缺血预适应现象对心肌梗死并发症的影响

目的探讨心肌缺血预适应对急性心肌梗死并发症的影响。方法对146例急性心肌梗死患者的并发症进行分析,按梗死前10d有无心肌缺血心绞痛分为有缺血预适应组(IP组)、无缺血预适应组(P组)两组。IP组86例,男60例,女26例,平均年龄(62.5±8.2)岁;P组60例,男42例,女18例,平均年龄(63.0±8.5)岁。结果IP组心肌酶峰值、并发心律失常、左心衰竭明显低于P组(P<0.05)。结论有心肌缺血预适应的患者,心肌梗死后能降低心律失常及左心衰竭的发生率。     

心肌缺血预适应对急性心肌梗死后临床及预后的影响

目的　探讨心肌缺血预适应 (IP)对急性心肌梗死 (AMI)临床及预后的近期影响。方法　根据心肌梗死前有无心肌缺血证据或 (和 )心绞痛病史将 198例患者分为A、B两组。对其临床资料进行回顾分析。结果　A组小面积心肌梗死发生率高于B组 ,而肌酸磷酸激酶 (CK)和同工酶 (CK MB)峰值、严重心脏并发症和梗死后心绞痛发生率、近期住院病死率均明显低于B组。结论　既往心绞痛促进冠状动脉侧支循环的建立 ,发病前心绞痛可能促进IP产生 ,二者协同对AMI后的心肌细胞起保护作用。     

心肌缺血预适应在急性心肌梗死中的临床意义

目的：探讨心肌缺血预适应性对急性心肌梗死的影响。方法：对75例急性心肌梗死患者按有无梗死前心绞痛分为两组,A组41例,B组34例,两组的性别、年龄无显著差异（P＞0.05)。观察两组梗死面积、心肌酶、并发症。结果：有心绞痛组,心肌梗死范围、心肌酶学峰值、左心衰明显低于无梗死前心绞痛组（P＜0.05)。结论：心肌缺血预适应可以限制梗死面积扩大,降低死亡率。     

心肌缺血预适应在急性心肌梗死中的临床意义

目的 :探讨心肌缺血预适应性对急性心肌梗死的影响。方法 :对 75例急性心肌梗死患者按有无梗死前心绞痛分为两组 ,A组 41例 ,B组 3 4例 ,两组的性别、年龄无显著差异 (P >0 0 5 )。观察两组梗死面积、心肌酶、并发症。结果 :有心绞痛组 ,心肌梗死范围、心肌酶学峰值、左心衰明显低于无梗死前心绞痛组 (P <0 0 5 )。结论 :心肌缺血预适应可以限制梗死面积扩大 ,降低死亡率。     

心肌缺血预适应对心肌梗死的临床影响

目的：研究心肌缺血预适应对心肌梗死的临床影响。方法：先取１３０例资料寒带的急性心肌梗死病例,接梗死前有无心肌缺血、心绞痛分为Ａ、Ｂ组,进行分析、比较。结果：Ａ组心肌梗死范围、心肌酶峰值、严重心律失常、左心衰竭、休克的发生率及病死率均明显低于Ｂ组。结论：心肌缺血预适应对心肌梗死的临床作用表现在限制梗死面积扩大,保护梗死后心脏功能,减少严重心律失常的发生。     

缺血预适应现象与心肌梗塞后左室重构的临床研究

目的：为探讨心肌缺血预适应对心肌梗塞后左室重构的影响。方法：用超声心动图观察比较心肌梗塞前２４小时内有心绞痛发作的３８例与３５例无心绞痛发作的急性前壁、前间壁、前间壁心肌梗塞患者的左室重构。结果：发现两组梗塞部位、溶栓治疗等都无差异，而心绞痛组左室重构比无心绞痛组轻。结论：心肌缺血预适应能减轻心肌梗塞后左室重构。     

缺血预适应减轻急性心肌梗死缺血再灌注损伤的临床观察

目的：探讨急性心肌梗死前心绞痛产生的缺血预适应对缺血再灌注心肌的保护作用。方法：将362例患者分为两组：Pre组（急性心肌梗死前有24h内有心绞痛发生）192例；非Pre组（急性心肌梗死前24h内无心绞痛发生）170例。观察两组患者CK及CK—MB峰值水平，超声心动图心功能指标，1个月内病死率及严重的充血性心衰的发生率的差异。结果：两组间各项指标差异有显著性（P〈0．05）。结论：缺血预适应能够减轻急性心肌梗死患者缺血再灌注损伤。     

心肌缺血预适应的临床观察

1996年 Murry等首先发现连续 4次冠状动脉阻断、再灌注 ,对随后的冠状动脉阻断引起的心肌梗死面积与对照组相比减少 30 %～ 70 % ,并称之为缺血预处理 [1 ] 。随着研究的进展 ,目前已将其定义为心肌缺血预适应 (IP)。急性心肌梗死前反复发作心绞痛对心肌具有缺血预适应的保护效应 ,近年来有多处报道。本文通过对 2 2 3例 AMI患者的分析 ,进一步探讨 AMI前有无心绞痛史对梗死面积、心肌酶的改变、严重心律失常发生率、心源性休克发生率、急性左心衰发生率及住院病死率等方面的影响。1　对象和方法1 .1　对象　将我院 1 990 - 0 1～ 2 0 0…     

心肌缺血预适应对急性心肌梗塞近期预后的作用

1986年Murry发现并提出心肌缺血预适应现象(ischemic conditioning)的新概念,是指一次或多次短时心肌缺血和再灌注可明显增强心肌对较长时间持续缺血和再灌注损伤的耐受能力。Orizi认为临床上心肌梗塞前多次发作不稳定心绞痛可使缺血心肌处于预适应状态。本文对100例急性下壁心肌梗塞或合并后壁、右室、前壁心肌梗塞患者,从临床上研究心肌梗塞前有无心肌缺血预适应现象对心肌梗塞的影响。 1 资料与方法 1993年1月～1997年5月收治的100例资料完整的急性下壁或合并后壁、右室和前壁心肌梗塞住院患者。其中男69例,女31例,平均年龄62岁。58例心肌梗塞前均有心绞痛发作史(A组),其心绞痛发作1天至10年不等,大多为2～4年。无心绞痛史者42例(B组)。     

心肌缺血预适应对心肌梗死的临床影响

目的 :研究心肌缺血预适应对心肌梗死的临床影响。方法 :选取 13 0例资料完整的急性心肌梗死病例 ,按梗死前有无心肌缺血、心绞痛分为A、B组 ,进行分析、比较。结果 :A组心肌梗死范围、心肌酶峰值、严重心律失常、左心衰竭、休克的发生率及病死率均明显低于B组。结论 :心肌缺血预适应对心肌梗死的临床作用表现在限制梗死面积扩大 ,保护梗死后心脏功能 ,减少严重心律失常的发生     

经静脉实时心肌造影超声心动图评估心肌梗死后存活心肌

目的探讨经静脉实时心肌造影超声心动图（RT-MCE）评估心肌梗死后存活心肌。方法18例准备进行血运重建术心肌梗死患者,于术前1-5天行RT-MCE检查,并于术后3个月再次行常规超声心动图检查,室壁运动分析采用18节段分析法,分为运动正常、运动减弱、无运动和反常运动。心肌存活定义为术后超声检查室壁运动明显改善。将造影结果分为3种情况：充盈缺损,造影剂充盈延迟、回声稀疏不均匀或心内膜下充盈缺损,回声均匀性增强。其中后两种情况定义为存活心肌。结果在18例心肌梗死患者中共检出109个室壁运动异常节段,运动减弱为47个,无运动为56个,反常运动为6个。注射造影剂后回声均匀性增强的心肌节段中有2个节段术前室壁运动减弱,术后运动均改善;回声不均匀或心内膜下充盈缺损的心肌节段中术前室壁运动减弱有24个节段,术后运动改善14个,术前室壁无运动有24个节段,术后运动改善20个;充盈缺损的心肌节段中术前室壁运动减弱有21个节段,术后运动均未改善,术前室壁无运动32个,术后运动改善2个。RT-MCE检出存活心肌的敏感性、特异性分别为94.7%、78.9%。结论RT-MCE能比较准确的判断心肌梗死后心肌的存活性。     

Drug-induced myocardial ischemia and acute myocardial infarction.

Myocardial infarction generally occurs in the presence of known risk factors and identifiable coronary artery disease. Atypical presentations due to therapeutic and illicit drug use are documented, however, and lead to the consideration of alternative pathophysiologic rationales for myocardial infarction. This article discusses central nervous system stimulants and other drugs that have the potential for myocardial damage and their nursing implications.     

Acute myocardial infarction in a child with myocardial bridge

BACKGROUND:

Myocardial infarction (MI) is rare in children, and Kawasaki disease is now recognized as the main cause for MI. In this report, we present a child with MI caused by myocardial bridge (MB).

METHODS:

A 7.5-year-old boy was admitted to Weifang People’s Hospital on September 16, 2008 for heart disease. By electrocardiogram, coronary CT angiography, emission computed tomography, and other examinations, he was initially diagnosed as having (1) acute inferior myocardial infarction and extensive anterior myocardial infarction; (2) fulminant myocarditis; or (3) coronary myocardial bridge. He was treated with oxygen, thrombolysis, myocardial nutrition, vitamin C (4.0 g per time), dexamethasone (7.5 mg per time), a large dose of gamma globulin, and interferon.

RESULTS:

Myocardial enzymes, liver function, C-reactive protein, and troponin-I returned to normal at 21 days after treatment. At 29 days, electrocardiogram indicated that II, III, aVF, V4 - V6 leads had abnormal Q wave, and ST-T changed. The patient was discharged.

CONCLUSION:

Myocardial bridge may be one of the causes of MI in children.KEY WORDS: Myocardial bridge, Electrocardiogram, Acute myocardial infarction     

心肌对比超声心动图估测心肌血流量的价值

目的评价心肌对比超声心动图测定心肌血流量的可行性.方法建立急性心肌梗死犬模型,以放射性微球测定的心肌血流量为"金标准”,经外周静脉持续滴注微泡造影剂,通过计算平台声强度(A)和微泡再充填速率(β)测定心肌相对血流量.结果放射性微球法所测的心肌血流量和心肌对比超声心动图测定的A*β值相关良好(r=0.81,P=0.001).结论经静脉持续滴注微泡造影剂行心肌对比超声心动图可估测心肌相对血流量.     

Noninvasive imaging of myocardial angiogenesis following experimental myocardial infarction

Noninvasive imaging strategies will be critical for defining the temporal characteristics of angiogenesis and assessing efficacy of angiogenic therapies. The αvβ3 integrin is expressed in angiogenic vessels and represents a potential novel target for imaging myocardial angiogenesis. We demonstrated the localization of an indium-111–labeled (¹¹¹In-labeled) αvβ3-targeted agent in the region of injury-induced angiogenesis in a chronic rat model of infarction. The specificity of the targeted αvβ3-imaging agent for angiogenesis was established using a nonspecific control agent. The potential of this radiolabeled αvβ3-targeted agent for in vivo imaging was then confirmed in a canine model of postinfarction angiogenesis. Serial in vivo dual-isotope single-photon emission–computed tomographic (SPECT) imaging with the ¹¹¹In-labeled αvβ3-targeted agent demonstrated focal radiotracer uptake in hypoperfused regions where angiogenesis was stimulated. There was a fourfold increase in myocardial radiotracer uptake in the infarct region associated with histological evidence of angiogenesis and increased expression of the αvβ3 integrin. Thus, angiogenesis in the heart can be imaged noninvasively with an ¹¹¹In-labeled αvβ3-targeted agent. The noninvasive evaluation of angiogenesis may have important implications for risk stratification of patients following myocardial infarction. This approach may also have significant clinical utility for noninvasively tracking therapeutic myocardial angiogenesis.     

心肌声学造影在急性心肌梗死中的临床应用

急性心肌梗死(AMI)的发生发展与心肌微循环障碍紧密相关,及时有效地评价微循环灌注情况对AMI的诊断、治疗和预后均有十分重要的意义。心肌声学造影是一种评估心肌微循环灌注的超声新技术,目前已成为临床评价AMI的重要方法。本文就心肌声学造影在AMI再灌注前后的应用、危险分层、疗效评估、存活心肌检测、造影剂安全性等方面进行综述。     

心肌梗死后心肌纤维化的研究进展

心肌纤维化是心肌梗死后主要的病理过程,特征是细胞外基质合成和降解失衡,而成纤维细胞和肌纤维母细胞在此过程中起重要作用。心肌梗死后,梗死区域替代性纤维化可以减少梗死区域进一步的扩张,维持心室结构完整性,防止心室壁破裂;而非梗死区域的反应性纤维化,则会改变心室顺应性,增加心室壁的硬度,影响心脏的收缩和舒张功能。因此,心肌梗死后理想的治疗是抑制非梗死区域反应性纤维化、诱导梗死区域心肌再生,从而改善心功能。     

急性心肌缺血对心脏电稳定性的影响

目的 应用长程晚电位及长程QT间期变异技术分别从心室除极、复极的角度探讨冠状动脉急性缺血对心电稳定性的影响。方法 选择我院住院的心绞痛频繁发作的冠心病患者47例，佩戴数字化Hoher记录仪，选取心绞痛发作时及症状缓解6h后的长程晚电位及QT间期变异各项参数指标，每一指标选取临近时间段的三个数值，取其均数用做统计数据。结果 在心绞痛发作时及症状恢复后，晚电位及QT间期变异各项参数均显示明显变化，差异有统计学意义（P〈0．05）。结论 冠状动脉血流情况与心电稳定性指标显著相关，短暂心肌缺血时心室除极、复极指标也有显著变化，其敏感性高于普通心电图，可以成为评价无创冠状动脉缺血事件的有益补充。     

The phenomenon of intermittent myocardial ischemia and characteristics of myocardial reserve in patients with myocardial infarction

AIM: To study coronary and myocardial reserves in myocardial infarction survivors (MIS) with consideration of development of intermittent ischemia during transesophageal pacing (TEP). MATERIAL AND METHODS: 320 MIS were examined 1.5-2 months after myocardial infarction onset. 30 healthy male volunteers served control. Stepwise overdrive TEP was made in all the examinees with parallel estimation of central hemodynamics by tetrapolar chest rheography with assessment of systolic and diastolic parameters. RESULTS: In the course of TEP, 39.4% MIS developed intermittent ischemia (II) at frequencies 120-140 imp/min. II presented as a significantly depressed ST segment on ECG. There was a simultaneous lengthening (1.4-fold) of diastole and a fall (1.5-fold) of end-diastolic pressure in the left ventricle (EDP). At frequencies 140-160 imp/min the length of the diastole shortened while EDP rose. CONCLUSION: The II phenomenon demonstrates a key role of coronary reserve. Changes in coronary and myocardial reserves during TEP in II development are interrelated. They may represent unknown adaptive mechanisms of the myocardium protecting against unfavourable outcomes of ischemic episodes.     

Relation between myocardial oxygen consumption and myocardial blood volume: a study using myocardial contrast echocardiography.

Myocardial blood volume (MBV) is the volume of blood residing in myocardial vessels, 90% of which is in capillaries. MBV can be measured in vivo using myocardial contrast echocardiography (MCE). It has been shown that when increases in coronary blood flow (CBF) are not associated with increase in myocardial oxygen consumption (MVO(2)), MBV does not increase. We hypothesized that MBV would increase when increases in CBF are associated with an increase in MVO(2). The atrioventricular node was ablated in 18 dogs and dual-chamber pacing was instituted. In group 1 dogs (n = 9), heart rate was altered from 50 to 150 bpm(-1) in increments of 20 bpm(-1) in random order. In group 2 dogs (n = 9), heart rate was kept constant, and dobutamine was infused at doses of 5, 10, 20, 30, and 40 microg/kg(-1)/min(-1). During each intervention, hemodynamic parameters and MVO(2) were measured, and MCE was performed. MVO(2) increased more (P <.01) with inotropic compared with chronotropic stimulation, resulting in a parallel increase in CBF. MBV fraction and MCE-derived myocardial blood flow increased significantly with increases in MVO(2) (P <.05 and P <.001, respectively) when dobutamine was infused, but remained unchanged when heart rate alone was increased. We conclude that when MVO(2) is increased substantially, the resulting increase in CBF and MCE-derived myocardial blood flow is mediated, in part, by an increase in MBV. Thus, capillary recruitment plays an important role in the physiologic regulation of CBF. Lack of increase in MBV during dobutamine stress may indicate the presence of coronary stenosis or microvascular disease.