中国现代临床心脏电生理学创始人-陈新

临床心脏电生理学的迅猛发展,给临床心电学注入了活力,使这门古老的心电学科焕发出勃勃生机,心电图临床应用从来也没有像今天这样应用广泛而深入。门诊与病房的内科、外科、儿科、妇科、介入科、中医科病人都要做心电图检查,数十亿人做过心电图。我国每年要做一亿人次的心电图和数万人     

腺苷的心脏电生理学：基础及临床概念

腺苷是一种具有强有力电生理效应的内源性核苷。它作为一种抗心律失常药,具有以下几个特性:①它是体内物质代谢过程的中间产物;②它具有很短的半衰期(小于1.5秒);③它的作用是通过特殊的膜受体连接鸟苷酸连接蛋白(G蛋白)来介导;④腺苷在心肌上有特异的活性部位对室上性和室性组织具有重要而特异的作用。腺昔在调节心肌氧气供/需平衡方面也有重要作用。它通过冠状动脉扩张而增加供氧并通过降低心肌收缩力而减少氧耗来完成这一平衡的调节,同时拮抗儿茶酚胺的作用,抑制窦房结和房室(AV)结之间的自律性和传导性。     

肝硬化病人的心脏电生理学异常（下）

4．QT间期延长 QT间期延长是肝硬化病人最常见并得到普遍认可的电生理异常。QT间期代表心室收缩期的时间，QT间期延长易引起室性心律失常的发生。QT间期可根据常规记录心电图的QRS起点到T波终点而确定。心电图中出现明显的U波其意义尚有争议，可能与除极后的心室有关，并使QT间期的测定发生困难。多数专家同意取T波和U波之间的最低点作为QT间期的终点。     

临床心脏电生理检查的常用方法和基本习形

临床心脏电生理学是应用同步记录心腔内和／或体表心电图结合程控电刺激等方法来研究心脏生物电活动变化的一门学科。通过心脏电生理检查可以了解心脏传导系统的电生理特性，探讨心律失常的发生机制，以协助选择治疗方案，并可判断预后与研究药物的疗效。近20年来射频导管消融治疗快速性心律失常的发展，使心脏电生理概念不断得到更新，对心律失常发生机制的认识有了重大提高，已成为诊治心律失常的重要技术。     

2001年第22届北美心脏起搏与电生理学会学术年会纪要

第 2 2届北美心脏起搏与电生理学会学术年会于 2 0 0 1年 5月 2～ 5日在美国波士顿举行 ,来自全世界的 6 30 0多名从事心脏起搏与电生理的医生和有关人员参加了这次大会。国内约有 10 0名医生代表参加了会议。大会共收到论文摘要 2 40 0余篇 ,其中 788篇被选出进行大会交流 ,包括39个分会场交流以及墙板交流。另外大会还安排了 32个中心发言 ,12个小型课程 ,6 9个临床教学讲座 ,以及 3个热点争论等。与以往不同的是 ,此次大会在报到当天增加了手术演示。在哈佛大学麻省总医院进行了射频消融术和双心室起搏器植入手术的现场演示。另外 ,在会…     

小儿心律失常的电生理学

小儿心律失常的电生理机制包括以下四个方面。 1自律性异常 :自律性是窦房结、心房传导束、房室交界区和希氏束 -浦肯野纤维系统心肌细胞的正常电生理特征。在正常心脏 ,窦房结的自律性比其他潜在起搏点的自律性都要高。当窦性心律降至次级起搏点自身频率以下时 ,或次级起搏点冲动频率超过窦性心律时 ,心脏的起搏点将从窦房结转向窦房结以外的次级起搏点。副交感神经受刺激或窦房结病变均可引起窦性频率减慢或受抑制 ,即发生“逸搏”。另外 ,很多因素可提高次级起搏点的自律性 ,使得在窦房结功能正常的情况下 ,也发生心脏起搏点的转移 ,称为…     

临床心脏不应期检测

不应期是心肌细胞及组织对兴奋或刺激能否发生反应的特性,是反映心脏各部位组织兴奋性和传导性的客观指标。检测不应期是临床心脏电生理检     

Pediatric cardiac electrophysiology

Over the past year, many advances have been made in the management of cardiac arrhythmias in the pediatric patient. It has become evident that the new surgical procedures for congenital cardiac disease can result in arrhythmia-associated morbidity and mortality. New pharmacologic agents such as adenosine have been shown to be efficacious in treating supraventricular tachycardias, and other agents such as flecainide, beta-blockers, and amiodarone are also of significant value in young patients with acute and chronic arrhythmias. Along with advances in the use of pharmacologic agents, pacing catheter techniques for the diagnosis and treatment of cardiac arrhythmias have also significantly progressed. Transcatheter ablation is safe and effective in our patient population, and an understanding of various pacemaker modalities and the physiologic parameters for optimum use have been defined. This review outlines the advances in all modes of treatment of cardiac arrhythmias.     

Clinical cardiac electrophysiology: history, rationale, and future

The discipline of clinical cardiac electrophysiology has evolved over the past 40 years. Intense interest has resulted in the clinical application of intracardiac electrophysiologic techniques over the past 20 years. Clinical cardiac electrophysiologic studies have developed since the demonstration that programmed electrical stimulation could be performed in the human heart to evaluate tachyarrhythmias and that cardiac electrical activity that could not be detected on the body surface could be measured with intracardiac electrodes. Clinical electrophysiologic techniques have evolved for the assessment of sinus nodal, AV nodal, and His-Purkinje system function. The evaluation of tachyarrhythmias has progressed rapidly, and pharmacologic, device, and surgical therapy can now be guided by electrophysiologic studies. Invasive electrophysiologic studies have confirmed the utility of noninvasive electrocardiographic analysis and in several circumstances have proved that invasive studies are not necessary. Alternatives to invasive electrophysiologic evaluation continue to be debated. It is clear that when performed by well-trained individuals in appropriately equipped laboratories, electrophysiologic studies are safe and can be shown to be beneficial. Clinical cardiac electrophysiology continues to evolve, and problems of uniformity of methods, definitions of terms, and protocols remain to be resolved. The future of clinical cardiac electrophysiology appears to be one of continued evolution of techniques, refinement of indications, and continued clinical applications.     

Clinical cardiac electrophysiology of indoramin, a post-synaptic alpha blocker

Indoramin is a selective post-synaptic alpha blocker. Animalexperiments had shown that it has antiarrhythmic effects, butwhether this is due to its alpha blocking effect or some othermechanism is not known. Fifteen patients (10 males) underwentelectrophysiological investigations before and 15 minutes afterintravenous indoramin injection (0.2-0.5 mg kg^–l). Theplasma level of indoramin was measured and the patients weredivided into two groups: group 1 (8 patients) whose plasma levelwas less than 100 µg ml^–1 (average 72 µg ml^–l)and group 2 (7 patients) whose plasma level was more than 100µg ml^–1 (average 151 µ ml^–1). In bothgroups there was a significant drop in the systolic blood pressureafter indoramin (129±22 to 111 ±23 mmHg, P<0.001).There was a marked improvement in the sinus node recovery timein group 1 only (253±92 to 163±40ms, P<0.01).Similarly there was a decrease in AH interval during fixed rateatrial pacing in group 1 only (128 ±33 to 100 ±37ms, P<005) and a significant decrease in the Wenckebach cyclelength after indoramin in group 1 only (372 ±85 to 347± 74 ms, P<005). At the atrial level there were nosignificant effects in either group but there was a significantincrease in the ventricular effective refractory period in group2 (231 ± 35 to 264 ± 64 ms, P< 0.05) but nochange in group 1. The QTc prolonged significantly in group2 (407 ±87 to 438 ±67 ms, P>0-05) but not ingroup 1. These findings suggest that indoramin has dual electrophysiologicaleffects: (1) an ‘excitatory’ effect as seen in group1 which is probably due to alpha blockade or enhanced beta stimulation,and (2) a ‘depressive’ effect: seen in group 2,which may be due to a direct effect.     

Arrhythmias and cardiac electrophysiology

This article contains a review of some of the most significant advances in cardiac arrhythmias that have taken place in the last year, particularly those concerning the most common clinical conditions associated with the risk of arrhythmia, such as sudden cardiac death, atrial fibrillation and syncope, and genetically determined and hereditary heart disease, as well as advances concerning the principal nonpharmacologic treatments, such as catheter ablation, and the use of implantable defibrillators and cardiac resynchronization therapy.     

Arrhythmias and cardiac electrophysiology

In the past few months, numerous articles have been published on arrhythmias and cardiac electrophysiology. As in previous years, a substantial proportion of researchers have concentrated on atrial fibrillation, both on catheter ablation of chronic and paroxysmal atrial fibrillation and on the development of new approaches to thromboembolism prophylaxis. The feasibility of atrial fibrillation ablation by remote control has been demonstrated and a step-wise approach to ablation has been proposed, which appears to improve outcome and reduce lesion size. In addition, multicenter randomized trials have shown that the improvements in functional class and left ventricular ejection fraction achieved by ablation in patients with chronic atrial fibrillation are greater than those resulting from pharmacological treatment. New strategies are being developed to improve the selection of patients for defibrillator implantation and to decrease the number of high-energy discharges occurring during follow-up. Controlled trials continue to demonstrate that pharmacological therapy is of little value in preventing recurrence of vasovagal syncope compared with maneuvers involving isometric muscular contraction. Finally, one of the most significant events in the last year was the publication of new clinical practice guidelines by European and American societies of cardiology. These provide important recommendations on the treatment and prevention of ventricular arrhythmias and sudden death and on the management of and thromboembolic prophylaxis in atrial fibrillation.