家兔急性心肌梗塞时高频心电频谱的变化

家兔32只,体重>2kg,常规麻醉。分别记录观察结扎冠脉左前降支(LAD),复制急性心肌梗塞前和心肌梗塞后的心肌单向动作屯位(MAP)高频心电图(HF-ECG)     

急性心肌梗塞时心肌单相动作电位变化的实验研究

本文通过结扎12支家兔左冠状动脉前降支造成实验性心肌梗塞模型,使用接触电极引导心外膜单相动作电位和同步记录体表心电图,并以微机实时分析。结扎LAD后,缺血区很快出现MAP减小,Vmax降低,负相波出现,平台期后段抬高,但MAPD不同程度延长,非缺血区MAP则无改变。实验发现,MAP的改变早于ECG的改变;     

高频心电图频谱分析用于识别家兔心肌缺血

用32只家兔观察结扎左冠状动脉前降支复制的急性心肌缺血模型上,ECG、心肌单向动作电位(MAP)率高频心电图(HF-ECG)和频谱图的变化。麻醉下家兔ECG律齐,ST-T无异常,心率224.4±91.8次/分,HF     

牛磺酸对大鼠心肌梗塞及血管活性物质的影响

本实验结扎在鼠左冠状动脉前降支建立心肌梗塞模型，观察牛磺酸对心肌梗塞的治疗作用及对血和活性物质的影响。结果显示外源性注射牛磺酸可减少大鼠心肌梗塞坏死面积和缩小梗塞范围：血清ＣＰＫ、ＣＫ ＭＢ活性下降，ＭＤＡ含量降低；牛磺酸还可使血浆内皮素、甘丙素、Ｐ物质、ｃＡＭＰ和ｃＧＭＰ水下下降，提示牛磺酸对急性心肌缺血坯死有明显的保护作用。     

通脉散对家兔急性心肌梗塞范围及血小板超微结构的影响

通脉散为治疗冠心病的纯中药制剂。为了探讨其作用机制而采用结扎家兔冠状动脉复制急性心肌梗塞动物模型（NBT染色法），观察通脉散对心肌梗塞范围和血小板形态及超微结构计量学指标的影响。结果表明：通脉散组的心肌梗塞范围和血小板超微结构指标的改变明显低于维拉帕米组（P＜0．05～0.01），通脉散缩小家兔急性心肌梗塞范围的机制可能与其稳定血小板形态及抑制血小板活性物质的释放有关。     

结扎犬前降支冠脉后的乳头肌血流量

结扎犬前降支冠脉是复制急性心肌缺血模型的主要方法之一。Blair利用冠脉铸型法证明犬左室前壁主要由左前降支冠脉供血,而左室前乳头肌主要由间隔动脉供血。本文目的在于观察当结扎左前降支冠脉后,左室前乳头肌和左室前壁的血流量将发生怎样的不一致性变化,并讨论该变化在实验性心肌缺血的研     

向量诊断心肌缺血的基础研究

目的：通过心电向量图（VCG）与心电图（ECG）两种方法描记犬心肌缺血，比较VCG和ECG的技术特征与图形特征，寻找心脏功能在病理状态下的准确表达途径，这对心肌梗塞的早发现、早治疗很有意义。方法：将31只正常犬的冠状动脉左前降支结扎，建立犬的心肌缺血模型。结扎60min、再灌注120min通过VCG、ECG两种方法记录每一时段的信息特征，以比较它们诊断心肌缺血异常项目的检出率。结果：心电向量图不管是结扎60min还是再灌注120min。对心肌缺血异常项目的检出率均明显地高于心电图。结论：对心肌缺血的诊断VCG优于ECG。     

飞龙掌血水提物对心肌缺血兔心功能和血液动力学的影响

目的:观察飞龙掌血(Toddalia asiatica Lam)水提物(飞龙一号,F01)对急性心肌缺血动物模型心脏功能和血液动力学的影响。方法:新西兰兔作不开胸膜冠脉左前降支高位结扎造成急性心肌缺血, 观测结扎后及F01 ip对动物心功、血液动力学的影响。结果:冠脉左前降支结扎后,LVEDP显著升高(P＜0.05),t-dp/dt max 无明显变化,其余各项参数均明显降低(P＜0.05或P＜0.01)。F01(268 mg/kg)腹腔注射后,除有关左室作功和心肌耗氧的参数(HR、TTI和TTI×HR)继续降低外,其余各项参数的变化均显著逆转,恢复或接近结扎前的水平, 用药后1.5 h的作用较0.5 h更明显。结论:F01可显著减少急性缺血心肌的作功和耗氧,通过纠正心脏对氧的供需平衡失调,改善心脏收缩、舒张功能和泵血功能,从而发挥对缺血心肌的保护作用。     

等容血液稀释对兔缺血—再灌注损伤时心肌细胞超微结构的影响

结扎兔冠脉左室枝45min，再灌注180min，复制急性心肌缺血－再灌注模型，观察等容血液稀释对再灌注损伤时心肌细胞超微结构的影响。20只兔随机分为两组：Ⅰ组（对照组）、Ⅱ组（稀释组）。结果：电镜下观察，Ⅰ组心肌细胞细胞器严重损伤，Ⅱ组心肌细胞超微结构有不同程度恢复。与此相对应，再灌注期间Ⅱ组心功能明显好于Ⅰ组，心肌梗塞面积亦小于Ⅰ组。提示：缺血－再灌注损伤时，心肌细胞的超微结构发生了异常改变，血液稀释疗法应用后细胞超微结构呈现出不同程度恢复且可缩小心肌梗塞范围，在心肌再灌注损伤的防治方面表现出良好的作用。     

三参维心胶囊经内质网应激通路抗心力衰竭的机制研究

<正>目的:本实验通过结扎大鼠冠状动脉左前降支复制心力衰竭模型。探讨心力衰竭发生发展过程中的分子机制。同时,研究三参维心胶囊抗心力衰竭的作用及其机制。方法:通过结扎大鼠冠状动脉左前降支(LAD)复制心力衰竭模型,将大鼠随机分为sham组、HF组(心力衰竭组)和Sanshen组(三参维心胶囊组),Sanshen组术后3 d给予三参维心胶囊0.8 g/kg治疗4     

微创球囊堵闭法建立猪心肌梗死模型及其手术并发症的预防和处理

目的 探讨运用微创冠状动脉球囊堵闭法建立猪急性心肌梗死模型的实验方法及其手术过程中并发症的处理.方法 猪麻醉后经右侧股动脉置入冠状动脉球囊导管至左前降支远端堵闭120 min,直至心电图证实心肌梗死形成.结果21只苏中幼猪均完成了冠状动脉造影及球囊封堵术,1只因术中失血过多在术后饲养过程中死亡,2只因封堵结束撤管时出现缓慢性心律失常和呼吸骤停,经抢救无效死亡.心电图监护显示典型急性心肌梗死图形演变过程,血清肌钙蛋白明显升高且呈动态变化,4周后病理标本显示疤痕形成,切片显示典型心肌梗死病理改变.结论 微创球囊冠状动脉堵闭法为一种简单安全的建立心肌梗死模型的方法,术中并发症的预防及处理是保证存活率的关键.     

Acute myocardial infarction caused by coronary artery dissection following blunt chest trauma

Chest trauma can lead to various cardiac complications ranging from simple arrhythmias to myocardial rupture. An acute myocardial infarction (AMI) is a rare complication that can occur after chest trauma. We report a case of 66-year-old male who suffered a blunt chest trauma from a traffic accident resulting in an AMI. The coronary angiography revealed an eccentric 50% narrowing of the ostium of left anterior descending artery (LAD) by a dissection flap with calcification. Intravascular ultrasonography (IVUS) revealed eccentric calcified plaque (minimal luminal diameter [MLD]=3.5 mm) with a dissection flap. Intervention was not performed considering the MLD and calcified flap, and he has been conservatively managed with aspirin and losartan for 2 years. The follow-up coronary angiography showed an insignificant luminal narrowing of the proximal LAD from the ostium without evidence of a dissection. An early coronary evaluation including an IVUS study should be considered for managing patients who complain of ongoing, deep-seated chest pain with elevated cardiac enzyme levels and an abnormal electrocardiogram (ECG) after a blunt chest trauma. Based on this case, some limited cases of traumatic coronary artery dissections can be healed with conservative management and result in a good prognosis.     

A case of acute myocardial infarction after blunt chest trauma in a young man

Coronary artery injury rarely occurs after blunt chest trauma, but it can lead to extensive myocardial infarction and be frequently overlooked. A 16-yr-old man was presented with comatose mental state and rapid respiration rate. He ran into guard rail while riding a motorcycle. In routine examination, his electrocardiogram showed Q wave and 2 mm ST segment elevation in all precordial leads, I and aVL. The cardiac enzymes were also elevated: creatine kinase (CK)-MB was 300 U/L, and cardiac specific troponin I was 5.7 ng/mL. Two-dimensional echocardiography showed anteroseptal akinesia with severely depressed left ventricular function, ejection fraction of 28%. He could not receive any anticoagulation or thrombolytic therapy because of his brain lesion. Three weeks later, his mental state improved. A diagnostic coronary angiogram revealed total occlusion in the proximal left anterior descending artery (LAD) with collaterals from the right coronary artery and left circumflex artery. We successfully performed a percutaneous coronary intervention for the LAD lesion, and the final angiogram showed a good coronary flow without residual stenosis.     

Hemorrhagic myocardial infarction after streptokinase treatment for acute coronary thrombosis

A 37-year-old man with an evolving anterior myocardial infarction received intracoronary thrombolytic therapy six hours after its onset. The restored coronary artery patency was recorded angiographically in the left anterior descending coronary artery (LAD). He died 28 hours after administration of the therapy. Uniform and severe interstitial hemorrhage was present in the area of myocardial necrosis. The distribution of hemorrhage and myocardial necrosis corresponded with the vascular bed of the LAD and was thus consistent with experimental studies that concluded that the hemorrhagic areas were probably confined to muscle that was already necrotic.     

Myocardial infarction in the C57BL/6J mouse: a quantifiable and highly reproducible experimental model.

INTRODUCTION: The laboratory mouse is a powerful tool in cardiovascular research. In this report, we describe a method for a reproducible mouse myocardial infarction model that would allow subsequent comparative and quantitative studies on molecular and pathophysiological variables. METHODS: (A) The distribution of the major coronary arteries including the septal artery in the left ventricle of the C57BL/6J mice (n=20) was mapped by perfusion of latex dye or fluorescent beads through the aorta. (B) The territory of myocardial infarction after the ligation of the most proximal aspect of the left anterior descending (LAD) coronary artery was quantified. (C) The consistency in the histological changes parallel to the infarction at different time points was analyzed. RESULTS: (A) The coronary artery tree of the mouse is different from human and, particularly, in regard to the blood supply of the septum. (B) Contrary to previous belief, the septal coronary artery in the mouse is variable in origin. (C) A constant ligation of the LAD immediately below the left auricular level ensures a statistically significant reproducible infarct size. (D) The ischemic changes can be monitored at a histological level in a way similar to what is described in the human. CONCLUSION: We illustrate a method for maximal reproducibility of experimental acute myocardial infarction in the mouse model, due to a consistent loss of perfusion in the lower half of the left ventricle. This will allow the study of molecular and physiological variables in a controlled and quantifiable experimental model environment.     

A case of successful primary coronary intervention for the total occlusion of left main stem with the aid of abciximab

A 61-yr-old male patient presented with severe chest pain with cardiogenic shock due to an extensive anterolateral myocardial infarction. Two-dimensional echocardiogram showed severe left ventricular systolic dysfunction (ejection fraction=17%). Emergent coronary angiogram obtained immediately after placing temporary pacing electrode revealed total thrombotic occlusion in the left main stem. We performed direct coronary intervention using kissing balloon technique with the aid of Abciximab (ReoPro) infusion. Residual stenosis with thrombus remained even after high pressure balloon dilatations, therefore we placed two stents, one in the ostia of left anterior descending (LAD) and the other in left circumflex artery (LCX). Coronary angiogram after kissing stents showed improved LAD and LCX flows without residual stenosis. Chest pain resolved and blood pressure normalized after coronary intervention. The whole procedure time was 15 min. Follow-up coronary angiogram taken one week later showed patent previous stented arteries, and echocardiography demonstrated 40% of left ventricular ejection fraction. The clinical course for one-year follow-up was uneventful.     

The significance of myocardial bridge upon atherosclerosis in the left anterior descending coronary artery

The relation between myocardial bridges (MB) and atherosclerosis in the left anterior descending coronary artery (LAD) was explored using morphometric methods in 642 hearts. The location of myocardial bridges in the LAD was classified according to distribution as proximal, middle and distal. Myocardial bridges were found in 48 per cent of males and 36 per cent of females. When proximal myocardial bridging was present intimal thickening and macroscopic raised lesion were increased just before the bridge as compared with the corresponding site in the other two categories. Underneath bridges eccentric plaques and raised lesions are absent although there is often concentric intimal thickening. The overall frequency of myocardial infarction was the same in patients with and without myocardial bridges. However, when infarction occurred in the patients having bridges, it was almost confined to those in the proximal group despite this being infrequent in the general distribution of myocardial bridges in the left anterior descending artery. It is postulated that hypertension may enhance infarction in the case of myocardial bridges in the very proximal left anterior descending artery. It is concluded that the location of myocardial bridges greatly alters the distribution of physical force against the arterial wall and influences the extent of atherosclerosis.     

Evaluation of coronary native and coronary collateral pressure gradients in the conscious dog

Sixteen dogs were instrumented chronically with a left circumflex (CIRC) Ameroid constrictor, and with CIRC, left anterior descending (LAD), aortic, left atrial and pulmonary artery (PA) catheters. Premature mortality was 12.5% prior to the last measurements of pressure at 50 +/- 3 days (mean +/- SE). Five animals developed closure of the Ameroid constrictor at 5 +/- 1 days with an LAD to CIRC pressure gradient of 57 +/- 8 mm Hg. Eleven animals developed closure of the Ameroid constrictor at 18 +/- 1 days with an LAD to CIRC pressure gradient of 29 +/- 3 mm Hg. Three animals in the former group had gross evidence of a myocardial infarction on postmortem examination. None of the animals in the latter group showed evidence of a myocardial infarction. Thus, closure of a CIRC Ameroid constrictor and subsequent collateral vessel development can be monitored chronically by the LAD to CIRC pressure gradient with a high survival, low infarction rate. This chronic model thus provides an accurate measure of coronary native and collateral pressures in unsedated dogs.     

False lumen stent placement during iatrogenic coronary dissection

A 38-year-old woman without significant cardiovascular risk factors was admitted in the coronary care unit with the diagnosis of acute coronary syndrome without ST-segment elevation. In coronary angiography, left coronary artery system was normal in the first contrast injection, but acute occlusion of the left main coronary trunk (LCT) due to iatrogenic dissection was observed in the following. The patient presented marked ST elevation, severe hypotension, hemodynamic collapse, and loss of consciousness. Cardiopulmonary resuscitation (CPR) was initiated, and two drug-eluting stents were consecutively placed in the LCT and the left anterior descending coronary (LAD), but the patient died after 60 min of continuous CPR. The autopsy showed dissection of the LCT and LAD coronaries with both stents placed in the false lumen and hyperacute myocardial infarction in the anterior left ventricular free wall. This case underlines the importance of careful indication of invasive procedures and of taking in consideration their potential risks.     

Morphology of coronary vessels in coronary heart disease. An analysis of 930 coronary angiograms

Coronary anatomy was analyzed in 930 patients who underwent coronary arteriography because of coronary artery disease. There was a slight predominance of single vessel disease, whereas double and triple vessel disease were equally distributed. A left main (LM) lesion was found in 5.2%, with an additional right coronary artery lesion in 3.3%. The left anterior descending (LAD) artery was involved most frequently, followed by the right coronary artery (RCA) and left circumflex (Cx). The LAD demonstrated more often a proximal stenosis than the RCA and Cx. If the LM is associated with a RCA-stenosis then the LAD and Cx are involved more commonly, suggesting a more advanced disease in all major vessels. The analysis of ventricular function revealed a significant deterioration according to the number of diseased vessels. If the LM is associated with a RCA lesion, then the hemodynamics are similar to a 3-vessel disease, whereas isolated LM lesions are associated with good ventricular function according to the lesser degree of coronary sclerosis. The deterioration of the hemodynamics in correlation with coronary vessel involvement is significant, however due to the large standard deviations conclusions for the individual patient can not be drawn.