美托诺尔对急性心肌梗死患者miRNA-423-5p与整合素连接激酶的影响

目的:分析美托诺尔对急性心肌梗死患者miRNA-423-5p及整合素连接激酶的影响。方法:以收治的140例急性心肌梗死患者为研究对象,利用随机数字表法将其分为试验组与对照组,每组70例。对照组采用常规治疗方式,试验组在对照组基础上加用美托洛尔。分析两组患者的治疗效果、心肌功能改善情况、miRNA-423-5p相对表达量、术后心室重构指标、生存率与整合素连接激酶指标。结果:治疗2周后,试验组治疗效果优于对照组,差异具有统计学意义(P0.05)。试验组心肌酶改善情况较为理想,组间差异较为显著(P0.05)。试验组miRNA-423-5p及整合素连接激酶均低于对照组,差异具有统计学意义(均P0.05)。试验组术后心室重构指标均优于对照组,差异具有统计学意义(均P0.05)。结论:在急性心肌梗死治疗中,美托诺尔具有一定疗效,能改善患者miRNA-423-5p与整合素连接激酶,促进患者恢复,值得临床推广。     

炎性细胞因子与急性心肌梗死后心室重构的关系

急性心肌梗死后心室重构过程是发生心力衰竭的重要病理生理基础,与患者临床症状、并发症和死亡率密切相关。现就心室重构中炎性细胞因子的促发因素,其对心室重构的早、晚期作用和目前临床意义作一综述。     

心肌梗死患者miR-150、miR-21-5p水平表达变化及其与心室重构、预后的关系分析

目的 探究急性心肌梗死（acute myocaridial infarction, AMI）患者miR-150、miR-21-5p水平表达变化及与心室重构、预后的关系。方法 选择2019年7月至2021年7月治疗的120例AMI患者为研究对象（AMI组）,另选取同期80健康体检者为对照组,比较2组患者外周血miR-150、miR-21-5p水平及心室重构指标[左室射血分数（left ventricular ejection fraction,LVEF）、左心室舒张末内径（left ventricular end-diastolic dimension,LVEDD）、左室收缩末容积（left ventricular end-systolic volume, LVESV）、左心室质量指数（left ventricular mass index,LVMI）],分析miR-150、miR-21-5p与心室重构指标相关性;患者经皮冠状动脉介入治疗（percutaneous coronary intervention,PCI）术后随访1年,统计不良心血管事件（major adverse cardi...     

心肌梗死后的心室重构

心室重构是指心肌损伤后基因组表达导致分子,细胞和间质的改变,梗死区伸展,心室肥厚和心室总体扩张是心室重构的主要形态学改变,受血流动力学,神经激素活化及其他因素影响,冠脉血管重建,血管紧张素转换抑制剂和β受体阻滞剂能减轻重构,改善心衰患者的预后。     

微小RNA-17-5p通过靶向调控TP53INP1的表达对急性心肌梗死后心室重构的影响

目的：探讨微小RNA(miRNA)mi R-17-5p通过靶向调控肿瘤蛋白53诱导性核蛋白1(TP53INP1)的表达对急性心肌梗死(AMI)后心室重构的影响。方法：选取成年miR-17-5p^-/-、miR-17-5p^+/+和正常型SPF级昆明种小鼠各20只,采用随机数字表法分为假手术组、AMI组、miR-17-5p^-/-假手术组、miR-17-5p^-/-AMI组,miR-17-5p^+/+假手术组和miR-17-5p^+/+AMI组,每组10只,雌雄各半。构建小鼠AMI模型,采用超声心动图检测舒张末期容积指数(EDVI)、收缩末期容积指数(ESVI)和左室射血分数(LVEF),红四氮唑(TTC)染色法检测小鼠心肌梗死面积,实时定量聚合酶链反应(qRT-PCR)检测小鼠心脏组织miR-17-5p和TP53INP1 mRNA表达水平,Western blot法检测小鼠心脏组织TP53INP1蛋白表达水平。结果：与假手术组比较,AMI组建模后7 d和14 d的ED...     

他汀类药物治疗急性心肌梗死后心室重构的研究进展

急性心肌梗死(AMI)后心室重构是梗死区的心肌发生扩张和变薄,非梗死区心肌代偿性变化,心肌节段变长,使左室整体扩大.急性心肌梗死后左室重构是反映心肌梗死后预后的敏感指标,也是远期发生心脏性死亡最重要的危险因素之一,决定心肌梗死患者疾病与生命转归,因此心室重构的临床治疗已成为焦点与热点问题.     

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。     

衰老影响心肌梗死后心室重构机制研究进展

心肌梗死（MI）后病理性心室重构的机制尚未完全明确,目前认为MI后心肌细胞凋亡,受损的心肌细胞自噬以及心肌细胞自我更新能力减低等机制在病理性心室重构中发挥重要作用,最终导致心脏功能降低,在老年人中表现更为突出。随着年龄的增长,心力衰竭（HF）发生率显著增高,亟需深入研究老龄患者心室重构的病理生理改变,为发展靶向治疗老龄患者MI后HF提供理论依据。     

急性心肌梗死患者侧支血流分数与左室重塑关系的临床研究

目的应用压力导丝,通过冠状动脉内压力测定,评价急性心肌梗死(AMI)患者侧支血流分数(QC/QN)与左室重塑的关系.方法 21例AMI患者,于经皮腔内冠状动脉成形术(PTCA)时,对梗死相关动脉远端侧支血流行Rentrop分级并记录梗死相关动脉病变远端嵌楔压(Pw)及主动脉压(Pa),据QC/QN值将21例患者分为A组(QC/QN≥0.25),B组(QC/QN<0.25).所有患者于AMI后3 d和1个月行二维超声心动图检查,并进行统计学分析.结果 AMI后3 d A、B两组间EF分别为(51.7±7.1)%和(45.6±5.8)%(P<0.05);ESVI分别为(25.0±5.4) ml/m2和(30.5±6.2) ml/m2(P<0.05);EDVI分别为(51.9±9.8) ml/m2和(55.4±7.5) ml/m2(P>0.05).AMI后1个月,两组间EF分别为(53.7±7.1)%和(43.9±8.1)%(P<0.01);ESVI分别为(27.1±5.8) ml/m2和(38.7±11.5) ml/m2(P<0.01);EDVI分别为(58.3±7.5) ml/m2和(67.8±13.0) ml/m2(P<0.05).AMI后1个月较3 d,A组患者EF有明显改善(P<0.05),B组EF变化不明显(P>0.05);A、B两组患者ESVI和EDVI均有显著增大.结论造影Rentrop分级对侧支循环的评价存在局限性;AMI时侧支循环的开放是影响左室重塑的重要因素,侧支血流分数的大小是决定AMI后左室重塑及其预后的重要指标.     

Circulating miR-133a and miR-423-5p fail as biomarkers for left ventricular remodeling after myocardial infarction

Background

Recent studies have suggested that the microRNAs miR-133a and miR-423-5p may serve as useful biomarkers in patients with left ventricular (LV) heart failure or with LV remodeling after myocardial infarction (MI). These results were however obtained in small series of patients and control subjects were used as reference groups. Whether these microRNAs may be indicators of the degree of LV remodeling after MI is unknown.

Methods

246 patients with a first anterior Q-wave MI were included. Serial echocardiographic studies were performed at hospital discharge, 3 months, and 1 year after MI and analyzed at a core laboratory. We investigated the temporal profile (baseline, 1, 3 and 12 months) of circulating miR-133a and miR-423-5p and their relations with cardiac biomarkers (B-type natriuretic peptide, C-reactive protein, and cardiac troponin I) and LV remodeling during the 1 year follow-up.

Results

There were time-dependent changes in the levels of circulating miR-133a and miR-423-5p with significant increase of miR-133a at 12 months compared to 3 months and significant increase of miR-423-5p at 1, 3, and 12 months compared to baseline. However, miR-133a and miR-423-5p were not associated with indices of LV function and LV remodeling serially assessed during a 1 year period after an acute anterior MI, nor with B-type natriuretic peptide.

Conclusions

Circulating levels of miR-133a and miR-423-5p are not useful biomarkers of LV remodeling after MI.     

Dynamics of left ventricular remodeling in patients with acute myocardial infarction

Dynamics of structural and functional left ventricular parameters was investigated in 51 patients with acute anterior myocardial infarction by means of serial (on days 1, 2, 3, 5, 7, 10 and 21 of infarction) echocardiographical study. Increase of end-diastolic volume index relative to initial values became significant on 5th-7th days and continued to progress until 3rd week of infarction. Left ventricular cavity became dilated and attained more occurred shape predominantly at the account of increased transverse diameters. Abnormalities of left ventricular contractile and pump functions were most pronounced during first 3 days of the disease. Between 5th and 10th days improvement and stabilization of myocardial functional state took place accompanied by progression of left ventricular dilation and increase of its sphericity with lessening of degree of myocardial asynergy.     

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。     

Relationship between transcardiac extraction of aldosterone and left ventricular remodeling in patients with first acute myocardial infarction: extracting aldosterone through the heart promotes ventricular remodeling after acute myocardial infarction.

OBJECTIVES: The purpose of this study was to evaluate whether plasma aldosterone (ALD) is extracted or produced through the heart in patients with acute myocardial infarction (AMI) and to determine the relationship between transcardiac extraction of plasma ALD and left ventricular (LV) remodeling. BACKGROUND: Although we demonstrated that circulating ALD was extracted through the failing heart and that transcardiac extraction of ALD correlated with LV end-diastolic volume index (LVEDVI) in patients with congestive heart failure, the existence and increase of ALD synthase in the hearts of infarct rats were reported, suggesting cardiac production of ALD in patients with AMI. METHODS: We measured plasma ALD in the aortic root (Ao) and coronary sinus (CS) in 57 consecutive patients who received successful revascularization and enalapril, with first AMI at acute phase and after one month. We also measured plasma procollagen type III aminoterminal peptide (PIIINP) in the CS. RESULTS: Plasma ALD was significantly lower in the CS than it was in the Ao at the acute phase (84.7 +/- 6.3 pg/ml vs. 105.5 +/- 8.0 pg/ml, p < 0.0001). Significant positive correlations exist between the transcardiac gradient of ALD at the acute phase and the LVEDVI at one month. Moreover, the transcardiac gradient of plasma ALD at the acute phase has a significant correlation with plasma PIIINP, a biochemical marker of fibrosis, after one month. Stepwise multivariate analysis showed that transcardiac extraction of plasma ALD at the acute phase had an independent and significant positive relationship with a large LVEDVI after one month. CONCLUSIONS: These results indicate that plasma ALD is extracted through the heart in patients with AMI at the acute phase and that the extracted ALD plays an important role in modulating post-infarct LV remodeling.     

High-sensitivity C-reactive protein and left ventricular remodeling in patients with acute myocardial infarction

 Inflammatory cytokines are suspected to play an important role in the pathophysiology of left ventricular (LV) remodeling. We investigated whether high-sensitivity C-reactive protein (CRP) (hs-CRP) is a predictor for LV remodeling in patients with acute myocardial infarction (AMI) with successful reperfusion, and also whether such a situation can be avoided by the administration of angiotensin-converting enzyme inhibitors (ACEI) or angiotensin II receptor blockers (ARB). The subjects were 139 patients with an initial attack of anterior myocardial infarction successfully treated by reperfusion therapy. They were randomly divided into the following two groups: an angiotensin (AG) group (91 patients treated with ACEI/ARB) and a NON-AG group (48 patients not treated with ACEI/ARB). Levels of hs-CRP, creatine kinase, human atrial natriuretic polypeptide, brain natriuretic peptide (BNP), fasting blood glucose, serum lipids, fibrinogen, fibrin degradation product, prothromloin time, and activated partial thromboplastin time were measured immediately after 1, 2, 3, and 7 days, and 1 months after the onset of AMI. ACEI or ARB administration lowered hs-CRP levels and prevented the development of LV remodeling. Peak CRP levels significantly correlated with BNP levels during the acute stage (r = +0.54, P < 0.0001), end-diastolic volume index (r = +0.78, P < 0.0001), end-systolic volume index (r = +0.36, P = 0.0405), ejection fraction (r = −0.45, P = 0.0052), left ventricular end-diastolic diameter (r = +0.61, P < 0.0001), cardiac output (r = −0.52, P = 0.0005), cardiac index (r = −0.41, P = 0.0099), and systolic pulmonary arterial pressure (r = +0.48, P = 0.0017) 1 month after the onset of AMI in the NON-AG group but not in the AG group. Logistic multivariate analysis revealed that peak CRP alone was an independent risk factor for the development of LV remodeling in the NON-AG group (odds ratio = 1.79, P = 0.002). These results suggest that hs-CRP is a useful factor for predicting LV remodeling. Furthermore, ACEI or ARB administration to AMI patients showing increased hs-CRP levels during the early stage of the disease could prevent LV remodeling. Received: October 18, 2002 / Accepted: February 7, 2003     

血管紧张素转化酶基因多态性与急性前壁心梗后患者左心室重塑及预后的相关性研究

目的 探讨血管紧张素转化酶(ACE)基因多态性与急性前壁心梗后患者左心室重塑及预后的关系。方法 选取164例急性前壁心肌梗死(AMI)患者作为研究对象。超声检测患者左心室收缩末期内径(LVSD)、左心室舒张末期内径(LVDD)、左室射血分数(LVEF)、左心室舒张末期容积(LVEDV)、左心室收缩末期容积(LVESV)、心肌做功指数(MPI)等指标。提取所有患者外周血DNA,多聚酶链反应检测ACE插入(I)/缺失(D)多态性。对所有患者随访1年,记录主要心血管事件(MACE)发生情况。比较不同ACE基因型与左室重塑及1年内MACE发生频率的关系。结果 164例AMI患者ACE基因I/I型80例、D/D 型67例、I/D型17例,分布频率分别为48.8%、40.8%、10.4%。第7天时,三组患者MPI、LVEDV、LVESV和LVSD差异有统计学意义(P＜0.05)。D/D基因型组患者第7 天MPI、LVESV、LVDD较第1天时显著下降,而LVEDV、LVEF较第1天显著升高(P＜0.05)。I/D基因型组患者第7 天MPI和LVEF与第1天时差异具有统计学意义(P＜0.05)。D/D基因型患者发生MACE的风险显著增加,其OR值为17.16,而I/I基因型患者发生MACE的风险显著下降,其OR值仅为0.39(P<0.05)。结论 ACE基因多态性可能会影响早期心肌梗死后重塑,而D/D型更易发生左室重塑并且1年内发生MACE的风险显著高于其余两种基因型。     

急性心肌梗死后螺内酯干预对左室重构的影响

目的　探讨急性心肌梗死(AMI)患者应用螺内酯干预对于左室重构(LVRM)的影响。方法　4家医院共入选AMI患者88例,采用多中心、随机、对照的方法,对46例AMI患者在常规治疗的基础上加用螺内酯40mg/d(螺内酯组),对照组(n=42)常规治疗。在6个月干预期内检测两组血清Ⅲ型前胶原氨基端肽(PⅢNP)、脑钠肽(BNP)及超声心动图,以评价左室纤维化、左室功能和左室容积。结果　88例中,急性前壁心肌梗死患者43例,螺内酯组23例、对照组20例;急性下壁心肌梗死患者45例,螺内酯组23例、对照组22例。急性前壁心肌梗死组在治疗3、6个月时螺内酯组与对照组相比,血清PⅢNP和BNP明显降低[PⅢNP分别为( 260 .2±59. 9 )ng/L比( 328 .0±70 .3 )ng/L, P=0 .001, ( 197 .1±46 .3 )ng/L比( 266. 7±52 .4 )ng/L, P<0. 001 ,BNP分别为( 347 .4±84 .0)ng/L比(430 .1±62 .9)ng/L, P<0 .001, (243 .7±79. 7)ng/L比(334. 6±62. 8)ng/L, P<0. 001]。治疗6个月时螺内酯组较对照组左室舒张末期内径、左室收缩末期内径明显降低[分别为(51. 0±5 .5)mm比(55. 6±4 .5)mm, P=0 .005, (35 .7±4 .6)mm比(39 .1±5 .6)mm, P=0 .046]。急性下壁心肌梗死组在治疗6个月时螺内酯组与对照组相比血清PⅢNP、BNP水平无统计学意义,(P>0 05),并且左     

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。     

急性心肌梗死早期左室重构与发病时间

目的 采用心肌静息门控单光子发射计算机体层摄影术（ＧＳＰＥＣＴ）研究了急性心肌梗列死（ＡＭＩ）早期左室的重构特点。方法 ＡＭＩ患者３７例,根据发病时间分作四个亚组,第一亚组（１６例）,第二亚组（７例）,第三亚组（１１例）和第四亚组（３例）,患者发病时间分别为≤３小时,〉３小时￣≤６小时,〉６小时￣≤１２小时和〉１２小时。患者入院后即注射显影剂＾９９ｍ锝甲氧基异丁基异腈,２小时后采用双探头ＧＳＰＥＣ