVEF、PER较直接PCI组增高(t=2.08和2.13,均P<0.05),同时TPER、PVI降低(t=2.10、2.49,均P<0.05)。③随访28周,易化PCI组和直接PCI组MACE发生率均低于溶栓组(8.33%:54.29%,χ2=35.05;8.45%:54.29%,χ2=34.49;均P<0.01);3组间主要脏器大出血和颅内出血的发生率均差异无统计学意义。结论:经桡动脉入径易化PCI治疗可早期充分、持久地开通IRA,能在AMI早期阻抑AMI急性左室重构过程,改善左室收缩功能,其效应优于直接PCI和单纯溶栓治疗。     

急性心肌梗死后择期冠脉介入治疗对左室重构和心功能的影响

目的探讨急性心肌梗死（AMI）后择期经皮冠状动脉介入（PCI）治疗对左心室重构和心功能的影响。方法112例AMI患者,分为PCI组和药物治疗组,PCI组于发病后1～2周内行PCI治疗,所有患者于发病后1～2周时、4周和24周时行超声心动图（UCG）检查,观察左心室收缩末容积指数（LVESVI）、左心室舒张末容积指数（LV-EDVI）和左室射血分数（LVEF）。结果行PCI治疗后,血管再通率为100%,术后4周和24周的LVESVI、LVEDVI和LVEF均明显优于术前,与药物治疗组比较有显著性差异（P<0.05）。结论AMI后择期PCI治疗能够有效抑制左心室重构,改善心功能。     

冠状动脉介入治疗再灌注时间对急性前壁心肌梗死左室重构及远期预后的影响

目的评价冠状动脉介入治疗(PCI)再灌注时间对急性前壁心肌梗死左室重构及远期预后的影响。方法选择113例首次急性前壁心肌梗死患者,冠状动脉造影证实梗死相关动脉(IRA)完全闭塞(TIMI0～1级)。依据PCI再灌注时间分为3组,A组35例,6h内IRA成功再灌注;B组40例,6～12h内IRA成功再灌注;C组38例,12～24h内IRA成功再灌注。分别于术后即刻和6个月行冠状动脉造影及左心室造影,对比分析3组左心室造影的心功能指标:左心室舒张末容积、左心室收缩末容积、左心室射血分数、每分输出量、心脏指数,并观察1年内主要不良心脏事件(MACE)的发生情况。结果成功再灌注即刻,3组之间各项心功能参数无显著性差异。6个月时A组和B组各项心功能参数较即刻有改善趋势;C组较前下降,但均无统计学意义。1年随访期间,A、B组无死亡及再次心肌梗死事件发生。心绞痛的发生在3组中无差别。C组心力衰竭及死亡的发生均明显高于A、B组。结论前壁心肌梗死后尽早行PCI,开通IRA,可阻抑左室重构,改善心功能,减少死亡等MACE的发生,从而改善预后。     

螺内酯抑制急性前壁心肌梗死患者的左室重构

目的探讨急性前壁心肌梗死患者口服螺内酯对于左室重构的影响。方法将急性前壁心肌梗死患者随机分为两组。对照组30例,接受血管紧张素转换酶抑制剂、β-受体阻滞剂、抗血小板、调脂药物等常规处理。螺内酯组30例,在常规治疗基础上加用螺内酯（40mg,每日1次）。随访1年,并检测脑钠尿肽（BNP）及超声心动图以评价左室功能和左室容积。结果6和12月时螺内酯组血清BNP水平明显低于对照组[（355±74）ng/Lvs（418±77）ng/L,P<0.05和（316±72）ng/Lvs（389±67）ng/L,P<0.05],且12月时螺内酯组较对照组左室舒张末期内径（LVEDD）、左室收缩末期内径（LVESD）明显缩小[LVEDD:（49±6）mmvs（53±5）mm,P<0.05;LVESD:（37±5）mmvs（40±4）mm,P<0.05]。结论螺内酯可抑制急性前壁心肌梗死患者左室重构。     

急诊PCI对老年急性心肌梗死患者的疗效及左室重构的作用

目的观察急诊PCI对老年急性心肌梗死患者的临床疗效及恢复期左室重构的作用。方法98例老年急性心肌梗死患者（≥60岁）随机分为2组,其中PCI组50例,对照组48例。PCI组于发病12h内行急诊PCI术;对照组给于尿激酶150万u静脉溶栓治疗。两组患者均长期服用抗凝、抗血小板药物及冠心病二级预防药物,并分别于发病后1个月、6个月做心脏彩超了解心功能及左室重构情况,观察1年内主要不良心脏事件的发生情况。结果两组患者在发病1个月后左心室容积及射血分数差异无统计学意义;发病6个月后,PCI组左心室容积小于对照组,射血分数大于对照组,差异有统计学意义。PCI组主要不良心脏事件的发生率低于对照组,差异有统计学意义。结论对于老年急性心肌梗死患者,急诊PCI能阻止患者的左室重构,改善患者的远期左室功能,并能减少主要不良心脏事件的发生。     

Effect of hepatocyte growth factor on left ventricular remodeling after acute myocardial infarction in canine

Background and objectives To investigate the effect of hepatocyte growth factor (HGF) on left ventricular (LV) remodeling after acute myocardial infarction (AMI). Methods AMI was produced by ligation of proximal left anterior descending coronary artery(LAD) in 12 mongrel canines. These animals were randomized into 2 groups. In HGF group (n=6), canines were injected with pcDNA3-HGF lml (about 300ug) at the margin of infarcted myocardium; in control group (n=6) canines were injected with equal volume of normal saline. Cardiac function and left ventricular remodeling were evaluated with echocardiography at 1, 4, 8 weeks after MI. LV myocardium specimens were obtained at 8 weeks and stained with hematoxylin and eosin for histological examination or with sirius red to assess the collagen content. Results Compared with control group, LVEF in HGF group was significantly higher at 4 weeks (49.61+6.66 vs 39.84+6.39; P＜0.05) and at 8 weeks (51.57+8.53 vs 40.61+7.67; P＜0.05) after AMI, while LVESV was significantly lower in HGF group than that in control group at 8 weeks after AMI (18.98+3.47 vs 25.66+5.86; P＜0.05). Posterior left ventricular wall thickness decreased significantly from 1 wk to 8 wks after AMI in control group, while remained unchanged in HGF group. Compared with control group, histological examination showed more neovascularization and less scar, and sirius red staining indicated higher volume of type Ⅲ collagen (7.10&#177;4.06% vs 3.77&#177;1.09%; P＜0.05) and lower collagen Ⅰ/Ⅲ ratio value (1.11&#177;0.52 vs 2.94&#177;2.48; P＜0.05)in HGF group. Conclusion HGF gene transfer might improve cardiac function and LV remodeling after acute myocardial infarction by stimulating angiogenesis, reducing fibrosis, and reducing myocardial scarring.     

Predictors of early and late ventricular remodeling after acute myocardial infarction.

BACKGROUND: The determinants of the early and late stages of the ventricular remodeling process after infarction are not well defined. HYPOTHESIS: The study was undertaken to evaluate the factors that condition the time course of left ventricular dilation during the first 6 months after infarction. METHODS: The study group consisted of 74 patients with a first intermediate-large (> or = 4 Q waves) acute myocardial infarction. Contrast left ventricular and coronary angiograms were performed at 7 +/- 1 and 175 +/- 25 days after infarction. Left ventricular volumes, regional function and infarction artery status were quantified. Percutaneous transluminal coronary angioplasty (PTCA) was performed in the early angiogram in 31 patients. RESULTS: In the early angiogram, 13 patients showed ventricular remodeling (end-diastolic volume > 90 ml/m2). A larger extent of dysfunction was the only predictor (p < 0.002) of early remodeling. At 6 months, a smaller, early end-diastolic volume (p < 0.0001) and a poorer regional function recovery (p < 0.05) were independently related to late diastolic enlargement, and a poorer regional function recovery (p < 0.0001) and a smaller, early end-systolic volume (p < 0.009) were independently related to late systolic enlargement. One patient with compared with 20 patients without early remodeling (p < 0.04) presented with late remodeling (increment of the end-diastolic volume > 20% at 6 months). In patients with early remodeling, the end-diastolic volume did not change significantly (101 +/- 13 vs. 94 +/- 22 ml/m2, NS) at 6 months; despite this, they maintained larger diastolic volumes than patients with late remodeling (81 +/- 12 ml/m2, p < 0.04) at 6 months. Infarction artery status did not influence the evolution of ventricular volumes and regional function. CONCLUSIONS: (1) A large infarct size is the main determinant of postinfarction remodeling. (2) Such infarct size-dependent ventricular dilation occurs early and does not tend to increase in late stage; in contrast, some cases of intermediate-large size infarcts without early remodeling exhibit late remodeling associated with a poor late recovery of regional function. (3) Recovery of regional function (indicating myocardial viability) rather than infarction artery status plays a role in the late ventricular remodeling process.     

肝细胞生长因子对急性心肌梗死后左室重构的预测作用

目的: 探讨血清肝细胞生成因子(HGF)对急性心肌梗死(AMI)后早期左室重构的预测价值。方法: 36例AMI患者入院时及发病7 d测定血清HGF水平;AMI其中的26例分别于发病后7~10 d及发病后3个月行超声心动图检查,3个月时左室舒张末期容积指数（LVEDVI）与7~10 d时比增加≥5 ml/m2定义为左室重构组(n=11),对两组血清HGF值进行比较。结果: AMI患者入院时血清HGF浓度较对照组明显升高［(809±288)ng/L vs.(620±162)ng/L,P<0.01］,7 d时升高更显著［(1 607±1 355)ng/L,P<0.01］。发病7 d时血清HGF浓度在左室重构组较非左室重构组升高［(2 216±1 522)ng/L vs.(1 176±593)ng/L,P<0.05］,而入院时两组浓度则无显著差异。结论: AMI时血清HGF浓度升高,AMI后7 d时增高的血清HGF可能预示心室重构。     

Left ventricular remodeling in patients with stress hyperglycemia after acute myocardial infarction

Background To investigate the association between left ventricular remodeling and stress hyperglycemia (SH) inpatients with acute anterior wall myocardial Infarction. Methods Patients with acute anterior myocardial infarction and a successful primary percutaneous coronary intervention (PCI) were enrolled and divided into two groups according to the presence or absence of SH. Patients with diabetes mellitus were excluded. Echocardiographic studies were performed on discharge and at 6 month follow-up. Left ventricular (LV) ejection fractions (EF), LV end-diastolic volume (EDV) and LV end-systolic volume (ESV) were obtained at baseline and at 6 month. Differences between changes of ESV (ΔESV) and changes of EDV (ΔEDV) in the two groups as well as EF improvement rate (ΔEF %) over six month were obtained. Correlation between SH and LV remodeling was investigated. Results (1) At baseline, the level of hemoglobin A1c was significantly higher in SH group (6.9±1.4 vs 6.2±0.8 P=0.04). Other baseline characteristics, including peak serum creatine kinase MB and LV function, were similar between two groups; (2) EF increased significantly over 6 months in both group with SH((41.1±7.2)% vs (52.7±8.4)%, P=0.02) and group without SH. ((43.6±8.7)% vs (54.5±9.3)%, P=0.03) (3) Only in SH group, EDV increased significantly at 6 month (139.6±26.7 vs 126.1±26.7 P=0.04); (4) There was a weak correlation between ΔEDV and the level of fasting plasma glucose on admission.(Pearson's r=0.35, P0.01). Conclusions (1) Previous glucose metabolism disorder is at least partially responsible for hyperglycemia on admission; (2) Given successful primary PCI within recommended time interval, left ventricular function improved regardless of whether SH is present or not; (3) The degree of glucose metabolic dysfunction on admission is weakly associated with the remodeling process in 6 months