心肌梗死后交感神经重构与室性心律失常

心肌梗死后早期即出现交感神经重构,交感神经的重构加重了心肌梗死后心肌的电生理异质性,从而导致室性心律失常发生增多,干预交感神经重构可影响心肌梗死后室性心律失常的发生。     

心脏自主神经重构与心肌梗死后室性心律失常

心肌梗死后心脏不同区域出现不同程度的去迷走神经支配、去交感神经支配以及交感神经过度再生。这种心脏自主神经的不均一重构加重了心肌梗死后心肌的电生理异质性,导致了室性心律失常易感性增加。多种针对自主神经重构的治疗手段可以有效预防及治疗心肌梗死后患者的室性心律失常,具有较大的临床应用前景。     

心肌边缘带及其电机械特性

心肌梗死发生后坏死心肌和正常心肌之间存在一个交界区域,被称为边缘带。边缘带具有特殊的解剖和生理特点,与心肌梗死后发生的心律失常、心室重构等病理生理改变密切相关。与脑梗死中的“缺血半暗带”一样,边缘带是心肌梗死治疗中必须重视的。     

心肌细胞与成纤维细胞间电耦联的研究进展

心肌纤维化这一病理过程存在于多种心血管疾病中,目前研究证明其与室性快速性心律失常以及心房颤动密切相关。了解心肌纤维化致心律失常的潜在病理生理学机制,对研究心律失常的发生和治疗具有重要意义。本文就心肌纤维化致心律失常的机制、心肌细胞与成纤维细胞间电相互作用的研究进展、细胞间电耦联微结构的探索进行综述。     

心肌边缘带及其电机械特性

心肌梗死发生后坏死心肌和正常心肌之间存在一个交界区域，被称为边缘带。边缘带具有特殊的解剖和生理特点，与心肌梗死后发生的心律失常、心室重构等病理生理改变密切相关。与脑梗死中的“缺血半暗带”一样，边缘带是心肌梗死治疗中必须重视的。     

白藜芦醇对大鼠心肌梗死后室性心律失常及长期存活率的影响

目的 研究白藜芦醇对大鼠心肌梗死后室性心律失常、心室重构和长期存活率的影响.方法 将SD大鼠随机分成假手术组、心肌梗死组、白藜芦醇治疗组(治疗组).心肌梗死组和治疗组开胸结扎冠状动脉左前降支,假手术组不结扎.植入性射频发射器记录24 h心电图,并分析心肌梗死后24 h内室性心律失常发病率;侵入性在体电生理检测评价室性心律失常的诱发率;全细胞膜片钳技术检测白藜芦醇对单个心室肌细胞的电生理作用;免疫荧光染色观察心肌细胞的结构改变.结果 与心肌梗死组相比,治疗组明显抑制了心肌梗死导致的室性心动过速和心室颤动发病率,治疗组室性心动过速的诱发率低于心肌梗死组,差异有统计学意义(46%vs 81%,P<0.01).14周后,治疗组心肌梗死面积和死亡率较心肌梗死组分别下降了20%和33%.膜片钳记录显示白藜芦醇抑制了L型钙电流.免疫荧光染色发现治疗组心肌细胞横断面积小于心肌梗死组.结论 白藜芦醇可以通过抑制大鼠心肌L型钙电流发挥抗心律失常作用,并抑制了左心室重构,提高了大鼠心肌梗死后的存活率.     

外源性电刺激诱导干细胞心肌向分化的研究进展

心肌梗死引起的缺血性心脏疾病是影响人类健康的重要问题.基于干细胞的心肌梗死治疗前景广阔,然而干细胞经定向诱导分化形成的心肌细胞具有分化率和成熟度低的特点,移植到受损心肌处可能会增加心律失常的风险.相关研究表明,施加电刺激可显著促进干细胞的心肌向分化.现综述不同电刺激参数对不同干细胞类型的影响及其中可能涉及的相关机制.     

心肌梗死后交感神经重构的研究进展

心肌梗死后心脏交感神经分布改变,使去神经支配和神经过度支配区域共存,引起电生理异质性增加.交感神经重构和电重构相互影响,成为心肌梗死后恶性心律失常发生和猝死的重要因素.交感神经重构的机制和干预已经成为研究的热点问题,可能为将来心肌梗死后心律失常的治疗提供一个新的方向.     

急性心肌梗死诱发心室颤动机制的研究进展

急性心肌梗死诱发的恶性心律失常是导致患者死亡的首要原因,其中最常见的是心室颤动。目前认为,心室颤动与多种因素所致的心肌组织电生理改变不均一性或电生理恢复不均一性有关,但急性心肌梗死诱发心室颤动的机制尚未完全阐明,是目前临床治疗的难点和疑点。本文将对这一机制的研究进展作一概述。     

溶栓疗法后室性心律失常对梗塞区供血冠脉再通的预测价值

动物试验证明,冠脉再灌注常伴有室性心律失常。但临床上,心肌梗塞(MI)开始后的心律失常中有些可能是缺血心肌电不稳定的表现,而不是再灌注的结果。急性心肌梗塞(AMI)57例,于症状开始后4小时内静脉滴注链激酶。溶栓后共21例(37%)发生室性心律失常,其中加速性心室自身节律13例、非持续性室性心动过速(室速)15例,     

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.     

Ventricular arrhythmia induced by programmed ventricular stimulation after acute myocardial infarction

The prevalence, characteristics and clinical significance of ventricular electrical instability with programmed ventricular stimulation was studied in 50 hemodynamically stable patients 17 to 40 days after acute myocardial infarction (AMI) using double extrastimuli at 2- and 10-mA intensity and from 2 right ventricular sites. Ventricular electrical instability was defined as induction of 10 or more consecutive intraventricular reentrant beats. Of 50 patients, 23 (46%) had ventricular electrical instability (10 of these had sustained ventricular tachycardia [VT] induced). No significant differences were observed between patients with and without ventricular electrical instability with respect to age, site of AMI, coronary prognostic index, maximal level of CK, number of narrowed coronary arteries and presence of severe wall motion abnormalities. During a mean follow-up of 11.2 months no patient died suddenly. During repeated Holter recordings patients with ventricular electrical instability had a higher incidence of nonsustained VT than did patients without ventricular electrical instability.     

心室电重构与临床

研究表明,心室电重构通过离子重构、Na /Ca2 交换体重构等机制产生相关临床症状,如心律失常等,同时,心肌肥厚、心肌梗死等也能引起心室电重构。鉴于其产生机制及与临床的密切联系,人们已开始探讨不同的干预措施。     

Influence of residual myocardial ischaemia on induced ventricular arrhythmias following a first acute myocardial infarction.

OBJECTIVES: The purpose of this study was to assess the possible effect of residual myocardial ischaemia on induced ventricular arrhythmia during programmed ventricular stimulation in survivors of a first acute myocardial infarction. BACKGROUND: Most deaths after hospital discharge for acute myocardial infarction are sudden and presumably arrhythmic. Sudden cardiac death results from a dynamic interaction of structural abnormalities and transient triggering factors. The role of myocardial ischaemia as a trigger for ventricular arrhythmias remains unclear. We hypothesized that residual myocardial ischaemia after a first acute myocardial infarction is a potent trigger for sustained ventricular tachyarrhythmias, particularly in the presence of an abnormal myocardium. METHODS AND RESULTS: In this prospective study, programmed electrical stimulation, coronary angiography and dipyridamole-thallium-201 scintigraphy single-photon emission computed tomography were performed in 90 consecutive survivors of a first acute myocardial infarction. Patients, divided in two groups - group 1 with induced ventricular tachyarrhythmia (n=24) and group 2 without induced ventricular tachyarrhythmia (n=66) - were compared regarding residual myocardial ischaemia. The two groups were comparable in terms of mean left ventricular ejection fraction, infarct size and location, gender ratio, peak creatine kinase value, and extent of coronary disease. Residual myocardial ischaemia was detected in 32 patients: 15 (42.5%) belonged to group 1 and 17 (25.7%) to group 2. There was a statistically significant difference between the two groups regarding the presence and the extent of residual myocardial ischaemia (P<0.05). CONCLUSION: Residual myocardial ischaemia, revealed by dipyridamole-thallium-201 scintigraphy following a first acute myocardial infarction, might contribute to electrical instability evaluated by programmed ventricular stimulation.     

Experiences with laser therapy in acute myocardial infarct

Our clinical and instrumental investigations showed that invasive laser therapy has a multiple therapeutic effect. Acting favourably on principal pathogenetic mechanisms of acute myocardial infarction, it decreases the pain syndrome, normalize electrical instability of the heart, limits myocardial ischemic damage area and accelerates scarring process. It leads to a decrease in mortality and in the incidence of severe complications of myocardial infarction such as ventricular fibrillation, cardiogenic shock, cardiac insufficiency. Thus, the new method of treating acute myocardial infarction with He-Ne laser irradiation significantly enhances treatment efficacy, improves the course and prognosis of myocardial infarction.     

Prognosis after myocardial infarction

A substantial number of patients die in the first year after myocardial infarction. The major determinants of risk during this period appear to be the extent of either damaged or potentially ischemic myocardium and the degree of electrical instability. Anterior infarction, early left ventricular failure, late significant arrhythmias, and markedly reduced radionuclide left ventricular ejection fraction are the major clinical markers of risk.     

Quantitative measurement of electrical instability as a function of myocardial infarct size in the dog

To investigate the relation between electrical instability and myocardial infarct size, 20 foxhounds were studied in the awake state 3 to 5 days after closed chest coronary occlusion. Programmed right ventricular stimulation was performed with use of an epicardial electrode. After six paced beats at 10 percent greater than control rate, single and then double extrastimuli were introduced, scanning from late diastole to ventricular refractoriness in steps of 10 to 20 ms. Abnormal responses observed after this provocation were repetitive ventricular response, unsustained ventricular tachycardia, sustained ventricular tachycardia and ventricular fibrillation. Scores for electrical instability were determined for each dog, with higher scores assigned for more hazardous tachyarrhythmias (ventricular fibrillation greater than sustained ventricular tachycardia greater than unsustained ventricular tachycardia greater than repetitive ventricular response) and for those provokable later in diastole. An electrical instability index derived from these scores correlated well with infarct size measured with tetrazolium staining (r = 0.94). When scores were given only for the type of abnormal response elicited, excluding the effect of diastolic timing and the number of extrastimuli or vice versa, there was no significant difference in correlation with infarct size (r = 0.85 versus 0.92). Thus the results demonstrate that inducible electrical instability early after infarction is directly related to infarct size. Further, these data demonstrate the usefulness of an electrical instability index derived from the results of programmed right ventricular stimulation in assessing the severity of ischemic damage to the heart.     

The clinical evaluation of the late potentials in patients with ventricular arrhythmias

We investigated the recognition of late potentials in patients with and without organic heart diseases and spontaneous ventricular arrhythmias. None of the normal subjects had late potentials and patients with ventricular arrhythmias but no organic heart diseases, also had no late potentials as well as patients with idiopathic ventricular tachycardias. Late potentials in patients with idiopathic cardiomyopathy were noted more frequently in the dilated type than in the hypertrophic type, especially in those with high grades of ventricular arrhythmias. Patients with old myocardial infarctions had a higher rate of late potentials recognition in cases of sudden death or ventricular tachycardias. On the other hand, we observed lower rates in patients during early stage of acute myocardial infarction in spite of the evidence of a higher rate of ventricular electrical instability. There was no association between ejection fractions, wall motion scores and late potentials. However, a higher recognition of late potentials was found in patients with inferior or posterior myocardial infarction and ventricular aneurysm. We concluded that the late potential must be evaluated in each of the different groups of organic heart diseases in order to estimate the clinical value of ventricular arrhythmias.     

Risk stratification of patients with complex ventricular arrhythmias. Value of ambulatory electrocardiographic recording, programmed electrical stimulation and the signal-averaged electrocardiogram

Currently, there are three prognostic indicators of ventricular electrical instability: long-term ambulatory ECG recording, programmed electrical stimulation and the signal-averaged electrocardiogram. Several clinical studies have suggested that frequent and complex ventricular premature contractions in patients with organic heart disease may identify future cardiac events, including sudden cardiac death although, with respect to prognosis, it is not likely that any grading system based on the ambulatory ECG will be without meaningful limitations. No study has adequately tested the hypothesis that decreasing ventricular arrhythmias after acute myocardial infarction reduces mortality. The inducibility of ventricular tachycardia during programmed electrical stimulation is regarded as an independent risk factor for sudden death. Predominantly due to the lack of standardized protocol and definitions, the actual relevance of current literature remains somewhat compromised. The indication for antiarrhythmic treatment in those patients in whom ventricular tachycardia can be induced has not been established with certainty since the effects of therapy on the prognosis are unknown. For patients with complex ventricular arrhythmias in whom sustained ventricular tachycardia cannot be induced, antiarrhythmic drug treatment does not appear indicated. Based on a number of studies, the presence of late potentials in the signal-averaged ECG has also been shown to be a meaningful prognostic indicator. The signal-averaged ECG, however, is not only subject to various technical problems but is also encumbered by limitations arising from electrophysiologic considerations. While no relationship could be established between late potentials and complex ventricular arrhythmias in the ambulatory ECG within the first two months after acute myocardial infarction, there was, however, a correlation between late potentials and the inducibility of ventricular tachycardia during programmed electrical stimulation. Consequently, the signal-averaged ECG may serve as a screening test to identify patients who should subsequently undergo programmed electrical stimulation for arrhythmia assessment or guided institution of treatment provided this proves to be effective in reducing the risk of future major arrhythmic events.     

Assessment, significance and mechanism of ventricular electrical instability after myocardial infarction

The mechanism of reentrant tachycardia was established nearly a century ago, but the relationships between myocardial infarction and predisposition to sudden death were not unravelled until much later. In the latter half of the twentieth century many studies sought to ascertain what variables were predictive of death following myocardial infarction. Approximately one half of all deaths during the year following myocardial infarction are sudden and due to ventricular tachycardia (VT) or ventricular fibrillation (VF). We aimed to utilise non-invasive signal-averaging, along with programmed electrical stimulation of the heart, to determine whether one could predict spontaneous ventricular tachycardia and sudden death late after myocardial infarction. The sensitivity of ventricular electrical instablility (inducible ventricular tachycardia or fibrillation) as a predictor of instantaneous death or spontaneous VT was 86%, and the specificity was 83%. When other variables (delayed ventricular activation at signal-averaging, ejection fraction at gated heart pool scan, ventricular ectopic activity at ambulatory monitoring and exercise testing) were taken into account, inducible VT at electrophysiological study was the single best predictor of spontaneous VT and sudden cardiac death after myocardial infarction. The Westmead studies of Uther et al. in the decade or so from 1980 established programmed stimulation as the best predictor of sudden death after myocardial infarction. Subsequent studies by others have demonstrated a survival advantage of defibrillator implantation in patients with low ejection fraction (and inducible ventricular tachycardia) after myocardial infarction.