Role of echocardiography in differential diagnosis of broad complex tachycardia

It is not always easy to distinguish between supraventricular tachycardia with aberration and ventricular tachycardia by electrocardiographic analysis alone. M mode echocardiography can often help by providing direct or indirect evidence of the relation between atrial and ventricular contraction. Sixteen consecutive patients with spontaneous sustained broad QRS complex tachycardia with heart rates of 120-225 beats/minute were examined. Echocardiographic evidence of 1:1 conduction was seen in three cases and 2:1 atrioventricular conduction in one (all four had supraventricular tachycardia, confirmed by intracardiac electrocardiography in three). Evidence of retrograde block was seen in 12 (all had ventricular tachycardia, with electrophysiological confirmation in 10). Satisfactory views of the mitral valve were obtained in all patients. Patients with ventricular tachycardia had a variable mitral valve opening time (range 42-110%) compared with those who had supraventricular tachycardia (9-15%). Aortic root and left atrial views gave direct evidence of atrial contraction in three cases, and subcostal right atrial wall views were diagnostic in four of five cases. Seven patients with ventricular tachycardia had been wrongly diagnosed elsewhere as having supraventricular tachycardia. This study confirms that echocardiography is a simple and rapid aid to accurate diagnosis in patients with broad QRS complex tachycardia.     

Role of echocardiography in differential diagnosis of broad complex tachycardia.

It is not always easy to distinguish between supraventricular tachycardia with aberration and ventricular tachycardia by electrocardiographic analysis alone. M mode echocardiography can often help by providing direct or indirect evidence of the relation between atrial and ventricular contraction. Sixteen consecutive patients with spontaneous sustained broad QRS complex tachycardia with heart rates of 120-225 beats/minute were examined. Echocardiographic evidence of 1:1 conduction was seen in three cases and 2:1 atrioventricular conduction in one (all four had supraventricular tachycardia, confirmed by intracardiac electrocardiography in three). Evidence of retrograde block was seen in 12 (all had ventricular tachycardia, with electrophysiological confirmation in 10). Satisfactory views of the mitral valve were obtained in all patients. Patients with ventricular tachycardia had a variable mitral valve opening time (range 42-110%) compared with those who had supraventricular tachycardia (9-15%). Aortic root and left atrial views gave direct evidence of atrial contraction in three cases, and subcostal right atrial wall views were diagnostic in four of five cases. Seven patients with ventricular tachycardia had been wrongly diagnosed elsewhere as having supraventricular tachycardia. This study confirms that echocardiography is a simple and rapid aid to accurate diagnosis in patients with broad QRS complex tachycardia.     

Double atrial responses to a single ventricular impulse due to simultaneous conduction via two retrograde pathways

Electrophysiologic studies were performed in two patients. In one patient (Case 1) with ventricular pre-excitation and paroxysmal supraventricular tachycardia, studies after diltiazem administration showed two QRS responses to a single atrial stimulus during atrial pacing at a cycle length of 300 ms. The first QRS response with full pre-excitation and short PR interval was consistent with accessory pathway conduction, while the second QRS response with a normal duration and an atrio-His bundle interval of 350 ms was consistent with normal pathway conduction. The second QRS response was followed by initiation of supraventricular tachycardia. Studies after verapamil administration on a separate day disclosed two atrial responses to a single QRS complex during ventricular pacing at cycle lengths between 330 and 280 ms, suggesting simultaneous retrograde accessory and normal pathway conduction. In Case 2 with a supraventricular tachycardia using a fast atrioventricular nodal pathway for anterograde and a slow ventriculoatrial pathway for retrograde conduction, two atrial responses to a single QRS complex were observed during ventricular pacing at cycle lengths between 500 and 400 ms. The first atrial response showed a stimulus to atrial interval of 120 ms and an atrial activation sequence with the low septal right atrium being earlier than other atrial sites, suggesting retrograde fast pathway conduction. The second atrial response showed a stimulus to atrial interval of 505 ms and an atrial activation sequence with low septal right atrium being simultaneous with the proximal coronary sinus, suggesting retrograde slow pathway conduction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Left posterior fascicular tachycardia: a diagnostic and therapeutic challenge

A wide QRS complex tachycardia with right bundle-branch block morphology and left axis deviation observed in a young patient without structural heart disease may pose a diagnostic and therapeutic challenge. The surface ECG may provide several diagnostic clues to make a correct diagnosis of left posterior fascicular tachycardia and may help to differentiate it from both a supraventricular tachycardia with aberrant conduction and a typical ventricular tachycardia related to coronary artery disease. Although this tachycardia is sensitive to verapamil, this medication may probably cause transient infertility in males. The presence of a Purkinje potential preceding the QRS complex during tachycardia and optimal pace mapping may guide radio-frequency ablation resulting in a definite cure.     

The value of the electrocardiogram in the differential diagnosis of a tachycardia with a widened QRS complex

To determine the value of the electrocardiogram for differentiating aberrant conduction from ventricular ectopy, findings were retrospectively reviewed from patients with a widened QRS complex during tachycardia in whom the site of origin of tachycardia was determined by His bundle electrography. Seventy episodes of sustained ventricular tachycardia from 62 patients and 70 episodes of aberrant conduction during supraventricular tachycardia from 60 patients were available for study. Findings suggesting a ventricular origin of tachycardia were (1) QRS width over 0.14 sec, (2) left axis deviation, (3) certain configurational characteristics of QRS and (4) atrioventricular (A-V) dissociation. Capture or fusion beats resulting from A-V conduction of dissociated atrial complexes during ventricular tachycardia were seen during only four of 33 episodes of sustained tachycardia.     

Brugada法联合Steurer法在宽QRS波心动过速鉴别诊断中的价值

为评价Brugada法联合Steurer法在宽QRS波心动过速 (WRT)鉴别诊断中的应用价值及存在的缺陷。对 1 0 1例WRT[室性心动过速 (VT) 5 8例 ,室上性心动过速 (SVT) 43例 ]进行分析。结果 :Brugada法诊断VT灵敏度、特异度、准确性分别为 85 .7%、89.5 %、87.1 % ;联合Steurer法后灵敏度、特异度、准确性分别升至 91 .5 %、90 .5 %、91 .1 %。进一步分析显示 :Brugada法对器质性原因所致VT、右束支阻滞型 (RBBB)特发性VT(IVT)、SVT伴室内差异性传导 (AC)或原有单侧束支阻滞 (BBB)者诊断符合率高 ( 95 .8%～ 1 0 0 .0 % ) ;对左束支阻滞型 (LBBB)特发性VT、SVT伴原有双支阻滞、心肌坏死或心肌梗死伴宽QRS波SVT及预激综合征伴旁道前传型SVT(WPW SVT)诊断的符合率低 ( 0～ 5 0 .0 % )。联合Steurer法可使WPW伴旁道前传型SVT得以明确诊断 ,但对前三者无鉴别意义 ,故不适合在前三者中应用。结论 :Brugada法联合Steurer法能提高WPW伴旁道前传型SVT的鉴别能力 ,是目前鉴别WRT的重要方法。     

Augmentation of QRS wave amplitudes in the precordial leads during narrow QRS tachycardia

INTRODUCTION: QRS morphology during narrow QRS supraventricular tachycardia in patients without ventricular preexcitation generally is considered the same as that seen during sinus rhythm. This study presents a new ECG observation that the QRS amplitude increased significantly in leads V2 through V5 during tachycardia. METHODS AND RESULTS: Using the same ECG machine and the same electrode patches applied to the same electrode positions, 12-lead ECGs during sinus rhythm and narrow QRS tachycardia were analyzed comparatively in 23 patients without ventricular preexcitation. Precordial QRS amplitudes were measured as the vertical distance from the peak of the R to the nadir of the S wave. The amplitudes also were measured during atrial rapid pacing and extrastimulation. Furthermore, ventricular excitation during sinus rhythm and tachycardia was studied using body surface mapping. Body surface distributions of QRS potentials and ventricular activation time (VAT) were displayed as maps. Gross area of QRS (AQRS, equivalent to the QRS amplitude) was compared during sinus rhythm versus tachycardia. During tachycardia, QRS amplitude significantly increased in leads V2 through V5, without any noticeable change in the transitional zone or QRS wave duration. Increase of QRS amplitude also was noted during atrial rapid pacing and extrastimulation. Gross AQRS values during tachycardia significantly increased in the left parasternal area, whereas QRS isopotential and VAT isochronal maps were similar during sinus rhythm and tachycardia, suggesting a minimal role of conduction delay in the increase of QRS amplitude. CONCLUSION: QRS wave amplitude significantly increased in leads V2 through V5 during narrow QRS tachycardia compared with QRS waves in sinus rhythm. Increase of QRS amplitude seemed unlikely due to a conduction delay within the ventricular myocardium.     

Evidence for a unidirectional retrograde communication between distal His bundle and atria.

Intracardiac electrogram recordings are presented suggesting the existence in one patient with recurrent supraventricular tachycardia of a functionally unidirectional retrograde connection between the distal His bundle and the low right atrium. Recordings obtained during junctional rhythm showed a short ventriculoatrial conduction time which did not lengthen during rapid or premature ventricular pacing. During an episode of supraventricular tachycardia induced by a single atrial premature stimulus, an infra-His Wenckebach period occurred during which retrograde ventriculoatrial conduction remained constant until ventricular capture was blocked, but atrial activation persisted with the same retrograde atrial activation sequence seen in the previous beats of supraventricular tachycardia. The findings appear to document participation in supraventricular tachycardia of a type of atrio-His fibre originally described by Brechenmacher.     

Case Report: Spontaneous Atriofascicular Pathway Automaticity Simulating Ventricular Tachycardia

Atriofascicular pathways most commonly present electrocardiographically as an antidromic reciprocating AV reentrant tachycardia. We report the case of a child who presented in infancy with a wide QRS complex tachycardia thought to be supraventricular tachycardia with aberrant conduction, associated with tachycardia-induced cardiomyopathy. Later in life the same patient represented with episodes of palpitations secondary to a wide QRS complex tachycardia, thought to be ventricular tachycardia. Electrophysiologic mapping demonstrated the origin of the wide QRS complex tachycardia was from automatic activity originating from a right anterolateral atriofascicular pathway, which also participated in a reentrant antidromic AV reciprocating tachycardia. Radiofrequency ablation of the atriofascicular pathway successfully eliminated both arrhythmias. The mechanism of the wide QRS complex tachycardia appeared to result from spontaneous automaticity of the atriofascicular pathway.     

A technique for the rapid diagnosis of atrial tachycardia in the electrophysiology laboratory

OBJECTIVE: The purpose of this study was to determine if the atrial response upon cessation of ventricular pacing associated with 1:1 ventriculoatrial conduction during paroxysmal supraventricular tachycardia is a useful diagnostic maneuver in the electrophysiology laboratory. BACKGROUND: Despite various maneuvers, it can be difficult to differentiate atrial tachycardia from other forms of paroxysmal supraventricular tachycardia. METHODS: The response upon cessation of ventricular pacing associated with 1:1 ventriculoatrial conduction was studied during four types of tachycardia: 1) atrioventricular nodal reentry (n = 102), 2) orthodromic reciprocating tachycardia (n = 43), 3) atrial tachycardia (n = 19) and 4) atrial tachycardia simulated by demand atrial pacing in patients with inducible atrioventricular nodal reentry or orthodromic reciprocating tachycardia (n = 32). The electrogram sequence upon cessation of ventricular pacing was, categorized as "atrial-ventricular" (A-V) or "atrial-atrial-ventricular" (A-A-V). RESULTS: The A-V response was observed in all cases of atrioventricular nodal reentrant and orthodromic reciprocating tachycardia. In contrast, the A-A-V response was observed in all cases of atrial tachycardia and simulated atrial tachycardia, even in the presence of dual atrioventricular nodal pathways or a concealed accessory atrioventricular pathway. CONCLUSIONS: In conclusion, an A-A-V response upon cessation of ventricular pacing associated with 1:1 ventriculoatrial conduction is highly sensitive and specific for the identification of atrial tachycardia in the electrophysiology laboratory.     

Adenosine-Sensitive Atrial Reentrant Tachycardia Originating from the Atrioventricular Nodal Transitional Area

Adenosine-Sensitive AT from AVN Area. Introduction : Atrial tachycardia shows wide variations in its electrophysiologic properties and sites of origin. We report an atrial tachycardia with ECG manifestations and electrophysiologic characteristics similar to an atypical form of AV nodal reentrant tachycardia (AVNRT).
Methods and Results : This supraventricular tachycardia was observed in 11 patients. It was initiated by atrial extrastimulation with an inverse relationship between the coupling interval of an extrastimulus and the postextrastimulus interval. Its induction was not related to a jump in the AH interval, and its perpetuation was independent of conduction block in the AV node. Ventricular pacing during tachycardia demonstrated AV dissociation without affecting the atrial cycle length. A very small dose of adenosine triphosphate (mean 3.9 ± 1.2 mg) could terminate the tachycardia. The earliest atrial activation during tachycardia was recorded at the low anteroseptal right atrium with a different intra-atrial activation sequence from that recorded during ventricular pacing, where the tachycardia was successfully ablated in 9 of 10 attempted patients. Bidirectional AV nodal conduction remained unatttched after successful ablation.
Conclusion : There may he an entity of adenosine-sensitive atrial tachycardia probably due to focal reentry within the AV node or its transitional tissues without involvement of the AV nodal pathways. This tachycardia can he ablated without disturbing AV nodal conduction from the right atrial septum.     

心电散点图在心律失常快速诊断中的应用

目的通过与诊断结果对比观察,探讨心电散点图在快速诊断心律失常方面的临床应用价值。方法应用动态心电图记录仪记录患者连续24h心电信号,利用计算机自动检测技术,进行心电分析,并同步绘制24h心电散点图。将诊断结果分为窦性心律、室上性早搏、室性早搏、心房颤动、差异性传导5组,分别将4组心律失常结果与心电散点图检测的诊断结果进行对照,计算出二者的符合率及各组的B线斜率,进行分析对比。结果室上性早搏组与室性早搏、心房颤动、差传组差异显著(p<0.001);室性早搏组与室上性早搏、心房颤动、差传组差异显著(p<0.001);心房颤动组与差传组差异不显著(p>0.05)。结论心电散点图在长程大样本心电数据中,快速诊断心律失常,尤其是室上性早搏、室性早搏、心房颤动等时具有较好的临床应用价值。     

Intracardiac electrode catheter recordings of atrioventricular bypass tracts in Wolff-Parkinson-White syndrome: techniques, electrophysiologic characteristics and demonstration of concealed and decremental propagation

Atrioventricular bypass tract deflections were recorded in five patients with the Wolff-Parkinson-White syndrome using standard, closely spaced (5 mm) electrode catheters. Three right paraseptal and two left-sided Kent bundles were recorded at the level of the tricuspid valve on the His bundle catheter and in the coronary sinus, respectively. Characteristics of the bypass tracts were studied during atrial pacing, programmed premature atrial stimulation, induction of supraventricular tachycardias and programmed ventricular stimulation. During atrial pacing, as pre-excitation increased, the stimulus to bypass tract deflection time remained unchanged. In five patients normalization of the QRS complex coincided with loss of the bypass tract deflection during incremental atrial pacing. Two patients demonstrated fragmentation of the bypass tract deflection before block. In one patient fragmentation of the bypass deflection coincided with normalization of the QRS complex. The effective refractory periods of the bypass tracts coincided with loss of bypass tract deflections in three of the five patients. In one patient, the effective refractory period of the bypass tract at its ventricular insertion preceded that at its atrial insertion, whereas in the remaining patient, the effective refractory period of the bypass tract was not attained because of atrial refractoriness. During orthodromic supraventricular tachycardia, the bypass tract deflections disappeared in the anterograde limb in all patients. In one patient, the bypass tract deflection was recorded during atrial fibrillation with pre-excitation. In conclusion: Bypass tract deflections can be recorded with a closely spaced electrode catheter. Right paraseptal bypass tracts are located close to the His bundle. The anterograde effective refractory period of the bypass tract usually reflects its atrial insertion, but concealment through the bypass tract can occur with block at the ventricular insertion. Decremental conduction within the bypass tract can occur before block, suggesting concealed and overt Wenckebach block within the bypass tract. Recordings of bypass tract deflections increase the potential of closed chest ablation of right paraseptal and left-sided bypass tracts.     

A transcardiac lead system for identification and termination of supraventricular and ventricular tachycardia

The value of a transcardiac lead system (coronary sinus to right ventricular apex) to record atrial and ventricular electrical activity and its pacing capabilities was assessed in 20 patients with a variety of tachycardias (atrial tachycardia in 3 patients, atrial flutter in 4, intranodal tachycardia in 6, circus movement tachycardia using an accessory pathway in 1 patient, and ventricular tachycardia in 9). The transcardiac lead invariably showed both atrial and ventricular electrical activity during sinus rhythm and tachycardias, allowing application of the same criteria as used when analyzing cardiac rhythm on the surface electrocardiogram. Atrial complexes had a mean amplitude of 4.2 mV during sinus rhythm and varied from 3.0 to 4.1 mV during the different types of tachycardia. Ventricular complexes had a mean amplitude of 9.8 mV during sinus rhythm, 13.8 mV during supraventricular tachycardia and 16.1 mV during ventricular tachycardia. The duration of the QRS complex on the transcardiac lead was equal to the duration of the QRS complex on the surface electrocardiogram during tachycardias with a small or wide QRS complex. By varying the intensity of current delivered through the transcardiac lead, only right ventricular pacing (mean current intensity 1.2 +/- 0.4 mA) or simultaneous atrioventricular pacing (mean current intensity 4.7 +/- 3.3 mA) could be achieved. Termination of all episodes of tachycardia was achieved with either ventricular pacing or simultaneous atrioventricular pacing. This transcardiac lead system allows clear identification of atrial and ventricular events, is suitable for tachycardia analysis using simple surface electrocardiographic algorithms and allows pacing termination of a variety of tachycardias.     

房室多旁道的电生理特征及其射频消融治疗

目的 探讨房室多旁道的电生理特点及射频消融方法。方法 23例患者经电生理检查确定房室多旁道，应用心房和心室刺激诱发室上速，确定每条旁道的电生理特征及与心动过速的关系，按照标测部位对相关旁道逐步消融，以射频消融成功确定旁道位置。结果 23例中检出旁道49条，其中三条旁道3例；左侧多旁道12例，右侧多旁道2例，双侧多旁道9例；左侧多旁道以隐匿性为主；右侧多旁道多为显性；未见心动过速时右侧旁道前传而同侧旁道逆传现象。结论 多旁道患者应首先确定和消融与心动过速相关旁道；左侧多旁道应以诱发心动过速或快速心室起搏方法标测；右侧多旁道应同步描记12导联体表心电图，旁道消融成功可能仅见于QRS波的变化，双侧多旁道应首先消融左侧旁道。     

Akuttherapie lebensbedrohlicher tachykarder Rhythmusstörungen

Life-threatening supraventricular tachyarrhythmias include atrial fibrillation, atrial flutter, AV-nodal reentrant tachycardia with rapid ventricular response and preexcitation syndromes combined with atrial fibrillation. Ventricular tachyarrhythmias still remain one of the leading causes of death; these arrhythmias include monomorphic and polymorphic ventricular tachycardia, torsade de pointes tachycardia, ventricular fibrillation and ventricular flutter. In all patients with tachycardias, an attempt should be made to differentiate between narrow (QRS duration < 0.12 s) or wide QRS complex (QRS duration ≥ 0.12 s) tachycardias. In the assessment of patients (pts) with supraventricular/ventricular tachyarrhythmias, attention should be given to identify whether the tachycardia is associated with worsening angina or low cardiac output. In pts with narrow QRS complex tachycardias or pts with atrial fibrillation and preexcitation syndromes immediate synchronized cardioversion should be performed if signs or symptoms of instability (hypotension, evidence of end-organ dysfunction, worsening angina) exist. In pts with a stable hemodynamic situation, vagal maneuvers, adenosine or calcium channel blockers can be used. Management of atrial flutter usually centers on cardioversion or rapid atrial pacing to normal sinus rhythm. In the treatment of patients with deemed unstable ventricular tachycardia (VT), electrical cardioversion is the treatment of choice. In more stable patients, ajmaline is the preferred agent after myocardial infarction and lidocaine if myocardial ischemia is present. In pts with torsade de pointes tachycardias aggressive steps must be taken to prevent degeneration of this rhythm to ventricular fibrillation (VF). Magnesium sulfate has recently been demonstrated efficacious and is currently considered first-line drug therapy. Transcutaneous overdrive pacing should be attempted if magnesium is unsuccessful. The pt with pulseless VT or VF demands early electrical countershock.     

Intractable paroxysmal tachycardia caused by a concealed retrogradely conducting Kent bundle. Demonstration by epicardial mapping and cure of tachycardias by surgical interruption of the His bundle.

Electrophysiological and epicardial mapping studies are described in a patient without pre-excitation who had intractable recurrent paroxysmal supraventricular tachycardia. Electrophysiological studies revealed fixed VA conduction times during both rapid ventricular pacing and coupled ventricular stimulation. Catheter mapping of atrial activation during retrograde conduction and during induced paroxysmal supraventricular tachycardia revealed early distal coronary sinus activation (posterior left atrium) relative to the low septal, low lateral, and high lateral right atrium. These studies suggested the presence of a concealed left-sided bypass tract. The patient underwent surgical interruption of the His bundle for control of paroxysmal supraventricular tachycardia. Epicardial mapping of the atria (during ventricular pacing) confirmed the presence of a concealed left-sided bypass tract. Surgery produced antegrade av block (while retrograde conduction was maintained) and total cure of paroxysmal supraventricular tachycardia. This is the first reported case of a concealed retrograde extranodal pathway documented by epicardial mapping.     

Determinants of QRS alternans during narrow QRS tachycardia

This study was designed to prospectively determine the incidence of QRS alternans during various types of narrow QRS tachycardia and to clarify the determinants of QRS alternans. An electrophysiologic study was performed in 28 consecutive patients with a narrow QRS tachycardia. Persistent QRS alternans was observed in 6 (43%) of 14 patients during orthodromic reciprocating tachycardia, 5 (71%) of 7 patients during atrial tachycardia and 3 (43%) of 7 patients during atrioventricular (AV) node reentrant tachycardia. Incremental atrial pacing during sinus rhythm resulted in QRS alternans in patients who had QRS alternans during tachycardia, unless the shortest pacing cycle length associated with 1:1 AV conduction exceeded the tachycardia cycle length. In patients without QRS alternans during narrow QRS tachycardia, incremental atrial pacing during sinus rhythm resulted in persistent QRS alternans in five patients in whom the shortest pacing cycle length associated with 1:1 AV conduction was 60 to 180 ms less than the tachycardia cycle length. In an additional 20 patients without a narrow QRS tachycardia, persistent QRS alternans was observed during incremental atrial pacing in 11 (55%) of the patients. In six of six patients who had QRS alternans during abrupt rapid atrial pacing, QRS alternans was not observed when the same pacing rates were achieved gradually. Among the patients with narrow QRS tachycardia, the mean tachycardia cycle length in those who had QRS alternans (mean +/- SD 288 +/- 44 ms) was significantly shorter than in those who did not (369 +/- 52 ms, p less than 0.001). The presence of QRS alternans was not related to the tachycardia mechanism, relative or functional refractory period of the His-Purkinje system (at a drive cycle length of 500 ms), age, presence of structural heart disease, direction of input into the AV node or concealed retrograde conduction in the His-Purkinje system. In conclusion, QRS alternans during narrow QRS tachycardias is a rate-related phenomenon that depends on an abrupt increase to a critical rate and is independent of the tachycardia mechanism.     

Continuous rapid atrial pacing to control recurrent or sustained supraventricular tachycardias following open heart surgery.

A technique is described to control recurrent or sustained supraventricular tachycardia associated with rapid ventricular rates following open heart surgery. The technique utilizes a pair of temporarily implanted atrial epicardial wire electrodes to pace the heart. In one group of patients with recurrent atrial flutter and 2:1 A-V conduction, continuous rapid atrial pacing at 450 beats/min produced and sustained atrial fibrillation. The ventricular response rate immediately slowed when compared to that during atrial flutter, and if further slowing was required, it was easily accomplished by the administration of digitalis. Another group of patients with different arrhythmias (recurrent paroxysmal atrial tachycardia, sustained ectopic atrial tachycardia, or sinus rhythm with premature atrial beats which precipitated runs of atrial fibrillation) was treated with continuous rapid atrial pacing to produce 2:1 A-V block. In all instances, the continuous rapid atrial pacing suppressed the supraventricular tachycardia and maintained the ventricular response rate in a therapeutically desirable range. It was demonstrated that the technique is safe, effective, and reliable.     

Reliability of retrograde atrial activation patterns during ventricular pacing for localizing accessory pathways

Definitive localization of accessory pathways is based on atrial activation patterns during orthodromic supraventricular tachycardia when retrograde conduction occurs exclusively through the accessory pathway. In some patients, supraventricular tachycardia cannot be induced or is deleterious. To determine whether accessory pathway sites can be identified accurately during ventricular pacing, retrograde atrial activation was assessed during orthodromic supraventricular tachycardia and ventricular pacing at multiple cycle lengths in 41 patients with a single accessory pathway. To obviate retrograde fusion due to concomitant conduction through the normal atrioventricular (AV) conduction system that may obscure the location of the accessory pathway, the difference in conduction time from the site of earliest atrial activation to the His bundle atrial electrogram (delta A-SVT) was measured during orthodromic supraventricular tachycardia and compared with values observed during ventricular pacing (delta A-VP). Characteristic values for the delta A-SVT interval were identified for left lateral (66 +/- 17 ms), left posterior (50 +/- 8 ms), posteroseptal (33 +/- 7 ms), right free wall (22 +/- 15 ms) and anteroseptal (0 +/- 0 ms) accessory pathway sites. During ventricular pacing, the site with the earliest atrial electrogram was used to define the accessory pathway location only if the maximal value of the delta A-VP interval over the range of cycle lengths assessed was comparable with the value of the delta A-SVT interval characteristic of that region. Values of the delta A-SVT interval correlated closely with the maximal values of the delta A-VP interval (r = 0.91). With this approach, 40 (98%) of 41 accessory pathway sites were identified correctly during ventricular pacing.(ABSTRACT TRUNCATED AT 250 WORDS)