Wide Complex Tachycardia in the Presence of Class I Antiarrhythmic Agents: A Diagnostic Challenge

We present two patients with paroxysmal atrial fibrillation on class 1C antiarrhythmic drugs without concomitant atrioventricular (AV) nodal blocking agents who developed atrial flutter with 1:1 AV conduction. Their electrocardiogram revealed wide complex tachycardia with rates >200/minute. Atrial flutter with 1:1 conduction in the presence of class IC antiarrhythmic drugs may present a diagnostic challenge. These cases illustrate the importance of coadministering an AV nodal blocking agent with class IC antiarrhythmic agents in patients with atrial fibrillation. The differential diagnosis of wide complex tachycardia in patients taking class IC agents should include atrial flutter with 1:1 AV conduction.     

AV nodal reentrant tachycardia with a bystander Mahaim fiber

A 13 year old boy had a wide QRS complex tachycardia. A discontinuity in the AV nodal functional curve was observed in the electrophysiologic study. The AV internal was prolonged in association with progressive ventricular preexcitation. At maximal preexcitation, the HV interval was -20 msec and the QRS complex was identical to that seen during clinical tachycardia. No VA conduction was found and atrial premature beats did not affect the tachycardia. The His deflection was found at variable timing when tachycardia was induced. These findings confirmed that tachycardia originated within the AV node and was conducted to the ventricle over the Mahaim fiber. The short effective period of the Mahaim fiber had clinical significance since when atrial fibrillation developed, a rapid ventricular response was observed.     

Intravenous adenosine triphosphate during wide QRS complex tachycardia: safety, therapeutic efficacy, and diagnostic utility

PURPOSE: Inappropriate administration of intravenous verapamil to patients with wide QRS complex tachycardia due to ventricular tachycardia or atrial fibrillation with Wolff-Parkinson-White syndrome occurs frequently because of misdiagnosis, and may precipitate a cardiac arrest. We evaluated the safety and the diagnostic and therapeutic utility of adenosine triphosphate administered to a consecutive series of 34 patients during wide QRS complex tachycardia due to a variety of mechanisms. PATIENTS AND METHODS: Patients who had a hemodynamically and electrically stable, monomorphic, wide (greater than 120 msec) QRS complex tachycardia induced during an invasive cardiac electrophysiologic test were studied. Hemodynamic stability was defined by a systolic blood pressure greater than 80 mm Hg and no clinical evidence of cerebral or myocardial ischemia. Adenosine triphosphate, 20 mg, was administered as a rapid intravenous bolus via a peripheral vein during wide QRS complex tachycardia. Five surface electrocardiogram leads, at least three intracardiac electrograms, and blood pressure were monitored. RESULTS: Ventricular tachycardia was present in 14 patients (mean age 50.6 +/- 19 years, cycle length 326 +/- 67 msec) and adenosine triphosphate terminated the arrhythmia in one case. Ventricular tachycardia cycle length did not change. Among 10 patients with supraventricular tachycardia with mechanisms not involving the AV node (average ventricular cycle length 346 +/- 82 msec), one case of ectopic atrial tachycardia was terminated. The ventricular rate was transiently increased in patients with Wolff-Parkinson-White syndrome and atrial fibrillation (average R-R interval 351 +/- 84 msec in control and 317 +/- 82 msec after adenosine triphosphate, p less than 0.001). Reentrant tachycardias involving the AV node (cycle length 302 +/- 52 msec) terminated in seven of 10 patients. The drug was well tolerated, and no patient developed hemodynamic compromise necessitating cardioversion as a result of adenosine triphosphate. CONCLUSION: In the setting of electrophysiology testing, adenosine triphosphate is a safe agent, even when administered inappropriately during arrhythmias for which it is relatively ineffective, such as ventricular tachycardia, and Wolff-Parkinson-White syndrome with atrial fibrillation. It is an effective agent in terminating supraventricular tachycardia involving the AV node. Tachycardia termination following adenosine triphosphate, when used as a diagnostic test to indicate obligatory participation of the AV node, had a sensitivity of 70%, specificity of 92%, and a positive predictive accuracy of 85%. Thus, adenosine triphosphate also has diagnostic utility, but should be used after the appropriate arrhythmia diagnosis has been made based on the clinical history and analysis of the 12-lead electrocardiogram.     

A new algorithm in the differential diagnosis of wide complex tachycardia.

A correct electrocardiographic diagnosis of the mechanism ofa wide complex tachycardia (WCT) is important when institutingemergent therapy and for long-term prognostic and therapeuticconsiderations. While any algorithm has the risk of oversimplifyinga complex problem, it is absolutely essential to have an initialstrategy for the acute evaluation of an arrhythmia. Causes of wide QRS tachycardia include (1) supraventriculartachycardia (SVT) with pre-existing or functional bundle branchblock, including sinus tachycardia, atrial tachycardia, atrialflutter, atrial fibrillation (AF) and AV nodal re-entry tachycardia,(2) orthodromic circus movement tachycardia with pre-existingor functional bundle branch block, (3) SVT with conduction overan accessory pathway, (4) Antidromic circus movement tachycardiausing an accessory pathway in the anterograde direction andAV     

Is This Atrial Fibrillation?

A 19‐year‐old girl was referred to our cardiology department for catheter ablation (isolation of the pulmonary veins) of paroxysmal atrial fibrillation (AF). The diagnosis was made upon a 12‐lead ECG of the arrhythmia documented in the emergency room. The ECG showed an irregular tachycardia without wide QRS complexes. Careful assessment revealed the irregularity of the rhythm was a sweep artifact due to a mechanic failure of the ECG‐machine to advance the article smoothly. During EP study a concealed anteroseptal accessory pathway causing an orthodromic AV reentrant tachycardia was eliminated by radio‐frequency ablation. This example emphasizes the need for careful assessment of an ECG tracing, including printed legends and technical data.     

Radiofrequency Catheter Ablation of an Atriofascicular Pathway During Atrial Fibrillation:

Atriofascicular Ablation During Fibrillation. Introduction: A male patient with an atriofascicular pathway underwent catheter ablation of the atriofascicular pathway during atrial fibrillation.
Methods and Results: The patient had preexcited atrial fibrillation both clinically and repeatedly during electrophysioiogic study. A preexcited tachycardia with a 1:1 AV relationship and regular RR intervals was also induced. Catheter ablation of the atriofascicular pathway could only be performed during persistent atrial fibrillation, based on mapping of the pathway's insertion into the right bundle branch. Following successful ablation and cardioversion to sinus rhythm, a regular QRS tachycardia (atrioventricular [AV] nodal reentry) having (he same rate, atrial activation sequence, and His-atrial time as the regular preexcited tachycardia noted preablation was initiated. An AV nodal slow pathway modification eliminated this tachycardia. Neither atrial fibrillation nor AV nodal reentry has recurred on follow-up.
Conclusion: This is the first report of atriofascicular mapping and ablation performed exclusively during atrial fibrillation and illustrates the utility of mapping the pathway's ventricular insertion. Other unusual features ("bystander" pathway activation during AV nodal reentry, possible role of the pathway in genesis of atrial fibrillation) are discussed.     

Ventricular tachycardia

The major differential diagnosis for VT is supraventricular tachycardia with a wide QRS complex due to aberrant conduction. Although VT may be slightly irregular, gross irregularities, such as those typically seen in atrial fibrillation, are uncommon during VT; such marked irregularities suggest atrial fibrillation. The QRS configuration is helpful in differentiating supraventricular tachycardia from VT. Supraventricular tachycardia with aberration generally produces QRS complexes that are less than 0.14 second in duration, whereas wider complexes are common in VT. The presence of an antiarrhythmic drug may, however, render this criterion unhelpful.     

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.     

食道心房调搏对窄QRS波室上性心动过速机制研究

目的：了解食道心房调搏（TEAP）对窄QRS波室上性心动过速机制的鉴别。方法：采用无创性TEAP技术,对145例有心动过速史但无器质性心脏病的患者进行检查,诱发窄QRS汉心动过速。结果：检出的窄QES波折返阵性发性室上性心动过速中,房室折返性心;动过速及房室结内折返性心动过速占约大多数,房性折返性心动过速极少。结论：TEAP是鉴别窄QRS波PSVT机制的一种安全,有效的方法。     

Spectrum of regular tachycardias with wide QRS complexes in patients with accessory atrioventricular pathways

Reciprocating tachycardia and atrial flutter or fibrillation are the rhythm disorders most frequently documented in patients with accessory atrioventricular (A-V) pathways. Reciprocating tachycardia typically results in a regular tachycardia (140 to 250/min) with a normal QRS pattern, although on occasion bundle branch block aberration occurs. Atrial flutter or fibrillation may result in an irregular ventricular response, with the QRS configuration being normal or exhibiting bundle branch block or various degrees of ventricular preexcitation, or both. Although much less common than either reciprocating tachycardia or atrial flutter/fibrillation, regular tachycardias with a wide QRS complex suggestive of ventricular preexcitation are observed in patients with accessory pathways. Excluding functional or preexisting bundle branch block, several arrhythmias may cause these electrocardiographic findings which may mimic those of ventricular tachycardia.In the present study a variety of arrhythmias that resulted in tachycardias with a wide QRS complex were examined in 163 patients with accessory pathways who underwent clinical electrophysiologic study for evaluation of recurrent tachyarrhythmias. Twenty-six patients (15 percent) manifested a regular tachycardia with a wide QRS complex suggesting ventricular preexcitation. Atrial flutter with 1:1 anterograde conduction over an accessory pathway (15 of 26 patients, 58 percent) was the most frequent arrhythmia and was usually associated with a heart rate of 240/min or greater (12 of 15 patients). Reciprocating tachycardia with conduction in the anterograde direction over an accessory pathway (antidromic reciprocating tachycardia) occurred in 7 of 26 patients (27 percent), and resulted in a slower ventricular rate than atrial flutter (217 ± 22 versus 262 ± 42, P < 0.01). Other arrhythmias included reciprocating tachycardia with reentry utilizing a fasciculoventricular or nodoventricular connection (two patients, 8 percent), reciprocating tachycardia with reentry in the atrium or A-V node and anterograde accessory pathway conduction (one patient, 4 percent) and ventricular tachycardia (one patient, 4 percent).In this study the clinical electrophysiologic diagnostic features of several arrhythmias which cause tachycardias with a wide QRS compex suggesting ventricular preexcitation are outlined. It is apparent that definitive arrhythmia diagnosis during these tachycardias is often complex and usually requires careful study using intracardiac electrode catheter techniques.     

Onset of atrial fibrillation during antidromic tachycardia: Association with sudden cardiac arrest and ventricular fibrillation in a patient with Wolff-Parkinson-White syndrome

Electrophysiologic evaluation in an 18 year old youth with the Wolff-Parkinson-White syndrome who had a sudden cardiac arrest while playing racquetball revealed two types of paroxysmal reciprocating tachycardia: (1) A normal QRS tachycardia with a short ventriculoatrial (V-A) interval fulfilled the criteria for reentry within the atrioventricular (A-V) node; and (2) a wide QRS tachycardia with a QRS configuration of maximal preexcitation was demonstrated to be the result of an antidromic mechanism.During laboratory study, the wide QRS tachycardia spontaneously degenerated into atrial fibrillation. In the basal state, the shortest R-R interval between preexcited QRS complexes was 270 ms, but after infusion of isoproterenol (1.6 μg/min intravenously), the shortest R-R interval became 180 ms. Consequently, this electrophysiologic study suggested that evolution of antidromic reciprocating tachycardia into atrial fibrillation with a rapid ventricular response during exercise-induced catecholamine release may have been the mechanism for ventricular fibrillation in this patient.     

Ventricular tachycardia masquerading as supraventricular tachycardia: A wolf in sheep''s clothing

It is generally assumed that if a wide QRS complex tachycardia has the same morphology on the 12-lead electrocardiogram as during sinus rhythm, the tachycardia is supraventricular. The author presents unique electrocardiographic data on four patients with QRS complex morphologies that are nearly identical during ventricular tachycardia and during sinus rhythm. The QRS complex duration during sinus rhythm was 140-180 msec and was the same as that of the tachycardia. The QRS complex morphology on the electrocardiogram was a right bundle branch block, left axis in three patients and right bundle branch block, normal axis in one patient. The mean ventricular tachycardia cycle length was 345 msec. The diagnosis of ventricular tachycardia was established by electrophysiologic testing in two patients and by atrial electrograms demonstrating AV dissociation in two patients. Thus, if the 12-lead electrocardiogram morphology of a wide QRS complex tachycardia is similar to that during sinus rhythm, it does not necessarily imply that the tachycardia is supraventricular. Ventricular tachycardia can occur with the same QRS complex morphology as occurs during sinus rhythm.     

Rapid wide QRS tachycardia with an unknown cause

One‐to‐one atrioventricular conduction during atrial flutter is one of the most severe life‐threatening arrhythmias and is hemodynamically perilous. Rapid wide QRS tachycardia often not only occurs in patients with ventricular tachycardia but is also found in supraventricular tachycardia/atrial flutter with preexistent QRS prolongation, supraventricular tachycardia/atrial flutter with QRS prolongation caused by an IC antiarrhythmic drug, and supraventricular tachycardia/atrial flutter with preexcitation. Furthermore, atrial flutter with 1:1 AVC via an accessory pathway is an uncommon presentation of Wolff‐Parkinson–White syndrome. We present a case of atrial flutter with 1:1 rapid AVC in the presence of Wolff–Parkinson–White syndrome. Physicians should be familiar with the rapid wide QRS complex ECG pattern associated with AFL with 1:1 AVC via an accessory pathway. Establishing the definitive diagnosis is essential for selecting an appropriate treatment strategy for improving outcomes.     

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.     

An approach to therapy of supraventricular tachyarrhythmias: An algorithm versus individualized therapy

Approaches to the treatment of supraventricular arrhythmias, including atrial fibrillation, atrial flutter, atrial tachycardia, atrioventricular (AV) reentrant tachycardia, and AV nodal reentrant tachycardia, continue to evolve. Within the past two decades, many new and effective treatments have become available. These include several new antiarrhythmic agents, ablative therapies, pacing and surgical modalities, and cardioversion/defibrillation techniques. This paper provides an algorithm for the treatment of these supraventricular arrhythmias which includes therapy for the acute episode as well as the prevention of subsequent episodes of the tachyarrhythmia.     

NASPE Plenary Lecture 2001. Catheter ablation: a personal perspective

Catheter ablation for control of cardiac arrhythmias was introduced 20 years ago. Since then, this technique has been applied successfully to virtually all cardiac rhythm disturbances. In this essay, some of the newer applications of ablative techniques for patients with AV nodal reentrant tachycardia, atrial flutter, and atrial fibrillation are emphasized. "AV nodal reentrant tachycardia" may involve a nodofascicular tract. A new classification of atrial flutter is proposed and various causes of atrial fibrillation are discussed.     

Incidence and clinical significance of inducible atrial tachycardia in patients with atrioventricular nodal reentrant tachycardia

INTRODUCTION: The purpose of this prospective study was to determine the prevalence and clinical significance of inducible atrial tachycardia in patients undergoing slow pathway ablation for AV nodal reentrant tachycardia who did not have clinically documented episodes of atrial tachycardia. METHODS AND RESULTS: Twenty-seven (15%) of 176 consecutive patients who underwent slow pathway ablation for AV nodal reentrant tachycardia were found to have inducible atrial tachycardia with a mean cycle length of 351+/-95 msec. The atrial tachycardia was sustained in 7 (26%) of 27 patients and was isoproterenol dependent in 20 patients (74%). The atrial tachycardia was not ablated or treated with medications, and the patients were followed for 9.7+/-5.8 months. Six (22%) of the 27 patients experienced recurrent palpitations during follow-up. In one patient each, the palpitations were found to be due to sustained atrial tachycardia, nonsustained atrial tachycardia, recurrence of AV nodal reentrant tachycardia, paroxysmal atrial fibrillation, sinus tachycardia, and frequent atrial premature depolarizations. Thus, only 2 (7%) of 27 patients with inducible atrial tachycardia later developed symptoms attributable to atrial tachycardia. CONCLUSION: Atrial tachycardia may be induced by atrial pacing in 15% of patients with AV nodal reentrant tachycardia. Because the vast majority of patients do not experience symptomatic atrial tachycardia during follow-up, treatment for atrial tachycardia should be deferred and limited to the occasional patient who later develops symptomatic atrial tachycardia.     

心房颤动伴预激综合征1例

患者,男,41岁,因持续心悸伴心动过速就诊。心电图示P波消失,心室率193次/min;QRS波的形态基本一致,但时限宽窄不一,可见最短的RR间距200ms。结合后期记录的窦性心电图及其QRS波起始部形态一致的特点,不难做出预激综合征合并心房颤动的诊断。     

An electrocardiographic criterion to detect AV dissociation in wide QRS tachyarrhythmias

A study was carried out on 12 patients with wide QRS tachycardia, 8 of whom presented with atrioventricular (AV) dissociation (Group A) and 4 with 1:1 AV association (Group B). This investigation aimed at assessing whether significant variations occurred in the QRS amplitude between the two groups. Group A showed more marked variations in QRS amplitude (31.7 +/- 13%) compared to Group B patients (6.2 +/- 1.2%) (p less than 0.001). The amplitude changes observed in Group A patients are probably related to variations in telediastolic volume resulting from the occasional contribution of the atrial systole. The findings suggest that variability in QRS amplitude during wide QRS tachyarrhythmias is a reliable sign of the presence of an AV dissociation. The possibility of diagnosing an AV dissociation on a surface ECG without visible P waves is an important finding, which though not pathognomonic of ventricular tachycardia, is a valid ECG criterion for assessing the ventricular origin of arrhythmias. This ECG criterion can be usefully applied in clinical practice along with others already used for the differential diagnosis of wide QRS tachyarrhythmias.     

Proarrhythmic effects of the new antiarrhythmic agent flecainide acetate

Flecainide acetate, a new potent class I antiarrhythmic agent, was given to 152 patients (46 orally and 106 intravenously) over a period of 22 months. Seven patients developed proarrhythmic effects. The only conduction abnormalities induced were PR interval prolongation and QRS complex widening, and no patient developed significant sinus bradyarrhythmias; patients with known serious abnormalities of impulse generation or conduction were excluded from this study. Five patients developed ventricular tachycardia or ventricular fibrillation of whom only three had preexisting ventricular arrhythmias. QT and QT_c interval prolongation was observed but was due to QRS complex widening rather than to an increase in the JT interval. A patient with the Wolff-Parkinson-White syndrome had an inducible orthodromic atrioventricular (AV) tachycardia prior to flecainide, but only an antidromic tachycardia was induced after the drug. In one patient flecainide administration resulted in an increase of atrial flutter cycle length which resulted in development of 1:1 AV conduction and overall faster ventricular rate. Two patients who developed ventricular arrhythmias were taking other antiarrhythmic agents, and in this series proarrhythmic effects occurred with both normal and high flecainide concentrations.