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This is a 26-year-old male, with no known congenital or other cardiovascular disease in the family. No known cases of premature (

In 37 (70%) of 53 patients with idiopathic ventricular tachycardia (VT), episodes were mainly related to exercise (group 1). These patients were younger (33 +/- 14 vs 44 +/- 18 years, p = 0.015) and more often had dizziness during VT (71 vs 40%, p = 0.003) than the 16 patients in whom VT was not exercise-related (group 2). Patients in group 1 needed cardioversion less often to terminate the arrhythmia (4 (11%) vs 6 (40%), group 2 [p = 0.04]). VT was initiated during exercise testing in 62% of patients in group 1 but in only 1 patient in group 2 (p = 0.0004). Induction of clinical VT during programmed stimulation was observed in a similar percentage in group 1 (49%) and group 2 (50%) patients. Isoproterenol infusion facilitated the induction of VT in 9 of 20 (45%) group 1 and in 2 of 8 (25%) group 2 patients (p = not significant). After a mean follow-up of 2.9 +/- 2.5 years, 8 (22%) group 1 patients and 5 (31%) group 2 had at least 1 episode of symptomatic VT. Only 1 patient died suddenly. Class III drugs were the most useful in preventing recurrences. Beta-blocking agents were of little value in both groups. Patients with VT and a structurally normal heart have a good prognosis despite recurrences of their arrhythmia. The relation of the arrhythmia to exercise has no prognostic implications.

In some patients with atrial fibrillation, atrial flutter develops after administration of class IC antiarrhythmic drugs, the so-called class IC atrial flutter. Radiofrequency ablation of the right atrial isthmus results in clinical improvement in 85% of patients and provides an alternative management strategy for a subset of patients with therapy-resistant atrial fibrillation.

This case report describes about a young, male patient with persisting syncope during physical therapy for complex regional pain syndrome type 1 after metatarsal fractures. The patient was referred to the Emergency Department, where Brugada syndrome was diagnosed. A cardioverter defibrillator was prophylactically implanted successfully. After this procedure, there were no contraindications for resuming further physical therapy for his painful foot. No clear causal inference with Brugada could be drawn from the complex regional pain syndrome type 1 or physical therapy described in this case report. Hyperthermia may, however, occur during such therapy, which is associated with dysrhythmia in general.

Antidromic circus movement tachycardia was documented in 36 of 345 consecutive patients with Wolff-Parkinson-White syndrome undergoing detailed electrophysiologic evaluation. Twenty-six patients were men and 10 were women (mean age +/- standard deviation 26 +/- 12 years [range 12 to 45]). Multiple accessory pathways were identified in 12 of these 36 patients (33%). Ten of the patients (67%) with clinically documented antidromic tachycardia had multiple accessory pathways. Dizziness and syncope occurred in 61 and 50% of patients with antidromic circus movement tachycardia. Six patients had clinical documentation of atrial fibrillation, and 4 patients (11%) were resuscitated from ventricular fibrillation. In the 36 patients, 56 distinct antidromic tachycardias were recorded and several different pathways were observed. Orthodromic tachycardia was the most frequently associated arrhythmia (72%). Dual atrioventricular nodal pathways were present in 12 patients (33%); however, atrioventricular nodal tachycardia could be initiated in only 2 of them. Interruption of the accessory pathway was successfully performed in all 20 patients undergoing surgery.

Seven of 17 patients with incessant supraventricular tachycardia caused by an accessory pathway with a long retrograde conduction time were seen with symptoms or echocardiographic signs of a tachycardia-induced cardiomyopathy. Three patients were in New York Heart Association functional class II with dyspnea and four were in class III. Eight patients (six with tachycardia-induced cardiomyopathy) underwent surgery because of failure of medical treatment (including one patient in functional class I) and one underwent direct current catheter ablation of the atrioventricular (AV) node. In six patients echocardiograms recorded before and after the procedure were available. Before surgery or direct current ablation the mean left ventricular ejection fraction was 36.3 +/- 8.7%, the left ventricular end-diastolic diameter 55.7 +/- 7.6 mm and the left ventricular end-systolic diameter 44.3 +/- 7.8 mm. A mean of 21.6 +/- 6.8 months after the procedure the mean left ventricular ejection fraction increased to 58.6 +/- 8.0%, the left ventricular end-diastolic diameter decreased to 49.0 +/- 3.6 mm and the left ventricular end-systolic diameter decreased to 32.2 +/- 2.7 mm; all six patients were in functional class I. These results confirm that control of incessant tachycardia leads to a regression of symptoms and signs of cardiomyopathy and progressive normalization of the dimensions of the heart. Because of these findings, surgery should be considered early in patients with an accessory AV pathway and incessant tachycardia. The presence of a tachycardia-induced cardiomyopathy should therefore be an indication for surgery rather than a contraindication.

The 12 lead electrocardiographic (ECG) findings were reviewed in 17 patients having two or more accessory pathways as documented during electrophysiologic study in all 17 patients and by intraoperative mapping in 8.Twelve patients had findings suggesting the presence of more than one atrioventricular (AV) pathway. These were 1) more than one P wave configuration during orthodromic circus movement tachycardia (four patients); 2) a “mismatch” between the location of the ventricular and atrial ends of the accessory pathway as assessed when comparing exclusive AV and ventriculoatrial conduction over the accessory pathway during antidromic and orthodromic circus movement tachycardia, respectively (seven patients); 3) atrial fibrillation showing more than one pre-excitation pattern (six patients); 4) a spontaneous change from orthodromic to antidromic circus movement tachycardia and vice versa (two patients); 5) a spontaneous change from one type of antidromic tachycardia to another (two patients); and 6) a change in pre-excitation pattern after administration of a drug that prolongs the anterograde refractory period of the accessory pathway (three patients).The retrospective nature of this study does not allow conclusions as to the true value of the ECG in predicting the presence of more than one accessory pathway. This issue needs to be evaluated in a prospective study.

Of the accessory pathways, partially or totally bypassing the atrio-ventricular conduction system, the bundle of Kent is the most common type. The electrocardiographic (ECG) expression of preexcitation depends upon the contribution of the activation fronts over the AV node and the accessory pathway. From the polarity of the delta wave in the surface ECG and from the behavior during electrophysiologic study, the location of the accessory pathway can be derived. The presence of an accessory pathway may induce circus movement tachycardia and, in case of atrial fibrillation, high ventricular rates possibly leading to sudden death. Noninvasive techniques are able to identify the patient at high risk. Treatment modalities are pharmacologic or surgical, whereas ablation techniques are still under investigation.

In a population of 690 patients with Wolff-Parkinson-White (WPW) syndrome referred to our hospital from January 1979 to February 1995, 15 patients (2.2%) had an aborted sudden death out of the hospital. This retrospective study examines their clinical and electrophysiologic characteristics. Gender, accessory pathway localization, and presence of multiple accessory pathways were compared between patients with and without spontaneous ventricular fibrillation (VF). Whereas gender and the presence of multiple accessory pathways did not significantly differ between both groups, septally located pathways occurred significantly more often in the VF group. In patients with aborted sudden death, spontaneous VF was found significantly more often in men (13 of 15). VF was the first manifestation of the WPW syndrome in 8 patients. The remaining 7 patients had documented episodes of atrial fibrillation, circus movement tachycardia, or both (n = 2). Ten of the 15 patients were exercising or under emotional stress at the time of aborted sudden death. Only 1 patient had 2 accessory pathways. The location of the accessory pathway was septal (midseptal or posteroseptal) in 11 patients, left lateral in 4, and right lateral in 1).

The importance of correct positioning of the catheter during mapping and radio frequency (RF) ablation is evident. Coupling between the fluoroscopic image and the electrogram is necessary to document that position. The authors developed a method for the acquisition of the fluoroscopic image and the integration of this data into the electrophysiologic (EP) system. For this purpose the EP system, the personal computer electrophysiologic measurement system (PC-EMS) is extended with a videoframe grabber. To document the dynamics of the catheter position during the cardiac cycle the authors implemented the cine-loop presentation; 8 sequential captured frames are displayed in an infinite loop. The acquisition of the cine-loop images proceeds concurrently with the acquisition of a 2 seconds period of surface ECG and intracardiac traces. The traces are marked at the actual moment of the frame captures to relate the individual frames with the exact moment in the cardiac cycle. The combined data is archived on CD. >

Background — The goal of this study was to test the hypothesis that the occurrence of atrial fibrillation (AF), in at least some patients with coexisting type I atrial flutter (AFL), is based on macro-reentry around the tricuspid valve orifice, including the right atrial (RA) isthmus, by evaluation of the AF recurrences after successful ablation of AFL. Methods and results — Eighty-two consecutive patients with type I AFL, with or without concomitant AF, underwent radiofrequency ablation (RFA) of the RA isthmus by an anatomical approach. The results were analyzed in 4 groups of patients: group 1 (only AFL; 29 patients), group 2 (AFL > AF; 22 patients), group 3 (AF > AFL; 15 patients), and group 4 (developing AFL while receiving class IC antiarrhythmic drug therapy for AF, the ‘class IC atrial flutter’; 16 patients). In all groups, RFA of type I AFL was performed with a high (≥ 93%) procedural success rate. In group 1, only 2 patients (8%) had AF after (18 ± 14 months) AFL ablation. These figures were 38% (20 ± 14 months) and 86% (13 ± 8 months) in groups 2 and 3, respectively. Group 4 patients (4 ± 2 months) had a 73% freedom of AF recurrences with continuation of the class IC agent. Conclusions — The low incidence of new AF during long-term follow-up after RFA of type I AFL makes it unlikely that radiofrequency lesions promote the development of AF. The impact of isthmus ablation on AF recurrences differs according to the clinically predominant atrial arrhythmia and suggests a possible role of the RA isthmus in the occurrence of AF in some patients. Ablation of class IC atrial flutter in patients with therapy-resistant AF is a novel approach to management of this patient subset. Careful classification of AF patients plays a role in the selection of the site of ablation therapy (Circulation 99: 1441-1445, 1999).

Background —After radiofrequency (RF) ablation of atrial flutter (AFL), the demonstration of bidirectional isthmus conduction (BIC) block is considered the hallmark of a successful procedure. The purpose of our study was to test the persistence of BIC block after isoproterenol administration and to evaluate the importance of this finding with regard to AFL recurrences. Methods and Results —RF ablation of AFL was performed in 44 consecutive patients with type I AFL by linear ablation of the posterior isthmus (n=29 patients), septal isthmus (n=4 patients), or both right atrial (RA) isthmi (n=11 patients). The procedural end point was complete BIC block and noninducibility of AFL. In case of noninducibility and apparent BIC block, the pacing protocol was repeated under isoproterenol infusion (1 to 3 μg/min). Reversal of apparent BIC block occurred in 7 (15.9%) of 44 patients. Six patients had bidirectional and 1 had unidirectional resumption of isthmus conduction. Counterclockwise AFL could be reinduced in 4 of these patients. Two to 24 (median, 4) additional RF applications were required to achieve permanent BIC block. At a mean follow-up of 7.3±7.6 months (range, 2 to 31 months), 2 (4.5%) of 44 patients had AFL recurrences. Conclusions —Partial linear RF ablation could possibly aggravate preexisting nonuniform anisotropic conduction in the RA isthmus, resulting in profound conduction slowing and apparent BIC block. Isoproterenol can unmask apparent BIC block, thus providing an opportunity to assess the possibility of reversal of BIC block and completeness of isthmus ablation during the same procedure. The low incidence (4.5%) of AFL recurrences at follow-up suggests that noninducibility and BIC block under isoproterenol infusion may be a better end point for successful AFL ablation.

Background —In patients with atrial fibrillation, intracardiac atrial defibrillation causes discomfort. An easily applicable, short-acting analgesic and anxiolytic drug would increase acceptability of this new treatment mode. Methods and Results —In a double-blind, placebo-controlled manner, the effect of intranasal butorphanol, an opioid, was evaluated in 47 patients with the use of a step-up internal atrial defibrillation protocol (stage I). On request, additional butorphanol was administered and the step-up protocol continued (stage II). Thereafter, if necessary, patients were intravenously sedated (stage III). After each shock, the McGill Pain Questionnaire was used to obtain a sensory (S), affective (A), evaluative (E), and total (T) pain rating index (PRI) and a visual analogue scale analyzing pain (VAS-P) and fear (VAS-F). For every patient, the slope of each pain or fear parameter against the shock number was calculated and individual slopes were averaged for the placebo and butorphanol group. All patients were cardioverted at a mean threshold of 4.4±3.3 J. Comparing both patient groups for stage II, the mean slopes for PRI-T ( P =0.0099), PRI-S ( P =0.019), and PRI-E ( P =0.015) became significantly lower in the butorphanol group than in the placebo group. Comparing patients who received the same shock intensity ending stage I and going to stage II, in those patients randomized to placebo the mean VAS-P ( P =0.023), PRI-T ( P =0.029), PRI-S ( P =0.030), and PRI-E ( P =0.023) became significantly lower after butorphanol administration. Conclusions —During a step-up internal atrial defibrillation protocol, intranasal butorphanol decreased or stabilized the value of several pain variables and did not affect fear. Of the 3 qualitative components of pain, only the affective component was not influenced by butorphanol. The PRI evaluated pain more accurately than the VAS.

Background —The goal of this study was to test the hypothesis that the occurrence of atrial fibrillation (AF), in at least some patients with coexisting type I atrial flutter (AFL), is based on macro-reentry around the tricuspid valve orifice, including the right atrial (RA) isthmus, by evaluation of AF recurrences after successful ablation of AFL. Methods and Results —Eighty-two consecutive patients with type I AFL, with or without concomitant AF, underwent radiofrequency ablation (RFA) of the RA isthmus by an anatomical approach. The results were analyzed in 4 groups of patients: group 1 (only AFL; 29 patients), group 2 (AFL >AF; 22 patients), group 3 (AF >AFL; 15 patients), and group 4 (developing AFL while receiving class IC antiarrhythmic drug therapy for AF, the “class IC atrial flutter”; 16 patients). In all groups, RFA of type I AFL was performed with a high (≥93%) procedural success rate. In group 1, only 2 patients (8%) had AF after (18±14 months) AFL ablation. These figures were 38% (20±14 months) and 86% (13±8 months) in groups 2 and 3, respectively. Group 4 patients (4±2 months) had a 73% freedom of AF recurrences with continuation of the class IC agent. Conclusions —The low incidence of new AF during long-term follow-up after RFA of type I AFL makes it unlikely that radiofrequency lesions promote the development of AF. The impact of isthmus ablation on AF recurrences differs according to the clinically predominant atrial arrhythmia and suggests a possible role of the RA isthmus in the occurrence of AF in some patients. Ablation of class IC atrial flutter in patients with therapy-resistant AF is a novel approach to management of this patient subset. Careful classification of AF patients plays a role in the selection of the site of ablation therapy.

The study described in this paper evaluated new tools for facilitating the development of criteria for ECG interpretation. Computer interpretation of the electrocardiogram (ECG) requires that numerous criteria related to diagnostic statements be defined. In the past, statistical techniques have been applied to derive and evaluate new criteria. More recently, some attempts have been made to incorporate artificial intelligence (AI) techniques such as expert systems in the computer interpretation of ECGs. In these systems the knowledge of the expert (facts, relations, heuristics) is stored in the knowledge base. With the help of the so-called inference engine this knowledge can be applied by a novice user. For instance, expert systems have been applied to improve arrhythmia detector performance in noise. ’ Such programs have also been used to evaluate the knowledge of human experts in determining the location of the accessory pathway in patients with Wolff-Parkinson-White syndrome.2 This study analyzed interpretation of guidelines given by five well respected authors for localization of the accessory pathway. The study demonstated that the information represented in these papers was incomplete, especially in regard to a frequent lack of heuristic information that distinguishes the expert from the novice user. In addition, the causal relationship between ECG measurements and the diagnosis was sometimes unknown.

Immediate Reinitiation of AF. Introduction: Although the recurrence rate of atrial fibrillation has been reported to be similar to that after external and internal cardioversion, little is known about immediate reinitiation of atrial fibrillation (IRAF) following internal cardioversion. Methods and Results: Thirty-eight patients (24 men; mean age 63 ± 13 years) underwent internal atrial defibrillation. Catheter-based defibrillation electrodes were positioned in the anterolateral right atrium and the coronary sinus. All patients were cardioverted at a mean threshold of 4.6 ± 3.4 J. Five of 38 patients (13%) had 1 to 4 episodes of IRAF. No difference in clinical and echocardiographic characteristics were observed when patients with and without IRAF were compared. Atrial fibrillation was always reinitiated by an atrial premature beat. When the earliest atrial endocardial activation time on the defibrillation catheters was analyzed, these atrial premature heats did not seem to originate from the defibrillation catheters. Twenty-one patients had atrial premature heats without IRAF. When the coupling intervals of the first atrial premature heat in patients without and with IRAF after conversion were compared, a significant difference was found (661 ± 229 vs 418 ± 79 msec, P < 0.05). IRAF was successfully treated with repeated shock delivery after the administration of atropine in 1 patient and intravenous flecainide in 2. Only repeated shock delivery was sufficient to treat IRAF in another 2 patients. Late recurrences of atrial fibrillation occurred in 3 of 5 with IRAK and in 19 of 33 patients without IRAF (P = NS). Conclusion: IRAF after internal atrial defibrillation occurred in 13% of patients, was always initiated by an atrial premature heat having a short coupling interval not originating from the defibrillation catheters, and was prevented by repeated shock delivery with or without preceding administration of pharmacologic agents. IRAF did not predict early recurrences of the arrhythmia after discharge from the hospital, emphasizing the necessity to treat immediate reinitiation promptly to achieve a successful cardioversion.

Cryoablation of the Proximal AV Node. Introduction: Radiofrequency (RF) is the most commonly used energy source for the treatment of cardiac arrhythmias. Surgical experience has shown that cryoablation also is effective for ablating arrhythmias. The aims of this study were to (I) investigate the feasibility of inducing permanent complete AV block (CAVB). (2) investigate the value of cold mapping to select the cryoablation site to produce permanent CAVB, (3) study the macro- and microscopic lesion characteristics 6 weeks later, and (4) compare them to those produced with RF energy. Methods and Results: A new steerable 8.5-French bipolar electrode catheter having a thermocouple with a 3-mm tip using N2O as the refrigerant controlled by a cryoconsole was used. Six mongrel dogs were anesthetized, and the catheter was positioned via the femoral vein across the tricuspid valve to record a large low right atrial and a small His-bundle potential. After cold mapping (-15° to -20°C tip temperature) resulted in ECG modifications, cryothermia (-70°C) was given twice, lasting 5 minutes each, to create permanent CAVB (Cryo group). Additionally, RF catheter ablation of the AV node was performed in two anesthetized mongrel dogs (RF group). In the Cryo group, a permanent proximal CAVB was created in four dogs (block occurred within 10 to 20 sec of cryothermia). Permanent right bundle branch block was obtained in one dog and transient CAVB in the remaining dog. In both dogs of the RF group, permanent CAVB was obtained. The cryolesions consisted of well-circumscribed, homogeneous areas of fibrotic tissue without viable cardiomyocytes. Lesions produced with RF were less circumscribed and inhomogeneous, with clear evidence of viable cardiomyocytes and cartilage formation (patchy lesions). Conclusions: (1) Permanent CAVB can he created by using a steerable cryoablation catheter. (2) Histologically, cryoablated sites were homogeneous and showed fibrotic tissue without signs of chronic inflammation and no evidence of viable myocytes. (3) Lesions created with RF were less homogenous and still contained viable myocytes within the lesion and cartilage formation. (4) The arrhythmogenic significance of these differences requires further study. (5) The technology of using reversible cold mapping has the potential to identify the successful ablation site and warrants further clinical study.

Shortly after in the introduction of programmed electrical stimulation (PES) of the heart to study and localize cardiac arrhythmias in the intact human heart, the technique was used for risk stratification of the arrhythmia patient. Two decades later we have to conclude that especially in ventricular arrhythmias the technique of PES did not live up to our expectations and the left ventricular function is a better long-term predictor than the induction of ventricular arrhythmias or the ability to find an antiarrhythmic drug able to prevent the initiation of the classically documented ventricular arrhythmia. Another sobering finding came from the analysis of the characteristics of the patient dying suddenly out-of-hospital, which showed that most of those patients could not be classified before the event as being at high risk using noninvasive or invasive testing, not even in those with a previous cardiac history. Monomorphic action potential (MAP) recordings have been of importance in our understanding of torsade de pointe arrhythmias in congenital and acquired QT prolongation. A major problem in case of a less generalized electrophysiological abnormality is the identification of the appropriate place where to put the MAP-electrode.

This study reports on predictors for successful radiofrequency (RF) ablation of idiopathic ventricular tachycardia (VT) in 48 patients--35 with right ventricular (RV) outflow tract and 13 with left ventricular VT. In RV outflow tract idiopathic VT, RF ablation was successful in 29 of 35 patients (83%). The following information allowed differentiation between patients with and without a successful RF ablation:1 induced VT morphology (O vs 3); presence of delta wave-like beginning of the QRS (2 vs 3) andor = 11 of 12 leads showing a "match" between the clinical VT and the pacemap (28 vs 1). Endocardial activation times were not different between both groups (-15 +/- 18 vs -4 +/- 5 ms). In left ventricle idiopathic VT, RF ablation was successful in 12 of 13 patients (92%). In patients who underwent successful ablation, 1 VT morphology was induced and no delta wave-like beginning of the QRS was present; a correlation between clinical VT and the pacemapor = 11 of 12 leads was found and the endocardial activation time preceded the QRS (range of -5 to -58 ms [mean -30 +/- 14]). Purkinje activity was observed in 5 of 7 patients with an idiopathic VT originating from the inferoposterior region but not from the inferoapical region of the left ventricle. Four patients (14%) with RV outflow tract idiopathic VT had recurrence during a mean follow-up of 2 to 50 months (mean 30 +/- 12). Thus, (1) in RV outflow tract idiopathic VT a good pacemap was more important than an early endocardial activation time; (2) an optimal pacemap as well as an early endocardial activation time were important predictors for successful ablation of the left ventricle idiopathic VT; (3) Purkinje activity was recorded in VTs arising in the inferoposterior region of the left ventricle; and (4) factors for unsuccessful ablation for idiopathic VT were1 induced VT morphology, a delta wave-like beginning of the QRS, and a VT/pacemap correlation11 of 12 leads. Idiopathic VT can be successfully ablated with both immediate and long-term success.

Answer to the rhythm puzzle The ECG shows a total atrioventricular block with junctional escape complexes, although the ninth QRS complex may be conducted. The second and eighth QRS complexes result from a retrogradely conducted P wave (Fig. 2). This mechanism, in which an escape complex is followed by a conducted complex, is called an escape-capture bigeminy. This only happens if the R-P interval of the retrograde P wave is long enough (along the slow AV nodal pathway) to be conducted back to the ventricles along the fast AV nodal pathway. When the P wave is caused by retrograde conduction along the fast AV nodal pathway, anterograde AV nodal conduction is blocked, resulting in a blocked P wave (after the third, fifth and (probably) tenth QRS complex). Fig. 2 Ladder diagram of a retrograde P wave conducted back to the ventricles and a blocked retrograde P wave Lithium intoxication was diagnosed based on the clinical symptoms (sinus node dysfunction and lethargy) and on a serum level of 0.88 mmol/l which is considered to be toxic at this age. Since lithium treatment was considered to be the most beneficial therapy for this patient, a DDD pacemaker was implanted. This was done successfully and without any complications, after which she was discharged from our centre.

Ablation of an Anterior Fascicular Idiopathic VT. Introduction: Idiopathic ventricular tachycardia (VT) originating in or close to the anterior fascicle of the left bundle is rare. A patient with no structural heart disease and VT with a right bundle branch block configuration and right-axis deviation underwent an electrophysiologic examination. Methods and Results: Both endocardial activation mapping during VT and pacemapping were performed via a transseptal approach to localize the site of origin of the VT. Endocardial recordings of the His bundle and the posterior and anterior fascicles of the left bundle branch revealed an origin of the VT in or close to the anterior fascicle. The Purkinje potential at that site preceded the QRS complex by 20 msec, with pacemapping showing an optimal match between the paced rhythm and the clinical VT. RF energy delivered at this site terminated the VT. A left anterior nemiblock appeared after RF ablation. Ten months later, the patient is free from recurrences of VT. Conclusions: Idiopathic VT originating in or close to the anterior fascicle was cured by RF ablation. A Purkinje potential preceding the QRS during tachycardia and an optimal pacemap were used to guide RF ablation.

OBJECTIVE: To determine the features that distinguish bundle branch reentry (BBR) ventricular tachycardia from a supraventricular tachycardia with aberration on the 12 lead electrocardiogram (ECG). PATIENTS: Three patients in whom premature beats (2 cases) or sustained tachycardia (2 cases) showed a QRS configuration identical to that observed during sinus rhythm. INTERVENTIONS: Programmed electrical stimulation. RESULTS: These arrhythmias were ventricular in origin and caused by a BBR mechanism, as suggested by the following data obtained during electrophysiological study: (a) an H-V interval shorter during tachycardia than during sinus rhythm; (b) A-V dissociation; (c) activation of the right bundle branch before activation of the bundle of His. The ECG of all 3 patients showed right bundle branch block with very prolonged QRS duration (0.16 to 0.20 s). Characteristically, all 3 had prolonged H-V interval during sinus rhythm. All patients had had a previous myocardial infarction and had a dilated left ventricle. CONCLUSION: The presence of (a) wide complex extrasystoles or tachycardia with a QRS morphology identical to that of sinus rhythm; (b) A-V dissociation; and (c) a very prolonged QRS duration (0.16 s or more) is suggestive of ventricular tachycardia caused by bundle branch reentry.

Ablation of Pacemaker Circus Movement Tachycardia. Introduction: Treatment of pacemaker circus movement tachycardia (PCMT) in patients with very long VA conduction times may present a problem. Methods and Results: PCMT occurred in a 46-year-old woman with an uncommon AV nodal reentrant tachycardia who developed 2:1 AV block after fast pathway radiofrequency catheter (RF) ablation performed at another institution. Due to the long VA conduction time, PCMT could not be prevented by reprogramming the pacemaker or by the addition of antiarrhythmic drugs. Cure of the PCMT was obtained after selective RF ablation of the slow AV nodal pathway. Conclusion: RF ablation of the retrograde conduction offers another alternative for treatment of PCMT.

Efficacy of procainamide and lidocaine in terminating spontaneous monomorphic ventricular tachycardia (VT) was assessed in a randomized parallel study. Patients with acute myocardial infarction and those with poor hemodynamic tolerance of VT were excluded. Procainamide 10 mg/kg was given intravenously with an injection speed of 100 mg/min, and lidocaine was administered at an intravenous dose of 1.5 mg/kg in 2 minutes. Fourteen patients were randomized to lidocaine and 15 to procainamide. Termination occurred in 3 of 14 patients after lidocaine and in 12 of 15 patients after procainamide (p

Ablation of interfascicular re-entrant tachycardia. Introduction: Fascicular re-entrant ventricular tachycardia (VT) using the anterior fascicle of the left bundle anterogradely is rare and may produce identical QRS morphology during sinus rhythm and VT. Catheter ablation of this type of VT has not been described in detail. Methods and results: In a postinfarct patient with dilated left ventricle and recurrent VT (showing a QRS configuration of right bundle branch, left posterior fascicular block), endocardial recordings from the His-Purkinje system showed that VT was due to interfascicular re-entry. Induction of VT occurred after progressive retrograde conduction delay on increasing the prematurity of the extrastimulus. Anterograde conduction occurred exclusively over the left anterior fascicle, which caused identical QRS morphology during sinus rhythm and VT. During VT, the left posterior fascicle was used retrogradely. The usual target for bundle branch re-entry ablation, the right bundle, did not participate in the re-entrant circuit. While performing left ventricular endocardial mapping, VT was interrupted when positioning the catheter on the left anterior fascicle, and ‘reversed1 nonsustained bundle branch re-entry occurred with anterograde conduction over the posterior fascicle and retrograde conduction over the anterior fascicle. Ablation of conduction in the anterior fascicle led to cure of the VT. Conclusion: Interfascicular re-entrant VT with right bundle branch block, right-axis QRS configuration can be cured by catheter ablation of anterior fascicle conduction.

To assess beat-to-beat behavior of QT interval under different conditions, high resolution recordings and computerized beat-to-beat analysis of the electrocardiogram were performed at rest, during recovery after short exercise, and during atrial pacing. Beat-to-beat variations of QT interval during sinus rhythm at rest and after short exercise were measured in ten healthy men. In an additional three patients with supraventricular tachycardia, beat-to-beat QT changes were studied after abrupt sustained acceleration and deceleration of heart rate by atrial pacing. Beat-to-beat changes in RR interval at rest are followed by minimal changes of the QT interval. The measured proportional change of the QT interval compared with the change in RR interval (delta QT/delta RR) was 0.02. This value represents 10% of the value expected for QT changes from Bazett's formula. Following short exercise QT interval did not change for 15 seconds and reached a maximal value 80 seconds later as compared to the RR interval (192 vs 115 secs, P < 0.001). The steady state of the QT interval during sustained atrial pacing was achieved after 132, 135, and 133 seconds for pacing intervals of 600, 500, and 600 msec, respectively. Our data indicate a relatively slow adaptation of the QT interval to changes in heart rate.

One hundred twenty-nine patients were prospectively studied after a first myocardial infarction. A first signal-averaged electrocardiogram (SAECG-1) was performed in the acute phase (within 48 hours after onset of symptoms) and a second one (SAECG-2) in the late phase (6 to 18 months after hospital discharge). We studied the influence of nine parameters on the evolution of the signal-averaged electrocardiogram: age, gender, myocardial infarction location, number of diseased coronary vessels, infarct-related coronary artery patency, use of thrombolytic therapy or percutaneous transluminal coronary angioplasty in the acute phase, left ventricular ejection fraction, and recurrence of ischemic events. No follow-up data were available in 15 patients. Of the remaining 114 patients, an ischemic event occurred in 25 (22%). The signal-averaged electrocardiogram remained unchanged in 97 (85%) (remaining normal in 78 and abnormal in 19). It became abnormal in 13 (11.5%) and became normal in 4 (3.5%). In patients with a normal SAECG-1, two factors were associated with the change to an abnormal SAECG-2: (1) an ischemic event occurred in 11 (85%) of 13 patients whose SAECG-2 was abnormal compared with only 13 (17%) of 78 patients whose SAECG-2 remained normal (p < 0.0001), and (2) 100% of patients with an abnormal SAECG-2 had an inferior myocardial infarction compared with 54% of patients with a normal SAECG-2 (p = 0.004).(ABSTRACT TRUNCATED AT 250 WORDS)

Supernormal Conduction. This report describes a patient with tachycardia-dependent left bundle branch block (LBBB) and atrial extrasystoles, some of which were followed by an unexpectedly narrow QRS complex. His-bundle recordings and premature atrial stimulation were performed to analyze the mechanism underlying the normalized intraventricular conduction of some of the early atrial impulses. The results suggested the presence of supernormal conduction in the left bundle branch (LBB), because(1) the HV interval was identical in LBBB complexes and in early narrow QRS complexes; (2) during single lest stimulation using different paced atrial cycle lengths, there was a well-defined range of H1, H2, intervals resulting in normalization of intraventricular conduction; and (3) atrial pacing with a cycle length of 500 msec resulted in alternation between wide and narrow QRS complexes. These findings rule out alternative mechanisms that could explain the unexpectedly normal intraventricular conduction of early impulses.

In 49 consecutive patients (27 men and 22 women, age range 44 to 86 years) presenting with acute symptoms and with subsequently proven pulmonary embolism, and without previous lung disease, the 12-lead electrocardiograms obtained at hospital admission were reviewed in a blinded fashion to identify electrocardiographic features suggestive of right ventricular overload. Pulmonary embolism was considered probable in 37 patients (76%), from the presence ofor = 3 of the following abnormalities: (1) incomplete or complete right bundle branch block (n = 33); which was associated with ST-segment elevation (n = 17) and positive T wave (n = 3) in lead V1; (2) S waves in leads I and aVL of1.5 mm (n = 36); (3) a shift in the transition zone in the precordial leads to V5 (n = 25); (4) Q waves in leads III and aVF, but not in lead II (n = 24); (5) right-axis deviation, with a frontal QRS axis of90 degrees (n = 16), or an indeterminate axis (n = 15); (6) a low-voltage QRS complex of5 mm in the limb leads (n = 10); and (7) T-wave inversion in leads III and aVF (n = 16) or leads V1 to V4 (n = 13), which occurred more often in patients with symptoms for7 days. In the 12 patients with normal electrocardiograms at admission, serial electrocardiograms revealed diagnostic features of embolism in an additional 3 patients. Two-dimensional Doppler echocardiography at admission revealed tricuspid valve regurgitation and an increased right ventricular end-diastolic diameter in all cases.(ABSTRACT TRUNCATED AT 250 WORDS)

The ECG (electrocardiography) shows a sinus bradycardia of 42 beats/min, a horizontal electrical heart axis and a narrow QRS complex. The second to fourth QRS complex is preceded by a P wave with a variation in the PQ time. The PQ time in the second QRS complex is 220 ms, in the third 200 ms and the fourth 140 ms. No P wave precedes the fifth QRS complex. In the sixth QRS complex, the P wave is incorporated in the S wave of the QRS complex. This pattern is suggestive for isorhythmic dissociation. The junctional rhythm (such as the fifth and sixth complex in this ECG) is temporarily faster than the sinus rhythm resulting in a pseudo-shortening of the PQ time. Since both the junctional and the sinus rate are nearly identical, there seems to be dissociation. However, during prolonged registration of the ECG 1:1 AV conduction, during a slightly faster sinus rhythm is present. This rhythm should not be confused with complete AV block when there is no relation between atrial and ventricular activation. Levy et al. have shown that a baroreceptor-initiated feedback mechanism is operative in isorhythmic dissociation. Elevated systolic pressure is the trigger of baroreceptor discharge, which produces sinoatrial slowing [1]. In our patient with symptomatic bradycardia and isorhythmic dissociation, we implanted a DDD pacemaker. After implantation, he had no further complaints of dizziness.

We performed radiofrequency catheter ablation of idiopathic ventricular tachycardia arising from the left ventricle, in two 15-year-old patients. Activation mapping during induced tachycardia revealed an origin from the mid-septal region of the left ventricle in both patients. Local activation times and pacemapping were used to select the target site for successful ablation. At follow-up, both patients are without symptoms.

Left ventricular (LV) function was studied in 30 patients with lone atrial fibrillation (AF) (paroxysmal [n = 27] and persistent [n = 3]) before and after ablation of atrioventricular conduction. In all patients, drug treatment did not control ventricular rate during AF or prevent recurrences of the arrhythmia, or both. LV ejection fraction, and LV end-systolic and end-diastolic, and left atrial dimensions were measured by echocardiography before (mean 7 +/- 10 months, range1 to 37) and after (14 +/- 20 months,1 to 77) ablation. Before ablation, LV ejection fraction wasor = 50% in 12 patients (group I) and50% in 18 (group II). After ablation, LV ejection fraction increased significantly in group I from 43 +/- 8% to 54 +/- 7% (p0.0001). There were also significant decreases in LV-end systolic and end-diastolic, and left atrial dimensions. No changes in these parameters were observed in group II. Groups I and II had a significant difference in the duration of AF (group I: mean 11 years, range 8 to 28; and group II: 5 years, 2 to 14) (p0.05). No difference was present in age, sex, New York Heart Association functional class for dyspnea, or type of ablation procedure. Thus, some patients with lone AF may show deterioration of LV function, which appears to be related to the duration of the arrhythmia; in these cases, LV function may improve significantly after ventricular rate control is accomplished by ablation of atrioventricular conduction.

In a patient with the Wolff-Parkinson-White syndrome, Ebstein's anomaly of the tricuspid valve, a right atrial Chiari net and a patent foramen ovale two unusual complications developed after surgical epicardial dissection combined with cryoablation of the anomalous pathway. The first complication was that ablation of the right atrial wall led to changes in interatrial pressure gradients and the development of a right to left shunt necessitating surgical closure of the atrial septal defect. The second complication was the development of a thrombotic mass in the Chiari net simulating on intracavity tumour, which also had to be removed surgically.

The 12-lead electrocardiogram during sinus rhythm was studied in 20 patients with arrhythmogenic right ventricular (RV) dysplasia with symptomatic ventricular tachycardia. Findings were analyzed, together with echocardiographic evaluation of site, extent and progression of RV wall abnormalities. Electrocardiographic abnormalities were found in 90% of patients. No correlation was found between abnormalities on the initial 12-lead electrocardiogram, and the echocardiographic extent and location of RV involvement. Over time, echocardiographic progression of the disease was observed; RV size increased in 6 of 7 patients from 34 +/- 3 to 39 +/- 3 mm (p = 0.01), and there was progression in the extent of RV wall motion abnormalities in 4 of 7 patients. Analysis of serial electrocardiographic recordings did not reveal changes indicative of progression of the disease during follow-up of 71 +/- 48 months. It is concluded that electrocardiographic abnormalities suggesting arrhythmogenic RV dysplasia are present in 90% of symptomatic patients on the first electrocardiogram recorded during sinus rhythm. However, serial electrocardiographic recordings in these patients do not provide information regarding anatomic progression of the disease.

One hundred twenty-nine patients were retrospectively analyzed and divided into 3 groups according to (1) the presence of a patent artery obtained either spontaneously or after thrombolytic therapy but without percutaneous transluminal coronary angioplasty (PTCA) (group I, n = 83), (2) the presence of a patent artery after opening by PTCA (group II, n = 29), or (3) absence of reperfusion despite thrombolytic therapy or PTCA (group III, n = 17). Thrombolytic therapy was given within 4 hours after onset of symptoms (mean 2.5 +/- 1.0 hours) and PTCA was performed within 24 hours after the onset of symptoms (mean 6 +/- 6 hours). Signal averaging was performed within 24 hours after cardiac catheterization. An abnormal signal-averaged electrocardiogram was present in 10 of 83 (12%) group I, 9 of 29 (31%) group II and 7 of 17 (41%) group III patients (p0.05 group I vs II, p0.01 group I vs III, no statistical difference group II vs III). Therefore, in contrast to reperfusion by thrombolytic therapy the incidence of abnormalities on the signal-averaged electrocardiogram early after myocardial infarction is not reduced by an early opening of the culprit vessel by PTCA.

Sex differences between certain types of arrhythmias have been reported. For example the Wolff-Parkinson- White syndrome is more frequent in male than female subjects. 1 Atrioventricular (AV) nodal tachycardia has been found to occur more frequently in female subjects. 2 Little is known about the age at onset of different types of supraventricular tachycardias. The purpose of this study was twofold: (1) to obtain insight into a possible relation between gender of patient and type of supraventricular tachycardia, and (2) to look for possible differences in age at the time of the first arrhythmic event in relation to the type of arrhythmia. The following 3 groups of patients were studied: those with atrial tachycardia, AV nodal tachycardia and tachycardias in the presence of an accessory AV pathway.

This study was designed to assess the influence of accessory atrioventricular (AV) pathway location on the clinical and electrophysiologic characteristics of 384 consecutive symptomatic patients having a single accessory pathway.Four locations were studied: left free wall (n = 270), posteroseptal (n = 52), anteroseptal (n = 29) and right free wall (n = 33). Ten clinical variables and 12 electrophysiologic variables were analyzed, including the effective refractory period of the accessory pathway and the different clinically occurring and inducible arrhythmias.Only two clinical findings were associated with accessory pathway location: 1) later age at onset of symptoms in the left free wall versus other accessory pathway locations (24 +/- 12 vs. 20 +/- 11 years, p = 0.02), and 2) later age at the time of electrophysiologic study in the left free wall accessory pathway location (36 +/- 13 vs. 32 +/- 11 years, p = 0.01). Six electrophysiologic variables showed a correlation with the accessory pathway location: 1) retrograde conduction only was found less frequently in right free wall (9%) and anteroseptal (10%) than in left free wall (26%) and posteroseptal (29%) accessory pathway locations (p = 0.05); 2) the retrograde effective refractory period of the accessory pathway was shorter in anteroseptal (253 +/- 52 ms) and left free wall (270 +/- 72 ms) as compared with right free wall (296 +/- 101 ms) and posteroseptal (301 +/- 76 ms) locations (p = 0.05); 3) retrograde decremental conduction over the accessory pathway was present in the posteroseptal (17%) and left free wall (3%) but absent in the other locations (p less than 0.001); 4) anterograde decremental conduction was only seen in the right free wall location (12%) (p less than 0.001); 5) orthodromic reentrant tachycardia was induced less frequently in the right free wall than in other locations (70% vs. 93%, p less than 0.001); and 6) inducibility of atrial fibrillation was greater in anteroseptal (62%) than in right free wall (21%), left free wall (44%) and posteroseptal (36%) locations (p = 0.01).The location of the accessory AV pathway is associated with specific electrophysiologic characteristics.

BACKGROUND Spontaneous sustained ventricular tachycardia (VT) occurring 16-24 hours after left anterior descending (LAD) coronary artery occlusion in the canine heart is most likely based on abnormal automaticity. In vitro, it has been demonstrated that the rate of the arrhythmia and the effect of overdrive pacing depends on the maximal diastolic potential (MDP). The MDP is also of importance in understanding the effect of antiarrhythmic drugs. To study 1) the possible presence of different responses to overdrive pacing and 2) the relation between the response to overdrive pacing and the effect of different antiarrhythmic drugs in the intact heart, we investigated the effect of 1) (prolonged) pacing and 2) lidocaine (3 mg/kg), verapamil (0.4-1.0 mg/kg), or flunarizine (2 mg/kg) during VT. METHODS AND RESULTS In 21 conscious dogs with chronic atrioventricular block, 60 sustained VTs were observed 1 day after LAD occlusion. During VT, pacing with interstimulus intervals of 400, 300, and 200 msec for 15, 60, and 120 seconds was done on 40 VTs. Based on their response to pacing, VTs were divided into a pacing-suppressible (PS group) and a pacing-nonsuppressible group (PNS group). The mean cycle length in the PS group was significantly longer (410 +/- 50 msec) than in the PNS group (360 +/- 35 msec, p less than or equal to 0.01). Suppression was directly related to the rate and duration of pacing. Spontaneous recurrence of VTs was observed after 26 +/- 45 seconds. Lidocaine and verapamil increased cycle length of the suppressible VTs and terminated them, whereas flunarizine had no effect. Except for verapamil, which increased cycle length of the VTs, no effects were seen in the PNS group. CONCLUSIONS In conscious dogs showing sustained VTs 16-24 hours after LAD occlusion, 1) the slower VTs can be suppressed by pacing, verapamil, and lidocaine but not by flunarizine, and 2) the faster VTs are not affected by pacing, lidocaine, and flunarizine, and are only slowed by verapamil. These findings are compatible with in vitro findings of abnormal automaticity, with the slower VTs originating from a higher MDP than the faster VTs.

In a small number of patients, cardiac arrhythmias are treated by transcoronary chemical ablation [1, 2]. Selective intracoronary injection of low amounts of pure ethanol results in permanent damage of the myocardial cells, being the substrate of the arrhythmia. Destroying the substrate can, however, result in deterioration of left ventricular function, especially in patients with ventricular tachycardia after myocardial infarction and a pre-existing low ejection fraction. However, assessment of the presence of viable tissue in and around infarcted areas is very difficult. We have studied the value of selective injections of technetium-99m (Tc-99m) sestaMIBI into main coronary arteries and into small arteries providing blood supply to the substrate of cardiac arrhythmias to detect the flow areas and to estimate the area at risk for chemical ablation. In a previous study [3, 4], we demonstrated that Tc-99m sestaMIBI is able to detect short episodes of ischemia, without the need for studying the patient immediately after injection of the radioactive tracer, which obviously is a prerequisite, when the nuclear agent is administered in the catheterization laboratory. The first part of the study was performed to determine whether intracoronary injection of Tc-99m sestaMIBI could demonstrate the flow area of the myocardium perfused by that artery. In the second part, we studied the value of selective injection of Tc-99m sestaMIBI into the artery providing blood supply to the substrate of the arrhythmia.

Chronic supraventricular tachycardias may lead to cardiac enlargement and depressed cardiac function[1–9]. That observation has resulted in the introduction of the term tachycardiomyopathy, indicating that deterioration in cardiac function can be caused by the arrhythmia per se and that normal heart function may be restored by cure of the arrhythmia.

Recently we reported on the chemical ablation of atrioventricular (AY) conduction by selective injection of pure ethanol into the AV nodal coronary artery. 1 In this communication we would like to report on the long-term follow-up of this intervention in 11 patients.

Ventricular fibrillation (VF) is a well-known but rare complication of the Wolff-Parkinson-White syndrome (WPW). Clinical and electrophysiological data of 23 patients with spontaneous VF were compared with data from 100 consecutive patients with WPW without VF but with symptomatic supraventricular tachycardia. The 23 patients were collected in a multicentre retrospective study in seven European centres. VF occurred in only one patient who was receiving antiarrhythmic drugs, and was the first manifestation of the syndrome in six. No significant differences were found between those with VF and without VF in age, complaints of palpitations, syncope, and presence of structural heart disease. The retrograde effective refractory period of the accessory pathway, the atrial refractory period and the fastest atrial pacing rate with 1:1 anterograde conduction over the accessory pathway were similar in both groups. Significant differences were found for sex, permanent pre-excitation on the electrocardiogram, type of documented supraventricular tachyarrhythmias, shortest RR interval less than or equal to 220 ms during spontaneous atrial fibrillation (AF), inducibility of supraventricular tachycardias, ventricular effective refractory period less than or equal to 190 ms, mean shortest RR interval during induced AF less than or equal to 180 ms and presence of multiple accessory pathways.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac arrhythmias can be successfully controlled nowadays in a remarkable percentage of patients. We have at our disposal new antiarrhythmic drugs with high efficacy and acceptable side-effect profiles [1]. Selected patients with selected arrhythmias not controllable with antiarrhythmic drugs [2] can be treated with electrical devices. Refined surgical techniques for the treatment of supraventricular [3–4] and ventricular arrhythmias [5–6] are available. The implantable defibrillator has become a reality [7]. Percutaneous electrical ablation is effective to create atrio-ventricular block in patients with atrial fibrillation with uncontrollable rapid ventricular rates [8]. Unfortunately, we are still far from controlling cardiac arrhythmias in all patients. Not all respond to antiarrhythmic drugs. Many are not amenable to antitachycardia pacing or control by an implantable defibrillator. Because of the important myocardial damage present in many patients surgery for ventricular tachycardia has a high perioperative mortality. Percutaneous electrical ablation of accessory pathways is still experimental and electrical ablation of ventricular tachycardia [9] has not offered the expected results [10].This technique creates lesions with a small size. Extensive myocardial damage can result when multiple shocks are given. However, surgery and percutaneous electrical ablation are forms of treatment that can destroy or remove the arrhythmia substrate, offering a definitive cure when successful. Antiarrhythmic drugs and electrical devices are palliative therapies. Techniques able to destroy the arrhythmia substrate overcoming the problems of percutaneous electrical ablation and surgery would represent an important addition to our antiarrhythmic armentarium.

The prognostic significance of serial signal-averaged electrocardiograms recorded during the first 3 days (period 1), in the second week (period 2) after a first acute myocardial infarction (AMI) and 6 months later (period 3) was prospectively assessed in 190 patients. No patients were treated with thrombolytic therapy. Patients with conduction disturbances were excluded. Mean age of the 190 patients was 57 years (range 34 to 74) and mean left ventricular ejection fraction was 40 + 6% (range 12 to 70). Eighty-four patients had an anterior wall AMI and the remaining 106 patients an inferior wall AMI. After a mean follow-up of 24 months, 16 patients developed sustained symptomatic monomorphic ventricular tachycardia, 7 patients were resuscitated from an episode of ventricular fibrillation, and 10 patients died suddenly. Multivariate regression analysis using continuous variables showed that the strongest predictor of sustained ventricular tachycardia and ventricular fibrillation was the left ventricular ejection fraction (p less than 0.0001) followed by the duration of QRS complex on the signal-averaged electrocardiogram recorded during the first 3 days of AMI (p less than 0.0005). Sudden death was only predicted by left ventricular ejection fraction (p less than 0.02).