The Role of Myocardial Anisotropy in Arrhythmogenesis Associated with Myocardial Ischemia and Infarction

Myocardial Anisotropy in Ischemia and Infarction . Anisotropy is defined as any property of a system that differs depending on the direction in which it is measured. In the heart, the structure of the cardiac myocytes and their electrical coupling via gap junctions confer an anisotropy in the intracellular resistance to current flow in myocardial tissue. This in turn is responsible for anisotropy in conduction in which the velocity and uniformity of impulse conduction is dependent on its direction relative to the normal myocardial fiber orientation and any underlying pathological nonuniformities in cell orientation and coupling. How cells are coupled also influences refractoriness and excitability. Recent experimental evidence has implicated uniform and nonuniform myocardial anisotropy as important substrates that play a role in the initiation and maintenance of arrhythmias in the setting of ischemia and infarction. These studies may provide a focus for the development of new antiarrhythmic modalities that depend on the modulation of cell electrical coupling.     

HIF-1对大鼠急性缺血心肌的保护作用

目的研究HIF-1对大鼠急性缺血心肌的保护作用及其作用机制。方法应用HIF-1活性诱导剂氯化钴预处理大鼠,观察预处理对大鼠急性心肌梗死面积和心肌VEGF、iNOS蛋白表达的影响。结果氯化钴预处理组大鼠较对照组和假手术组急性心肌梗死面积显著减少(P<0.01),VEGF、iNOS蛋白表达显著增高(P<0.01)。结论HIF-1可以减少大鼠急性心肌梗死面积,对大鼠急性缺血心肌具有保护作用,其机制可能与HIF-1促进VEGF、iNOS蛋白表达增加有关。     

自噬在心肌缺血再灌注中作用的研究进展

自噬是指细胞内的自身物质被溶酶体所降解的过程,为普遍存在的生命现象,是细胞处于饥饿状态时的一种自我保护机制。既往研究表明,在心肌缺血再灌注过程中,自噬被诱导激活,自噬体明显增多。自噬在缺血再灌注中的作用表现出双面性,缺血期主要发挥保护作用,但再灌注时期自噬过度激活则表现出损伤作用,可导致自噬性细胞死亡。自噬具体是如何被激活,怎样发挥其影响作用,至今尚无清楚的答案。本文就自噬在心肌缺血再灌注中作用的研究进展进行综述。     

醒脑静对兔心肌缺血再灌注损伤的抗炎性因子和改善凝血-纤溶功能障碍的作用

目的探讨醒脑静预处理对心肌缺血再灌注损伤（MIRI）的抗炎性因子的影响和改善凝血-纤溶功能障碍的作用。方法20只新西兰兔随机分成安慰剂组与醒脑静组，各10只。结扎冠状动脉造成MIRI模型，分别在冠状动脉结扎前、结扎后1h、再灌注后1h，取心房血分别检测肿瘤坏死因子-α（TNF-α）、组织型纤溶酶原激活物（t-PA）、纤溶酶原激活物抑制物-1（PAI-1）、肌酸激酶（CK）水平。同时观察各组梗死范围。结果冠状动脉结扎后醒脑静组TNF-α、PAI-1、CK水平较安慰剂组显著降低（P〈0．01），心肌梗死面积显著小于安慰剂组（P〈0．01）。结论醒脑静预处理对MIRI有良好的抗心肌缺血再灌注损伤作用。     

Reversible T‐Wave Inversions and Neurogenic Myocardial Stunning in a Patient with Recurrent Stress‐Induced Cardiomyopathy

A 72‐year‐old female was diagnosed as a stress‐induced cardiomyopathy from apical ballooning pattern of left ventricular dysfunction without coronary artery stenosis after the mental stress. ECG showed the transient T‐wave inversions after the ST‐segment elevations. By the mental stress after 1 year, she showed a transient dysfunction with similar ECG changes again. T‐wave inversions recovered earlier, and cardiac sympathetic dysfunction showed a lighter response corresponding to the less severe dysfunction than those after the first onset. Wellens’ ECG pattern was associated with the degree of neurogenic myocardial stunning with sympathetic hyperinnervation caused by mental stress.     

Stress‐Induced Drinking in Parents of Adolescents with Externalizing Symptomatology: The Moderating Role of Parent Social Support

Parenting adolescents with externalizing symptomatology has been repeatedly shown to be stress‐inducing for parents. One possible coping strategy for parents dealing with this chronic stress may be drinking. The current study extended previous research by examining the prospective relations between adolescents' externalizing behaviors and parents' negative affect and alcohol consumption. Additionally, the present study tested whether this mediated effect is a function of parental social support. Adolescents' externalizing symptoms prospectively predicted mothers' negative affect. Interestingly, however, mothers' negative affect prospectively predicted mothers' drinking only for those mothers with low social support. Furthermore, the mediated effect (Wave 1 adolescent externalizing symptoms → Wave 2 mother negative affect → Wave 3 mother drinking) was significant only for mothers with low social support. There were no effects of adolescents' externalizing symptoms on fathers.     

Detection of Exercise‐Induced Myocardial Ischemia by Multichannel Magnetocardiography in Single Vessel Coronary Artery Disease

Background: Detection of myocardial ischemia was studied with multichannel exercise magneto‐cardiography (MCG). A surface gradient method was applied to analyze cardiac magnetic fields. Methods: We studied 27 patients with single vessel coronary artery disease (CAD) and 17 healthy volunteers. The MCG was recorded over anterior chest during supine bicycle ergometry. The two‐dimensional direction of the maximum spatial magnetic field gradient was determined during the ST segment and at the T‐wave apex at different phases of stress test. Results: The CAD patient group was separated from controls by the orientation of the magnetic field gradient during the ST segment at cessation of exercise (CAD 167 ± 68° vs controls 106 ± 49°; P < 0.005) and at 4 minutes postexercise, but not at rest. The‐CAD patient group was separated from controls also by the orientation of the magnetic field gradient at the T‐wave apex at 4 minutes postexercise (CAD 87 ± 60° vs controls 58 ± 18° P < 0.05), but not at rest. The change in the orientation of the field gradient at the T‐wave apex 4 minutes postexercise, compared to baseline, was greater in CAD patients (31 ± 43°) than in controls (9 ± 8° P < 0.05). This change was larger in the patient group with stenosis in the right than in the left coronary artery (P < 0.05). Conclusions: Transient acute myocardial ischemia causes well‐recognizable changes in the magnetocardiogram at the ST segment and the T wave. The orientation of the maximum spatial gradient of the magnetic field can be used as a parameter to determine these changes.     

二氮嗪对异丙肾上腺素诱发的大鼠心肌缺血损伤的保护作用

目的 :评价线粒体三磷酸腺苷敏感性钾通道 (mitoKATP)开放剂二氮嗪 (diazoxide ,Diaz)对大鼠心肌缺血损伤的保护作用。　　方法 :选用Wistar大鼠 3 6只 ,分为对照组 8只、异丙肾上腺素 (ISO)组 10只、二氮嗪 10mg/kg组 9只和二氮嗪2 0mg/kg组 9只。用ISO 5mg/kg皮下注射复制大鼠心肌缺血损伤模型 ,2 4h后采血测定血清乳酸脱氢酶 (LDH)和肌酸激酶 (CK)活性及乳酸含量 ,同时监测心电图、血压和心率的变化 ,并观察心肌组织形态学改变。　　结果 :ISO引起大鼠心肌缺血损伤时 ,ISO组与对照组比较 ,血清LDH、CK活性和乳酸含量明显增加 ,有极显著性差异 (P <0 0 1) ,组织形态学也发生明显改变 ,心肌细胞损伤严重 ,有极显著性差异 (P <0 0 1)。预先口服二氮嗪 10～ 2 0mg/kg可逆转血清LDH、CK和乳酸的升高 ,有显著性差异 (P <0 0 5～ 0 0 1) ,减轻心肌细胞损伤程度。二氮嗪 10mg/kg不影响收缩压和心率。　　结论 :二氮嗪对ISO诱发的大鼠心肌缺血损伤具有保护作用     

超声背向散射积分量化犬心肌缺血再灌注致心肌纤维化程度的研究

目的应用超声背向散射测定结合胶原代谢物评估犬心肌缺血再灌注致心肌纤维化程度。方法 12只成年杂种犬随机分为2组:假手术组和缺血再灌注组,每组6只。测定两组血流动力学指标,于再灌注120 min后经颈内静脉采血,用超声背向散射测定技术检测室间隔和左心室后壁背向散射积分值(IBS)和背向散射积分周期变化值(CVIB)。以酶联免疫吸附法检测患者血清结缔组织生长因子(CTGF)和Ⅰ型前胶原氨基端肽(PⅠNP)。行Masson染色观察胶原纤维组织结构变化,用免疫组织化学方法检测Ⅰ型胶原蛋白表达。结果缺血再灌注组CTGF和PⅠNP水平均高于假手术组,差异有统计学意义(P0.05)。与假手术组比较,缺血再灌注组室间隔和左心室后壁的IBS明显增加,CVIB明显减小,差异有统计学意义(P0.05)。CTGF和PⅠNP水平与IBS呈正相关(P0.05),与CVIB呈负相关(P0.05)。Masson染色显示缺血再灌注组心肌纤维化明显增加。缺血再灌注组Ⅰ型胶原蛋白表达呈强阳性。结论缺血再灌注组犬超声背向散射参数IBS增加,CVIB减少,胶原代谢物CTGF和PⅠNP水平增加,心室肌纤维化参与了缺血再灌注损伤,导致心室重构。超声背向散射测定结合胶原代谢物可早期无创性检测缺血再灌注阶段心室肌纤维化程度。     

缝隙连接阻滞剂预防缺血性室性心律失常及其机制的研究

目的观察缝隙连接阻滞剂类Heptanol对局部心肌缺血性室性心律失常发生率的影响,并探索可能的作用机制。方法①结扎离体SD大鼠冠状动脉前降支,造成左心室前壁局部缺血,观察不同浓度Heptanol对缺血所致室性心律失常发生率的影响。②取缺血部分心肌进行免疫荧光染色及RT PCR检测,应用图像分析系统半定量分析CX43蛋白及mRNA的水平。③实验动物随机分为5组,每组12只,分别为对照组、缺血组、0.1mMHeptanol组、0.3mMHeptanol组、0.5mMHeptanol组。结果①Heptanol可明显降低由于缺血引起的室性心动过速(室速)和心室颤动(室颤,缺血组45%;0.1mMHepta nol组10%;0.3mMHeptanol组0;0.5mMHeptanol组10;P<0.05)。②缺血心肌CX43蛋白表达面积比正常心肌明显减少,Heptanol可使缺血所致的CX43蛋白的减少发生部分逆转(对照组1706±397;缺血组561±147;0.1mMHeptanol组1027±215;0.3mMHeptanol组1112±301;0.5mMHeptanol组1179±425,P<0.05)。mRNA表达与蛋白水平的变化相一致。结论①Heptanol可以减少由于局部缺血引起的室速和室颤发生率。②Heptanol可以部分逆转缺血引起的CX43mRNA和蛋白表达下调。     

热休克蛋白对短暂心肌缺血所致蛋白质聚集的影响

为了观察短暂心肌缺血后心肌中蛋白质聚集物的产生，探讨热休克蛋白70及αB-晶状体蛋白对心肌中蛋白质聚集物的影响，采用雄性Wistar大鼠制备在体心缺血—再灌注损伤模型。通过乙醇磷钨酸电镜观察蛋白质聚集物产生，采用免疫电镜观察热休克蛋白70及αB-晶状体蛋白对蛋白质聚集物的影响。结果发现：①缺血15min再灌注30min时，心肌细胞中开始出现形态不规则的蛋白质聚集物，聚集物主要分布在核周、线粒体周围及其两极。再灌注4h，蛋白质聚集物达到高峰，24h后逐渐减少，72h基本恢复正常。②大鼠经热休克预处理及缺血预适应后，15min缺血及4h或24h再灌注所致的心肌蛋白质聚集物的产生明显减少，恢复速度加快，再灌注24h已基本恢复正常。③通过免疫电镜观察，在假手术对照组，心肌中热休克蛋白70表达水平很低。大鼠经热休克预处理后，心肌中热休克蛋白70表达增多，经缺血15min再灌注4h后，热休克蛋白70与心肌中蛋白质聚集物共分布。在假手术对照组心肌中，αB-晶状体蛋白有一定量的组成型表达，并均匀分布于胞浆之中。经热休克预处理、缺血预适应后缺血15min再灌注4h心肌中，αB-晶状体蛋白向肌丝移位，主要位于z线两侧的明带，且与蛋白质聚集物共分布。本研究首次揭示了缺血—再灌注损伤时心肌细胞中蛋白质聚集物的形成、空间分布及其动态变化规律；证实了热休克预处理及心肌缺血预适应可明显减轻缺血—再灌注所致心肌蛋白质聚集。     

Role of Echocardiography in the Emergency Department for Identifying Patients with Myocardial Infarction and Ischemia

Echocardiography is a valuable, noninvasive diagnostic tool that can provide information on systolic function and valvular abnormalities and can provide alternative explanations for causes of chest pain. Experimental as well as clinical studies have shown that wall motion abnormalities have a high sensitivity for predicting myocardial infarction. More recent studies, performed in the emergency department on patients evaluated for myocardial ischemia, have reported similar results. An important aspect is that necrosis is not necessary to cause wall motion abnormalities; therefore, echocardiography can also be used to identify patients with ischemia without infarction. Importantly, sensitivity is significantly higher than that for electrocardiography and is comparable to that for myocardial perfusion imaging. Newer developments, such as digital transmission over telephone lines, may lead to more widespread routine use in the emergency department. Acute emergency department echocardiography appears to be a promising tool when used in the evaluation of patients with chest pain.     

心肌缺血后心肌存活性的评价

心肌缺血后如何评价其存活性的问题近年来日益引人注目,存活心肌主要指急性心肌缺血时间＜20分钟后引起的“顿抑心肌”及慢性心肌缺血后导致的“冬眠心肌”两种状况。本文从心肌代谢、超声心动图及心电图三个方面总结了目前常用的评价心肌存活性的方法。