Cardiac involvement in genetically confirmed facioscapulohumeral muscular dystrophy

In a series of 100 patients exhibiting clinical and molecular features of facioscapulohumeral muscular dystrophy (FSHMD), five patients had conduction defects or arrhythmia in the absence of cardiovascular risk factors--namely, intraventricular conduction delay and supraventricular arrhythmia induced by electrophysiologic investigations (two patients), palpitations associated with supraventricular arrhythmia (one patient), severe atrioventricular block leading to pacemaker implantation (one patient), and ventricular tachycardia related to arrhythmogenic right ventricular cardiomyopathy (one patient). Patients with FSHMD may have cardiac involvement.     

Ventriculo-atrial conduction time during reciprocating tachycardia with intermittent bundle-branch block in Wolff-Parkinson-White syndrome

Records from patients with the Wolff-Parkinson-White syndrome were reviewed with particular emphasis on the occurrence of bundle-branch block aberration during reciprocating tachycardia and the significance of this observation with respect to accessory pathway location. Increase by greater than 25 ms in the ventriculoatrial interval during reciprocating tachycardia with bundle-branch block, when compared to reciprocating tachycardia with normal intraventricular conduction, occurred only with right or left free wall accessory pathways. No patient with a septal accessory pathway proven by epicardial mapping showed a ventriculoatrial interval prolongation greater than 20 ms during bundle-branch block aberration. Measurement of ventriculo-atrial interval during bundle-branch block abe-ration also helped to diagnose accessory pathways AH and HV intervals as well as ventriculo-atrial times, may give midleading information. In one patient increase in cycle length during left bundle-branch block was the result of prolonged HV interval rather than prolonged ventriculo-atrial interval. In another patient cycle length remained the same during bundle-branch block while the ventriculo-atrial interval increased by an increment identical to the decrease in AH interval.     

Wolff-Parkinson-White syndrome type B with tachycardia-dependent (phase 3) block in the accessory pathway and in left bundle-branch coexisting with rate-unrelated right bundle-branch block

A patient with Wolff-Parkinson-White syndrome type B developed 2:1 atrioventricular block resulting from the association of persistent right bundle-branch block with tachycardia-dependent (phase 3) left bundle-branch block. Electrophysiological studies disclosed the coexistence of a tachycardia-dependent (phase 3) block in the accessory pathway. This conduction disturbance was exposed, not by carotid sinus massage as in previous studies, but by pacing-induced prolongation of the interval between two consecutively conducted atrial impulses. Furthermore, the surface electrocardiogram showed, at different times, ventricular complexes resulting from: (1) exclusive atrioventricular conduction through the normal pathway without bundle-branch block; (2) predominant, or exclusive, atrioventricular conduction through a right-sided accessory pathway; (3) exclusive atrioventricular conduction through the normal pathway with right bundle-branch block; (4) exclusive conduction through the normal pathway, with left bundle-branch block; (5) fusion between (1) and (2); and finally, (6) fusion between (2) and (3) However, QRS complexes resulting from simultaneously occurring Wolff-Parkinson-White syndrome type B and left bundle-branch block could not be identified. Future electrophysiological investigations should re-evaluate the criteria used to diffrentiate between true and false patterns of Wolff-Parkinson-White syndrome type B coexisting with left bundle-branch block.     

Analysis of the onset and termination of repeated pattern ventricular arrhythmias

A group of algorithms has been developed to investigate the characteristics of beat-to-beat intervals preceding and following the onset and termination of repeated pattern ventricular arrhythmias (RPVA) such as bigeminy and trigeminy. Eighty-five patients, each with more than 3000 ventricular ectopic beats in a 24-hour Holter recording and with more than 10 episodes of RPVA, were evaluated. A statistically significant prolongation of sinus intervals preceding the onset of bigeminy and trigeminy and shortening of postectopic intervals after the onset were observed. In addition, shortening of postectopic intervals before the termination of bigeminy and trigeminy and lengthening of sinus intervals following their termination were also seen. A significant presence of these characteristics was not observed in arrhythmias with a greater number of sinus beats between ectopic beats. These dynamics provide information which may be utilized in the assessment of mechanisms involved in the onset and termination of RPVA.     

Incidence and clinical relevance of the occurrence of bundle-branch block in patients treated with thrombolytic therapy

BACKGROUND: Whether thrombolytic therapy alters the incidence and clinical outcome of bundle-branch block is unclear. METHODS AND RESULTS: We examined the occurrence of new-onset bundle-branch block, both transient and persistent, in 681 patients with acute myocardial infarction enrolled in the Thrombolysis and Angioplasty in Myocardial Infarction 9 and Global Utilization of Streptokinase and t-PA for Occluded Arteries 1 protocols. Each patient underwent continuous 12-lead ECG monitoring for 36 to 72 hours with the Mortara ST monitoring system. Bundle-branch block was characterized as right, left, alternating, transient, or persistent. The overall incidence of bundle-branch block was 23.6% (n = 161), with transient block in 18.4% (n = 125) and persistent block in 5.3% (n = 36). Right bundle-branch block was found in 13% (n = 89) of the population; left bundle-branch block was found in 7% (n = 48). Alternating bundle-branch block was seen in 3.5% (n = 24) of patients. Left anterior descending artery infarcts accounted for most bundles (54%, n = 79). Patients with bundle-branch block had lower ejection fractions, higher peak creatine phosphokinase levels (P < .0001), and more diseased vessels (P < .019). Mortality rates in patients with and without bundle-branch block were 8.7% and 3.5%, respectively (P < .007). A higher mortality rate was observed in the presence of persistent (19.4%) versus transient (5.6%) or no (3.5%) bundle-branch block (P < .001). CONCLUSIONS: Thrombolytic therapy reduces the overall mortality rate associated with persistent bundle-branch block. However, persistent bundle-branch block remains predictive of a higher mortality rate than either transient or no bundle-branch block. Continuous 12-lead ECG monitoring provides an accurate characterization of the incidence and type of conduction disturbances after acute myocardial infarction.     

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

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

Advances in the understanding of conduction disturbances

The interest towards intraventricular conduction defects started some 10 yr after the introduction of the string galvanometer by Einthoven. As early as 1910, it was known that conduction blockade could occur along either branch of the intraventricular conducting pathway. It took some 20 yr to identify properly the electrocardiographic manifestations of right and left bundle branch blocks. A further 30 yr were needed to obtain a sound correlation between these functional disorders and the presence of anatomical lesions. The more recent introduction of the concept of left hemiblocks further improved our understanding of intraventricular conduction defects. The latter concept is based on the hypothesis of the anatomical and functional bifascicularity of the left bundle branch, a hypothesis which cannot be accepted without some reservations. Later developments indicated that left hemiblocks associated with right bundle branch block represent manifestations of bilateral conduction disturbances (incomplete bilateral bundle branch block). Such an association may constitute a forerunner of complete atrioventricular block, or an indicator of the possibility of sudden death. Whether these complications occur frequently or unfrequently in the setting of incomplete bilateral bundle branch block remains an unsettled question.     

Diagnosis of right ventricular infarction: experimental study through the use of body surface isopotential maps

This investigation was designed to diagnose right ventricular infarction, which is difficult to diagnose by the standard twelve-lead ECG, through the use of body surface isopotential maps which have significant diagnostic information. Right ventricular infarction was experimentally caused by ligation of the canine right coronary artery. Each dog had a series of maps recorded before and a week after experimentally-induced myocardial infarction. The common features of maps in right ventricular infarction are: 1. In the early stage of the ventricular depolarization the negative area occupies a comparatively large part of the right anterior chest surface, and in the middle stage, the larger part of the right anterior surface is also occupied by the negative area. 2. A minimum appears on the right anterior chest surface in the early stage. The delayed excitation resulting from intraventricular conduction disturbance caused by infarction, as verified by the epicardial isochronic map, is also well represented by the body surface isopotential map. In conclusion, through the use of body surface isopotential maps, it is much easier to diagnose right ventricular infarction and intraventricular conduction disturbance caused by infarction even in cases in which the standard twelve-lead ECG does not show the abnormalities clearly.     

Evolution of flightless land birds on southern continents: transferrin comparison shows monophyletic origin of ratites

In 34 successive patients with Wolff-Parkinson-White syndrome premature beats were induced from the right ventricular apex during reciprocating tachycardia (RT) at progressively shorter coupling intervals. The presence of an accessory pathway was confirmed by a reduction in the atrial cycle length (A-A interval) during which the premature ventricular beat was introduced. This retrograde preexcitation occurred at a time when the His-AV node pathway was refractory; i.e. there was premature activation of the atria over a pathway other than the His-AV node. 3 patients were excluded because of unsatisfactory or unstable H-H intervals. In the remaining 31 patients with constant preceding H-H intervals, the A-A interval shortened; (a) 35-65 msec in 4 patients with right-sided pathways and normal conduction during RT and by 110 msec in a 5th patient with a right-sided pathway, in whom bundle branch block aberration persisted during RT, (b) 45 msec in the single patient with both a right-sided and a septal accessory pathway, (c) 35-65 msec in 5 patients with septal pathways, and (d) 15-35 msec in only 4/20 patients with left-sided pathways and normal conduction during RT. Left-sided ventricular premature beats were introduced in 5 patients with left-sided pathways and normal conduction in RT. In 4/5, left-sided premature beats shortened the A-A interval 40-75 msec whereas right-sided premature beats at the same coupling interval failed to do so. In the fifth case, the left-sided premature resulted in a 65 msec abbreviation of the A-A interval compared to 30 msec from the right ventricular outflow tract and 15 msec from the right ventricular apex. In 5 patients with left-sided pathways, right ventricular premature beats were introduced during RT with left bundle branch block aberration, and shortened the A-A interval 30-50 msec in all of these, whereas right-sided premature beats in 4 of the 5 during normal conduction failed to do so. This technique is useful to confirm the participation of accessory pathways in reciprocating tachycardias associated with the preexcitation syndromes, and emphasizes the importance of the site of stimulation used relative to the location of the accessory pathway. Because of the possibility of multiple accessory pathways, stimulation of the left ventricle should be performed in patients undergoing surgery for preexcitation unless the left ventricle is already inplicated by right-sided studies.     

Electrophysiological mechanism of the characteristic electrocardiographic morphology of torsade de pointes tachyarrhythmias in the long-QT syndrome: detailed analysis of ventricular tridimensional activation patterns

BACKGROUND: The long-QT syndrome (LQTS) is an electrophysiological (EP) entity characterized by prolongation of cardiac repolarization and the occurrence of polymorphic ventricular tachyarrhythmias (VTs), sometimes with a twisting QRS morphology, better known as torsade de pointes (TdP). In the present study, detailed analysis of ventricular tridimensional activation patterns during nonsustained TdP VT was performed to provide an EP mechanism of the periodic transition in QRS axis. METHODS AND RESULTS: The studies were conducted with the anthopleurin-A canine model of LQTS. Tridimensional isochronal maps of ventricular activation were constructed from 256 bipolar electrograms obtained from the use of 64 plunge needle electrodes. In 26 episodes of nonsustained TdP VT, detailed activation maps could be accurately constructed during QRS-axis transitions in surface ECGs. The initial beat of all VTs consistently arose as a subendocardial focal activity, whereas subsequent beats were due to reentrant excitation in the form of rotating scrolls. The VT ended when reentrant excitation was terminated. In 22 of 26 episodes, the transition in QRS axis coincided with the transient bifurcation of a predominantly single rotating scroll into two simultaneous scrolls involving both the right ventricle and left ventricle separately. The common mechanism for initiation or termination of bifurcation was the development of functional conduction block between the anterior or posterior right ventricle free wall and the ventricular septum. In 4 of 26 episodes, a fast polymorphic VT, with an apparent shift in QRS axis, was due to a predominantly single localized circuit that varied its location and orientation from beat to beat, with the majority of ventricular myocardium being activated in a centrifugal pattern. CONCLUSIONS: The study provides for the first time an EP mechanism for the characteristic periodic transition of the QRS axis during TdP VT in the LQTS.     

Arrhythmogenic marker for the sudden unexplained death syndrome in Thai men

BACKGROUND: Between 1981 and 1988, the Centers for Disease Control and Prevention reported a very high incidence of sudden death among young male Southeast Asians who died unexpectedly during sleep. The pattern of death has long been prevalent in Southeast Asia. We carried out a study to identify the clinical markers for patients at high risk of developing sudden unexplained death syndrome (SUDS) and long-term outcomes. METHODS AND RESULTS: We studied 27 Thai men (mean age, 39.7+/-11 years) referred because they had cardiac arrest due to ventricular fibrillation, usually occurring at night while asleep (n=17), or were suspected to have had symptoms similar to the clinical presentation of SUDS (n=10). We performed cardiac testing, including EPS and cardiac catheterization. The patients were then followed at approximately 3-month intervals; our primary end points were death, ventricular fibrillation, or cardiac arrest. A distinct ECG abnormality divided our patients who had no structural heart disease (except 3 patients with mild left ventricular hypertrophy) into two groups: group 1 (n=16) patients had right bundle-branch block and ST-segment elevation in V1 through V3, and group 2 (n=11) had a normal ECG. Group 1 patients had well-defined electrophysiological abnormalities: group 1 had an abnormally prolonged His-Purkinje conduction time (HV interval, 63+/-11 versus 49+/-6 ms; P=.007). Group 1 had a higher incidence of inducible ventricular fibrillation (93% for group 1 versus 11% for group 2; P=.0002) and a positive signal-averaged ECG (92% for group 1 versus 11% for group 2; P=.002), which was associated with a higher incidence of ventricular fibrillation or death (P=.047). The life-table analysis showed that the group 1 patients had a much greater risk of dying suddenly (P=.05). CONCLUSIONS: Right bundle-branch block and precordial injury pattern in V1 through V3 is common in SUDS patients and represents an arrhythmogenic marker that identifies patients who face an inordinate risk of ventricular fibrillation or sudden death.     

Right and left ventricular geometry and myocyte contractile processes with dilated cardiomyopathy: myocyte growth and beta-adrenergic responsiveness

OBJECTIVES: Comparison of the effects of supraventricular tachycardia-induced dilated cardiomyopathy on left and right ventricular isolated myocyte geometry and function. BACKGROUND: Chronic ventricular tachycardia and supraventricular tachycardia cause left ventricular dilation and dysfunction in humans. However, it is unknown whether supraventricular tachycardia-induced dilated cardiomyopathy is a homogenous process for both the left and right ventricles. METHODS: Dilated cardiomyopathy was induced by rapid atrial pacing (240 beats/min, 3 weeks) in 5 pigs. Five age- and weight-matched pigs served as controls. Ventricular mass was measured, myocyte dimensions were obtained, and isolated right and left ventricular myocyte contractile performance was evaluated at baseline and after beta-adrenergic receptor stimulation. RESULTS: With the development of dilated cardiomyopathy, there was no change in left ventricular mass. In contrast, right ventricular mass was increased, as was right ventricular myocyte cross-sectional area. In the control group, baseline right ventricular myocyte contractile function was increased compared to left ventricular myocytes. beta-adrenergic receptor stimulation increased myocyte contractile function in both left and right ventricular myocytes. With supraventricular tachycardia-induced cardiomyopathy, both left and right ventricular myocyte contractile function and beta-adrenergic responsiveness were reduced. CONCLUSIONS: This study demonstrated differences in left and right ventricular myocyte growth with supraventricular tachycardia-induced dilated cardiomyopathy and this differential growth response was associated with changes in contractile performance. Thus, in this model of cardiomyopathic disease, left and right ventricular growth and changes in contractile performance are not a homogenous process.     

The retrograde His bundle deflection: its recognition and value in the analysis of tachyarrhythmias induced by stimulation on the T wave

Interpretation of deflections presumably retrograde His bundle in origin has to be performed in context considering the coexisting changes in simultaneously recorded intracardiac and surface leads. His bundle electrocardiography thus conceived is helpful in the analysis of the runs of ectopic beats elicited by premature ventricular stimulation during the antecedent T wave in patients without coronary artery or primary myocardial disease. Identification of AV nodal echoes within the paroxysms as well as the subsequent runs of reciprocating tachycardias, was possible in patients with and without preexcitation, although a thorough study of these cases also requires recording of coronary sinus and low lateral right atrial electrograms. The behavior of the retrograde H deflection in respect to the first extra beat following the premature QRS complex helped in excluding bundle branch reentry. The latter is improbable in patients with 'complete' bundle branch block pattern, if extra beats show a contralateral bundle branch morphology. However, in absence of bundle branch block, retrograde H deflections were not helpful in elucidating the mechanisms of pacemaker-induced intraventricular (bundle branch, fasicular or vulnerability-related) reentry.     

"Peripheral infarction blocks". Vectocardiographic analysis and electrogenetic hypothesis (author's transl)]

500 vectorcardiograms of variously located myocardial infarctions were analysed. Abnormalities of the afferent limb of QRS loop, consistent with intraventricular conduction disturbances, were detected in 42 cases. This pattern, according to Rosenbaum, was called "infarction block"; it was always associated with inferior and/or posterior infarction. This kind of block is shown by a large downward, righward and backward-directed vector, which always appears about 50 msec after the onset of ventricular activation. Total ventricular depolarization time was not significantly prolonged. The pattern was explained as a variant of "peri-infarction block" and its origin is hypothesized as the interruption of a peripheral ramification of LBB posterior fascicle.     

"The athlete's heart": most common electrocardiographic findings

The morphological and functional cardiac adaptations induced by physical training may be reflected in several athlete's electrocardiographic variants. Rhythm and heart rate disturbances are the most common findings, and sinus bradycardia is the most frequent adaptation. Non-specific intraventricular conduction delay and incomplete right bundle branch block are also frequent, but other bundle branch and fascicular blocks are extremely rare. While the atrioventricular conduction may be prolonged, the occurrence of first degree and type I second degree atrioventricular blocks depends on the individual's susceptibility. Advanced second and third degree atrioventricular blocks are exceptional, and when present, the possibility of underlying heart disease must be excluded. High QRS voltage is more frequent in male athletes, but its correlation with left ventricular hypertrophy is low. The ST segment elevation in the so called "early repolarization" pattern is typical of the athlete's electrocardiogram. Vagotonic or high T wave voltages and U waves are also frequent when sinus bradycardia is present. Tachyarrhythmias and increased automatism arrhythmias are rare and usually benign. The increased vagal tone is responsible for the suppression of the physiological and ectopic pacemakers. While Wolff-Parkinson-White syndrome per se does not exclude an athlete from sports activity, the risk of a sudden death makes it mandatory to perform an exhaustive cardiac evaluation. We may conclude that no sport can be considered arrhythmogenic or as a predisposing factor for malignant ventricular arrhythmias.     

The significance of fetal electrocardiography in the diagnosis of intrauterine bradyarrhythmia

From 11 cases of fetal bradycardia diagnosed by monitoring of 130 fetal electrocardiograms (ECG's) in high-risk pregnancies we have presented our experience in three selected cases of fetal bradyarrthythmia. Case 1 revealed on ECG blocked atrial premature beats simulating an extreme sinus bradycardia sequentially followed by conducted atrial premature beats. In case 2 we diagnosed ventricular premature beats in the form of persistent bigeminy which was controlled by intravenous propranolol. The last case illustrated the phenomenon of aberrant ventricular conduction known to occur in adult cardiology. The electrophysiologic basis of the variable arrhythmias was discussed. Detailed analysis of repeated direct fetal ECG's provided us with the diagnosis and understanding of the electrophysiologic mechanisms underlying the rhythm disturbances. This consequently determined the pharmacologic therapy and the obstetric approach relevant to each case. We have shown that by direct fetal electrocardiography it is possible to analyze accurately the rhythm disturbances. Persistent fetal bradycardia does not always signify fetal distress. We hope that this will lead to closer teamwork between the obstetrician and the cardiologist which will give an impetus to the future development of "fetal cardiology," thereby enhancing our understanding of the electrophysiology of the fetal heart.     

Atrioventricular conduction during long-term follow-up of patients with sick sinus syndrome

BACKGROUND: It has been claimed that patients with sick sinus syndrome have an increased risk of developing AV block, but this has never been assessed prospectively. The aim of the present study was to evaluate in a prospective trial AV conduction during the long-term follow-up of patients with sick sinus syndrome. METHODS: Two hundred twenty-five consecutive patients with sick sinus syndrome and intact AV conduction were randomized to undergo single-chamber atrial pacing (110 patients) or single-chamber ventricular pacing (115 patients). Follow-up after 3 months and then yearly included measurement of the PQ interval and, in patients with atrial pacemakers, determination of the atrial stimulus-Q intervals at pacing rates of 100 and 120 bpm. The occurrence of AV block in the atrial group was recorded. During follow-up (mean, 5.5+/-2.4 years), there was no change in PQ interval in either group and no change in atrial stimulus-Q intervals or Wenckebach block point in the atrial group. Four of 110 patients in the atrial group developed grade 2 to 3 AV block that required upgrading of the pacemaker (0.6% per year). Two of these 4 patients had right bundle-branch block at pacemaker implantation. CONCLUSIONS: AV conduction, estimated as PQ interval and atrial stimulus-Q interval at atrial pacing rates of 100 and 120 bpm and the Wenckebach block point, remains stable during long-term follow-up. Thus, treatment with single-chamber atrial pacing is safe and can be recommended to patients with sick sinus syndrome without bundle-branch block.     

Adenosine-sensitive atrial reentrant tachycardia originating from the atrioventricular nodal transitional area

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

Progressive familial heart block--two types

Two types of heart block which occur extensively in families in the Republic of South Africa are reported. A type I heart block tends to have the pattern of a right bundle-branch block and/or left anterior hemiblock occurring individually or together, and manifesting clinically when complete heart block supervenes, either with syncopal episodes, Stokes-Adams seizures or sudden death. The condition is inherited as an autosomal dominant gene and appears to be progressive in nature; the risk to life appears to be greatest at 3 particular periods:at or soon after birth, during puberty and the early 20s, and again towards middle age. The type II condition also appears to be progressive and is inherited as an autosomal dominant gene. The pattern, however, tends to develop along the lines of a sinus bradycardia with a left posterior hemiblock, again presenting clinically as syncopal episodes. Stokes-Adams seizures or sudden death when complete heart block supervenes. Both conditions are likely to be widely prevalent throughout the Republic of South Africa. The pathogenesis is discussed in relation to the patterns of the conduction disturbances.     

Recurrent polymorphic ventricular tachycardia complicating radiofrequency catheter ablation of the atrioventricular junction

Recurrent ventricular tachycardia and ventricular fibrillation were observed immediately after RF ablation of the AV junction in a 64-year-old man. This arrhythmia was preceded by ventricular bigeminy and a long-short sequence. It was not associated with prolongation of the QT interval compared to baseline, and recurred 3 months later despite ventricular pacing at 90 beats/min. This is the first reported case of sustained ventricular arrhythmia complicating RF AV junction ablation despite rapid ventricular pacing, and recurring 3 months after discharge. It may explain the rare cases of sudden death complicating this procedure.