脑梗塞患者血清抗心磷脂抗体含量变化的研究

目的探讨脑梗塞患者血清中抗心磷脂抗体(ACA)含量变化的意义。方法采用酶联免疫吸附试验(ELISA)对80例脑梗塞患者血清中ACA含量进行检测,并与40例作为对照组进行比较。结果脑梗塞组血清中ACA阳性率明显高于对照组(P<0.01);ACA分型中,脑梗塞组血清中IgG阳性率明显高于对照组(P<0.01)。结论检测血清中ACA含量,可作为研究ACA与脑梗塞关系的一项可靠指标,对脑梗塞的病理机制研究以及对疾病的预防、治疗和预后判断可能有一定帮助。     

眼科以咽部瘙痒为首发症状的心肌梗死1 例- 附文献复习

目的:提高异位疼痛为首发症状心肌梗死的临床警惕性与确诊率。方法:通过我院不典型心肌梗死病例1例就诊过程进行回顾性追溯分析,进行相关文献复习,总结提高诊断准确性,减少误诊的经验方法。结果:因诊断及时,患者经积极的抢救治疗,症状改善,治愈出院。结论:提高对异位疼痛为首发症状心肌梗死的警惕,拓宽诊断思维,全面体检,尤其注意心电图:动态心电图、心肌酶谱的监测,及时确诊,以尽量减少不典型心肌梗死的误诊。     

大鼠心肌梗死模型构建和评价方法的改良

目的 优化和改良大鼠心肌梗死模型的构建和评价方法,提高模型的可靠性和稳定性.方法 取雄性SD大鼠结扎左冠状动脉前降支建立心肌梗死模型,在模型的构建过程中从麻醉、插气管、保温、手术操作、术后护理等环节进行优化和改进,并观察不同的麻醉方法和术后时间对心肌梗死程度的影响,用不同的染色方式进行心肌梗死模型的评价.结果 对比大鼠心肌梗死模型构建过程中各组大鼠麻醉时间、术后恢复以及心肌梗死面积的结果,戊巴比妥钠是更合适的麻醉药;结扎手术后时间对模型心肌梗死范围无明显影响（P＆gt;0.05）,但心肌缺血危险区面积随术后时间的延长明显减少（P〈0.01）;TTC与依文思蓝双重染色相对TTC染色能明显观察到心肌缺血危险区和梗死区范围.结论 优化和改进后的大鼠心肌梗死模型,提高了动物福利,制备和评价方法更加客观准确.     

Internal synchronization of the main 0.1-Hz rhythms in the autonomic control of the cardiovascular system

Synchronization parameters of 0.1-Hz rhythms isolated from the heart rate and the oscillations of the blood volume in microcirculatory vessels were studied in 12 healthy subjects and 32 patients with acute myocardial infarction. Recordings of the electrocardiogram and the pulsogram from the distal phalanx of the index finger, as well as mechanical recording of respiration with the body in a horizontal position, were performed. In patients with myocardial infarction, the recordings were performed during the first three to five days and the third week after the infarction. Synchronization was tested by plotting phase differences and calculating the total percentage of phase synchronization. Synchronization parameters of 0.1-Hz rhythms were high in healthy subjects. In patients with acute myocardial infarction, synchronization of 0.1-Hz rhythms was considerably poorer. The data obtained suggest that the studied 0.1-Hz rhythms are two independent oscillatory processes that are synchronized in healthy subjects. However, this interaction may be disturbed in cardiovascular pathologies, e.g., myocardial infarction.     

Disorder of the contractile function of the nonischemic portion of the heart in experimental infarct and its prevention by the phospholipase inhibitor chloroquine

Contractility of an isolated rat right auricle was studied one day after producing one day after producing experimental infarction in the left cardiac region, there was a pronounced decrease in elasticity, and contractility was depressed, which manifested in an approximately two-fold decline in the developing tension. These originally stress-induced disturbances were prevented by administering the phospholipase inhibitor chloroquine to the animals prior to infarction. The data obtained indicate that activation of phospholipases might play a role in contractility disturbances of cardiac nonischemized regions under infarction.     

Ultrastructure of cardiomyocytes in the peri-infarct zone during the treatment of experimental myocardial infarct in rats using the hexapeptide dalargin

The experiments on white rats with induced myocardial infarction have studied the influence of dalargin on the infarction size and peri-infarction zone ultrastructure. 24 hours later the decrease in the infarction zone size was detected in rats who had received dalargin in a dose of 50 and 100 micrograms/kg. In the peri-infarction zone the increase in glycogen quantity, the lower degree of lipid infiltration, the increase in mitochondrial number and mitochondrial energy effectiveness coefficient were noted, as compared to control animals. Sarcolemma of cardiomyocytes from the peri-infarction zone in rats on dalargin was impermeable for colloidal lanthanum. The decrease in the infarction size under the effect of dalargin is explained by its influence on the survival of cardiomyocytes in the peri-infarction zone.     

The morphofunctional state of the neurons in the nodose ganglia of the normal vagus nerves and in experimental myocardial infarct

Basing on a complex approach with the use of general morphological and morphometrical methods, a morphofunctional characteristics of the nodose ganglia neurons of the nervus vagus has been presented in 203 dogs, both normal and at an experimental myocardial infarction. The neurons in question react to the myocardial infarction with a complex of changes in the intracellular structure parameters and their chemical markers. Their manifestation degree is higher and lasts longer, when the myocardial infarction happens at day time.     

Effect of Eleutherococcus on the subcellular structures of the heart in experimental myocardial infarct

The effect of Eleutherococcus on subcellular heart organization in rats with or without myocardial infarction was investigated. It was found that Eleutherococcus decreases ultrastructural lesions in the ischemic area, intensifies regeneration of subcellular structures and accelerates the recovery after myocardial infarction. The accumulation of glycogen, lipids and lysosomes is observed in lipocytes. It is suggested that positive effect of Eleutherococcus during myocardial infarction is related to lipid transformation into glycogen.     

Dynamics of the strength of the rat left ventricle wall in experimental uncomplicated myocardial infarction

Left ventricular wall stability was studied in 131 normal rats at different terms of uncomplicated experimental myocardial infarction. Left ventricular wall stability was estimated by the normal effort required for its destruction. Normal left ventricular wall could stand the pressure of 1.1 X 10(5) Pa. During ischemic phase of myocardial infarction the wall stability in the infarction area increased up to 1.5 X 10(5) Pa. It diminished during necrotic phase, however timely started repair processes did not let it drop lower than 1.0 X 10(5) Pa. The mechanisms of preserving ventricular wall stability in the infarction area were studied in detail.     

急性心肌梗死患者肠道优势菌群分析

目的探讨急性心肌梗死患者肠道优势菌群的改变及其与疾病严重程度的关系。方法共筛选急性心肌梗死患者71名及正常健康体检者33名,急性心肌梗死患者根据是否心衰分为急性心肌梗死组36名和急性心肌梗死伴泵衰竭组35名,所有入选者收集大便及血清标本,分别采用qPCR及化学发光仪测定肠道优势菌群改变和血清脑钠肽前体及肌钙蛋白水平。结果急性心肌梗死患者肠道优势菌群显著改变,肠道肠杆菌以及肠球菌细菌数量较对照组显著增加,均与脑钠肽前体、肌钙蛋白、Killip分级显著正相关,而双歧杆菌、乳酸杆菌等细菌数量显著降低,与脑钠肽前体、肌钙蛋白、Killip分级显著负相关。结论急性心肌梗死患者呈现典型的肠道菌群紊乱,且与患者疾病严重程度相关。     

Infarction in the territory of the anterior cerebral artery: clinical study of 51 patients

Background

Little is known about clinical features and prognosis of patients with ischaemic stroke caused by infarction in the territory of the anterior cerebral artery (ACA). This single centre, retrospective study was conducted with the following objectives: a) to describe the clinical characteristics and short-term outcome of stroke patients with ACA infarction as compared with that of patients with ischaemic stroke due to middle cerebral artery (MCA) and posterior cerebral artery (PCA) infarctions, and b) to identify predictors of ACA stroke.

Methods

Fifty-one patients with ACA stroke were included in the "Sagrat Cor Hospital of Barcelona Stroke Registry" during a period of 19 years (1986–2004). Data from stroke patients are entered in the stroke registry following a standardized protocol with 161 items regarding demographics, risk factors, clinical features, laboratory and neuroimaging data, complications and outcome. The characteristics of these 51 patients with ACA stroke were compared with those of the 1355 patients with MCA infarctions and 232 patients with PCA infarctions included in the registry.

Results

Infarctions of the ACA accounted for 1.3% of all cases of stroke (n = 3808) and 1.8% of cerebral infarctions (n = 2704). Stroke subtypes included cardioembolic infarction in 45.1% of patients, atherothrombotic infarction in 29.4%, lacunar infarct in 11.8%, infarct of unknown cause in 11.8% and infarction of unusual aetiology in 2%. In-hospital mortality was 7.8% (n = 4). Only 5 (9.8%) patients were symptom-free at hospital discharge. Speech disturbances (odds ratio [OR] = 0.48) and altered consciousness (OR = 0.31) were independent variables of ACA stroke in comparison with MCA infarction, whereas limb weakness (OR = 9.11), cardioembolism as stroke mechanism (OR = 2.49) and sensory deficit (OR = 0.35) were independent variables associated with ACA stroke in comparison with PCA infarction.

Conclusion

Cardioembolism is the main cause of brain infarction in the territory of the ACA. Several clinical features are more frequent in stroke patients with ACA infarction than in patients with ischaemic stroke due to infarction in the MCA and PCA territories.     

The Significance of Ventricular Premature Beats in the Diagnosis of Septal Infarction

Two hundred and twenty electrocardiograms containing premature ventricular beats were reviewed. Twenty of these contained premature ventricular beats of a myocardial infarction pattern, that is, one consisting of a significant Q wave followed by an R wave. A review of the case histories of these 20 patients disclosed that all 20 had angina pectoris and/or myocardial infarction. Postmortem examinations were performed in seven, and the presence of myocardial infarction was verified. In three instances, only the premature ventricular beat disclosed the myocardial infarction pattern while the normally conducted beats did not. In these three cases the postmortem examination confirmed the presence of septal infarction.     

Correlations between the endothelium-dependent relaxation of the aorta and arterial pressure in rats with myocardial infarction

The effect of experimental myocardial infarction on endothelium-dependent relaxation was studied on isolated rat aorta and compared with the dynamics of arterial pressure (AP). It was shown that the endothelium-dependent relaxation of aorta was increased 1.8 times 3 h following the myocardial infarction. Simultaneously the drop in AP which had begun immediately following the experimental infarction became maximal. In 24 h both the indices were restored practically to the initial level. There was a significant negative correlation between the extent of endothelium-dependent relaxation and AP. It was suggested that the increase in endothelium-dependent relaxation could influence vascular tone, the drop in AP, and, finally, the development of cardiogenic shock in myocardial infarction in man.     

175例侧脑室体旁脑梗死的发病部位与临床对照研究

目的：探讨侧脑室体旁脑梗死的发病部位与临床关系的特点及发病机理,以便给予相应治疗对策。方法：收集175例侧脑室体旁脑梗死的患者,均经头颅CT或MRI证实为侧脑室体旁的梗死,其中小梗死120例,大梗死55例,结合文献就两者的临床症状及影像学表现进行分析,通过这些分析推测出在侧脑室体旁放射冠处锥体束排列与躯体存在定位关系。同时,对其发病机理进行探讨,以采取不同的相应治疗对策。结果：小梗死与大梗死的临床表现略有差别,发病机制有所不同。小梗死以腔隙性脑梗死为多,发病机制同腔隙性脑梗死类似;大梗死以分水岭脑梗死为多,发病机制同分水岭脑梗死类似。但就目前研究上来说,以上两种脑梗死的病因及发病机理仍存在不小的争议,本文就研究所见一并加以探讨。结论：侧脑室体旁放射冠区由前向后依次排列着支配头面部、上肢及下肢的锥体束纤维。可推测皮质脑干束与皮质脊髓束经侧脑室体旁放射冠区纤维由前向后重叠排列,支配感觉的传导束纤维则排列于放射冠的中部至后部,锥体束的后外侧。Broca区语言中枢和Wernicke区语言中枢的皮质下白质传导束在侧脑室体旁放射冠区由前向后排列,Broca区的纤维可能主要走行于放射冠的前部,Wernicke区的纤维可能主要走行于放射冠的后部,而侧脑室体旁放射冠的中部可能存在两种纤维的重叠。同时,针对发病的不同的病理生理机制,采取不同的相应治疗对策。     

Time of regression of the Q wave in patients with myocardial infarction]

A rate of Q wave regression was assessed in 72 patients with ischaemic heart disease, including 46 patients after the infarction of the inferior wall and 26 patients after anterior wall infarction. All patients were followed-up for two years. Complete regression of Q wave was noted in 19 patients (41.3%) after inferior wall infarction and in one patient (3.8%) after anterior wall myocardial infarction. Partial regression of Q wave was seen in 9 patients (19.6%) after inferior wall, and in 2 patients (7.6%) of patients with anterior wall myocardial infarction. It seems that the regression of Q wave in ECG does not improve prognosis in these patients. Six out of 10 deaths which occurred in the followed up group of patients involved those in whom no electrographic features of the past myocardial infarction were seen.     

Effect of adaptation to short-term stress exposure on the fibrillation threshold and ectopic activity of the heart in experimental myocardial infarct

Preliminary adaptation to short-term stress was shown to prevent the decrease in the heart fibrillation threshold and an increase in ectopic activity which is usually observed in experimental myocardial infarction. This protective effect involves an enhanced activity of the antioxidant system. Therefore, a synthetic antioxidant ionol was applied to prevent disturbances of the heart electrical stability in infarction. It was established that ionol completely prevents the decrease in the electrical threshold and the increase in ectopic activity of the heart in experimental infarction. Thus, it can be concluded that ionol possesses an antiarrhythmic effect.     

Possible role of lipid peroxidation in the pathogenesis of arrhythmias in myocardial infarct

The effect of myocardial infarction sustained by rats on the resistance of their isolated auricles to H2O2, an inductor of lipid peroxidation (LP), was studied. Atrial resistance to the LP inductor depends on the level of developed tension (DT) and the decrease of DT leads to augmentation of atrial resistance to the arrhythmogenic effect of LP. The experimental myocardial infarction causes appreciable disturbances in the function of automatism of the auricles, 60% of which lose their capability of spontaneous contractile activity. When compared with the control under equal DT, the auricles of the "infarction" series are less resistant to H2O2: the time of arrhythmias and arrests in them are 2.3 times as much as in the control. In infarction, the pretreatment with ionol reduces both the quantity of the auricles which stopped before H2O2 administration and the quantity of the auricles responding by arrhythmia to LP induction. The data point to the possibility of the use of antioxidants for preventing arrhythmias in experimental myocardial infarction.     

Comparative analysis of the X-ray morphology of coronary atherosclerosis and the results of endovascular interventions performed in the subacute period and 6 months after prior myocardial infarction

The study was undertaken to analyze the morphology of coronary lesion and the angiographic results of interventions made in the subacute period and 6 months after prior myocardial infarction. It included 593 patients with and without prior Q-wave myocardial infarction. The X-ray morphological parameters of the coronary bed were analyzed in the patients who had undergone invasive studies within a month (n = 362) and 6 months (n = 231) after sustained myocardial infarction. In both groups, the successful intervention rate was also estimated during endovascular treatment. The study showed that the number of stenoses with the complicated morphology (type B) was significantly more 6 months after sustained myocardial infarction than that in the subacute period. The number of occluded segments with the characteristics that were unfavorable for endovascular intervention (bridge collaterals, extended occlusions) was also significantly more in the late periods. In the subacute period, the angiographic success rate of endovascular recanalizations of chronic occlusions was 83.4%, which was significantly higher than that (62.6%) 6 months following infarction. The findings have led us to the conclusion that it is necessary to make routine coronary angiography in all postinfarction patients during their hospital stay in order to define the potentialities of early revascularization.     

Enhanced expression of angiopoietin-2 and the Tie2 receptor but not angiopoietin-1 or the Tie1 receptor in a rat model of myocardial infarction

Modulation of Tie2 receptor activity by angiopoietin ligands is crucial for angiogenesis, blood vessel maturation, and vascular endothelium integrity. The role of the angiopoietin (Ang) and Tie system in myocardial infarction is not well understood. To investigate the participation of the Ang/Tie in myocardial infarction, adult Sprague-Dawley rats with ligation of the left anterior descending coronary artery to induce myocardial infarction were studied. Ang1, Ang2, Tie1, and Tie2 were measured immediately after ligation of the coronary artery, and at 6 h, 1 and 3 days, and 1, 2, 3 and 4 weeks after ligation by Northern blotting, Western blotting, and immunohistochemical staining. Ang2 mRNA significantly increased from 2 weeks (2.1-fold) to 4 weeks (2.9-fold) after the infarction in the left ventricular free wall. Tie2 mRNA increased significantly from 1 week (2.1-fold) to 4 weeks (3.8-fold) after the infarction. Ang2 protein also significantly increased from 3 days (1.9-fold) to 4 weeks (3-fold) after the infarction in the left ventricular free wall. Tie2 protein increased 2.4-fold at 3 weeks and 2.8-fold at 4 weeks after the infarction. Neither Ang1 nor Tie1 mRNA or protein showed any significant change at any time point after the infarction. The ratio of Ang2/Ang1 mRNA and protein in the study group was higher than that in the control group. Ang2 and Tie2 expression in nonischemic myocardium showed no significant change. Immunohistochemical study also showed increased immunoreactivity of Ang2 and Tie2 at the infarct border. In conclusion, Ang2 and Tie2 expressions significantly increased both spatial and temporal patterns after myocardial infarction in the rat ventricular myocardium, while Ang1 and Tie1 receptor expression did not.     

Increased preproenkephalin A gene expression in the rat heart after induction of a myocardial infarction.

The expression of preproenkephalin A (ppENK) gene was investigated in the rat heart, following the onset of myocardial infarction induced by ligation of the left anterior descending coronary artery. The relative abundance of ppENK mRNA and the level of enkephalins were measured by Northern blot analysis and radioimmunoassay, respectively, in the ventricles from control-unoperated, sham-operated, and operated rats. Three hours after the surgery, a comparison between rats with infarction and sham-operated rats revealed that the relative abundance of ppENK mRNA and the level of enkephalins were increased three- to four- and two- to three-fold, respectively, in the ventricles of rats with infarction. No difference was observed between rats with infarction and sham-operated rats 24 h after the surgery, or between rats with infarction compared at time intervals of 3 and 24 h following the surgery. The abundance of the ppENK mRNA in the polysomal fraction of the ventricular septum was also measured 3 h after the surgery and found to be threefold higher in rats with infarction as compared with sham-operated rats. These results indicate that the level of enkephalins rapidly increases in the ventricles of rats following myocardial infarction, and that this higher level may be ascribed to a stimulation of the local synthesis of enkephalins.