Dr. Gallagher et al  wrote 22Baseline electrocardiogram of patients with atriofascicular or atrioventricular pathways (pseudo-Mahaim)  are charElectrocardiogram of fasciculoventricular pathway is characterized by normal frontal plane axis like an anteroseptal accessory pathway (0° to +75°)  with a sThe major findings are the slow conducting and decremental properties that can be assessed during right atrial pacing: AH interval lengthens, HV interval shortens and QRS widens until a steady value is achieved. Faster atrial stimulation does not increase preexcitation, but can prolong AV conduction time until block occurs . DecremeVentricular stimulation usually discloses ventriculoatrial conduction from the A-V node. The vast majority of atriofascicular and atrioventricular pathways have only anterograde conduction ,31. AdenThere are plenty of electrophysiologic and anatomic data supporting the concept that at least atriofascicular pathways are accessory AV nodes. We have seen a patient with an electrophysiologic profile suggestive of the presence of an atriofascicular pathway without conduction through the AV node. This patient had unexplained syncope with a baseline ECG showing LBBB-like pattern with normal PR interval . Atrial Associated conditions: Mahaim fibers (AF/ AV) very often occurs in the setting of Ebstein's disease 10 to 40%) and associated accessory pathways are a commom finding (up to 30%). Fasciculoventricular pathways also occurs very often in association with accessory pathways. I have reviewed the cases reported since 1981 0 to 40% ,23,33,34® SR2 or SR3, which improves stability. The potential may be as large as the His bundle potential or small, narrow with low amplitude. Catheter ablation at a site with "M" potential is likely to be successful (Searching for the "M" (Mahaim) potential  along thccessful . We 20]® SR2 or ccessful , but ocaccessful . We haveActivation mapping of the earliest local ventricular potential is feasible in short atrioventricular pathways like in fast conducting AV accessory pathways. Atrioventricular decremental pathways with a long course often shows extensive arborization over a wide area of ventricular muscle . TargetiShortest stimulus-QRS interval as assessed by atrial stimulation at a constant pacing rate along the atrial aspect of the annulus was the gold standard mapping method before mapping of "M" potential had been reported. Stimulation sites remote from the atrial insertion of the accessory pathway result in long stimulus-QRS interval due to the amount of interposed atrial tissue. We do not use this method because it is time consuming and very inaccurate because it is difficult to stimulate from many sites at the same distance from the annulus and stimulating atrial tissue requires good contact with the tip, which is not always possible.Extrastimulus mapping during antidromic tachycardia. Finding an atrial site where the longest coupled premature extrastimulus causes resetting, or assessing the amount of advancement of the QRS following application of a fixed atrial extraestimulus coupling interval. Similar to the previous technique it looks for a site in the atrial annulus with the least interposing tissue separating it from the accessory pathway proximal insertion. Likewise shortest stimulus-QRS technique is an inaccurate and tedious method.Some authors ,37 reporElectroanatomic mapping (noncontact mapping) ,38 can bSome particular features are unique to Mahaim fibers: Mapping of the atrial insertion by ventricular stimulation is usually not possible because those decremental pathways do not conduct retrogradely. Atrioventricular connections can be located by mapping the site of earliest ventricular activation on the annulus, as with other anterogradely conducting accessory AV pathways. On the contrary, atriofascicular pathways or even the long atrioventricular pathways with distal (nonannular) insertion cannot be mapped in this way. To worse matters these decremental pathways are unusually sensitive to mechanical trauma. Inadvertent knocking of the ablation catheter against the annulus can result in transient abolition of conduction through the pathway from minutes to hours ,35. The Radiofrequency current should be applied during atrial pacing to enhance preexcitation and making it easier to assess conduction block at the AP. Stability is improved during atrial pacing as compared with ablation during antidromic tachycardia when catheter is likely to move with tachycardia termination. MAT is a common and expected event and can also cause catheter displacement. Before "M" potential mapping technique became the gold standard mapping technique some authors favored targeting the ventricular insertion to avoid MAT and maintain a better catheter stability .Catheter ablation have been very successful particularly when ablating at a site with "M" potential or assessing earliest delta-V interval in atrioventricular decremental pathways .


Fascicular ventricular tachycardia (VT) is an idiopathic VT with right bundle branch block morphology and left-axis deviation occuring predominantly in young males. Fascicular tachycardia has been classified into three subtypes namely, left posterior fascicular VT, left anterior fascicular VT and upper septal fascicular VT. The mechanism of this tachycardia is believed to be localized reentry close to the fascicle of the left bundle branch. The reentrant circuit is composed of a verapamil sensitive zone, activated antegradely during tachycardia and the fast conduction Purkinje fibers activated retrogradely  during tachycardia recorded as the pre Purkinje and the Purkinje potentials respectively. Catheter ablation is the preferred choice of therapy in patients with fascicular VT. Ablation is carried out during tachycardia, using conventional mapping techniques in majority of the patients, while three dimensional mapping and sinus rhythm ablation is reserved for patients with nonmappable tachycardia. The first report of fascicular ventricular tachycardia was in 1979 by Zipes et al  in 1981 Zipes et al  postulatFascicular tachycardia has been classified into three subtypes  (1) leftFascicular tachycardia can be induced by programmed atrial or ventricular stimulation. Administration of isoprenaline by infusion may be needed to facilitate induction in some cases; however this tachyarrhythmia may be non inducible in a significant number of patients ,11. It iThe tachycardia circuit can be constructed from the observations during VT. During tachycardia two distinct potentials can be observed before the ventricular electrogram, namely the purkinje potential (PP) and pre Purkinje potential (Pre-PP), also designated P2 and P1 respectively  13,14].,14.13,14During VT, the antegrade limb of the circuit proceeds through the specialized, verapamil sensitive zone from the basal to the apical site of the left ventricular septum, giving rise to the Pre PP. Therefore the earliest Pre-PP is seen in the basal septum and the latest pre-PP is seen in the apical septum. The lower turn around site of the reentrant circuit occurs in the lower third of the septum with the capture of the fast conduction Purkinje fibers which are rapidly activated in either direction during tachycardia. Antegrade activation occurs down the septum to break through in the posterior septal myocardium below, and retrograde activation occurs over the posterior fascicle from apical to basal septum forming the retrograde limb of the tachycardia. The reentrant circuit of fascicular tachycardia is completed by a zone of slow conduction between Pre PP and PP areas in the basal interventricular septum. The slow conduction zone which is the upper turn around point of the circuit is located close to the main trunk of the left bundle branch .  The opFascicular VT is frequently misdiagnosed as supraventricular tachycardia with aberrancy on account of the narrow-QRS duration during tachycardia (120 ms), responsiveness to intravenous verapamil, and the occurrence in young patients with structurally normal hearts . HoweverInterfascicular VT, which is a type of bundle branch reentrant VT, has a typical RBBB morphology and left or right axis deviation during VT mimicking fascicular VT. However, interfascicular VT is most commonly seen in patients with an anterior infarction and either left anterior or posterior hemi fascicular block. During EP study, the ventricular depolarization is preceded by His bundle depolarization in interfascicular VT which is not seen in fascicular VT .Idiopathic mitral annulus VT has RBBB morphology with right axis deviation of the frontal QRS vector and hence mimics anterior fascicular VT. Tada et al  describeThe first report of ablation of fascicular VT was in 1987 by Fontaine et al  by the aUsually ablation of this tachycardia is performed during VT because the electrophysiologic targets are clear and the end point of ablation is termination of tachycardia. Various investigators have used different targets for ablation during tachycardia.Nakagawa et al  preferreAiba et al  and NogaIn patients with non-inducible tachycardia and in those with ill sustained tachycardia during the study, mapping and ablation during tachycardia is not possible. Moreover, the critical substrate of the tachycardia is amenable to mechanical injury due to catheter manipulation, thus making the tachycardia non-inducible during the study. Various methods of mapping and ablation of fascicular VT in such patients have been described.In general, pace mapping is more useful in mapping focal tachycardias whereas outcomes in reentrant tachycardia ablation are less favourable ,24. In tAnatomic data gathered together with endocardial electrogram data by various electroanatomic mapping systems have facilitated ablation of this arrhythmia in sinus rhythm. Chen et al  reportedCatheter ablation is the preferred choice of therapy in patients with fascicular VT. The success rate for ablation is more than 80% and complications are infrequent. Most of the patients with fascicular VT can ablated during tachycardia, using conventional mapping techniques. Three dimensional electro anatomical mapping and sinus rhythm ablation is to be reserved for patients with non - inducible or illsustained tachycardia and in patients with recurrences.


Although interventional electrophysiology and the use of radiofrequency energy to cure various arrhythmias primarily developed in the adult population, similar applications in children have grown dramatically over the last decade. The anatomic basis for various arrhythmias is critically important for the pediatric ablationists to appreciate. Such understanding allows the use of alternative technique to affect cure while avoiding complications. Further, because of the relatively small heart and less thick myocardium in children, without the appreciation of the underlying cardiac anatomic relationships, collateral injury, for example to the arterial system, may occur. In this review, the cardiac anatomic consideration important in approaching various supraventricular and ventricular arrhythmias in the normal heart is discussed. The last two decades have witnessed tremendous change in the care of children with symptomatic cardiac arrhythmia. The anatomic basis for various cardiac arrhythmias (in children and adults) has been much better understood, particularly for common supraventricular tachyarrhythmia.While cardiac electrophysiology still forms the basis for electrophysiological study and radiofrequency ablation for supraventricular arrhythmia, pure anatomic approaches are evolving with appropriate adjunctive electrophysiological maneuvers performed prior to energy delivery. Radiofrequency ablation for AV node reentry and paroxysmal atrial fibrillation is performed almost entirely as an anatomy-based ablation in many centers -2.Radiofrequency ablation was initially reported as a feasible, successful, and safe therapy that could be used in children as an alternative to drug therapy in 1991 . There aOver 90% of supraventricular arrhythmia in children is a result of a reentrant mechanism . The secwithout necessarily effecting the His bundle electrogram, yet either advancing or delaying the subsequent atrial electrogram [In the initial few decades of cardiac electrophysiology, AVNRT was thought to represent a reentrant arrhythmia arising entirely from the compact AV node. This was because there was nearly simultaneous activation of the ventricle and atrium observed from the earliest recorded demonstration of this arrhythmia. If this were to have been the case (entire circuit in AV node), radiofrequency ablation for this arrhythmia without heart block would not have been possible. It later became recognized that AV node reentry could be reset and entrained from the atrium particularly the posteroseptal annular atrial tissue . Importactrogram . PioneerThe circuit for this arrhythmia, however, is far from completely understood. While it is accepted that atrial inputs to the AV node are necessary components to the circuit (see below), certain less commonly observed phenomena do suggest a distinct difference from AVNRT and any other macroreentrant atrial tachycardia. AVNRT can be dissociated from the ventricle either with block occurring in an infra-Hisian location (more common) or above the bundle of His. Also clearly observed and well documented are cases of AV node reentry with dissociation of the tachycardia from all recorded atrial tissue .The sinus impulse originates epicardially at the junction of the crista terminalis and the superior vena cava, where as the atrioventricular conduction system is located anteriorly and septally on the annulus. Specifically, the penetrating bundle of His is consistently found at the junction of the noncoronary cusp and right coronary cusp of the aortic valve where it meets the commissure of the anterior and septal leaflets of the tricuspid valve (membranous intraventricular septum). The compact AV node itself is located relatively more atrial and more posteriorly (closer to the coronary sinus) in the mid-septal tricuspid annulus when compared to the penetrating bundle of His. Although the compact AV node is relatively atrial to the His bundle, it is always found ventricular to the Eustachian ridge and the underlying tendon of Todaro within the so-called triangle of Koch. This triangle is bounded anteriorly by the tricuspid annulus, posteriorly by the tendon of Todaro, and inferiorly by the coronary sinus.The atrial inputs into the AV node that carry the sinus node impulse (or paced impulse) are not diffuse but along distinct anatomic pathways. This is because of the anatomic obstacles in the atrium (particularly right atrium) that the impulse must circumvent to reach the AV node. The atrial myocardial input to the AV node that occurs superior to the fossa ovalis and through the apex of the triangle of Koch is referred to as the fast pathway. The posterior inputs to the AV node traverse to this structure along the interatrial septum. These posterior inputs may involve the myocardial sleeves along the coronary sinus and the posteroseptal right atrium in the region of the coronary sinus ostium. The posterior inputs are referred to as the slow pathway and may be more than one in number (right and left-sided slow pathways). The actual junction of these posterior inputs into the AV node is likely through extensions of compact AV nodal and transitional AV nodal tissue called the posterior horns. This anatomic distinction between the atrial myocardial inputs to the AV node forms the essential substrate for AV node reentrant tachycardia.fast pathway.It should be noted that the distinction between the fast and slow pathways, while although partially reflective of the different conduction and refractory properties, is fundamentally an anatomic distinction . In otheThis anatomic distinction of the fast and slow pathway is not easily ascertained in the antegrade direction and involves complex entrainment maneuvers during AV node reentry to provide evidence. On the other hand, retrograde activation of the atrium during AV node reentry or ventricular pacing is straightforward in demonstrating proof of the anatomic separation of the two limbs of the AVNRT circuit. During typical AV node reentry or during ventricular pacing with retrograde activation of the fast pathway, the earliest recordable site of atrial activation is just behind the tendon of Todaro, close to the apex of the triangle of Koch. Whereas with atypical AV node reentry or retrograde activation via the slow pathway during ventricular pacing, the earliest recorded atrial electrograms are in the region of the coronary sinus ostium (posterior).The fact that atrial myocardium is essential to the circuit of AV node reentry is more than semantics and forms the basis for all atrial AVNRT ablation procedures. While ablating either the anatomic fast or slow pathway will prevent future AVNRT, the exit site of the fast pathway is fairly close to the compact AV node and separated only from this structure by the tendon of Todaro. The slow pathway, however, (see below) can be ablated 4 of 5 cm from the compact AV node with little or no risk of AV block. This distinction in the anatomy of the two pathways to the AV node is critical for safe ablation in young children.It is important for ablationists to understand the fluoroscopic anatomy of the fast pathway. In the RAO projection as anticipated, the fast pathway site is more atrial (behind the Eustachian ridge) than the compact AV node and, of course, the penetrating bundle of His. The characteristic fluoroscopic appearance, however, when mapping the fast pathway, is best noted in the LAO projection . As the The slow pathway fibers are funnel-like and triangular in section with the apex of the triangle inserting into the compact AV node and the base fanning out into the posterior interatrial septum both involving the fibers of the coronary sinus and the right posterior septal atrium . Thus, tBecause of the relatively smaller hearts and thus closer proximity of the compact AV node to the atrial input sites, ablation in children should be performed as far away from the compact AV node as possible ,7. UnderBecause of relatively rapid conduction times in children, it can be difficult to distinguish whether retrograde activation is via the slow pathway or fast pathway. Thus, there is often simultaneous activation of the atrium as recorded on the His bundle catheter and the proximal coronary sinus catheter. Specific mapping, understanding the fluoroscopic anatomy as detailed above of the fast pathway will clarify the situation.In children who have a persistent left superior vena cava, the coronary sinus including the ostium can be very large. This can make ablation of the slow pathway difficult. This difficulty is because of the lack of catheter stability created by the large coronary sinus ostium and the fact that multiple slow pathway inputs related to the diverse musculature of the enlarged coronary sinus will require attention. Again, linear ablation including careful ablation within the coronary sinus is most likely to be effective .In children, because of relatively rapid conduction times through the fast pathway, typically AVNRT may present as a long R-P tachycardia. This is because in AVNRT, activation of the atria and ventricle occur from a common turnaround point likely within the compact AV node or next to it (slower common pathway). When fast pathway activation is rapid, then atrial activation proceeds ventricular activation, giving rise to a long R-P interval. The P wave will be narrow and negative in leads 2, 3, and aVF unlike the wide P waves that result from slow pathway activation . Once catheters are placed, specific mapping of the fast pathway will show earlier activation than the anatomic slow pathway region .Activation of the left atrium in sinus rhythm or any right atrial rhythm occurs primarily through Bachmann's bundle and through the coronary sinus musculature. In children, Bachmann's bundle activation can be rapid. This occurrence can give rise to unusual activation patterns in the coronary sinus in children with typical AVNRT . If one Wolff-Parkinson-White syndrome results when an accessory pathway is present that electrically connects ventricular and atrial myocardium and gives rise to reentrant supraventricular tachycardia. The electrocardiographic recognition and electrophysiological approach to management of this syndrome in children is discussed elsewhere . SpecifiAccessory pathways in children, as well as adults, is sometimes classified into endocardial and epicardial types. In a strict anatomic sense pathways are always epicardial. That is the atrioventricular connection occurs exterior to the fibrous annulus . However, most of these pathways can be ablated either on the pathway itself or its atrial or ventricular insertion with standard endocardial techniques. In a few exceptional circumstances the pathway is truly epicardial in that the atriovenous connection occurs through another epicardial structure . In an analogous fashion, pathways that course through the fibrous trigone represent situations where standard endocardial ablation is unlikely to be successful for an anatomic reason.Muscular extensions  into most cardiac veins including the superior vena cava, pulmonary veins and the coronary sinus exist ,12. ThisWhile technically atrioventricular connections (accessory pathways) should be possible at any point along the atrioventricular annulus, an exception occurs in the region of the aortic mitral continuity. Thus, left anteroseptal accessory pathways (and left anterior) are exceedingly rare compared to other locations. This is because of the unique position of the aortic valve preventing direct atrioventricular connections as could occur across the annulus in other locations. For accessory pathways to occur here, the cardiac muscle (pathway) would have to apparently cross the central fibrous trigone. While this may occur another possibility more evident from recent case description is a connection from the atrial myocardium to the supra-aortic valvar myocardial extension (see below) under ventricular tachycardia and from there to the ventricular myocardium . The sitAnother non-annular anatomic situation where atrial and ventricular myocardial tissue is apposed is with respect to the appendages. Accessory pathways that involve electrically active myocardial connection occur between the appendages and the underlying ventricle. Although rare, when seen, these connections constitute an accessory bypass tract as conduction can proceed through these fibers independent of the AV node. When such tracts are diagnosed in children, the optimal approach is to ablate in a circumferential manner isolating a portion of the left or right atrial appendage close to its ostium. While the actual connection may also be targeted deep in the appendage, the risk of perforation in children is high. Targeting the ventricular insertion is typically futile as it is often multiple.Some accessory pathways may be located in the typical atrioventricular annular location, however, demonstrate unusual physiological properties such as decremental conduction or lack of typical responses to decremental atrial pacing etc. The nomenclature for these pathways is confusing with historical and contemporary usage significantly different . The anaIn present electrophysiology terminology, a Mahaim fiber is a true accessory bypass tract connecting the free wall of the right atrium to either ventricular myocardium or the infra-Hisian conduction system. Unlike a typical accessory pathway, however, Mahaim fibers have AV node-like characteristics near the annulus and connect to relatively apical myocardium or the infra-Hisian right bundle-branch system through an insulated fascicle similar to the His bundle/right bundle-branch.These pathways, when they occur in children with relatively rapid AV nodal conduction, can be exceedingly difficult to recognize as accessory pathways ,16. TheyWhile Mahaim fibers do not conduct retrograde, pathways that conduct either exclusively retrograde or bidirectionally occur and are responsible for the syndrome labeled PJRT . These pathways are distinguished from Mahaim fibers by having the ventricular and atrial insertions close to the annulus and conducting retrograde. There is no relationship anatomically with these pathways and the normal conduction system. For unclear reasons, retrograde decremental pathways are often found in the region of the pyramidal space, close to the coronary sinus ostium in the posterior right or left atrium . PathwayUnlike a Mahaim fiber that connects atrial myocardium to the ventricular myocardium, nodoventricular pathways connect compact AV nodal tissue either to the fascicular system (right or left bundle branch) or the ventricular myocardium. For these pathways to occur and participate in tachycardia, some form of longitudinal dissociation in the AV node is required, that is antegrade conduction through the AV node and then down the nodoventricular/fascicular tract and then retrograde to AV nodal tissue occurs over a conduction interval too short to be allowed by the usual refractory period of the AV node. The anatomic basis for such dissociation or in fact a convincing example of the anatomy/pathology of these connections is lacking and has prompted some electrophysiologists to question their existence ,20. AlthNormally, there is a fibrous sleeve of insulation on the penetrating bundle of His and the right and left bundle branches until this sleeve disappears and the bundle branch tissue connects to the ventricular myocardium (bundle branch exit). In some patients, there is a breach in this insulation and ventricular excitation occurs closer to the base on the septum either directly from the His bundle or from the proximal bundle branches. This is termed a fasciculoventricular connection or pathway. The reader should note that these do not represent true atrioventricular accessory bypass tracts since anatomically there is no direct connection from the atrium to ventricular myocardium. Importantly, when the AV node blocks, there is no pre-excitation and progressive decrement in AV nodal conduction is not associated with progressive pre-excitation as seen with typical atrioventricular bypass tracts. The pediatric electrophysiologist should be cognizant of this anatomic variant and differentiate these electrophysiologically from true bypass tracts since fasciculoventricular tracts are not associated with tachycardia and should not be targeted for ablation.In the pediatric population, in patients without prior cardiac surgery or congenital heart disease, atrial flutter and atrial fibrillation are uncommon. While atrial flutter is one of the most frequent causes of fetal tachycardia, after birth, the arrhythmia is rarely seen without coexisting cardiac disease. Similarly, atrial fibrillation in the pediatric age group is unusual without coexisting disease such as the Holt-Oram syndrome or with familial/inherited atrial fibrillation. From the anatomic perspective, a few important differences are significant with pediatric ablation and are outlined below .The cavo-tricuspid isthmus also referred to as the subeustachian isthmus is the critical zone for the typical atrial flutter circuit . This isRecognizing the occurrence of this pouch is also important when attempting to cannulate the coronary sinus including for cardiac resynchronization procedures, and this issue if explained more fully in another manuscript in this series.When ablating atrial fibrillation in children, the pulmonary veins are typically isolated. However, the veins tend to be smaller in children and the sleeve of myocardium entering the vein is also smaller . FurtherBecause of the small pulmonary veins and branches, acute occlusion of one of the venous branches may occur during ablation. When venography is performed, it can be difficult to know whether a branch has been occluded or did not exist at all. A simple anatomic rule of pulmonary vein branching can assist the operator in making this decision. Daughter veins that tend to coalesce into a parent trunk have a consistent relationship in terms of the diameter or circumference. The diameter (or circumference) of the daughter veins (tributaries) when added up always is greater (110%) than the diameter (or circumference) of the main vein .Although ventricular tachycardia ablation in children has gone from a rarely performed procedure to more frequently done, it still remains most likely required in children with congenital heart disease or other structural abnormalities. When significant structural abnormality is present , a defibrillator has often been placed, and the ablation procedure performed to minimize frequent shocks. The use of defibrillators in children and principles of radiofrequency ablation in pediatric scar-related VT are covered elsewhere in these discussions and this supplement. In this paper, we will expand on the anatomic basis of the two most common ventricular tachyarrhythmias found in children with otherwise structurally normal hearts.Outflow tract ventricular tachycardia is characterized by exercise-related wide QRS tachycardia that mostly occurs in active older boys and less commonly as paroxysmal VT in postmenarchal girls. In a few children with right ventricular outflow tract tachycardia, underlying cardiomyopathy, particularly arrhythmogenic right ventricular cardiomyopathy is found, but the vast majority have no obvious structural heart disease. An accurate understanding of the underlying anatomy of the outflow tracts is critical to safe catheter manipulation, mapping, and ablation of this arrhythmia in children. Pediatric ablationists should familiarize themselves with the relative positions of the right and left ventricular outflow tracts, myocardial sleeves that extend beyond the semilunar valves, and knowledge of the coronary arterial systems relative to both the left and right ventricular outflow tracts.rightward and posteriorly should prompt consideration of left ventricular outflow tract mapping. Similarly, when mapping the left ventricular outflow tract, leftward and anterior activation sites should prompt reconsideration of meticulous mapping of the posterior right ventricular outflow (a site where catheter positioning is not straightforward)  .Myocardial sleeves have been well described that extend beyond the semilunar valves to various lengths endocardial to the great arteries. While these occur in all age groups, the relative lengths of these myocardial sleeves appear to be longer in infants and young children . When maleft main coronary artery. While it is common for ablationists to consider performing coronary angiography when ablating in the left ventricular outflow tract, the proximity of the ostium and initial course of the left main coronary artery is closer to the a catheter position to deliver radiofrequency energy in the posterior right ventricular outflow tract close to the pulmonic valve. Because of the relatively shorter angle formed in very young patients and the lack of thick myocardial separation, particular care when ablating at these locations in children is required. When doubt exists, either intracardiac echocardiography to carefully document the separation between the ablating catheter and the coronary arteries  or coronary angiography should be performed [Because the pulmonic valve is cephalad and leftward of the aortic valve, the posterior portion of the right ventricular outflow tract just above and at the level of the pulmonic valve is very close to the erformed .Exercise-related ventricular tachycardia in structurally normal hearts that exhibit a right bundle branch block superior access morphology is usually mapped and ablated in the region of the left posterior fascicle (Belhassen's VT). While the heart is typically structurally normal, tissue that traverses the left ventricular cavity from the septum to the free wall is sometimes found close to the region of successful ablation. These have been variously referred to as false tendons, interpapillary muscle chords, left ventricular chords, or lancisi fibers. While such structures are commonly found even in patients without ventricular tachycardia that has been documented when clearly recognized with an imaging modality (echocardiography), their presence can guide the ablationist, particularly when tachycardia has been difficult to induce.An important trend in contemporary electrophysiology is anatomy-based ablation. Although the pediatric electrophysiologist still needs to clearly understand the physiological principles underlying various mapping, diagnostic, and ablation maneuvers, an appreciation of the underlying cardiac anatomy has become critical.Understanding cardiac anatomy will help minimize complications including collateral damage to the AV conduction system, pulmonary veins, and neighboring structures in the pyramidal space of the heart. Further, an appreciation of the complex anatomy of the ventricular outflow tracts, particularly in children allows accurate correlation between mapping, electrocardiographic, and imaging data. Such understanding again decreases the likelihood of damage to the coronary arteries while facilitating successful ablation.


Retrograde ventriculoatrial conduction in persons with implanted dual chamber pacemakers can cause two types of responses. One is the familiar pacemaker mediated endless loop tachycardia. Another less known response is the repititive non-rentrant ventriculoatrial synchrony (RNRVAS). Both conditions produce similar symptoms due to the loss of atrial booster function and the presence of the reverse atrial kick, which initiates neurocardiogenic responses.In this form of tachycardia, the pacemaker actively participates in the tachycardia circuit. Retrograde conduction of a ventricular beat causes a P wave which is sensed by the the pacemaker circuit, triggering off the next ventricular stimulus at the end of the programmed AV delay. This cycle is repeated and results in an endless loop tachycardia at the programmed upper rate of the dual chamber pacemaker. This situation is more common in those who have been implanted a pacemaker for sinus node dysfunction, though retrograde conduction can be rarely intact in those with anterograde AV block. The trigger for the tachycardia is usually an appropriately timed ventricular premature beat. Occasionally it could be triggered by an atrial premature beat occurring within the post ventricular atrial refractory period. Pacemaker mediated endless loop tachycardia can be terminated by the application of a magnet and prevented by re-reprogramming the post ventricular atrial refractory period (PVARP). Interestingly, Barold et al  have repRNRVAS  is less A long AV interval as well as a fairly fast programmed lower rate favour the development of RNRVAS . The fas


Forty-four-year-old male patient with surgical closure of ostium secundum type atrial septal defect at the age of 9 years had undergone radiofrequency catheter ablation of the cavotricuspid isthmus because of recurrent drug-resistant typical isthmus-dependent atrial flutter, with bi-directional isthmus block achieved. Only few days later he started to suffer again high-rate tachycardia. An atypical atrial flutter was diagnosed on ECG . This onA second ablation was attempted, with 20-polar catheter deployed in the right atrium around the tricuspid annulus such that its tip was in the inferolateral part of the cavotricuspid isthmus, 6-polar catheter in the coronary sinus, and use of EnSite NavX electroanatomic mapping system . Surprisingly, the intracardiac recordings showed activation sequence resembling the same counter-clockwise atrial flutter that was previously ablated , althoug Electroanatomic activation map showed macroreentrant atrial tachycardia with the wave-front circulating around the presumed post-operative scar on the right atrial free wall . The volPatients with previous congenital heart surgery not infrequently develop atrial tachycardias late after the operation. These tachycardias are predominantly macroreentrant and the cavotricuspid isthmus often is part of the reentrant circuit. The incisional scar in the right atrial free wall and the cavotricuspid isthmus make together long protected corridor potentiating the occurrence and the perpetuation of peritricuspid reentry. Gaps in the scar predispose to the occurrence of reentrant tachycardias in the right atrial free wall with the scar acting as the central obstacle of the circuit . The sam


Arias et al in the article 'A narrow QRS complex tachycardia with an apparently concentric retrograde atrial activation sequence' describe a case with spontaneous intra atrial block along the mitral isthmus to explain the change in atrial activation . This ph


We report an unusual presentation of supraventricular tachycardia, in an infant, with cyanosis. The child had atrial septal defect with hypoplastic right ventricle. Radiofrequency ablation was performed in view of drug resistant SVT Cardiac arrhythmias are relatively uncommon in the younger population, accounting for approximately 5% of all emergency cardiac admissions. ParoxysmA 10-month-old male born at full term of non-consanguineous marriage presented with episodic listlessness associated with bluish discoloration of the lips. He had recurrent respiratory tract infections and a failure to thrive.2 saturation of 95% at rest); a normal-sized heart; quiet precordium, and a Grade II/VI short ejection systolic murmur in the left parasternal region. A chest X-ray showed mild cardiomegaly with normal vascularity. An echocardiography revealed a large ostium secundum atrial septal defect (ASD) with bidirectional shunt. There was no pulmonic stenosis or pulmonary hypertension. However, the right ventricle was hypoplastic [During one such episode, the pediatrician noted rapid heart beats and an ECG revealed narrow QRS tachycardia at the rate of 260 beats per minute. Oxygen saturation was 80% on room air. Adenosine terminated the tachycardia. A post-termination ECG in sinus rhythm did not reveal preexcitation. A clinical examination during sinus rhythm revealed an absence of cyanosis  study with a view to radiofrequency (RF) ablation. Amiodarone was omitted for 10 days prior to the EP study. At the time of the procedure, the child was 1 year old and weighed 7.2 kg. The procedure was performed under general anesthesia.A 5F sheath was introduced in the left femoral vein through which a 5F deflectable decapolar catheter was introduced in the coronary sinus. A 4F sheath was used in the right femoral vein and a 4F quadripolar catheter was introduced in the bundle region. The HV interval was normal. The ventriculo-atrial (VA) conduction was eccentric via a concealed left lateral accessory pathway (AP). An orthodromic AVRT  could beAn additional 5F sheath was introduced in the right femoral vein. A 5F radiofrequency ablation catheter was used. Mapping was performed during left ventricular pacing (via the ASD) using the quadripolar catheter. The mitral annulus was mapped and the site of AP identified. Radiofrequency energy was applied in the temperature controlled mode with a cut-off of 60 degrees centigrade and power limit of 25 watts. Successful RF ablation  was perfAccessory pathway mediated tachycardias constitute 80% of all the tachyarrhythmias during infancy. In some infants they resolve as the child grows. Most SVTRadiofrequency ablation is uncommonly performed under 5 years of age. This is because some SVTs resolve spontaneously. Also, arrhythmias may get suppressed under the influence of anesthesia at the time of RF ablation. Patient size poses limitations in using multiple electrode catheters and there is an increased possibility of cardiac/valve damage with ablation. The risks of ablation are acceptable only if the child has recurrent, drug-resistant SVT especially if it results in tachycardiomyopathy or life-threatening cardiovascular compromise.‐8Our case of SVT is unique in its presentation with cyanosis. This 1-year-old child had recurrent, drug-resistant SVT. The large ASD and hypoplastic RV resulted in hypoxia during SVT. The right to left shunt may have increased during rapid heart rates because of the shortening of diastole and increased trans-tricuspid gradient-almost similar to what one sees during tachycardia in mitral stenosis. Propafenone or flecainide are probably more effective agents for managing these tachycardias; however, these are not easily available in India. Adenosine responsiveness of the tachycardia suggested AV node dependant SVT and therefore is more likely to be successfully ablated. The large ASD provided easy access to the left heart for ablation without the need for arterial access.Left-sided accessory pathways has been accessed by the antegrade  or the retrograde trans-aortic route (via the aorta and left ventricle). In young children, the antegrade approach is preferred to avoid damage to the aortic/mitral valves and also avoiding arterial access. Radiofrequency ablation by the antegrade approach was facilitated in our patient because of the ASD. Tackling the SVT before ASD closure in patients with left-sided AP avoids the inconvenience of a septal puncture through the ASD patch. Mapping and RF ablation was performed in our patient during LV pacing. The latter allowed VA conduction exclusively over the left lateral AP.The current case highlights a rather unusual presentation of SVT with cyanosis. The resistant nature of the tachycardia and non availability of a certain group of anti-arrhythmics prompted us to undertake RF ablation in this young child. The presence of an ASD certainly facilitated the approach to the AP located on the left lateral wall.


Cardiac rhythm disturbances such as bradycardia (heart rate < 50/min) and tachycardia (heart rate > 100/min) require rapid therapeutic intervention. The supraventricular tachycardias (SVTs) are sinus tachycardia, atrial tachycardia, AV-nodal reentrant tachycardia, and tachycardia due to accessory pathways. All SVTs are characterized by a ventricular heart rate > 100/min and small QRS complexes (QRS width < 0.12 ms) during the tachycardia. It is essential to evaluate the arrhythmia history, to perform a good physical examination, and to accurately analyze the 12-lead electrocardiogram. A precise diagnosis of the SVT is then possible in more than 90% of patients. In ventricular tachycardia (VT) there are broad QRS complexes (QRS width > 0.12 s). Ventricular flutter and ventricular fibrillation are associated with chaotic electrophysiologic findings. For acute therapy, we will present the new concept of the five ‘A's, which refers to adenosine, adrenaline, ajmaline, amiodarone, and atropine. Additionally, there are the ‘B,’ ‘C,’ and ‘D’ strategies, which refer to beta-blockers, cardioversion, and defibrillation, respectively. The five ‘A’ concept allows a safe and effective antiarrhythmic treatment of all bradycardias, tachycardias, SVTs, VT, ventricular flutter, and ventricular fibrillation, as well as of asystole. Emergency medicine and critical care are fields that call for rapid diagnosis and intervention in specific situations. In cardi3Bradycardia, defined as a heart rate < 50 beats/min, may be caused by different mechanisms and have various etiologies . Sinoatr5Narrow-QRS tachycardia is a cardiac rhythm with a rate faster than 100 beats per minute and a QRS duration of less than 0.12 s. The patient with narrow-QRS tachycardia usually seeks medical attention because of palpitations, light-headedness, shortness of breath, or anxiety. In many patients with narrow-QRS tachycardia, the heart rate is very high (180-240 beats per min) and therefore, after onset of the tachycardia, the patient will arrive very soon in an intensive care unit for diagnosis and treatment.The narrow-QRS complex indicates that AV conduction occurs through the AV node. ECG documentation of the tachycardia is extremely important so that the mechanism of the tachycardia can be diagnosed and the patient can be given the correct emergency treatment. Causes of narrow QRS tachycardia are sinus tachycardia, atrial tachycardia, atrial flutter, atrial fibrillation, AV nodal reentry tachycardia (AVNRT), and orthodromic circus movement tachycardia (CMT) . There aBecause a drug given for the treatment of SVT may be deleterious to a patient with ventricular tachycardia (VT), the differential diagnosis in broad-QRS tachycardia is critical. Wide-QRS complex tachycardias (QRS duration > 0.12 s) often pose a difficult diagnostic and therapeutic problem . Errors Approximately 1,000 people suffer from cardiac arrest each day in the US, most often as a complication of an acute myocardial infarction with accompanying ventricular fibrillation (VF) or unstable VT . In 200510In emergencies due to arrhythmias, rapid and correct diagnosis is necessary for adequate therapy. The clinical symptoms, the physical examination, and the 12-lead electrocardiogram are important sources of information for making a correct diagnosis . Of courIn patients with ventricular flutter or ventricular fibrillation, syncope following cardiac arrest is the leading clinical sign.ECG documentation is one of the most important steps for correct diagnosis and treatment. It is necessary to divide tachycardias into those with narrow QRS complexes (QRS < 0.12 s) and those with wide QRS complexes (QRS > 0.12 s) Figures  and 4. SSometimes, in emergencies, treatment of bradyarrhythmias, tachyarrhythmias, ventricular flutter, or ventricular fibrillation can be difficult. Younger colleagues and those not familiar with clinical electrophysiology sometimes do not know what to do when a patient develops an arrhythmia. Therefore, we would like to present a new concept for the treatment of arrhythmias in an emergency, a concept that involves only five drugs, all beginning with ‘A’ - adenosine, ajmaline, amiodarone, adrenaline, and atropine - the five ‘A’ concept .vs 91%, P = ns).[In regular narrow-QRS complex tachycardia, vagal maneuvers should be initiated to terminate the arrhythmia or to modify AV conduction. If this fails, intravenous antiarrhythmic drugs should be administered for arrhythmia termination in hemodynamically stable patients. Adenosine, calcium channel blockers, or beta- blocking agents are the drugs of first choice. Adenosine was approved by the Food and Drug Administration in 1990 and is today the treatment of choice for acute therapy of SVT . Adenosi16 P = ns). Higher dThe initial approach in patients with wide-QRS complex tachycardia depends on the hemodynamic stability and the symptoms associated with the tachycardia. When the patient is hemodynamically unstable or has pulmonary edema, the tachycardia should be promptly cardioverted with a direct current (DC), synchronized shock. Once the hemodynamically stable patient has been cardioverted and stabilized, it is important to evaluate the preconversion 12-lead ECG for the QRS configuration and signs of AV dissociation as described elsewhere in this manuscript. In patients with sustained (duration > 30 s), hemodynamically stable, monomorphic VT, amiodarone  plays an important role in terminating the arrhythmia; this drug is discussed in detail later. An alternative treatment is the administration of procainamide (10 mg/kg i.v.) or ajmaline (50-100 mg i.v. over 5 min), both of which can provide high termination rates . In patiP = 0.03).[Amiodarone is currently regarded as the most effective antiarrhythmic drug available for the treatment of patients with both supraventricular and ventricular tachyarrhythmias. It is considered to be particularly useful in patients with life-threatening ventricular tachyarrhythmias . The mos = 0.03). The role = 0.03). Today, a = 0.03).24 Despitet al.[P = 0.84), basic life support  and time to first defibrillation  were significantly correlated with good neurologic outcome. In addition to the better neurologic outcome, among the patients who did not receive basic life support, the average cost per patient with good neurologic outcome significantly increased with the delay of the first defibrillation (P < 0.001). The importance of cerebral perfusion and pressure and cerebral tissue oxygen tension during cardiopulmonary resuscitation has been described elsewhere.[1 and α2 receptors almost equally, and β1 and β2 receptors in a ratio of approximately 1: 4.[et al.[The importance of vital organ perfusion in patients suffering cardiac arrest makes arterial vasomotor tone, and the resultant perfusion pressure, critical in resuscitation from sudden death. After failure of DC countershock, ventilation, and oxygenation, the target organ for resuscitation pharmacotherapy is the arterial vascular smooth muscle cell. There is general agreement that bystander first aid, defibrillation, and advanced life support are essential for good neurologic outcome in patients after a cardiac arrest. Bur et al. evaluatelsewhere. Over theely 1: 4. The Amerely 1: 4. Few of tely 1: 4. This sol4.[et al. They com1 receptors. Wenzel et al.[vs 43.0%) or pulseless electrical activity were present (33.7% vs 30.5%) (P = ns). In accordance with these results, the guidelines of the American Heart Association and European Resuscitation Council recommended 40 units vasopressin intravenously and 1 mg adrenaline intravenously as equally effective for the treatment of patients with ventricular fibrillation [Another important vasopressor drug is vasopressin. It acts directly on contractile elements by way of Vel et al. studied illation . There i33.7% vs .5% (P = Atropa belladonna), jimsonweed (Datura stramonium), mandrake (Mandragora officinarum), and other plants of the family Solanaceae. It is a secondary metabolite of these plants and serves as a drug with a wide variety of effects. It is a competitive antagonist for the muscarinic acetylcholine receptor. It is classified as an anticholinergic drug. Atropine increases firing of the SA node and conduction through the AV node, opposes the actions of the vagus nerve, blocks acetylcholine receptors, and decreases bronchiole secretions. In general, atropine lowers the parasympathetic activity of all muscles and glands regulated by the parasympathetic nervous system. This occurs because atropine is a competitive antagonist of the muscarinic acetylcholine receptors. Acetylcholine is the main neurotransmitter used by the parasympathetic nervous system. Atropine may cause swallowing difficulties and reduced secretions. Atropine works because the main action of the vagus nerve of the parasympathetic system on the heart is to decrease the heart rate. Atropine blocks this action and, therefore, may increase the heart rate. Indications for atropine administration are vagus-mediated sinus bradycardia, blocks in the AV node, and vagus-mediated asystole.[Atropine is a tropane alkaloid extracted from deadly nightshade (asystole. For sympasystole.. Atropinasystole.Emergency medicine and critical care are fields that often require rapid diagnosis and intervention for specific situations. It is well known that in all patients with tachyarrhythmias, evaluation of the underlying etiology and the degree of left ventricular dysfunction is essential. Correct treatment of arrhythmias in the intensive care setting is based on an understanding of the mechanisms that cause the situation. The therapeutic role of antiarrhythmic drugs in the management of atrial fibrillation or cardiac arrest is debatable. For acute therapy, there is the new concept of the five ‘A's, which refers to adenosine, adrenaline, ajmaline, amiodarone, and atropine. The five ‘A's concept will enable safe and effective treatment of all bradycardias, tachycardias, SVTs, VT, ventricular flutter, ventricular fibrillation, and of asystole.


Primary tumors of the heart are rare, but they are often associated with refractory arrhythmias. Vascular tumors of the heart comprise a small minority of primary cardiac tumors. In patients with structurally normal hearts, ventricular tachycardia (VT) originating from the right ventricular outflow tract (RVOT) can be sensitive to adenosine, vagal maneuvers, and calcium channel blockers. In this report, we describe a case of ventricular tachycardia originating from within a hemangioma in the RVOT that was ultimately controlled with verapamil. A 15 year old girl presented with a recurrence of ventricular tachycardia after having been externally cardioverted twice in a 24 hour period at a referring hospital. She had been diagnosed with a cardiac hemangioma when a murmur was noted at 5 years of age on a routine physical exam. Echocardiogram at that time showed a large mass in the RVOT with mild obstruction. Endomyocardial biopsy showed a non-specific vascular proliferation. A histopathologic diagnosis was confirmed when the tumor was resected shortly after the initial presentation. The tumor was infiltrative and encroached on the RVOT free wall and tricuspid valve, and hence was only incompletely resected. She continued to do well, and at 10 years of age, non-sustained polymorphic VT was noted on a routine screening Holter monitor. An EP study was performed and ventricular double extrastimuli (600:290:270) provoked sustained polymorphic VT. At that time, a transvenous single-chamber internal cardioverter defibrillator (ICD) was placed for primary prevention and the patient was started on Nadolol.She remained asymptomatic for the next five years. Frequent episodes of non-sustained polymorphic VT were noted, but there were no ICD therapies or episodes of sustained VT. At 15 years of age, she presented to the emergency room with palpitations and 12-lead ECG demonstrated wide complex tachycardia at 180 bpm .During sustained ventricular tachycardia, 3D mapping with CARTO was initially performed using a Biosense Webster EZ Steer catheter (4mm tip). Earliest areas of ventricular activation in tachycardia were noted along the border of the tumor, and earliest ventricular activation preceeded the QRS by 41 msec. Initial lesions placed along the tumor border were unsuccessful. Pace mapping from these sites showed paced QRS morphology similar to VT morphology in 11 of 12 surface leads. With similar findings at several points on the tumor border, the conclusion was made that tachycardia originated from within the tumor. Attempts to isolate the tumor with a series of lesions using an irrigated Navistar ThermoCool catheter were ultimately unsuccessful and tachycardia persisted. The case was ended and the patient was transferred back to the PICU in sinus rhythm. She underwent an upgrade to a dual chamber ICD with the intention of giving aggressive beta-blocker therapy.Sustained tachycardia recurred and intravenous verapamil, which had previously not been tried, was given and tachycardia terminated.  Oral verapamil was continued and there were no further tachycardia recurrences. She was started on oral Verapamil SR 240 mg daily and discharged from the hospital. She continued on Verapamil and did not have any recurrent episodes for one year. Subsequently, during a vigorous exercise the patient experienced two appropriate shocks. She had been noncompliant and was not taking verapamil at the time. Electrograms from the device demonstrated sinus tachycardia prior to an episode of VT .Cardiac hemangiomas are composed of a benign proliferation of endothelial cells and blood vessels, and they are histologically identical to hemangiomas found elsewhere in the body. Hemangiomas account for less than 3% of primary cardiac tumors ,2.Ventricular arrhythmias and sudden cardiac death are associated with a variety of cardiac tumors and are independent of tumor size ,4. TumorVentricular tachycardia arising from the RVOT in patients with structurally normal hearts has been characterized by cAMP-mediated triggered activity . These aThis case illustrates that ventricular tachycardia arising from a hemangioma in the RVOT can act similar to VT arising from the RVOT in patients with structurally normal hearts. Tumor-associated ventricular tachycardias can be difficult to control with medication, and can also be difficult to treat with radiofrequency ablation. Verapamil should be considered before proceeding to tumor resection or other invasive therapies.


We report an unusual association of persistent atrial flutter and bundle branch re-entrant ventricular tachycardia in a young patient without structural heart disease. Atrial flutter masked the infra-Hisian conduction disease, was fundamentally dependent on a long PR interval, and could be a possible trigger of ventricular tachycardia. A 28-year-old female with a recent diagnosis of persistent atrial flutter (AFL) and no structural heart disease, was undergoing treatment with betablocker while waiting for ablation . She wasDuring the EPS, the patient was in persistent AFL with a cycle length of 255 ms associated with a typical isthmus-dependent circuit. The AV conduction was variable with a HV interval 90 msec. Cavotricuspid isthmus ablation stopped the tachycardia  restorinBBR VT is often encountered in patients with dilated cardiomyopathy and with less frequency in valvular, ischemic and other structural heart disease, but is rarely seen in patients with a normal heart . The tacIn our patient, without structural heart disease or bundle branch block and with persistent AFL, His-Purkinje system disease could be suspected only by a mild non-specific intraventricular conduction delay. This is highly unusual, the absence of the typical clinical and ECG features in this setting makes it difficult to consider the final diagnosis, and invasive testing is essential. Several reports have related BBR VT induction with atrial stimulation as well as with AFL/fibrillation . We supp


We report a patient with an implantable cardioverter defibrillator (ICD) for arrhythmogenic right ventricular dysplasia (ARVD) who received inappropriate shocks for atrioventricular node reentry tachycardia (AVRNT). Patient had multiple shocks for tachycardia with EGM characteristics of very short VA interval and CL of 300 msec. An electrophysiologic (EP) study reproducibly induced typical AVNRT with similar features. The slow AV nodal pathway ablation resolved the ICD shocks. Despite increasingly sophisticated discrimination algorithms available in modern ICDs, the ability to differentiate SVT from VT can be challenging. Our patient received inappropriate shocks for AVNRT. When device interrogation alone is not conclusive, an EP study may be necessary to determine the appropriate therapeutic course. Arrhythmogenic right ventricular dysplasia (ARVD) is an inherited degenerative disorder involving progressive replacement of the myocardium by fibro fatty tissue. This is seen predominantly in the right ventricle though left ventricular involvement is not uncommon. The fibrofatty replacement provides the substrate for life threatening arrhythmias such as monomorphic ventricular tachycardia, polymorphic ventricular tachycardia (torsades de pointes), ventricular fibrillation and / or electrical storm  are sophisticated devices with arrhythmia discrimination algorithms that reliably differentiate SVT from VT and provide appropriate therapy. We report a patient with ARVD who had inappropriate shocks for AVNRT.A 47-year old male presented with 3 ICD shocks for persistent ventricular tachycardia. He had known history of polysubstance abuse and coronary artery disease with angioplasty. Eight months prior to this admission he had presented with symptomatic monomorphic ventricular tachycardia (Cycle length 360 msec). A 2D-echo showed an ejection fraction of 40% followed by a coronary angiogram which showed non-obstructive disease with previously placed patent right coronary stent. Cardiac MRI confirmed a diagnosis of ARVD. He received a Biotronik Lexos DR ICD (model # 347000). Device interrogation during the current admission revealed a wide complex tachycardia (WCT) that received 3 ineffective shocks but resolved spontaneously. The WCT as shown by the Electrograms (EGMs) during ICD interrogation showed a short VA interval, a Cycle length (CL) of 300msec which were completely different from the VT seen during his initial clinical presentation . ICD shoDuring EP study, no arrhythmia was inducible at baseline. With RV stimulation and Isoproterenol (2mcg) provocation, a typical AVNRT with a pacing cycle length of 500 msecs and 3 extra stimuli of 290-280-270 ms, identical to the arrhythmia seen on ICD interrogation strips was easily and reproducibly induced . PresencOur patient presented with sustained monmorphic VT, was diagnosed as ARVD by cardiac MRI, requiring ICD implantation. Subsequently he had inappropriate shocks due to AVNRT . Due to differences in the characteristics of the two arrhythmias an appropriate diagnosis of the arrhythmia responsible for the inappropriate shocks could be established only with programmed electrical stimulation during an EP study.ARVD has an increased incidence of ventricular arrhythmias and SCD requiring ICD implantation. It has been estimated that about 20 percent of SCD among patients <35 years is due to ARVD .In spite of a high specificity, inappropriate shocks have been seen in ARVD patients with ICD especially with atrial arrhythmias. In a study of 653 arrhythmia episodes in patients with dual chamber ICDs, inappropriate detection of atrial arrhythmias (with a stable atrioventricular relationship) was seen in 42% of patients, of which atrial flutter or fibrillation were more often misdiagnosed [Most modern ICDs have sophisticated discrimination algorithms to differentiate atrial and ventricular arrhythmias. While ventricular arrhythmias are recognized and treated with precision, atrial arrhythmias can be misdiagnosed and receive inappropriate shock therapy. An EP study may thus be necessary in establishing an accurate diagnosis and delivering appropriate therapy.


Spontaneous pneumothorax is usually caused by the rupture of subpleural blebs/bullae in the underlying lung and is one of the most common elective applications of video-assisted thoracoscopic surgery (VATS). VATS has been used as an alternative to thoracotomy in the treatment of spontaneous pneumothorax. Recurrent pneumothorax and persistent air leakage are quite often indications for spontaneous pneumothorax, and bilateral spontaneous pneumothorax is also considered to be an indication for surgical intervention. The goals of surgical intervention are to eliminate intrapleural air collection and prevent recurrence. Diverse procedures have been reported in the surgical treatment for spontaneous pneumothorax. We review the literature regarding the VATS approach for spontaneous pneumothorax. With advances in videothoracoscopic equipment, most operations for spontaneous pneumothorax are usually performed with a minimally invasive technique that involves video-assisted thoracoscopic surgery (VATS) . AdditioPatients with spontaneous pneumothorax, which is usually caused by a rupture of a subpleural bleb or bulla in the underlying lung, most commonly present with ipsilateral sudden chest pain and dyspnea. Spontaneous pneumothoraces are classified as primary or secondary -7. PrimaThe generally accepted indications for surgical intervention in pneumothorax are as follows ,9,13-15:Randomized clinical trials that have compared the clinical results of a VATS procedure to thoracotomy for spontaneous pneumothorax have shown that the VATS procedure was superior to thoracotomy with regard to postoperative pain, hospital stay, and pulmonary function -46. VATSAccording to the recent development of technology in the videoscopic field, several reports have shown that needlescopic VATS is feasible in the treatment of spontaneous pneumothorax ,49. The Simultaneous bilateral spontaneous pneumothorax is an infrequent phenomenon that reportedly accounts for approximately 1% of all cases of spontaneous pneumothorax ,51. AlthMedian sternotomy or bilateral axillary thoracotomy has been traditionally performed for the bilateral treatment of pneumothorax ,60. WithRecently, a few researchers -66 have The author declares that they have no competing interests.The author performed a literature search, and wrote and approved the final manuscript.


Unlike the adult population, arrhythmias occur less commonly in childhood. Only 5% of the emergency hospital admissions in the paediatric population is attributed to symptomatic arrhythmias . MajoritThe symptomatology of arrhythmias in children depends on the underlying rhythm disorder and the age at presentation. Typically, neonates and infants with arrhythmias tend to present with congestive cardiac failure secondary to tachycardiomyopathies. This is particularly known to occur following PJRT, AET and VT. Palpitation and or syncope are the mode of presentation in older children. Complete heart block is the bradyarrhythmia of significance seen in childhood. This is either of congenital etiology or a sequela to cardiac surgery. Infrequently, sudden cardiac death (SCD) occurs due to arrhythmias particularly when they are of ventricular origin. SCD of arrhythmogenic etiology in children is reported with HCM, LQTS, Type B WPW syndrome, complete heart block and ventricular arrhythmias post cardiac surgery.Atrioventricular reentry (AVRT) remains the most common mechanism for fetal tachyarrhythmias. Infrequently atrial reentry tachycardias are seen. With sustained tachycardia there is a 50% risk of the fetus developing congestive cardiac failure and 50% risk of fetal death with untreated hydrops . SustainThe supraventricular tachycardia (SVT) occurring in earlier life is commonly accessory pathway mediated. Atrioventricular reciprocating tachycardia (AVRT) represents 85% of the arrhythmias in fetal life and 82% of the arrhythmias occurring during infancy. In most cases tachycardia will resolve spontaneously by the end of infancy although there may be late recurrences . The incWolff-Parkinson-White (WPW) syndrome is a typical example of AVRT in children. The population prevalence of ventricular pre-excitation is around 1.5 per 1000 in the adolescent age group and probably lower during the early childhood [hildhood . A signihildhood . The ovehildhood . SCD in hildhood . Radio fhildhood .Permanent Junctional Reciprocating Tachycardia is the commonest form of incessant supraventricular tachycardia in children. This is an orthodromic AVRT with RP>PR and presents typically at 3-4 years of age. These are likely to persist for a long time and are known to cause tachycardiomyopathy. Although pharmacological control is possible with amiodarone or verapamil or in combination with digoxin, the best long-term management is reportedly by RF ablation [ablation .Atrial tachycardias in childhood are commonly seen as a result of postoperative atrial scarring, distortion of anatomy, changes in the wall stress and changes in the atrial refractoriness associated with sinus node dysfunction. Atrial tachycardia with one to one conduction can cause SCD. In a collaborative study of atrial flutter of 380 cases by electrophysiological study, significantly more young people with atrial flutter died when no drug control was achieved, compared to those with pharmacologically controlled atrial flutter. Surgical intervention to improve the cardiac haemodynamic function showed a significant decrease in the incidence of atrial flutter and this should be considered whenever feasible [feasible . Atrial Ventricular premature contractions (VPC) are the commonest ventricular conduction anomaly seen in neonates. Up to 33% of neonates have VPCs in the first week of life and these usually resolve by two weeks of age. However, if they persist beyond this period then further investigation is warranted to rule out an underlying structural heart defect. Ventricular arrhythmias are rare in childhood and may be benign or malignant. Benign VT is a condition diagnosed by exclusion and these children usually have normal ECG, chest X-Ray, and echocardiography and in some cases when performed, a normal EP study. The VT is suppressed by exercise and is usually refractory to medical management with a good long-term prognosis. Incessant idiopathic infant VT presents in the first two years of life with a male preponderance and is considered to be secondary to a left ventricular hamartoma. The children present with CCF or collapse. The VT best responds to pharmacological treatment with flecainide and amiodarone and usually resolves spontaneously by school age facilitating withdrawal of drugs. RVOT tachycardia is occasionally seen in teenagers and is distinct from arrhythmogenic right ventricular dysplasia or cardiomyopathy. The ECG shows LBBB with a vertical or right axis. This VT is usually produced by exertion or emotion, can be reproduced by isoprenaline or burst pacing and is amenable to RF ablation. Idiopathic LV tachycardia is rare and arises from the posterior fascicle of the left bundle branch and is thought to originate from the Purkinje network. It responds to treatment with verapamil and is also amenable to RF ablation. Catecholaminergic VT, first described by Coumel, is induced by emotion or exertion and can result in torsades associated with syncope. The resting ECG is normal. Isoprenaline administration or exercise testing can reproduce the VT. This is a dangerous form of VT and the prognosis is greatly improved by beta blocker therapy .Long QT syndrome (LQTS) is a familial disease characterized by prolonged and abnormal ventricular repolarisation and by the risk of life threatening ventricular arrhythmias. Recent molecular genetic studies in LQTS families have identified aberrations in genes encoding for cardiac ion channels. Dysfunction of these cardiac ion channels leads to prolongation and inhomogeneity of the action potential, which leads to arrhythmias, based on abnormal impulse propagation as well as sensitizes the heart to the arrhythmogenic effects of catecholamines. At least 5 genes located on chromosomes 11, 7,3,4 and 21 have been identified with aberrations in encoding for cardiac ion channels in families with LQTS. Romano-Ward syndrome, the autosomal dominant LQTS is sub classified in to LQT 1, which is the commonest form of LQTS and where the mutation is in the gene KVLQT1 on chromosome 11, LQT 2 in HERG on chromosome 7, LQT 3 in SCN5A on chromosome 3, LQT 4 in chromosome 4 and LQT 5 with mutation in Min K on chromosome 21. Jervell-Lange-Nielsen syndrome, the autosomal recessive LQTS is due to mutation in KVLQT1 on chromosome 11 and is associated with deafness. The main diagnostic criteria has been a prolonged QT on ECG but it is to be noted that genetically proven LQTS patients may have normal QT interval. Other diagnostic criteria include a slow heart rate for age, T wave alternans and abnormal T wave morphology. Patients usually present with syncope or cardiac arrest precipitated by emotional or physical stress. The syncope is usually due to "torsade de pointes" frequently degenerating in to ventricular fibrillation. Neonates with LQTS may be identified by a partial AV block and slow heart rate due to prolonged repolarisation. History of syncope, virulent family history, T wave alternans, a QTc exceeding 0.54 s and associated AV block in neonates carry a higher risk. The mortality among untreated symptomatic patients reaches 70% within 15 years from the time of the first syncopal episode. Treatment options include beta-blockade, other anti arrhythmic drugs, stellate ganglionectomy and automatic implantable cardiac defibrillator with marked improvement in survival [survival .Hypertrophic Obstructive Cardiomyopathy (HOCM) is much less prevalent in children than in adults. A Japanese screening programme estimates the prevalence in children at 1 in 15000 compared to an adult prevalence rate of 1 in 500. The overall risk of SCD in HOCM is low and is around one per million in the age specific population under 20 years. The mechanism of SCD in HOCM is believed not to be due to an arrhythmia but ventricular fibrillation has been implicated in some [ in some .Junctional Ectopic Tachycardia (JET) is the commonest (22%) arrhythmia seen in the immediate post-operative period following intracardiac repair mostly following Tetralogy of Fallot correction. The etiology is thought to be due to resection of right ventricular outflow tract (RVOT) muscle bundles, relief of RVOT obstruction through the right atrial approach and an extended bypass time. The risk factors predisposing to post-operative JET have been identified as lower age and body weight at the time of surgery, higher Aristotle basic score, longer cardiopulmonary bypass time and cross clamp time, use of deep hypothermia and total circulatory arrest [y arrest . The undLate post-operative arrhythmias are the commonest medical problem encountered after repair of congenital heart defects. The incidence relates to the complexity of the underlying heart defects and the clinical significance depends on the interaction between the arrhythmia and the cardiac status. The arrhythmias are attributed to variety of reasons.An underlying electrical substrate associated with specific structural heart defects such as atrial isomerisms, Ebsteins anomaly, corrected TGA.Acquired due to the pre-operative natural history as with myocardial fibrosis, cyanotic congenital heart diseaseDue to the surgical suture lines as in Sennings repairDue to post-operative haemodynamics as with right atrial dilatation following classical Fontan surgery, TOF repair.Up to 50% of adult patients who have undergone TOF repair reveal late non-sustained arrhythmias during ambulatory ECG monitoring. Occasionally, symptomatic sustained ventricular arrhythmia is documented in these patients. EP studies have shown these ventricular arrhythmias to be due to re-entry, which requires areas of slow conduction within the myocardium. Pulmonary valve regurgitation seen commonly after TOF repair, results in chronic right ventricular overload and diastolic dysfunction and this has been shown to correlate with QRS prolongation on the ECG. It has also been shown that right ventricular QRS prolongation correlates with a higher incidence of symptomatic arrhythmia and a QRS duration exceeding 180 ms on the resting ECG is the most sensitive predictor of life threatening ventricular arrhythmias .Congenital complete heart block (CCHB) is reported to occur with an incidence of 1 per 25000 live births. When it occurs without an associated underlying heart defect and the diagnosis is made at birth, then the mortality is reported at 15%. The risk of death is significantly less at 3.5% when the diagnosis is made beyond the first year of life. In this study by Michaelsson and Engle, the risk of dying is reportedly greatest in early infancy with half of all deaths occurring early in the first year of life. The overall survival rate was 92% in this group. However, the group with CCHB and associated structural heart defect exhibited a higher mortality of 42.4% in those diagnosed at birth [at birth . Anotherat birth . The ris


Dual ventricular response to a single supraventricular impulse is an interesting possibility in the  presence of dual atrioventricular nodal physiology. Double His bundle and ventricular responses to a single atrial impulse caused by a simultaneous fast and slow pathway conduction is the hallmark of this condition. One of the earliest descriptions of simultaneous conduction through both atrioventricular (AV) nodal pathways was by Csapo G , who desThe major determinants of simultaneous anterograde fast and slow pathway conduction during sinus rhythm are: 1) Retrograde unidirectional block in both pathways 2) Critical conduction delay in the slow pathway and a long enough His-A interval to allow sequential conduction of impulse from both pathways . The criA mistaken diagnosis of atrial fibrillation may be entertained if the dual response is intermittent. Dixit S et al  found thNon-reentrant supraventricular tachycardia due to 1:2 AV conduction has been described between 44 - 74 years of age and with duration of symptoms of up to 7 years . It may Even tachycardiomyopathy secondary to non-reentrant atrioventricular nodal tachycardia has been described recently . TreatmeIn this issue of the journal Laszlo R et al  describe


We report on an atrial tachycardia (AT), emanating from the non-coronary (NC) aortic cusp, ablated with the aid of an electro-anatomical navigation system. In this setting, the electrocardiographic, electrophysiologic (EP), anatomical, and ablative considerations are discussed.Although NC aortic cusp focal ATs are an uncommon EP finding, their ablation is effective and safe, especially from an atrio-ventricular (AV) conductive point of view. This origin of AT must be invoked and systematically disclosed when a peri-AV nodal AT origin is suspected, in order to avoid a potentially harmful energy application at the vicinity of the AV conductive tissue. A 37 year-old woman, without any structural heart disease, was referred to our institution for management of symptomatic supra-ventricular tachycardia. Three anti-arrhythmic drugs had failed before the patient was considered for catheter ablation. Baseline 12-lead electrocardiogram (ECG) and echocardiogram were both normal. After written informed consent was obtained, an EP study was undertaken. A narrow complex tachycardia was easily induced by simple catheter manipulation . Upon ceIt has been shown that the right and left aortic coronary cusps can give rise to ventricular tachycardia ,2 while On the other hand, the fact that the interatrial septum and the NC aortic cusp are immediately adjacent 5], led some investigators to postulate that some aborted AT ablations presumed to emerge from the peri-AV nodal region could have been in fact related to a NC aortic cusp origin . Accordi, led somWhen mapping the posterior and left-sided aspects of the NC aortic cusp, large atrial electrograms must be recorded whereas, when the catheter approaches the commissure with the right coronary cusp, His bundle electrograms and large ventricular electrograms appear. Although, atrial NC aortic cusp atrial electrograms have been described as fractionated ,7 in ourTypically, NC aortic cusp focal AT 12-lead ECG shows positive P waves in V1, while an anterior tricuspid valve origin or/and a RA appendage origin, both exhibit a negative P wave pattern in V1 . InteresRegarding the energy used for NC cusp ablation, recent publications, either experimental or clinical, have assessed the security of standard RF energy, cooled-tip RF energy and cryothermal ablation -8. In ouConcerning electroanatomical navigation systems, although non-indispensable, they can depict comfortably the activation of all the chambers mapped and allow the reproducible repositioning of the ablation catheter at the "spot of interest". These systems have therefore the potential to render easer the ablation procedures. Moreover, merging the computed tomography of the heart with the electro-anatomic reconstruction may add further information, enhance the understanding of the complex anatomic relationship between structures, and increase safety at the level of coronary cusps ,10.Finally, the distance between the ablation catheter and the origin of the coronary arteries should be absolutely disclosed by means of a prior coronary angiogram, in order to avoid a serious coronary complication .Although ATs originating from the NC aortic cusp are uncommon, their ablation is feasible and safe. NC aortic cusp ATs must be invoked and systematically disclosed when a peri-AV nodal AT origin is suspected, in order to avoid a potentially harmful energy application at the vicinity of the AV conductive tissue.


Mahaim fiber exhibits atrio-ventricular node like properties and generally is localized at the lateral aspect of the tricuspid annulus. Of the varying methods for localization, ablation at the site of Mahaim potential is the most accepted and successful method. Radiofrequency ablation of Mahaim fiber has high success rates. Mahaim fiber tachycardia is not an uncommon cause of wide QRS tachycardia in young having no structural heart disease. Mahaim and Winston were the first to describe Mahaim fiber, as a tract, which connects the atrio-ventricular (AV) node to the ventricular myocardium . It was  Mahaim Fiber conducts only antegrade and has decremental conduction property. Due to its AV node like EP property it is also known as an ectopic AV node ,8. MahaiAnatomically Mahaim Fiber is located at the lateral tricuspid annulus in most instances. Location of the pathway in occasional cases may be variable along the tricuspid annulus especially when associated with Ebstein's anomaly which is a common associated structural anomaly along with Mahaim fiber tachycardia ,11,14-20Once Mahaim fiber related tachycardia is confirmed by EP study, mapping is generally performed along the lateral tricuspid annulus, which is the most common localization site. Because of their conduction properties and anatomic location, it is difficult to map both the proximal  and distal (ventricular) insertion of Mahaim fibers. Mahaim fibers do not conduct retrogradely so the proximal insertion cannot be identified by ventricular pacing. They tend to have generally a long course and often show extensive arborization over a wide area of ventricular muscle making ablation at the ventricular insertion site difficult . There a Mahaim (M) potentials  appear aMechanical trauma induced loss of conduction via Mahaim fiber has also been described. Mahaim fiber is located very close to the endocardium and thus catheter movement related mechanical trauma resulting transient loss of conduction is not uncommon. Mapping and RF ablation guided by this method has been useful ,20. UninActivation mapping of the earliest local ventricular potential targeting distal branches is a time consuming task. It is possible to ablate some of them using this technique but mostly a complete elimination is very unlikely. Some patients with atriofascicular pathway who underwent ablation at the distal insertion had developed a pro-arrhythmic response with facilitation of antidromic tachycardia occurrence due to slow conduction induced by radiofrequency ablation ,10. Also Shortest interval from stimulus to ventricular activation is defined as the shortest interval between the pacing sites at different sites at the RA side of the tricuspid annulus to the earliest preexcited QRS. The result of RF ablation at the site of the shortest interval has remained inconsistent as seen in various studies and varies from 0 to 100% -20.  ThiSimilar to the previous technique, atrial extra-stimulus mapping during antidromic tachycardia is a time consuming method for finding an atrial site where the longest coupled premature extra-stimulus causes resetting. The site in the atrial annulus with the least interposing tissue separating it from the accessory pathway proximal insertion is obtained which is a suitable site for attempting ablation.Electro-anatomic mapping ,24 can b "Mahaim" automatic tachycardia (MAT), is generally brought about during radiofrequency current delivery , though Ablation catheter should be moved slowly and carefully along the annulus, avoiding bumps on the tissue so as to avoid a mechanical trauma and accidental loss of preexcitation, for which long sheaths can be used for improving stability. Ablation, if possible, should be done during atrial pacing. Stability is improved during atrial pacing as compared with ablation during antidromic tachycardia when catheter is likely to move with tachycardia termination. MAT can also cause catheter displacement and therefore atrial pacing during ablation is beneficial. Also radiofrequency current applied during atrial pacing increases preexcitation and hence make it easier to assess conduction block.In occasional patients in spite of all attempts to localize the pathway, ablation may not be successful ,20. This Coexistence of other tachycardias, especially atrioventricular nodal reentrant tachycardia (association of up to 10-40%) and WPW syndrome due to Kent bundle has been described in literature ,14,16-20Summarizing, Mahaim fiber exhibits AV node like properties and generally is localized at the lateral aspect of the tricuspid annulus. Successful ablation of the accessory pathway is achieved using varying methods, the most successful being the site of the M Potential. MAT is generally obtained along with a successful ablation. Radiofrequency ablation of Mahaim Fiber has a high success rate.


In Wolff-Parkinson-White Syndrome (WPW), presence of accessory pathways causes various tachyarrhythmias that lead to different symptoms and clinical conditions in patients. Atrial fibrillation is observed in about 20-30% of this group of patients. Life threatening malignant ventricular arrhythmias and sudden cardiac deaths are observed in patients having rapid conduction in accessory pathways and short antegrade refractory periods (<250 msn). We present a WPW syndrome case that presented to the emergency service with narrow QRS tachycardia and later developed malignant ventricular arrhythmia. A 32 years old male with no previous cardiac evaluation and clinical complaints presented to the emergency service with palpitation. Due to narrow QRS complex tachycardia, emergency service physicians  administWPW syndrome is a clinical entity characterized by presence of an electrical signaling accessory pathway between atrium and ventricular that may cause tachyarrhythmia's sometimes and sudden cardiac death. Studies have shown that SCD occurs at the rate of 0.15% per year in patients with WPW. These deaths are caused by atrial fibrillation with rapid ventricular response that leads to ventricular fibrillation (VF) .The most frequently encountered tachycardia in WPW syndrome is the reentrant tachycardia. The degeneration of reciprocating tachycardia to atrial fibrillation is not uncommon . It has Risks factors for sudden death in WPW are presence of more than one AP, development of AVRT along with AF and the shortest preexcitation RR interval less than 260 msn ,2,7. DevAs a result, Using AV node suppressive medicines in patients with WPW syndrome may cause atrial fibrillation followed by development of fatal cardiac arrhythmias. We believe that it is important to acquaint all the clinicians, especially the emergency service and ambulance physicians who are the first to face SVT patients in daily practice, with this issue.


We describe a patient with an implanted pacemaker for impaired AV conduction who presented with  an incessant tachycardia. EP study showed that the tachycardia was atrioventricular nodal reentrant tachycardia (AVNRT) with repeated spontaneous initiation because of poor or absent antegrade fast pathway conduction. Slow pathway ablation was successful in terminating the tachycardia and making it non-inducible. During a follow-up visit in the pacemaker clinic, a 45-year-old male complained of persistent palpitations for the past 2 months. He had undergone implantation of a permanent single chamber pacemaker with a ventricular lead 18 years back for trifascicular block with intermittent complete heart block and had subsequently undergone pulse generator replacement twice. His heart rate in the clinic was 130 bpm. Echocardiogram showed normal LV function without any abnormalities. He was not on any drugs. Electrocardiogram showed a broad complex tachycardia with a right bundle branch block (RBBB) morphology, 1:1 ventriculo-atrial (VA) association and a short RP interval. An electrophysiology study was planned in view of the persistent tachycardia.In the electrophysiology lab, he had tachycardia at the beginning of the procedure. The tachycardia could be easily terminated with ventricular overdrive pacing, and on termination of the tachycardia he was found to have sinus rhythm with a PR interval of 380 ms and broad QRS of RBBB morphology. However, tachycardia would always reinitiate spontaneously after a few beats of sinus rhythm . During Intracardiac electrograms during tachycardia showed 1:1 VA association with VA interval of 95 ms and central atrial activation. RV overdrive pacing at a cycle length (CL) slightly shorter than the tachycardia CL showed a ventricle-atrium-ventricle (VAV) response on termination of pacing with post pacing interval 216 ms longer than the tachycardia cycle length and VA interval was 150 ms longer than stimulus-atrial (SA) interval, all consistent with typical slow-fast atrioventricular nodal reentrant tachycardia (AVNRT) .Due to the incessant nature of the tachycardia, mapping had to be performed in tachycardia in the region of the slow pathway guided by fluoroscopy and electrograms. Ablation near the os of the coronary sinus was accompained by junctional beats. Post ablation, patient remained in sinus rhythm. AH and HV intervals were 228 ms and 50 ms respectively. Atrial programmed stimulation showed no dual pathway physiology and tachycardia could not be induced with atrial premature stimuli or burst pacing.AVNRT usually presents as a paroxysmal form of tachycardia with each episode lasting for a short period of time. We could find only one report of incessant presentation of AVNRT . In pati


Major spontaneous variation in cycle length during supraventricular tachycardia is quite an uncommon phenomenon, which sometimes can mislead a correct diagnosis. We describe a patient who developed spontaneous variation in cycle length during electrophysiologic study in whom the coronary sinus cannulation was extremely difficult. In this situation, careful inspection of the mechanisms associated with this variation and classic pacing maneuvers are important to make a correct diagnosis of the supraventricular tachycardia. Major cycle length (CL) variations are unusual in supraventricular tachycardia. These variations can occur due to several mechanisms, which are not always obvious . In patiA 20-year-old man underwent EPS for evaluation of recurrent palpitations. Baseline 12-lead electrocardiogram was normal. Catheter positioning induced a sustained narrow QRS complex tachycardia with 1:1 ventriculo-atrial (VA) relationship. Coronary sinus (CS) cannulation was extremely difficult due to anatomical reasons and could not be performed in the beginning of the study. During the tachycardia, there was a spontaneous change in CL from 346 to 265 ms. A significant QRS voltage alternans was also observed . What arMinor CL variations are frequently seen during supraventricular tachycardia, but oscillations above 15 ms are unusual. These changes can occur by a variety of mechanisms, particularly due to autonomic influences. In a re-entrant mechanism, a shift in either the antegrade or the retrograde limb, or a change in the conduction time along these limbs can contribute to the CL change. In tachycardias due to enhanced automaticity, either a shift in the automatic focus or varying degrees of exit block from the focus can contribute to the change in CL -5.In the beginning of tachycardia CL 346 ms), the AH, HA and VA intervals are 198 ms, 175 ms and 107 ms respectively. When the tachycardia CL changes (265 ms), the intervals are 118 ms, 150 ms and 105 ms respectively. So, it is possible to conclude that the change in tachycardia CL is predominantly due to change in conduction along the antegrade limb, which is in this case the AV node. Additionally, retrograde atrial activation sequence remains the same during the CL change. These findings are highly suggestive of a change in the antegrade conduction through the AV node. Overdrive ventricular pacing was done to entrain the tachycardia and the response on stopping the entrainment was VAV: further evidence against AT. The post pacing interval minus tachycardia cycle length (PPI-TCL) was 126 ms and the difference  was 96 ms. Also there is evidence of progressive fusion during tachycardia entrainment by ventricular pacing. These findings are in favour of a pathway as the tachycardia mechanism.  . W ms, the The present case illustrates an ORT using a concealed left lateral bypass in a patient with dual AV node physiology, which has been previously reported .  The inThe challenging component of this case was the significant delay in CS cannulation, which can make the diagnosis difficult. The tachycardia was successfully terminated by accessory pathway ablation. Moreover, AV nodal slow pathway ablation strategy could be considered even in patients with no inducible AVNRT in special populations  in order to reduce the risks due to multiple EPS for recurrent arrhythmias .Although the exact mechanism associated with change in tachycardia CL is unknown, it is suggestive that antegrade conduction modification through the AV node was the causal factor. AV node accommodation is possible, but not the most probable explanation for the change in CL, since a gradual increase in heart rate would be expected . Thus, a