异常电位在特发性流出道室性心律失常中的机制及意义

流出道起源室性心律失常是临床最常见的特发性室性心律失常之一,射频消融可达到根治性效果。常规电生理标测技术的局限性限制了其在非持续性、难诱发性心律失常中的应用。近年研究显示异常电位与流出道起源特发性室性心律失常的消融靶点相关,被认为是致心律失常的基质,可作为一个新的靶点预测指标。尽管产生机制不明,现认为异常电位或为微小病变或分化不完全的残留原始心肌,特殊的细胞电生理特性使该处成为保护异位起源点的缓慢传导区,而不同组织类型心肌共存表现为三维电压图上的低电压区和电压移行区。该区域的细胞电生理学研究将成为探究特发性流出道室性心律失常发生/维持基质的新方向。     

导管消融室性心律失常的现状和未来

运用导管消融的方法治疗室性心律失常已经广泛用于临床。术前运用心电图、心脏超声、计算机断层摄影术(CT)和磁共振成像(MRI)等辅助检查手段和起搏标测、激动标测、基质标测、电压标测和起搏拖带等标测方法,对判断室性心律失常的发生机制、起源点位置和制定合理的室性心律失常导管消融策略具有很大的帮助。导管消融治疗特发性室性心律失常,成功率高、风险和并发症发生率低,目前已成为一线治疗。而对于疤痕介导性室性心律失常,导管消融只是药物治疗和植入型心律转复除颤器(ICD)治疗的辅助手段。目前导管消融治疗室性心律失常的临床终点和对患者的临床长期受益,还需要进行前瞻性、随机的多中心研究。     

乳头肌起源的特发性室性心动过速的研究和治疗进展

近年来的研究发现,除心室流出道、动脉瓣和二尖瓣环外,心室乳头肌也参与了特发性室性心动过速的发生和维持,起源于乳头肌的特发性室性心动过速有其电生理学和心电图表现的特点,使用各种手段对乳头肌实施消融是这类心律失常有效的治疗手段,但其治疗特点和难点与一般心律失常有所不同。现对这种类型心律失常的研究和治疗的现状做一综述。     

特发性QT延长综合征研究进展

<正> 特发性QT延长综合征(The idiopathic long QT syndrome,LQTS)是一种以心电图QT间期延长和发生恶性室性心律失常性晕厥及猝死为特征的家族遗传性疾病。随着对猝死和室性心律失常研究的深入,国际上对特发性LQTS的研究倍加重视,认为对特发性LQTS的研究是打开与交感神经刺激有关的恶性室性心律失常机制的敲门砖。一、临床表现特发性LQTS的典型临床表现是以晕厥为主要症状并伴有心电图QT间期延长。患者往往在精神紧张或剧烈运动的情况下发生晕厥,可反复发生甚至引起心脏骤停。家族史调查往往     

射频消融术对特发性室性心动过速患者QT离散度的影响

ＱＴ离散度（ＱＴｄ）反映了心室肌复极的不均匀性,许多研究表明,室性心律失常患者的ＱＴｄ显著高于无心律失常者。Ｇｉｌ等的研究也证实特发性室性心动过速（特发性室速）伴晕厥患者的ＱＴｄ显著增加。射频消融是目前治疗特发性室速的最有效的根治性手段,本研究旨在通...     

室性心动过速新分类的临床意义

<正>如电解质紊乱和心肌缺血等情况下发生的室性心律失常,可能存在分子和组织水平的异常。特发性室性心律失常指既无结构性心脏病,也无任何原因的室性心律失常,故不包括各种遗传性室性心律失常;所谓特发性是相对的。未来可能找到病因。新近将无结构性心脏病的室性心律失常分为无生命威胁的室性心律失常和有生命威胁的室性心律失常两大类。笔者     

特发性室性心律失常

已往认为频发室性期前收缩与室性心动过速(VT)可以转变成心室颤动而致命 ,故一经发现立刻收入院 ,进行严格的心电监护及治疗。近 2 0年 ,特别在开展射频电消融后 ,发现许多室性心律失常患者经各种检查均未发现器质性心脏病 ,而且病程长达数十年也未发生心室颤动 ,预后较好 ,这种心律失常称之特发性室性心律失常。它不仅见于成年人 ,也见于儿童。区别特发性与病理性室性心律失常有 3个要点 :①特发性室性心律失常病史长达数月至数年 ,无明显临床症状。②经各种检查 ,包括临床体检、心电图系列检查、超声心动图、X线摄片、CT或MRI,以及心…     

交感神经与特发性右室流出道室性心律失常相关性的研究进展

正长期以来人们对特发性右室流出道(RVOT)室性心律失常的机制研究不仅集中在电生理学方面,也更多的开始关注自主神经作用。随着临床数据和基础实验结果的累积,人们越来越意识到自主神经异常是一个诱发特发性RVOT室性心律失常并使其维持的因素~([1]),其中交感神经分布及其功能异常与心室肌细胞密切的相互作用,构成了触发室性心律失常的潜在基质~([2])。1右室流出道交感神经的分布心脏同时受到交感神经与迷走神经的支配。支配心脏     

非结构性心脏病恶性室性心律失常射频消融治疗现状

射频消融起源于浦氏纤维系统和右室流出道,少数起源于其他部位的室性早搏,治疗无结构性改变的心脏病恶性室性心律失常,包括特发性心室颤动,多形性、儿茶酚胺敏感性室性心动过速,Brugada综合征,长QT综合征和短QT综合征等引起的恶性室性心律失常,取得了良好效果,能有效减少恶性室性心律失常发生,并减少埋藏式心脏转复除颤器放电。     

经导管主动脉窦内射频消融治疗心律失常的现状

主动脉窦(ASC)由无冠窦、左冠窦和右冠窦组成,位于心脏的中心部位,与心脏各腔室在解剖上发生联系。在ASC内消融根治的快速性心律失常的解剖基质有两方面:直接起源于心室或心房肌与ASC之间的心肌纤维连接;源于邻近组织的心内膜深处或心外膜。在无冠窦消融治疗局灶性房性心动过速的报道较多;而主动脉三个窦内消融治疗室性早搏/特发性室性心动过速有报道,而以左冠窦多见,上述心律失常发生时的心电图和电生理往往有其特征性。消融时应避免损伤冠状动脉。     

Ventricular tachycardia ablation.

The role of catheter ablation in the treatment of ventricular arrhythmias has been changing in the last decade, and this form of therapy now aims at curing multiple ventricular tachycardia morphologies and complex substrates in patients with structural heart disease (post-infarction and idiopathic dilated cardiomyopathy). Under these circumstances, conventional mapping is not feasible and accurate, and the development of new diagnostic methods has become necessary. The non-contact mapping system has been introduced to study the activation pattern of any ventricular arrhythmia by a "single-cycle" analysis, and has brought to the characterization of unstable and of non-sustained forms of arrhythmia. The evaluation of the arrhythmogenic substrate has similarly become more precise by the more common use of the electroanatomic mapping (CARTO), which is being applied to identify areas of scarred tissue responsible for ventricular arrhythmias, to map stable tachycardias and to validate the creation of a line of block. By means of this technological advancement, the identification of critical isthmi and deep intramural circuits has also led to new ablation strategies, frequently simplifying the procedure and minimizing complications.     

室性心律失常的导管消融——“百尺竿头，更进一步”

Catheter ablation is now an important option to control drug-refractory ventricular arrhythmias.Ablation is highly effective for ventriculal arrhythmia originating from outflow tract and idiopathic left ventricular tachycardias(VT).Catheter ablation of hemodynamically unstable scar-related VT,which frequently occurs in patients with remote myocardial infarction,dilated/hypertrophic cardiomyopahties and after surgical correction of congenital heart disease,is still a challenge for electrophysiologists.In the last decade,catheter ablation in this field has rapidly evolved and has made a big progression with a introduction of 3-D mapping system and new ablation catheter.However,it requires further investigation to identify the high-risk patients and to understand the arrhythmia substrate and improve lesion formation in the ventricle.     

Sex Differences in Cardiac Electrophysiology and Clinical Arrhythmias: Epidemiology,Therapeutics, and Mechanisms

Sex differences in cardiac electrophysiological properties and arrhythmias are evident in epidemiologic and investigative studies as well as in daily patient care. At the supraventricular level, women are at increased risk of sick sinus syndrome and atrioventricular (AV) node re-entrant tachycardia, whereas men manifest more AV block and accessory pathway–mediated arrhythmias. At the ventricular level, women are generally at higher risk of long QT–associated arrhythmias, whereas men are more likely to present with early repolarization, idiopathic ventricular fibrillation, and Brugada syndromes. Great advances have been made in unraveling the fundamental mechanisms underlying sex differences in ventricular arrhythmias, particularly those associated with abnormal repolarization. Conversely, the basis for male-predominant arrhythmia risk in structural heart disease and differences in supraventricular arrhythmia susceptibility are poorly understood. Beyond biological differences, arrhythmia occurrence and patient care decisions are also influenced by gender-related factors. This article reviews the current knowledge regarding the nature and underlying mechanisms of sex differences in basic cardiac electrophysiology and clinical arrhythmias.     

Spontaneous sustained ventricular tachyarrhythmias during treatment with type IA antiarrhythmic agents

Twenty-six patients who developed their first clinical episode of sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) while taking type IA antiarrhythmic agents for more benign rhythm disturbances were rechallenged with the identical drug during electrophysiologic testing. Patients with these new drug-associated spontaneous ventricular arrhythmias often manifested a preexisting substrate for such arrhythmias: sustained VT or VF was induced in 65% of patients at baseline, and in 58% of patients when tested with their previously taken antiarrhythmic drug. Among those without inducible sustained ventricular arrhythmias in the drug-free state, 78% remained free of inducible sustained arrhythmias when tested with the same drug they had been taking at the time of the clinical arrhythmia. Even patients without a definable electrophysiologic substrate for sustained VT or VF remained at risk for arrhythmia recurrence if treated with alternative antiarrhythmic medications: 40% of such patients who continued to receive an antiarrhythmic agent different from that being administered when their clinical VT or VF occurred had recurrent spontaneous ventricular tachyarrhythmias during follow-up. Thus, patients with drug-associated clinical sustained ventricular tachycardias form a heterogenous group that should be evaluated individually and not empirically managed for a "proarrhythmic effect" simply by antiarrhythmic drug withdrawal or drug substitution.     

Familial polymorphic ventricular arrhythmias: a quarter century of successful medical treatment based on serial exercise-pharmacologic testing

OBJECTIVES

We sought to determine whether objective tests of antiarrhythmic drug efficacy could produce favorable short- and long-term outcomes in a family with idiopathic malignant ventricular arrhythmias.

BACKGROUND

In 1973 a family presented with a history of several generations of syncopal spells and sudden death. Some individuals had nonspecific electrocardiographic (ECG) changes. Their QT intervals were normal at rest and with exercise. Autopsies in two young family members showed no cardiac abnormalities, specifically no evidence of arrhythmogenic right ventricular dysplasia, other cardiomyopathy, myocarditis or gross abnormality of the conduction system.

METHODS

Available family members had screening ECGs. Symptomatic members had a battery of tests, including electrophysiologic studies, ambulatory ECGs, audiograms, exercise stress testing, serum catecholamine levels during rest and exercise and isoproterenol infusion. Serial exercise-pharmacologic testing was performed in symptomatic family members until induction of an arrhythmia during exercise required higher work loads or became impossible.

RESULTS

Arrhythmias were not induced during electrophysiologic studies. In several family members tested, ventricular premature beats and then rapid polymorphic ventricular arrhythmias occurred whenever the sinus rate exceeded 130 beats/min. Emotional stress, isoproterenol infusion and exercise all elicited similar arrhythmias. Catecholamine levels during exercise were, however, unequivocally normal in two of three family members tested. Beta-blockers appeared to be the most effective pharmacologic agent for prevention of these arrhythmias. The efficacy of treatment has been confirmed during a follow-up of 25 years.

CONCLUSIONS

This family appears to have catecholamine hypersensitivity as the basis for their ventricular arrhythmias. Guided therapy using serial exercise-pharmacologic testing provided reliable protection for this familial ventricular arrhythmia during a 25-year follow-up.     

Catheter-based Ablation for Ventricular Arrhythmias

Catheter ablation for patients with recurrent ventricular arrhythmias has emerged as an important and effective treatment option. The approach to ablation, and the risks and likely efficacy are determined by the nature of the severity and type of underlying heart disease. Although implantable defibrillators remain the corner stone for prevention of sudden cardiac death, ablation successfully reduces tachycardia recurrences and storms of ventricular arrhythmias triggering defibrillator shocks in patients with structural heart disease. Our understanding of idiopathic ventricular tachycardia (VT) has grown substantially with several new sites of VT origin recognized in recent years. Ablation is often curative for idiopathic VT. This review discusses common mechanisms and clues to diagnosis of the various VTs, and current advances in ablation options. In particular, endocardial ablation techniques have been complemented by newer approaches such as percutaneous epicardial ablation. In rare cases, transcoronary alcohol ablation can be effective for life-threatening arrhythmia.     

Cerebral Venous Sinus Thrombosis: Update on Diagnosis and Management

Ventricular arrhythmias (VA) are a significant contributor to morbidity and mortality in patients with heart failure (HF). Implantable cardioverter defibrillators are effective in reducing mortality, but do not prevent arrhythmia recurrence. There is increasing recognition that frequent premature ventricular contractions or repetitive ventricular tachycardia may also lead to new onset ventricular dysfunction or deterioration of ventricular function in patients with pre-existing HF. Suppression of the arrhythmia may lead to recovery of ventricular function. Catheter ablation has emerged as a safe and effective treatment option for reducing arrhythmia recurrence and for suppression of PVCs but its efficacy is governed by the nature of the arrhythmias, the underlying HF substrate and the accessibility of the arrhythmia substrates to ablation.     

Ventricular arrhythmias initiated by programmed stimulation in four groups of patients with healed myocardial infarction

Programmed electrical stimulation of the heart was prospectively used in 160 patients with healed myocardial infarction to study the incidence and characteristics of ventricular arrhythmias induced. Thirty-five patients had neither documented nor suspected ventricular arrhythmias (Group A); 37 patients had documented nonsustained ventricular tachycardia (Group B); 31 patients had been resuscitated from ventricular fibrillation (Group C); and 57 patients had documented sustained monomorphic ventricular tachycardia (Group D). No electrophysiologic differences were found between patients in Group A and Group B, but patients in both groups differed significantly from patients in Group C and Group D. In the last two groups, sustained monomorphic ventricular tachycardia was more frequently induced, the cycle length of the induced ventricular tachycardia was slower and a lesser number of premature stimuli was required for induction. No differences were found in the incidence, rate or mode of induction of nonsustained monomorphic ventricular tachycardia, but nonsustained polymorphic ventricular tachycardia and ventricular fibrillation were more frequently induced in Groups A and B. It is concluded that the substrate for sustained ventricular arrhythmia is present in at least 42% of patients after myocardial infarction. The electrophysiologic characteristics of the substrate for ventricular tachycardia seem to be the major determinant of the clinical occurrence of sustained ventricular arrhythmia. Changes in the electrophysiologic properties of the substrate of ventricular tachycardia, either spontaneously with time or induced by ischemia or antiarrhythmic drugs, can contribute to the clinical occurrence of sustained ventricular arrhythmias in patients with an old myocardial infarction.     

Significance and reproducibility of exercise-related idiopathic ventricular arrhythmias

Fifty-five patients with a severe idiopathic ventricular arrhythmiawere subjected to a follow-up study three to seven years afterthe discovery of the arrhythmia. During this time only one suddencardiac death had occurred. Special attention was paid to comparingthe clinical significance and reproducibility of arrhythmiaseither aggravated or suppressed by exercise. For this reason,20 of the patients, 10 with aggravation and 10 with suppressionof the arrhythmia by exercise, were studied more extensivelyby repeated exercise stress testing, pulse tracings, and echo-and phonocardiography. Patients with an arrhythmia aggravatedby exercise exhibited a significantly higher frequency of latentor manifest cardiovascular disease as compared to patients witharrhythmias suppressed by exercise (10 v. three patients; P< 0.05). A high intra-individual inter-test reproducibilityof ventricular arrhythmias was seen in this group of patientswith very pronounced arrhythmias. Also the arrhythmia patternon exercise, i.e. aggravation or suppression of arrhythmia respectively,showed a good reproducibility. Although patients with aggravatingarrhythmia during exercise had a higher frequency of cardiovasculardisease, the three to seven year prognosis for these patientsdid not differ from that of patients with arrhythmias suppressedby exercise.     

Importance of the atrial channel for ventricular arrhythmia therapy in the dual chamber implantable cardioverter defibrillator

INTRODUCTION: Performance of dual chamber implantable cardioverter defibrillator (ICD) systems has been judged based on functioning of the ventricular tachycardia:supraventricular tachycardia (VT:SVT) discrimination criteria and DDD pacing. The purpose of this study was to evaluate the use of dual chamber diagnostics to improve the electrical and antiarrhythmic therapy of ventricular arrhythmias. METHODS AND RESULTS: Information about atrial and ventricular rhythm in relation to ventricular arrhythmia occurrence and therapy was evaluated in 724 spontaneous arrhythmia episodes detected and treated by three types of dual chamber ICDs in 41 patients with structural heart disease. Device programming was based on clinically documented and induced ventricular arrhythmias. In ambulatory patients, sinus tachycardia preceded ventricular arrhythmias more often than in the hospital during exercise testing. The incidence of these VTs could be reduced by increasing the dose of a beta-blocking agent in only two patients. In five patients in whom sinus tachycardia developed after onset of hemodynamic stable VT, propranolol was more effective than Class III antiarrhythmics combined with another beta-blocking agent with regard to the incidence of VT and pace termination. In all but three cases, atrial arrhythmias were present for a longer time before the onset of ventricular arrhythmias. During atrial arrhythmias, fast ventricular rates before the onset of ventricular rate were observed more often than RR irregularities and short-long RR sequences. Dual chamber diagnostics allowed proper interpretation of detection and therapy outcome in patients with different types of ventricular arrhythmia. CONCLUSION: The advantages of the dual chamber ICD system go further than avoiding the shortcomings of the single chamber system. Information from the atrial chamber allows better device programming and individualization of drug therapy for ventricular arrhythmia.