Cardiac arrhythmias in childhood. Diagnostic considerations and treatment.

Determining safe and effective antiarrhythmic therapy in paediatric patients requires definition of the mechanism of the arrhythmia, determination of associated risk factors for treatment (such as the presence of congenital cardiac defects, myocarditis or cardiomyopathy), and monitoring for potential drug side effects related to the treatment. A number of modalities for non-invasive evaluation of arrhythmias is available, including ECG, 24-hour ambulatory Holter monitoring, and transtelephonic ECG transmission. Arrhythmias requiring medical treatment in children with normal cardiac anatomy and function include supraventricular tachycardia (SVT), ventricular tachycardia (VT) and primary atrial tachycardias. SVT is treated acutely with vagal manoeuvres or drugs which slow AV conduction [adenosine (adenine riboside), edrophonium, phenylephrine or verapamil]. When medical conversion is not achieved, transoesophageal overdrive pacing or direct current (DC) cardioversion may be required. Long term drug therapy for SVT includes first-line treatment with digoxin, verapamil or propranolol. Ventricular tachycardia is managed acutely with DC cardioversion and intravenous lidocaine (lignocaine). Chronic drug regimens include mexiletine, propranolol or amiodarone. In children with structural congenital heart disease or myocardial dysfunction, hazards of drug therapy for arrhythmias include depression of cardiac function, proarrhythmia (drug-induced worsening of arrhythmias), and conduction abnormalities. Care must be taken to choose medication regimens which are likely to be effective with minimum risk of potentiating abnormal haemodynamics or conduction.     

射频消融治疗心动过速116例分析

目的 总结射频消（ＲＦＣＡ）治疗１１６例各类心动过速的效果。方法 左房室旁道肖融二尖瓣室侧,右旁道消融三尖瓣房侧;房室结双径路通过下位能量递增消融法,改良房室结慢径;室速采用心内膜激动时间及起博标测相结合办法,标测起源点消融;房扑采用三尖瓣与下腔静脉之间的峡部行线性消融的方法;房速采用双大头电极顺序标测法。结果 房室折返性心动过速７１例,右侧旁道２５条,左侧旁道４９条,共７４条,消融成功７３条,成功率９８．７％;房室结双径路改良全部成功;房速消融成功率达１００％;房扑１例折驼环变异,消融未成功。结论 射频消融治疗各类心动过速安全、有效、复发率低。     

Clinical cardiac electrophysiologic effects of adenosine

Adenosine is very useful for the acute diagnosis and treatment of tachycardias in humans. Adenosine's major cardiac effect, when given as a bolus, is to produce transient atrioventricular block. It can be used either to terminate tachycardias that involve the atrioventricular node or to transiently reveal an atrial tachycardia by slowing the ventricular response, and so to allow the diagnosis to be made. Adenosine is effective in the diagnosis of broad complex tachycardias, revealing and terminating supraventricular tachycardias, with usually no effect on ventricular tachycardia. Adenosine's great advantages over verapamil are its safety, especially in haemodynamically unstable patients, and its short half-life. Is major disadvantage is the somatic side effects it produces: chest pain, deep breathing, flushing, and a variety of other sensations. Adenosine's effects on other tachycardias also gives an insight into their mechanisms. Right ventricular outflow tachycardia is terminated by adenosine, which supports the thesis that it is due to triggered afterdepolarizations. This may be the explanation for the termination of some atrial tachycardias by adenosine. Sinus node reentry tachycardia is slowed and terminated by adenosine, suggesting that at least part of the tachycardia circuit is in the sinus node. To conclude, the ability of adenosine to selectively block atrioventricular conduction, combined with its very short half-life, make it a very useful drug both clinically and in the electrophysiology laboratory. © 1993 Wiley-Liss, Inc.     

室上性心动过速特殊病例的射频消融结果评价

目的研究室上性心动过速(SVT)合并风心病、冠心病及电生理检查(EPS)不能诱发心动过速等特殊病例行EPS及导管射频消融(RFCA)治疗的有效性及安全性。方法共26例,男12例,女14例,年龄21～76岁;SVT合并风心病5例(心功能Ⅱ～Ⅲ级),合并冠心病7例,EPS心动过速不能诱发14例(其中11例存在房室结双径路);常规行EPS及RFCA,合并单纯二尖瓣狭窄者(2例)同时行经皮二尖瓣球囊扩张术(PBMV),合并冠心病冠脉造影病变较重者(2例)择期行经皮冠脉内干预治疗(PCI),SVT不能诱发但有房室结双径路(DAVNP)证据者行经验性房室结改良术(AVNM)或放弃RFCA。结果5例SVT合并风心病患者RFCA均成功,其中2例同时行PBMV也均成功(瓣口面积分别由术前1．04与1．16扩大至2．30与2．42cm^2),随访1例心动过速复发,再次RFCA成功,心功能持续改善;7例SVT合并冠心病RFCA也均成功,其中2例术后1个月与3个月成功施行PCI术,随访无心动过速复发,冠心病症状无或轻微;6例经验性AVNM均成功阻断慢径传导,随访无一例心动过速复发,另5例未予干预患者中4例心动过速复发。所有病例均无重要手术相关并发症发生。结论SVT合并风心病、冠心病患者在术前相应药物治疗下能够耐受EPS及RFCA过程,其有效性及安全性与无器质性心脏病并存者类同,适应证病例可同时或择期行PBMV或PCI治疗;经典AVNM术可使EPS不能诱发心动过速的DAVNP患者获根治目的。     

Supraventricular tachycardia in infants, children and adolescents: diagnosis, and pharmacological and interventional therapy

Supraventricular tachycardia is the most frequent form of symptomatic tachydysrhythmia in children. Neonates and infants with paroxysmal supraventricular tachycardias generally present with signs of acute congestive heart failure. In school-aged children and adolescents, palpitations are the leading symptom. Chronic-permanent tachycardia results in a secondary form of dilated cardiomyopathy. Therapy for episodes of tachycardia depends on the individual situation. In severe haemodynamic compromise, or if ventricular tachycardia is suspected, tachycardia should immediately be terminated by external cardioversion during deep sedation. Vagal manoeuvres are effective in patients with atrioventricular reentrant tachycardias. Adenosine is the drug of first choice in any age group for tachycardias involving the atrioventricular node; its advantages include short half-life and minimal or absent negative inotropic effects. Adenosine may also be used in patients with wide QRS complex tachycardia. Intravenous verapamil is contraindicated in neonates and infants because of the high risk of electromechanical dissociation. In older children (>5 years) and adolescents, verapamil may be administered with the same restrictions as in adult patients (wide QRS complex tachycardia, significant haemodynamic compromise). Spontaneous cessation of tachycardia can be expected in most neonates and infants during the first year of life. Prophylactic pharmacological treatment in this age group is advisable because recognition of tachycardia is often delayed until the occurrence of symptoms. Withdrawal of drug treatment should be attempted around the end of the first year. However, in older children, spontaneous cessation of tachycardia is rare. Prophylactic drug therapy is performed on an empirical basis. Digoxin may be administered in all forms of supraventricular tachycardia in which the atrioventricular node is involved, except in patients with pre-excitation syndrome aged >1 year. In patients with atrioventricular reentrant tachycardia, class IC drugs such as flecainide and propafenone are effective. Sotalol is also effective in atrioventricular reentrant tachycardia, as well as in primary atrial tachycardia. Although amiodarone has the highest antiarrhythmic potential, it should be used with caution because of its high rate of adverse effects. In school-aged children and adolescents, radiofrequency catheter ablation of the anatomical substrate is an attractive alternative to drug therapy, with a rate of permanent cessation of the tachycardia of up to 90%. Despite the clear advantages of this procedure, it should be performed only with unquestionable indication; the long term morphological and electrophysiological sequelae on the growing atrial and ventricular myocardium are still unknown.     

Effects of a novel class III antiarrhythmic agent, E-4031, on reentrant tachycardias in rabbit right atrium.

Effects of a new antiarrhythmic agent, E-4031, on reentrant types of tachycardias in rabbit right atrial preparations were studied using the microelectrode technique. E-4031 at concentrations of 0.1 and 1.0 microM prolonged the refractory period (RP) of the atrium and atrioventricular node (AVN) without affecting the intraatrial conduction time. In 13 of 17 preparations, premature stimulation repeatedly induced tachycardias lasting more than 10 beats. Twelve of 13 preparations exhibited a smooth AV conduction curve and showed activation patterns compatible with intraatrial reentry (IAR) during tachycardias, whereas the remaining preparation started tachycardia with a jump on the AV conduction curve, indicating dual AVN reentrant tachycardia (AVNRT). Application of 0.1 and 1.0 microM E-4031 completely prevented the initiation of both types of tachycardias by producing intraatrial conduction block due to prolonged effective refractory period (ERP) of the atrium. The results indicated that E-4031 exhibiting pure class III antiarrhythmic properties is effective for prevention of reentrant type of supraventricular tachycardias (SVTs).     

Effects of verapamil on accessory pathway properties and induction of circus movement tachycardia in patients with the Wolf-Parkinson-White syndrome

The electrophysiological effects of 0.2 mg/kg of intravenously administered verapamil (mean plasma level, 51.3 ng/ml) were evaluated using intracardiac recordings and electrical stimulation in 10 patients with the concealed or manifest Wolff-Parkinson-White syndrome. Verapamil produced a minimal effect on both the antegrade and retrograde effective refractory periods of the accessory pathway and the retrograde conduction time over the accessory pathway, but significantly lengthened the intranodal conduction time as well as the effective and functional refractory periods of the atrioventricular (AV) node. Reproducible sustained circus movement tachycardia was initiated in 8 patients before administration of verapamil and in 2 after verapamil. The sustained tachycardia could no longer be initiated in 6 patients because of an increase in AV nodal refractoriness. In 4 patients, atrial echoes were induced at longer premature beat intervals due to a greater AV conduction delay of the atrial impulse. The cycle length of the tachycardia was lengthened in 2 patients, reflecting an increase in the A-H interval after verapamil administration. In conclusion, these results show that verapamil has no apparent effect on either antegrade or retrograde accessory pathway properties and suggest that verapamil does indeed prevent sustained circus movement tachycardia by increasing the AV nodal refractoriness in some patients with the Wolff-Parkinson-White syndrome.     

Wolff-Parkinson-White syndrome. Identification and management.

Patients with Wolff-Parkinson-White (WPW) pattern of ventricular pre-excitation may develop paroxysmal re-entrant tachyarrhythmias through the Kent bundle and, less commonly, atrial fibrillation. WPW patients are at risk of sudden death when a rapid ventricular response occurs during atrial fibrillation due to conduction through the accessory pathway. Conduction properties of the accessory pathway and atrial vulnerability, which is the propensity to develop atrial fibrillation, are important parameters for evaluation in these patients. The former can be assessed by means of noninvasive tests, such as stress and pharmacological tests, and with electrophysiological study; the latter only by electrophysiological study. There is no indication for treatment of asymptomatic patients. Antiarrhythmic prophylaxis is required in patients with previous episodes of atrial fibrillation with rapid ventricular response, in patients with paroxysmal re-entrant tachycardias and rapid conduction through the accessory pathway, and in patients with frequent episodes of re-entrant tachycardias of long duration. Vaughan-Williams class IC anti-arrhythmic drugs (propafenone, flecainide) are the first choice for drugs in patients with rapid anterograde conduction through the accessory pathway due to their high efficacy and low incidence of adverse effects, while beta-blockers (atenolol, nadolol) are indicated for patients with re-entrant tachycardias and low conduction capacity through the bypass tract. When pharmacological therapy is ineffective, surgical or catheter ablation of the accessory pathway may be considered.     

A dual model for cardiac arrhythmias: coexistence of re-entry and abnormal automaticity and effects of antiarrhythmic agents.

1. We have developed a dual model for arrhythmia anaesthetized dogs. The model consists of an inducible re-entrant atrial tachycardia and spontaneous ventricular ectopies in the same heart. 2. The model for re-entrant atrial tachycardia was created by crushing the right atrium longitudinally in the intercaval region and transversely in the front free wall parallel to the atrioventricular groove. Ventricular abnormal automaticity was produced by prior (20 approximately 24 h) left anterior descending coronary artery occlusion. The ventricular arrhythmia was partially suppressed during rapid pacing-induced atrial tachycardia and resumed after atrial re-entry was terminated. 3. Mapping experiments indicate that the atrial tachycardia was due to circus movement occurring in the tissue around the tricuspid ring. This re-entrant circuit was identical to that induced in the model created by the incision method. 4. Clofilium (0.75 mg kg-1, n = 5) increased the cycle length of atrial re-entry by 14 +/- 4% from 139 +/- 12 to 159 +/- 18 ms (P less than 0.05). Flecainide (1.8 +/- 0.9 mg kg-1, n = 5) prolonged the cycle length of the tachycardia by 114 +/- 57% from 158 +/- 11 to 332 +/- 66 ms (P less than 0.05). 5. Both drugs terminated the atrial arrhythmia, but re-entry could be reinduced only in flecainide-treated dogs. Flecainide reduced ventricular ectopies by 89 +/- 19%, whereas clofilium did not change ventricular abnormal automaticity or maximum pacing cycle length that is necessary to overdrive the ventricle fully.(ABSTRACT TRUNCATED AT 250 WORDS)     

Changes in hemodynamics and contractility during supraventricular tachycardias and after electrical or aprindin-induced termination (author's transl)]

Alterations of hemodynamics and contractility were studied in 6 patients in whom two consecutive runs of supraventricular tachycardias (SVT) were electrically induced. Following initiation there was an abrupt decrease of arterial blood pressure, left ventricular systolic pressure, dp/dtmax, cardiac index and stroke work index (SWI). These parameters -- with the exception of SWI -- increased in the course of the SVT, however, control values were not reached. Mean pulmonary artery pressure steadily increased and remained on an elevated level until the tachycardia was stopped. When the SVT was electrically terminated, there was a transient overshoot of mean arterial and left ventricular systolic pressure, while mean pulmonary artery pressure slowly returned to control values. When the tachycardia was stopped by i.v. infusion of N-)diethylamino-3-propyl)-N-phenyl-indanamine-2 (aprindin, Amidonal) -- started at the 7th minute -- there was no statistically significant difference, neither during the SVT nor after cessation as compared to the values of the first run. Only mean pulmonary artery pressure remained at a higher level after SVT was stopped. It may, therefore, be concluded that in patients with otherwise normal hearts aprindin applied in a dosage sufficient to stop the SVT, does not exhibit noteworthy inotropic side effects.     

胎儿室上性心动过速的超声心动图诊断及治疗干预评价

目的胎儿心动过速的宫内胎儿超声心动图诊断及干预治疗室上性心动过速(SVT)评价。方法对已检出的1 911名心律失常胎儿中的126例快速心律失常者,分为窦性心动过速、SVT、SVT合并心衰3组,对后两组胎儿进行宫内地高辛转律治疗。结果胎儿心动过速126例(心率≥180bpm)中SVT 29例(含房颤、房扑10例),窦性心动过速97例。SVT组中合并复杂先天性心脏病者7例、胎儿水肿5例。合并先天性心脏病7例均于检查后中止妊娠,其余22例行常压氧治疗或经胎盘给药,首选药物为地高辛。新生儿随访期最长者16个月,头颅CT、超声心动图等各项生理指标均正常。结论胎儿超声心动图是目前惟一可迅速检出胎儿心律失常并明确性质的诊断手段,且重复性好。地高辛经胎盘治疗可有效转律并同时控制胎儿心衰减轻水肿且无致畸作用。     

Effect of tiapamil in the Wolff-Parkinson-White syndrome

The effect of tiapamil was studied in 9 patients with the Wolff-Parkinson-White syndrome using programmed stimulation of the heart. Before the drug, sustained orthodromic tachycardias could be initiated in 7 patients and antidromic tachycardia in 2 by premature atrial and/or ventricular stimulation. An intravenous bolus of tiapamil, 2 mg/kg, terminated the tachycardia in 7 out of 8 cases by a block in the atrioventricular (AV) node. Tiapamil lengthened the effective refractory period of the AV node in the only patient in whom it could be measured and the atrial effective refractory period in 1 out of 9 cases, but the drug had no influence on antegrade or retrograde refractory periods of the accessory pathway or on that of the ventricle. The AV nodal conduction time (A-H interval) was prolonged. Following tiapamil, it was not possible to initiate the tachycardia in 4 cases, in 2 patients the tachycardia zone widened, and in 3 it was unaltered. In the latter cases, the cycle length of the tachycardia was increased. Tiapamil appears to be useful for the termination of tachycardia and also for its prevention in some cases. In others, it may facilitate the inhibition of tachycardia. The delayed AV nodal conduction during sinus rhythm augments the area of ventricular preexcitation, which may facilitate the electrocardiographic localization of the accessory pathway.     

Sinus node disease. Current concepts in diagnosis and therapy.

Sinus node disease (SND) encompasses a number of abnormalities of sinus impulse generation and transmission within the atria and may lead to both bradyarrhythmias and tachycardias. Such abnormalities may be due to primary atrial electrophysiological abnormalities, or be secondary to drugs or abnormal autonomic control. The diagnosis may be readily established from the surface ECG or Holter recordings in many cases, but invasive electrophysiological study or assessment of the effects of autonomic blockade may be required in symptomatic patients in whom the diagnosis is suspected but not confirmed by simple electrocardiographic monitoring. Treatment should be restricted to those patients in whom clear correlation between symptoms and electrocardiographic or electrophysiological abnormalities has been established. Although a number of pharmacological agents have been assessed, the treatment of bradyarrhythmias should be permanent pacing. There is now substantial evidence that physiological (atrial or dual chamber) pacing reduces atrial arrhythmias, systemic embolisation, progression to heart failure and mortality, compared to single chamber ventricular pacing. Antiarrhythmic therapy may be required to control atrial tachyarrhythmias if they persist following pacing. In patients with uncontrolled atrial arrhythmias, especially those with ventricular pacemakers, long term oral anticoagulation should be considered to reduce the risk of systemic embolisation which is a common complication in patients with the bradycardia/tachycardia syndrome.     

射频导管消融法治疗室上性心动过速108例临床分析

目的通过分析射频导管消融术(RFCA)治疗室上性心动过速(SVT)108例患者的临床资料,总结其临床疗效、并发症和复发情况。方法根据体表心电图(ECG)或食管心房调搏(TEAP)诱发的心电图的特点和心内心电图的精确标测,确定最佳消融靶点后进行放电,直到旁路、双径路现象消失,SVT不能诱发。结果108例患者中房室折返性心动过速(AVRT)87例,其中左侧旁路66例均消融成功,但有1例发生心包填塞,右侧旁路21例中有1例消融失败;房室结折返性心动过速(AVNRT)21例,全部消融成功,未发生并发症。消融成功后患者1年内随访,无一例复发。结论RFCA治疗SVT是一种可靠的根治手段,成功率高、并发症少、复发率低,值得在中小医院推广。     

老年人动态心电图290例分析

目的探讨老年人动态心电图检查时各种心律失常、心肌缺血的检出率及最低心率。方法对2007年至2011年间我院290例老年人的动态心电图资料进行分析。结果老年人单发室上性早搏的检出率为96.90%,成对为95.86%;非阵发性及阵发性房性心动过速的检出率分别为55.86%和17.93%;老年人单发室性早搏的具体检出概率是85.17%,成对概率是15.17%;而老年人阵发性以及非阵发性出现心动超速的具体检出概率分别是1.72%和5.86%。最低心率<30次/分者8例(1.5%),最低心率并不随年龄增长而下降。心肌缺血67例(23%),其中63例(97%)为完全无症状性心肌缺血。结论单纯室上性及室性早搏在老年人中很常见,可能并无病因和预后价值。对最低心率过慢(<30次/分)及伴有心肌缺血者,应采取必要措施,以防意外发生。     

History of arrhythmias

A historical overview is given on the techniques to record the electrical activity of the heart, some anatomical aspects relevant for the understanding of arrhythmias, general mechanisms of arrhythmias, mechanisms of some specific arrhythmias and nonpharmacological forms of therapy. The unravelling of arrhythmia mechanisms depends, of course, on the ability to record the electrical activity of the heart. It is therefore no surprise that following the construction of the string galvanometer by Einthoven in 1901, which allowed high-fidelity recording of the body surface electrocardiogram, the study of arrhythmias developed in an explosive way. Still, papers from McWilliam (1887), Garrey (1914) and Mines (1913, 1914) in which neither mechanical nor electrical activity was recorded provided crucial insights into re-entry as a mechanism for atrial and ventricular fibrillation, atrioventricular nodal re-entry and atrioventricular re-entrant tachycardia in hearts with an accessory atrioventricular connection. The components of the electrocardiogram, and of extracellular electrograms directly recorded from the heart, could only be well understood by comparing such registrations with recordings of transmembrane potentials. The first intracellular potentials were recorded with microelectrodes in 1949 by Coraboeuf and Weidmann. It is remarkable that the interpretation of extracellular electrograms was still controversial in the 1950s, and it was not until 1962 that Dower showed that the transmembrane action potential upstroke coincided with the steep negative deflection in the electrogram. For many decades, mapping of the spread of activation during an arrhythmia was performed with a "roving" electrode that was subsequently placed on different sites on the cardiac surface with a simultaneous recording of another signal as time reference. This method could only provide reliable information if the arrhythmia was strictly regular. When multiplexing systems became available in the late 1970s, and optical mapping in the 1980s, simultaneous registrations could be made from many sites. The analysis of atrial and ventricular fibrillation then became much more precise. The old question whether an arrhythmia is due to a focal or a re-entrant mechanism could be answered, and for atrial fibrillation, for instance, the answer is that both mechanisms may be operative. The road from understanding the mechanism of an arrhythmia to its successful therapy has been long: the studies of Mines in 1913 and 1914, microelectrode studies in animal preparations in the 1960s and 1970s, experimental and clinical demonstrations of initiation and termination of tachycardias by premature stimuli in the 1960s and 1970s, successful surgery in the 1980s, the development of external and implantable defibrillators in the 1960s and 1980s, and finally catheter ablation at the end of the previous century, with success rates that approach 99% for supraventricular tachycardias.     

Electrophysiologic effects and antiarrhythmic efficacy of recainam in patients with supraventricular tachycardia.

Recainam is a new antiarrhythmic agent with class Ic properties. To evaluate its electrophysiologic effects and antiarrhythmic efficacy in patients with recurrent supraventricular tachycardia (SVT), programmed electrical stimulation was performed in 10 patients before and after intravenous recainam (loading dose 0.8 mg/kg, infusion 1 mg/kg/h), and in four patients on oral recainam 1,200 mg/day. Five patients had atrioventricular (AV) node reentrant tachycardia; five had AV-reciprocating tachycardia. There were no significant changes in electrocardiographic and intracardiac intervals after either intravenous or oral recainam. After intravenous recainam, the ventricular effective refractory period (ERP) shortened (231 +/- 14-219 +/- 9 ms, p less than 0.05). The antegrade ERP of all three bidirectional accessory pathway markedly prolonged, but the effect on retrograde accessory pathway and AV node ERPs was unremarkable. SVT induction was prevented in three of 10 patients and SVT cycle length increased modestly in seven (357 +/- 44-374 +/- 42 ms, p = 0.07). On oral recainam, an increase in the frequency of spontaneous SVT occurred in two patients. At the doses given, recainam caused less electrophysiologic change than expected, had modest antiarrhythmic efficacy, and might have significant arrhythmogenic potential.     

The effect of intravenous disopyramide phosphate on recurrent paroxysmal tachycardias.

1 Reccurent paroxysmal atrial, atrioventricular and ventricular tachycardias in 50 patients without acute coronary insufficiency, heart failure or metabolic abnormlity were treated with disopyramide phosphate in a dose of 2 mg/kg body weight infused over 5 min. 2 Conversion to sinus rhythm within 10 min of the completed infusion occurred in 10 of 14 (71%) patients with paroxysmal 'lone' atrial fibrillation, 3 of 7 (43%) patients with paroxysmal atrial flutter, 6 of 9 (67%) patients with paroxysmal atrial tachycardia, 5 of 9 (56%) patients with paroxysmal atrioventricular tachycardia associated with the Wolff-Parkinson-White syndrome and 8 of 11 (73%) patients with paroxysmal ventricular tachycardia. 3 Side effects: significant systemic hypotension in 3, high grade AV block in 1, an increased ventricular response producing symptoms in 4, post conversion asystole in 1 land sinus bradycardia in 2. 4 The anti-arrhythmic effect and arrhythmogenic side effects may be related to both the direct membrane stabilizing effect and the anticholinergic effect of disopyramide.     

慢径消融治疗房室结折返性心动过速无交界性心律出现的电生理特点

目的　探讨射频消融房室结慢径时 ,治疗房室结折返性心动过速 (AVNRT)无交界性心律出现的电生理特点及其可能机制。方法　将 32 5例 A VNRT患者分为两组 :A组 30 4例 ,消融房室结慢径时出现交界性心律 ;B组 2 1例 ,消融慢径时无交界性心律出现。比较两组慢径消融时消融导管电极所在部位 ,A/ V比值 ,有无碎裂波或慢径电位 ,以及好发于何种 AVNRT。结果　 B组多为快 -慢 (Fast- Slow) AVNRT患者 ;B组 A/ V>A组A/ V比值 ;B组患者消融导管电极大多位于后区 ,且较少记录到碎裂波或慢径电位。结论　消融慢径时 ,极少数病例无交界性心律出现 ,也可成功地打断房室结慢径使治疗 AVNRT获得成功。