12-Kanal-Elektrokardiogramm

The surface electrocardiogram (ECG) is an important diagnostic tool for the diagnosis of arrhythmias and acute coronary syndrome. Supraventricular tachycardias (SVT) are paroxysmal tachycardias as are sinus tachycardia, atrial tachycardia, AV nodal reentry tachycardia, and tachycardia due to accessory pathways. All SVT are characterized by a ventricular heart rate >100/min and small QRS complexes (QRS width <0.12 s) during tachycardia. It is important to analyze the relation between P wave and QRS complex to look for an electrical alternans as a leading finding for an accessory pathway. Wide QRS complex tachycardias (QRS width ≥ 0.12 s) occur in SVT with aberrant conduction and SVT with bundle branch block or ventricular tachycardia (VT). In broad complex tachycardias, AV dissociation, negative or positive concordant pattern in V₁–V₆, a notch in V₁ and QR complexes in V₆ in tachycardias with left bundle branch block morphologies are findings indicating VT. In addition, an R/S relation <1 in V₆ favors VT when right bundle branch block tachycardia morphologies are present. By analyzing the surface ECG in the right way with a systematic approach, the specificity and sensitivity of correctly identifying a SVT or VT can be raised by >95%. The 12-lead surface ECG allows the coronary culprit lesion to be located in 97% due to determination of the 12-lead ST segment deviation score.     

Differenzialdiagnostik und Therapie tachykarder Herzrhythmusstörungen

The 12-channel surface electrocardiogram (ECG) is an important diagnostic tool for diagnosis of arrhythmias and acute coronary syndrome. Supraventricular tachycardia (SVT) is a paroxysmal tachycardia as are sinus tachycardia, atrial tachycardia, atrioventricular (AV) nodal reentry tachycardia and tachycardia due to accessory pathways. All SVTs are characterized by a ventricular heart rate >?100 beats/min and small QRS complexes (QRS width <?0.12 s) during tachycardia. It is important to analyze the relation between p-wave and QRS complex, to look for an electric alternans as a main finding for an accessory pathway. Wide QRS complex tachycardia (QRS width ≥?0.12 s) occurs in SVT with aberrant conduction, SVT with bundle branch block or ventricular tachycardia (VT). In broad complex tachycardia, AV dissociation, negative or positive concordant patterns in V1–V6, a notch in V1 and qR complexes in V6 in tachycardia with left bundle branch block morphology, are findings indicating VT. In addition, an R/S relation <?1 in V6 favors VT when right bundle branch block tachycardia morphologies are present. By analyzing the surface ECG in the correct way with a systematic approach, the specificity and sensitivity of correctly identifying SVT or VT can be raised to >?95?%. Therapy of tachycardia is possible with few antiarrhythmic drugs (concept of the 5As), beta-blocking agents, cardioversion and defibrillation. Using these approaches termination of tachycardia is possible in the majority of cases with high success rates.     

Regelm??ige Tachykardien mit breitem Kammerkomplex

Differential diagnosis of regular tachycardia with broad QRS complex can be challenging in daily practice. There are four different arrhythmias that have to be taken into account when being confronted with a broad QRS complex tachycardia: (1) ventricular tachycardia (VT); (2) supraventricular tachycardia (SVT) with bundle branch block (BBB); (3) SVT with AV conduction over an accessory AV pathway; (4) paced ventricular rhythm. Due to potentially fatal consequences, the correct diagnosis is important in view of both the acute treatment and the long-term therapy. Since SVT with accessory conduction is rare and a paced ventricular rhythm can be identified easily by stimulation artifacts, in most cases, a VT has to be differentiated from an SVT with BBB. Several ECG criteria can be helpful: (1) QRS complex duration > 140 ms in right BBB tachycardia or > 160 ms in left BBB tachycardia; (2) ventricular fusion beats; (3)“Northwest” QRS axis; (4) ventriculoatrial dissociation; (5) absence of an RS complex or RS interval > 100 ms in leads V₁-V₆; (6) a positive or negative concordant R wave progression pattern in leads V₁-V₆; (7) absence of an initial R wave or an S wave in lead V₁ in right BBB tachycardia; (8) absence of an R wave or an R/S ratio < 1 in lead V₆ in right BBB tachycardia; (9) absence or delay of the initial negative forces in lead V₁ in left BBB pattern (R wave duration > 30 ms in V₁; interval between onset of R wave and Nadir of S wave > 60 ms in V₁); (10) presence of Q wave. Any of these variables favor VT. However, none of the criteria has both a sufficient sensitivity and specificity when utilized on its own. Therefore, various diagnostic algorithms have been proposed using a number of the above criteria consecutively. By doing so, the specificity and sensitivity of correctly identifying a VT or an SVT with BBB can be raised to > 95%.     

Diagnostic Clues From the Surfaee ECG to Identify Idiopathic (Fascicular) Ventricular Tachycardia: Correlation with Electrophysiologic Findings

ECG in Idiopathic Fascicular VT. Introduction : An RS interval > 100 msec in precordial leads has been recently described for the diagnosis of ventricular tachycardia (VT). The aim of this study was to assess the value of this criterion when applied to patients with right bundle branch block pattern, left-axis deviation (fascicular) VT sensitive to verapamil.
Methods and Results : Eleven patients (mean age 31 ± 11 years; range 16 to 51) had a mean heart rate of 164 ± 37 beats/min (range 107 to 230) during VT, The QRS complex axis was -92°± -15° (range -80 to -115). The mean QRS duration was 121 ± 9 msec (range 105 to 140). The mean RS interval was 67 ± 9 msec (range 60 to 80). Fusion beats were present in 2 patients (18%), and AV dissociation confirmed by electrophysiologic study was found on ECG in 8 (73%) of 11. During tachycardia, the QRS-H'interval was 19 ± 10 msec (range 10 to 30) in 6 of 11 patients. In seven patients, a fast, unique (or double) presystolic potential lasting 32 msec (range 12 to 40) occurring before the onset of the QRS complex was found at the site of origin of VT, localized in the inferior apical left ventricular septum. In all cases, VT was successfully treated by catheter ablation.
Conclusion : A wide QRS complex tachycardia with right bundle branch block and left-axis deviation sensitive to verapamil observed in a young patient without structural heart disease should not be confused with supraventricular tachycardia with aberrancy but rather suggests the presence of fascicular VT. As opposed to VT associated with structural heart disease, the RS interval is < 80 msec in all precordial leads in all cases. Independent of this parameter, AV dissociation detectable on surface ECG has a sensitivity of 73%, which increases to 82% in the presence of fusion beats.     

Functional Bundle Branch Block as a Delayed Manifestation of Retrograde Concealment in the His-Purkinje System

Delayed Manifestation of Retrograde HPS Concealment. Introduction: The mechanism of functional bundle branch block induced at the onset of supraventricular tachycardia (SVT) is well established. However, no data exist to address the underlying mechanism of functional bundle branch block occurring in the second beat of SVT, when the first beat is conducted with a narrow QRS morphology and preceded by ventricular stimulation. Methods and Results: Two patients showing such a phenomenon form the basis of this report. Patient 1 with AV nodal reentrant tachycardia of the common variety persistently demonstrated functional right bundle branch block in the second SVT complex when a short train of ventricular pacing was introduced during SVT. This occurred without any discernible change in the SVT cycle length. Patient 2 bad a manifest posteroseptal accessory pathway and inducible orthodromic reentrant tachycardia. Functional bundle branch block during propagation of the second SVT complex invariably occurred either in the left bundle when SVT was induced by a bundle branch reentrant complex during premature ventricular stimulation, or in the right bundle when SVT was induced with a short train of ventricular pacing. The development of functional bundle branch block was preceded by minimal or no cycle length variations in the His-bundle inputs. Conclusion: These observations suggest that the type of functional bundle branch block occurring in the second SVT complex as a de novo phenomenon may be related to the relative timing of the retrograde penetration of the right versus left bundle during ventricular pacing or bundle branch reentrant complex. Therefore, due to its longest cycle length of activation and refractoriness, the earliest site of retrograde penetration is the most likely site of functional block during propagation of the second SVT complex. This delayed manifestation of retrograde concealment may provide new information regarding the electrophysiologic behavior of the His-Purkinje system.     

Transitory or permanent regular wide QRS complex tachycardia induced by atrial stimulation in patients without apparent heart disease. Significance

Objectives. - The purpose of the study was to evaluate the frequency of transitory or permanent bundle branch block (BBB) associated with a paroxysmal tachycardia induced by atrial stimulation in patients without heart disease and its significance.Methods. - Esophageal atrial stimulation was performed in 447 patients suspected to have supraventricular tachycardias (SVT). Sustained regular tachycardia was induced in all of them but three, either in control state (75%) or after administering isoproterenol. In 346 patients, only narrow complex SVTs were induced (77%); in 259 of them, the reentry occurred in the AV node and in remaining patients within a concealed accessory pathway. In 62 patients, a transitory functional BBB was recorded at the onset of the tachycardia (14%). In 33 of them, the reentry occurred in the AV node and in the remaining 29 patients within a concealed accessory pathway. In 36 patients (8%), a permanently wide QRS complex tachycardia was induced. Three patients had also inducible narrow complex SVT. Atrial pacing induced a BBB similar to the aberrancy in tachycardia in 22 patients: the reentry occurred in the AV node in 17 patients, within a concealed accessory pathway in three patients and in a Mahaim bundle in two patients. In other patients, QRS complex remained normal during atrial pacing: all 14 patients had a ventricular tachycardia (VT), either a verapamil-sensitive VT (n = 7) or catecholamine-sensitive VT (n = 4) or bundle branch reentry (n = 3). Followed from 2 to 12 years, the prognosis of these patients was excellent.Conclusion. - Transitory BBB at the onset of an SVT is noted in 14% of the population, is more frequent in patients with accessory pathway reentrant tachycardia, but is helpful for this diagnosis in only 12% of cases. A regular tachycardia with permanent left or right bundle branch morphology induced by atrial stimulation in a patient without heart disease and without BBB during atrial pacing is due to a VT even if this patient has also narrow complex tachycardias. This mechanism does not affect the excellent prognosis of this population.     

Value of preexisting bundle branch block in the electrocardiographic differentiation of supraventricular from ventricular origin of wide QRS tachycardia

The relation between the morphologic configuration of QRS complexes during wide QRS tachycardia induced during electrophysiologic studies and sinus rhythm was examined in 18 patients who had preexisting left or right bundle branch block. Representative QRS complexes during sinus rhythm and during tachycardia were isolated from each patient and juxtaposed for comparison. The QRS complexes that constituted each pair were judged by 4 observers as being identical, different or, if the decision was equivocal, similar. Nine patients had supraventricular tachycardia (SVT). In 8 of the 9 patients, all 4 observers found the QRS complexes during sinus rhythm and SVT identical in morphologic configuration. In the other patient, 2 observers found the QRS complexes identical and 2 found them similar. In 12 patients ventricular tachycardia (VT) was induced. In 11 of these 12, all 4 observers found the QRS complexes during VT different from their respective sinus beats. In the other patient, 3 observers found the QRS complexes different, whereas the fourth found them similar. During SVT, the QRS duration was unchanged from the corresponding value during sinus rhythm, whereas in patients with VT, QRS width increased by a mean of 56 +/- 20 ms (p less than 0.001). The results of our study suggest that the electrocardiographic differentiation of wide QRS tachycardia in patients with preexisting bundle branch block can be accomplished easily and accurately by comparing the QRS complexes during tachycardia with those during sinus rhythm: If the complexes are identical, the tachycardia is supraventricular, but if they are different, the arrhythmia is ventricular in origin.     

Electrophysiologic characteristics of ventricular extrastimulation-induced dissipation of functional bundle branch block associated with supraventricular tachycardia

INTRODUCTION: Linking-related anterograde functional bundle branch block during supraventricular tachycardia (SVT) is due to repetitive concealed retrograde conduction of impulses from the contralateral bundle branch and can be eliminated by a critically timed premature ventricular beat (PVB). We assessed the electrophysiologic characteristics of PVB-induced dissipation of functional bundle branch block during SVT. METHODS AND RESULTS: During SVT with functional bundle branch block, PVB was delivered from the right ventricular apex, scanning the tachycardia cycle length (CL) with 10-msec decrements in the coupling interval in 14 patients (3 AV nodal reentrant tachycardia and 11 orthodromic AV reciprocating tachycardia). Dissipation was achieved in group 1: functional right bundle branch block (RBBB) in 4, functional left bundle branch block (LBBB) in 4, and both functional RBBB and LBBB in 1 with a dissipation zone occupying 4% to 13% (mean 8.5%) of the tachycardia CL. The outer limits were 22+/-16 msec and 68+/-14 msec < tachycardia CL; the inner limits were 56+/-18 msec and 90+/-24 msec < tachycardia CL for RBBB and LBBB, respectively (both P < 0.05). Dissipation could not be achieved in group 2 (4 RBBB and 1 LBBB) due to CL-dependent bundle branch block and/or local ventricular refractoriness. CONCLUSION: During SVT, functional bundle branch block due to "linking" often can be dissipated by timely PVB delivered from the right ventricular apex within a narrow zone of the tachycardia CL. Our findings suggest that the dissipation zone is affected by the pattern of functional bundle branch block relative to the site of PVB delivery.     

Ventricular tachycardia induced by atrial stimulation in patients without symptomatic cardiac disease

Ten patients with an unusual form of ventricular tachycardia (VT) are described. All were young (mean age 21 years) at the onset of VT, symptoms were of long duration (mean 7 years), none had symptomatic organic heart disease, VT was induced by atrial and ventricular stimulation, VT had a characteristic QRS morphologic picture resembling right bundle branch block with left-axis deviation and 9 had early retrograde His deflections during VT. Supraventricular tachycardia (SVT) was excluded in every patient by electrophysiologic study, although QRS morphologic characteristics and clinical stability of these patients during tachycardia frequently led to the diagnosis of SVT before referral. Four patients received verapamil during electrophysiologic testing. Verapamil slowed and terminated VT in all. Three patients are being treated chronically with oral verapamil, 3 patients with conventional antiarrhythmic agents and 1 with a radiofrequency ventricular pacemaker.     

Conventional Electrocardiogram in Arrhythmogenic Right Ventricular Dysplasia-Cardiomyopathy and Idiopathic Right Ventricular Outflow Tract Tachycardia

Objective: Arrhythmogenic right ventricular dysplasia up to now is a rare cardiomyopathic entity with certain difficulties in clinical definition of diagnostic criteria. In 42 patients with major and minor criteria of arrhythmogenic right ventricular dysplasia and 25 patients with idiopathic ventricular arrhythmia, the role of conventional ECG in the diagnosis of arrhythmogenic right ventricular dysplasia was reevaluated. Methods: In standard 12-lead ECG, QRS duration was measured in limb lead D₁, and in V₁-V₆. A ratio of the sum of right (V₂+ V₃) and left (V₄+ V₅) was calculated. T wave inversions, Epsilon wave, and mechanisms of advancing right bundle branch block were analyzed. Results: In 39 out of 42 patients (93%) with the diagnosis of arrhythmogenic right ventricular dysplasia, a ratio of right and left precordial QRS duration of >1.2, a maximum right precordial QRS duration of > 100 ms in 10 cases (26%) and >110 ms in 29 cases (74%) could be found. Incomplete right bundle branch block with right precordial T inversions was found in one case. The ECG in two patients revealed a precordial R/S transition in V₁ or V₂; in all other cases, R/S transition was localized in V₃ or V₄. R peak time was normal (< 0.04 s) in all cases, a “notching” or “slurring” of the S wave was striking in 16 cases. T wave inversions were found in 27 cases and definite Epsilon wave in only one case. Although incomplete right bundle branch block and certain preforms could also be disclosed in four patients with idiopathic right ventricular outflow tract (RVOT) tachycardia, localized right precordial QRS prolongation could be excluded in all but one of these cases. Localized right precordial QRS duration prolongation in one case was probably due to a rotation of the heart with a precordial R/S transition between V₁ and V₂. Conclusion: Localized right precordial QRS prolongation in a normal precordial R/S transition: (a) seems to be the most important aspect of arrhythmogenic right ventricular dysplasia at conventional ECG, with a sensitivity of 93% and a specificity of 96% in order to distinguish idiopathic RVOT tachycardia; (b) can appear with (64%) or without (36%) secondary T wave inversions; and (c) is due to a “parietal” block sparing the specialized conducting system.     

QRS Alternans with 2:1 Atrioventricular Conduction Block: What Is the Mechanism?

An 81‐year‐old woman was admitted for symptomatic bradycardia. On admission, the ECG exhibited QRS alternans, narrow QRS complex and left bundle branch block with 2:1 AV block. The patient soon had complete AV block and underwent a pacemaker implantation. An appropriate mechanism for explaining those ECG findings might be 4:1 conduction over the left bundle branch and 2:1 conduction over the right bundle branch. An ECG pattern exhibiting QRS alternans with a narrow QRS complex and bundle branch block with 2:1 AV block may suggest the coexistence of both bundle branch blocks and a high risk of complete AV block.     

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     

Electrocardiogram during tachycardia in patients with anterograde conduction over a Mahaim fiber: old criteria revisited.

OBJECTIVES: The aim of this study was to prospectively evaluate the sensitivity, specificity, and positive and negative predictive values of previously described ECG criteria to identify preexcited tachycardia due to decrementally conducting accessory pathways (QRS axis between 0 and -75 degrees , QRS width < or = 0.15 seconds, an R wave in lead I, an rS pattern in lead V(1), RS > 1 QRS transition > V(4), and cycle length between 220 and 450 ms). BACKGROUND: Preexcited tachycardia associated with decrementally conducting right-sided accessory pathways usually shows a rather "narrow" QRS complex and can be difficult to differentiate from supraventricular tachycardia (SVT) with left bundle branch block (LBBB) aberrant conduction. METHODS: We analyzed three groups of patients: 32 patients with an atriofascicular pathway (group I); 8 patients with long (n = 3) or short (n = 5) decrementally conducting right-sided AV pathway (group II); and a control group that consisted of 35 patients with SVT and LBBB (group III). RESULTS: Presence of all six criteria had 87.5% sensitivity in group I and a 0% sensitivity in group II. There were four false negatives in group I. The negative predictive value was 82.5%, with six false positives in group III (five patients with an aberrant LBBB-shaped tachycardia with ventriculoatrial conduction over an accessory AV pathway). The criterion cycle length was not helpful. CONCLUSIONS: Criteria for identifying a tachycardia with anterograde conduction over a Mahaim fiber are helpful only in atriofascicular pathways, with a sensitivity of 87.5% and a negative predictive value of 82.5%. The major cause of false positives was a tachycardia with aberrant LBBB conduction and ventriculoatrial conduction over an accessory AV pathway.     

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。     

Are wide complex tachycardia algorithms applicable in children and patients with congenital heart disease?

Introduction

Several algorithms have been developed to help determine the etiology of wide complex tachycardias (WCTs) in adults. Sensitivity and specificity for differentiating supraventricular tachycardia (SVT) with aberration from ventricular tachycardia (VT) in adults have been demonstrated to be as high as 98% and 97%. These algorithms have not been tested in the pediatric population. We hypothesize that these algorithms have lower diagnostic accuracy in children and patients with congenital heart disease.

Methods

A retrospective review of the pediatric electrophysiology database at Stanford from 2001 to 2008 was performed. All children with WCT, a 12-lead electrocardiogram (ECG) available for review, and an electrophysiology study confirming the etiology of the rhythm were included. Patients with a paced rhythm were excluded. The ECGs were analyzed by 2 electrophysiologists blinded to the diagnosis according to the algorithms described in Brugada et al,² and Vereckei et al.⁵ Additional ECG findings were recorded by each electrophysiologist.

Results

A total of 65 WCT ECGs in 58 patients were identified. Supraventricular tachycardia was noted in 62% (40/65) and VT in 38% (25/65) of the ECGs. The mean age was 13.5 years (SD ± 5.1), the mean weight was 51.8 kg (SD ± 22.4), and 48% (31/65) were male. The mean tachycardia cycle length was 340 milliseconds (SD ± 95). Congenital heart disease (CHD) was present in 37% (24/65) of patients (7 tetralogy of Fallot, 6 Ebstein's, 4 double-outlet right ventricle, 3 complex CHD, 2 d-transposition of great arteries, 1 status-post orthotopic heart transplantation, 1 ventricular septal defect). The Brugada algorithm correctly predicted the diagnosis 69% (45/65) of the time, the Vereckei algorithm correctly predicted the diagnosis 66% (43/65) of the time, and the blinded reviewer correctly predicted the diagnosis 78% (51/65) of the time. There was no difference in the efficacy of the algorithms in patients with CHD vs those with structurally normal hearts. The findings of left superior axis deviation (P < .01) and a notch in the QRS downstroke of V₁ or V₂ (P < .01) were more common in VT than SVT, whereas a positive QRS deflection in V₁ (P = .03) was more commonly present in SVT than VT.

Conclusion

The Brugada and Vereckei algorithms have lower diagnostic accuracy in the pediatric population and in patients with congenital heart disease than in the adult population. Left superior axis deviation and a notch in the QRS downstroke were more commonly associated with VT, whereas a positive QRS deflection in V₁ was more commonly associated with SVT in this population.     

Application of a new algorithm in the differential diagnosis of wide QRS complex tachycardia.

AIMS: The Brugada criteria proposed to distinguish between regular, monomorphic wide QRS complex tachycardias (WCT) caused by supraventricular (SVT) and ventricular tachycardia (VT) have been reported to have a better sensitivity and specificity than the traditional criteria. By incorporating two new criteria, a new, simplified algorithm was devised and compared with the Brugada criteria. METHODS AND RESULTS: A total of 453 WCTs (331 VTs, 105 SVTs, 17 pre-excited tachycardias) from 287 consecutive patients with a proven electrophysiological (EP) diagnosis were prospectively analysed by two of the authors blinded to the EP diagnosis. The following criteria were analysed: (i) presence of AV dissociation; (ii) presence of an initial R wave in lead aVR; (iii) whether the morphology of the WCT correspond to bundle branch or fascicular block; (iv) estimation of initial (v(i)) and terminal (v(t)) ventricular activation velocity ratio (v(i)/v(t)) by measuring the voltage change on the ECG tracing during the initial 40 ms (v(i)) and the terminal 40 ms (v(t)) of the same bi- or multiphasic QRS complex. A v(i)/v(t) >1 was suggestive of SVT and a v(i)/v(t) 相似文献   

Arrhythmogenic effect of ajmaline on the atrial level

The aim of this study was to determine whether an antiarrhythmic, Ajmaline, could have proarrhythmic effects on the atrium and to compare the results with those of other antiarrhythmic drugs. A total of 1950 patients without cardiac failure or recent (less than 6 weeks) myocardial infarction were given 1 mg/kg of Ajmaline intravenously during electrophysiological investigation. A proarrhythmic effect was defined as the occurrence of supraventricular tachycardia (SVT) in a patient without this arrhythmia before the test or the facilitation of its induction. Fifty five patients developed SVT (mainly atrial tachyarrhythmias: 48 cases, and some junctional tachycardia: 7 cases) which occurred spontaneously in 22 patients and during fixed atrial pacing in 33 patients. Fifteen patients developed ventricular tachycardia (VT). The predisposing factors for the development of SVT were: a previous history suggesting spontaneous SVT (28 patients; 51 p. 100); sinoatrial block (14 patients--the only abnormality in 10 cases). Seventeen patients had none of these factors but 8 had known cardiac pathology and the other 9 were relatively elderly patients (79 years). Twelve of the patients developing VT had known cardiac disease, bundle branch block in 12 cases and previous VT in 6 cases. In conclusion, proarrhythmic effects of Ajmaline are infrequent if its contraindications are respected, but they do exist at both atrial (2.8 p. 100) and ventricular levels (0.8 p. 100): the risk factors are comparable: previous spontaneous arrhythmias or ECG changes (SA block at the atrial and bundle branch block at the ventricular level).     

Wide complex tachycardias. Differential diagnosis and management.

The majority of wide complex tachycardias are secondary to VT. The differential diagnosis of wide complex tachycardia also includes SVT with aberrancy or underlying bundle branch block and antegrade SVT conduction over an accessory pathway (antidromic SVT). VT is usually the result of reentry and most commonly arises in an area of diseased myocardium in the setting of previous myocardial infarction or cardiomyopathy. VT, however, can also occur in patients with structurally normal hearts. Criteria useful in diagnosis of wide complex tachycardia include clinical criteria (presence of structural heart disease or a history of previous myocardial infarction) and electrocardiographic criteria (the presence of capture or fusion beats, relation of atrial or ventricular activity, QRS duration and axis, and morphology). The acute management of wide complex tachycardia includes cardioversion and intravenous pharmacologic therapy. Almost all patients with VT require chronic therapy, although in rare patients treatment of acute precipitating factors may be sufficient. While pharmacologic therapy has been the mainstay of treatment for these patients, there have been many exciting advances using surgical, device, and ablative therapies.     

Wolff-Parkinson-White syndrome in children: electrophysiologic and pharmacologic characteristics.

Intracardiac electrophysiologic studies were performed on 28 infants and children, ages 1 month to 18 years, with the Wolff-Parkinson-White syndrome to try to determine 1) the electrophysiologic characteristics of the accessory connection and 2) the mechanisms of associated supraventricular dysrhythmias. Although the antegrade refractory periods of the normal conduction system were shorter than those found in adults, those of the accessory connection were slightly longer. Reciprocating supraventricular tachycardia (SVT), which had been a clinical problem in 26 of 28, could be induced in the laboratory in all 26 subjects. The mechanism involved reentry with antegrade conduction through the atrioventricular (AV) node and retrograde through the accessory connection in 22. Eleven of these 22 had a wide QRS during tachycardia due to a bundle branch block. Three other subjects had wide QRS tachycardia, but the mechanism involved antegrade conduction through the accessory connection and retrograde through the AV node. The other patient had AV node reentry tachycardia. Two patients did not have clinical SVT, and in these two, SVT could not be induced. Neither patient had retrograde conduction through the accessory connection. The site of the accessory connection could be identified in 26 subjects by the sequence of retrograde activation of the atrium during SVT or ventricular pacing. Digitalis shortened the refractory period of the accessory connection in five of the eight patients studied.     

Intermittent bundle branch blocks in a patient with uncommon-type atrioventricular nodal reentrant tachycardia and enhanced atrioventricular nodal conduction

We report on a patient with uncommon-type atrioventricular (AV) nodal reentrant tachycardia with a short tachycardia cycle length (235-270 ms), in whom transient wide QRS tachycardia with both left bundle branch block and right bundle branch block aberrancy were followed by narrow QRS complexes. In addition, His-ventricular (H-V) block and a sudden prolongation of the H-V interval occurred during the tachycardia. As the determinant of these unusual findings, the possibility that the anterograde limb of the reentry circuit has an enhanced AV nodal conduction property is discussed, as is the clinical significance of this type of tachycardia.