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。     

心肌梗死并心功能不全患者冠状动脉介入治疗的作用

目的 :评价心肌梗死 (MI)并左心功能不全患者经皮冠状动脉介入术 (PCI)对左心收缩功能和左心室重构的作用。方法 :5 2例MI并左心功能不全患者 ,急性心肌梗死 (AMI) 30例 ,陈旧性心肌梗死 (OMI) 2 2例 ,行经皮腔内冠状动脉成形术加支架术治疗 ,术后随访 3个月 ,超声心动图测定左室舒张末内径 (LVEd)、左心房内径(LAd)、左室舒张末容积 (LVEDV)、左室收缩末容积 (LVESV)、左室射血分数 (LVEF)和左室短轴缩短率 (LVFS) ,比较治疗前后各参数的变化。结果 :PCI治疗后LVEd、LAd、LVEDV、LVESV较治疗前均明显减少 (均P <0 .0 1)、LVEF和LVFS明显增高 (P <0 .0 1) ,尤以AMI组明显 ,并且冠状动脉血运重建的时间越早 ,心功能恢复越好。结论 :MI并左心功能不全患者尽早PCI治疗可明显改善左心室收缩功能 ,部分阻抑左心室重构。     

急性心肌梗死后早期左室形态变化的研究

目的 :探讨急性心肌梗死 (AMI)发病后 1～ 3周内左室形态、构型的动态变化。方法 :应用二维超声心动图 (2 - DE)对 32例 AMI患者分别于发病后第 1周、第 2周和第 3周连续测量并计算左室形态、构型的各项指标 ,对其结果进行对比分析 ,并与 33例正常人进行对照。结果 :32例 AMI患者中 ,14例 (44 % )发生左室重构(L VR) ,有明显的左室形态及构型变化 ,从 1周到 3周 AMI患者左室形态的变化呈进行性加重 ,以第 3周最为显著 ,且重构组的改变较非重构组为明显。结论 :AMI后左室形态、构型的改变与 AMI后早期 L VR密切相关     

急性心肌梗死患者血浆B型钠尿肽浓度与心肌梗死面积的相关性

目的:研究急性心肌梗死(AMI)患者血浆B型钠尿肽(BNP)浓度与心肌梗死(MI)面积的相关性。方法:AMI患者80例为AMI组,30例健康志愿者为对照组,2组均行血浆BNP检测、心脏磁共振检查,分析BNP浓度与MI面积的关系。结果:AMI组血浆BNP与MI面积呈正相关(r=0.645,P<0.01),与左室射血分数呈负相关(r=0.297,P<0.05)。多元回归分析显示仅MI面积是BNP的独立相关因素(r2=0.32,f=7.712,P<0.01)。将BNP水平设在150 ng/L时,诊断MI面积>10%的敏感性为85.1%,特异性为70.4%。结论:AMI患者血浆BNP浓度与MI面积密切相关,检测BNP浓度可以粗略评估MI面积。     

急性心肌梗死与左室重构

急性心肌梗死(AMI)后左室发生细胞学,分子学及细胞间质的变化,进而引起左室在大小、形态、组织结构和功能状态的改变,此即目前许多研究所提及的AMI后的左室重构.AMI后左室的重构贯穿于整个病程的始终,成为影响AMI患者近远期预后的主要原因之一.     

首次前壁心肌梗死后血清C-反应蛋白水平升高与左室血栓形成的联系

左室附壁血栓是急性心肌梗死 (AMI) ,尤其是前壁Q波形AMI室壁瘤形成时的重要并发症之一。大多数血栓形成于AMI后 2周内。血栓形成的确切机制未明 ,推测AMI后 ,表现为血清C 反应蛋白 (CRP)升高的炎症反应增强可能与左室血栓形成有关。方法 :1995年 2月～ 2 0 0 1年 9月首发急性前壁MI中 ,列为研究对象者 160例。分别测定血清肌酸激酶 (CK)及CRP ,症状发作后平均 12天时行经胸超声心动图检查 ,评价血清CRP水平与左室血栓形成的联系。结果 :160例平均年龄 63± 13 ( 19～ 93 )岁 ,共检出左室附壁血栓 13例 ( 8% )。左室有附壁血栓与…     

小面积心肌梗死后左室扩大、射血分数下降的原因初探

目的 探讨小面积心肌梗死后左室扩大，射血分数下降(左心室重构)病人的原因。方法 回顾性分析我院1998年1月1日至2001年12月31日住院的192例心肌梗死病人的病案有关记录资料，病人心肌梗死的面积、首次急性心肌梗死(AMI)的年龄、首次AMI到发展为左心室重构的时间、心肌梗死后反复心绞痛史、高血压病史、糖尿病史和吸烟史及患者血胆固醇的平均值。结果 192例病人中符合左心室重构33例，占17．2％。在33例患者中，心绞痛、高脂血症发生率高于未发生左心室重构的患者，大面积心肌梗死和小面积心肌梗死病人对比发现第1次急性心肌梗死后到发生左心室重构的时间、反复心绞痛发作、高血压合并高脂血症均有显著差异。结论 心肌梗死后范围大小与左心室重构成正相关，左心室重构为多因素共同作用的结果，小面积心肌梗死后在梗死后早期左心室功能正常，3年～4年后才逐渐出现左心室重构。     

急性心肌梗塞后左室重构：危害与对策

急性心肌梗塞(AMI)以后,大多数病人左室梗塞区域和非梗塞区域的心肌结构和形态会发生一系列变化,称为左室的重构(ventricular remodeling)。近年来,左室的重构问题已越来越受到重视。不少心血管病学家观察到,左室重构不仅使心肌梗塞(MI)病人左室功能严重减退,并发症出现率明显增加,而且病人的死亡率也明显增加。因此,限制或减少AMI后的左室重构已成为当前心血管领域中最重要研究内容之一。本文综述AMI后左室重构的机理及其危害和目前所采取的对策。 1急性心肌梗塞后左室重构的发生机理 1.1梗塞区的膨胀:梗塞区的膨胀是AMI后左室重构的第一个原因。在心肌坏死后的     

微小RNA调控心肌梗死后心肌肥大的研究进展

心肌梗死( MI)是世界范围主要死亡原因之一,欧美国家因MI致心力衰竭( HF)在所有HF的发病率和死亡率占首位〔1〕,中国MI是继高血压致HF的第二大病因;对于MI患者,现临床主要通过溶栓、介入和搭桥术挽救患者生命;虽然大部分患者得到救治,但MI后心室壁结构不断重新构建,使心脏结构和功能从代偿逐步向失代偿方向发展,在...     

左室造影对急性心肌梗死后左室重构发生的评价

目的 :探讨左室造影对急性心肌梗死 (AMI)后左室重构发生的评价及其临床意义。方法 :用左室造影投影系统计算出心肌梗死 (MI)急性期及恢复期左室容积指标 ,根据左室容积指标将患者分为重构组和非重构组 (均为 2 0例 ) ;用漂浮导管测定血流动力学指标 ;用99m 锝心血池扫描测定左室射血分数 (LVEF) ;用2 0 1铊心肌血流扫描测定梗死的面积积分 (ES)和重症度积分(SS)。结果 :重构组恢复期左室舒张末期及收缩末期容积均显著高于非重构组 (P <0 .0 1) ,亦显著高于该组急性期左室容积 (P <0 .0 1)。重构组急性期肌酸磷酸激酶峰值、急性期及恢复期肺小动脉嵌压、恢复期左室舒张末压力以及恢复期ES和SS均显著高于非重构组 ,而LVEF显著低于非重构组。重构组恢复期左室收缩末期容积及舒张末期容积与LVEF之间存在有意义的相关关系 (r =- 0 .72 ,P <0 .0 1;r =- 0 .6 7,P <0 .0 1)。结论 :AMI后进行左室造影能较准确地评价左室重构的发生及严重程度。发生左室重构的患者其心肌坏死量较大 ,且其恢复期左室功能显著降低。恢复期左室功能与左室容积指标之间存在密切相关。     

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。     

The Angiotensin-converting Enzyme Inhibition Post Revascularization Study (APRES)

OBJECTIVE: This study was performed to assess the effect of treatment with ramipril on the incidence of cardiac events after invasive revascularization in patients with asymptomatic moderate left ventricular dysfunction. BACKGROUND: In patients with angina pectoris and left ventricular dysfunction, both invasive revascularization and treatment with angiotensin-converting enzyme inhibitors reduce cardiac mortality and morbidity. Whether there is a benefit from combining the two treatment strategies has never been evaluated prospectively. METHODS: After invasive revascularization, 159 patients with preoperative chronic stable angina pectoris, left ventricular ejection fraction between 0.30 and 0.50 and no clinical heart failure were randomly assigned to receive double-blind treatment with either ramipril or placebo and subsequently followed for a median of 33 months. RESULTS: Ramipril reduced the incidence of the triple-composite end point of cardiac death, acute myocardial infarction or clinical heart failure (risk reduction 58%; 95% confidence interval 7% to 80%, p = 0.031). The incidence of the quadruple-composite end point of cardiac death, acute myocardial infarction, clinical heart failure or recurrent angina pectoris was not altered with ramipril. These findings were consistent across subgroups with respect to left ventricular ejection fraction below or above 0.40, and whether coronary artery bypass grafting or percutaneous transluminal coronary angioplasty was performed. CONCLUSIONS: In patients with angina pectoris and asymptomatic moderate left ventricular dysfunction, long-term treatment with ramipril after invasive revascularization significantly reduced the incidence of the composite end point of cardiac death, acute myocardial infarction or clinical heart failure, indicating that the beneficial effects of angiotensin-converting enzyme inhibitor treatment may be extended to include treatment of this patient group.     

Can the mode of death be predicted in patients with angiographically documented coronary artery disease?

To determine whether sudden versus non-sudden cardiac death could be predicted in high risk patients, 1157 medical patients were followed for an average of 46 months after a diagnostic coronary angiogram and 18 clinical, hemodynamic, and angiographic variables known to be associated with a high risk of mortality were analyzed. The total group of 141 deaths was classified into 3 subgroups: (1) 82 sudden deaths (less than 1 hour after onset of symptoms); (2) 46 deaths due to acute myocardial infarction with or without heart failure, and (3) 13 deaths unrelated to cardiac symptoms. In a subset of 64 patients, the duration of electrical systole (QTc) was calculated before angiography and before death. A comparison was made of QTc measurements at entry with QTc values of subjects with normal coronary arteries and normal left ventricular function. Deaths from cardiac causes could often be predicted from older age, male sex, history of myocardial infarction, unstable angina, congestive heart failure, abnormal cardiothoracic ratio, multivessel disease, abnormal left ventricular contraction, and abnormal ejection fraction. However, these variables did not discriminate between sudden and nonsudden cardiac deaths and both modes of death were characterized by depressed left ventricular function and multivessel coronary disease. During follow-up the incidence of acute myocardial infarction was not different in patients with cardiac and noncardiac deaths and in long-term survivors. However, patients dying from cardiac causes had a higher incidence of heart failure. Patients dying suddenly did not present new infarctions during follow-up whereas patients dying from acute myocardial infarction had a 13% incidence of prior infarction and a higher incidence of heart failure. In addition, QTc at entry was longer in nonsurvivors than in normal subjects (p less than 0.0001) and patients experiencing sudden death exhibited the highest incidence of QTc prolongation (greater than or equal to 440 ms) during follow-up (p less than 0.05). We conclude that: (1) although the severity of coronary disease and left ventricular dysfunction are closely related to cardiac mortality, they do not discriminate between sudden and nonsudden cardiac deaths; (2) patients experiencing sudden death are characterized by a low incidence of new myocardial infarction or congestive heart failure and prolongation of the QTc interval during follow-up.     

Effects of angiotensin-converting enzyme inhibition with perindopril on left ventricular remodeling and clinical outcome: results of the randomized Perindopril and Remodeling in Elderly with Acute Myocardial Infarction (PREAMI) Study

BACKGROUND: Angiotensin-converting enzyme inhibitors reduce mortality and remodeling after myocardial infarction in patients with left ventricular dysfunction. METHODS: Perindopril and Remodeling in Elderly With Acute Myocardial Infarction (PREAMI), a double-blind, randomized, parallel-group, multicenter, placebo-controlled study, determined whether similar benefits occur in elderly postinfarction patients with preserved left ventricular function. A total of 1252 patients 65 years or older with a left ventricular ejection fraction of 40% or higher and recent acute myocardial infarction were randomized to receive perindopril erbumine or placebo (8 mg/d) for 12 months. The combined primary end point was death, hospitalization for heart failure, or left ventricular remodeling. Secondary end points included cardiovascular death, hospitalization for reinfarction or angina, and revascularization. RESULTS: The primary end point occurred in 181 patients (35%) taking perindopril and 290 patients (57%) taking placebo, with a significant absolute risk reduction of 0.22 (95% confidence interval, 0.16 to 0.28; P<.001). A total of 126 patients (28%) and 226 patients (51%) in the perindopril and placebo groups, respectively, experienced remodeling. The mean increase in left ventricle end-diastolic volume was 0.7 mL with perindopril compared with 4.0 mL with placebo (P<.001). In the perindopril group, 40 deaths (6%) and 22 hospitalizations (4%) for heart failure occurred, whereas 37 deaths (6%) and 30 hospitalizations (5%) occurred in the placebo group. Treatment did not affect death, whereas the hospitalization rate for heart failure was slightly reduced (absolute risk reduction, 0.01; 95% confidence interval, -0.01 to 0.02). No treatment effect on other secondary end points was detected. CONCLUSION: We found that 1-year treatment with 8 mg/d of perindopril reduces progressive left ventricular remodeling that can occur even in the presence of small infarct size, but it was not associated with better clinical outcomes.     

Rhythmusstörungen während der Remodelingphase nach Herzinfarkt

BACKGROUND: The effect of mechanical on electrical remodeling or electrical instability of the heart shows that it is essential for the prevention of sudden death to avoid or delay mechanical remodeling and neurohumoral activation after myocardial infarction. In other words, patients after myocardial infarction prone to neurohumoral activation need to be treated with ACE inhibitors or perhaps AT1-receptor blockers and beta blockers to maintain electrical stability. ICD INDICATION: MADIT I and MUSTT study showed that patients with severe ventricular dysfunction after myocardial infarction are at high risk of sudden death, especially in presence of electrical instabilities indicated by ventricular arrhythmias. These patients certainly need an automatic implantable cardioverter defibrillator (ICD). It is not clear so far whether or not the indication needs to be extended according to the MADIT II study. In other words, need all postmyocardial infarction patients with reduced pump function an ICD? There is no doubt that many patients with an ejection fraction below 30% have ventricular arrhythmias and fulfil therefore the inclusion criteria for the MADIT I or MUSTT study. In MADIT I, a run of three ventricular premature beats force was sufficient to fulfil the inclusion criteria. CONCLUSION: Another important consequence of the temporal correlation between mechanical and electrical remodeling is that specific attention must be directed to these interrelations in patients after myocardial infarction. Patients who die of sudden death show in comparison to surviving patients a substantial dilatation of the left ventricular during 6 months of observation which parallel the increasing incidence of ventricular premature beats. The consequence for therapy would be that in patients who present with left ventricular dilatation during 6 months after myocardial infarction, electrical instability is present and a high risk of sudden death exists. These patients probably will benefit from an ICD.     

Heart failure after myocardial infarction: clinical implications and treatment

Heart failure is a frequent complication of myocardial infarction. Several factors, such as recurrent myocardial ischemia, infarct size, ventricular remodeling, stunned myocardium, mechanical complications, and hibernating myocardium influence the appearance of left ventricular systolic dysfunction after myocardial infarction. Importantly, its presence increases the risk of death by at least 3‐ to 4‐fold. The knowledge of the mechanisms and clinical features are essential for the diagnosis and treatment of left ventricular dysfunction and heart failure after myocardial infarction. Therefore, this review will focus on the clinical implications and treatment of heart failure after myocardial infarction. © 2011 Wiley Periodicals, Inc. The authors have no funding, financial relationships, or conflicts of interest to disclose.     

缺血性心肌病的外科治疗进展

缺血性心肌病(ischemic cardiomyopathy,ICM)发病率逐年增高,它是导致心力衰竭最常见的原因。尽管药物治疗ICM不断发展,但无法逆转心肌重构。通过外科手段来治疗ICM,仍是目前逆转心肌重构、改善患者预后的主要方向。ICM的外科治疗策略包括心肌血运重建、左心室重建、二尖瓣成形、心室辅助装置和心脏移植等5方面。本文就ICM的最新外科治疗现状及进展作一述论。     

Heart failure and left ventricular remodeling after reperfused acute myocardial infarction in patients with hypertension

In the thrombolytic era, hypertension has been shown to adversely affect the development of heart failure after acute myocardial infarction (AMI). We sought to examine the relation between antecedent hypertension and heart failure after mechanical reperfusion and to test the impact of postinfarction left ventricular remodeling on heart failure in hypertensive patients. A series of 953 patients (324 hypertensives) with AMI treated with successful primary percutaneous coronary intervention underwent a 5-year follow-up. A subgroup of 325 subjects underwent 2D echocardiography at admission, 1 month, and 6 months. From day 1 to 6 months, despite similar improvement in regional and global left ventricular function and similar 6-month infarct artery patency rate, left ventricular end-diastolic volume increased in the normotensives (122+/-36 mL to 131+/-47 mL; P<0.001) but not in the hypertensives (127+/-41 mL to 128+/-31 mL; P=0.768). At 6 months, the incidence of left ventricular remodeling in hypertensive and normotensive patients was not different (22% versus 28%; P=0.210). However, at 5 years, the incidences of hospitalization for heart failure (7% versus 3%; P=0.014) and of New York Heart Association functional class > or =2 (53% versus 40%; P<0.001) were higher in hypertensive as compared with normotensive patients. Hypertension was found to be a predictor of heart failure (hazard ratio, 2.23; P=0.015). In conclusion, patients with antecedent hypertension are at higher risk to develop heart failure after AMI, even when successfully reperfused by primary percutaneous coronary intervention. However, the increased incidence of heart failure in hypertensive patients is not associated with a greater propensity to postinfarction left ventricular remodeling.     

Impact of early changes in left ventricular filling pattern on long-term outcome after acute myocardial infarction

BACKGROUND: In patients with heart failure due to chronic ischemic heart disease improvement of diastolic function indicates improved survival and a reduced morbidity, but whether this is also the case after acute myocardial infarction is not known. METHODS: To assess the prognostic importance of changes in left ventricular filling pattern, assessed with mitral deceleration time and colour M-mode flow propagation velocity, on cardiac death and readmission due to heart failure serial Doppler echocardiography was carried out in 103 patients with a first myocardial infarction. Based on echocardiography on hospital admission and after 1 month, patients were divided into three groups: group A (n=29) comprised patients with normal filling at either examination, group B (n=29) comprised patients with improvement of initially abnormal filling, and group C (n=45) patients with deterioration or no change of an abnormal filling pattern. RESULTS: One-year survival free of cardiac death or hospitalisation for heart failure was 97% in group A, 86% in group B and 64% in group C (P<0.0001). In Cox analysis persistence of abnormal filling or deterioration of left ventricular filling was still a predictor of the combined endpoint (risk ratio 4.4, 95% CI 1.8-12.0, P=0.003) after adjustment of LV filling on admission, left ventricular systolic function and clinical variables. Serial analyses of left ventricular systolic function demonstrated a significant improvement after 1 year in ejection fraction in groups A and B, whereas ejection fraction remained unchanged in group C. CONCLUSION: Patients with a persistently abnormal or a deterioration of left ventricular filling pattern as opposed to improved or normal filling are at increased risk of cardiac death and readmission due to heart failure after acute myocardial infarction.     

Incidence and significance of pericardial effusion in acute myocardial infarction as determined by two-dimensional echocardiography

To determine the incidence and clinical significance of pericardial effusion after acute myocardial infarction, two-dimensional echocardiography was serially performed in 66 consecutive patients. Pericardial effusion was observed in 17 (26%); the effusion was small in 13 patients, moderate in 3 and large with signs of cardiac tamponade in 1. In this patient, two-dimensional echocardiography strongly suggested myocardial rupture. The observation of pericardial effusion was not associated with age, sex, previous myocardial infarction, atrial fibrillation or treatment with heparin. It was more often a complication of anterior than of inferior acute infarction. Patients with pericardial effusion had higher peak levels of creatine kinase and lactic dehydrogenase and a higher wall motion score index. More patients with pericardial effusion had congestive heart failure or ventricular arrhythmias, developed a ventricular aneurysm or died within 1 year after their infarction. In conclusion, pericardial effusion is frequently visualized by two-dimensional echocardiography after acute myocardial infarction and its presence is associated with an increased occurrence of complications and cardiac death.