The concept of reentry within the sinus node is by no means new. In their 1943 report, Barker and co-workers postulated that “…a circus rhythm could be accommodated in auricular muscle and in one of the specialized nodes at known rates of conduction and with cycle lengths such as occur in paroxysmal tachycardia” . In a suSymptoms of SART vary widely. Patients may present with paroxysmal palpitations, dyspnoea, dizziness, (near-) syncope, chest discomfort and other symptoms . Given tIn contrast to inappropriate sinus tachycardia and atrial tachycardias, SART rarely responds well to β-blockers. Digoxin, calcium channel blockers such as verapamil and amiodarone are the drugs of choice . In drugSinoatrial reentry tachycardia is a relatively uncommon arrhythmia in the literature, but may be prone to underdiagnosis due to electrocardiographic similarity to sinus tachycardia and misinterpretation of symptoms as psychosomatic. Awareness of the diagnosis, and hence differentiation of SART from inappropriate sinus tachycardia, atrial tachycardia or non-cardiac diagnoses paves the way for adequate therapy. While medication  may be successful or even desirable under certain conditions, radiofrequency catheter ablation offers curative therapy in most cases with few adverse effects.


We report a 26-year-old woman with frequent episodes of palpitation and dizziness. Resting electrocardiography showed no evidence of ventricular preexcitation. During electrophysiologic study, a concealed right posteroseptal accessory pathway was detected and orthodromic atrioventricular reentrant tachycardia incorporating this pathway as a retrograde limb was reproducibly induced. After successful ablation of right posteroseptal accessory pathway, another tachycardia was induced using a concealed right posterolateral accessory pathway in tachycardia circuit. After loss of retrograde conduction of second accessory pathway with radiofrequency ablation, dual atrioventricular nodal physiology was detected and typical atrioventricular nodal reentrant tachycardia was repeatedly induced. Slow pathway ablation was done successfully. Finally sustained self-terminating atrial tachycardia was induced under isoproterenol infusion but no attempt was made for ablation. During 8-month follow-up, no recurrence of symptoms attributable to tachycardia was observed. Several reports demonstrated the existence of double tachycardia such as atrioventricular reentrant tachycardia (AVRT) and atrioventricular nodal reentrant tachycardia (AVNRT) -3, or AVA 26-year-old woman, with no evidence of structural heart disease, was referred to our center for evaluation of palpitation and dizziness. Despite frequent occurrence of palpitation, she had no chance to capture any 12-lead electrocardiogram (ECG) during palpitation. The only evidence of arrhythmia in this patient was a sustained SVT with heart rate about 185 beats/min recorded in one of her 24-hour holter monitoring. Two antiarrhythmic agents  were tried in our patient with no success.The baseline standard 12-lead ECG showed no any abnormality. The physical examination and transthoracic echocardiography were unremarkable.After obtaining of written informed consent, electrophysiological study (EPS) was done in post absorptive, and non-sedated state. All antiarrhythmic drugs were interrupted for at least five half-lives before procedure. Three 6F diagnostic catheters  were inserted via left femoral vein and placed in the high right atrium (HRA), His bundle position, and right ventricular apex (RVA), respectively. A 7F decapolar catheter with 2/2/2 mm electrode spacing  positioned retrogradely via right femoral vein into the coronary sinus (CS) for coronary sinus mapping. During programmed electrical stimulation (PES) from RVA, nondecremental retrograde conduction was seen with earliest atrial activity on the proximal pole of CS catheter (located at the ostium of CS). No ventricular preexcitation was observed on atrial incremental pacing, compatible with a concealed right posteroseptal (RPS) accessory pathway. During atrial extrastimulation, a sustained narrow complex tachycardia (cycle length=320 ms) was induced reproducibly with earliest retrograde atrial activity in the proximal CS . This taApplication of RF energy at right posteroseptal area resulted in loss of conduction over the accessory pathway (AP) Figure 2ADuring 8-month’s follow-up, she was free of symptoms with no antiarrhythmic drugs and no recurrence of tachycardia was seen.The combination of AVNRT-AVRT -3 (incluAs atrioventricular (AV) bypass tract is a congenital abnormality due to developmental defect in the AV rings, it is not surprising that multiple bypass tracts can be present in the same patient. Incidence of multiple bypass tracts ranges from 3.1-30% -8, and tDual AV nodal physiology is known to occur in 8-40% of patients with AP, leading to a variety of possible reentrant circuits ,11. In tIn the study of 176 consecutive patients who underwent SP ablation for AVNRT, Sticherling et al . demonstBecause of easy and reproducible induction of AVNRT after successful ablation of bypass tracts and absence of clinically documented tachycardia compatible with one of the specific types of SVT, we decided to ablate SP in this patient. Because the majority of patients with inducible AT without clinically sustained AT do not experience symptomatic atrial tachycardia during follow-up , ablatioOur report demonstrated: 1) complexity of symptom origin in the patients with recurrent palpitations, 2) the importance of detailed electrophysiological assessment in the patients with AP before and after ablation, and 3) feasibility and efficacy of radiofrequency catheter ablation of multiple SVTs in single session.


Incisional atrial tachycardias have been described most frequently in patients with previous corrective surgery for congenital heart defects and mitral valve disease. Less information is available on atrial tachycardias appearing late after isolated aortic valve surgery. We report the case of a patient who developed a left figure-8 tachycardia after undergoing aortic valve replacement. During electrophysiologic study the entire cycle length of the tachycardia was mapped within a low voltage area confined to the left anterior atrial wall. However, during ablation a transmural lesion could not be attained. The mapping and ablation strategy along with the mechanism of the tachycardia are discussed. A 57-year-old man with dilated cardiomyopathy and chronic heart failure, who had undergone aortic valve replacement 26 years ago, was referred to our department for a third attempt at radiofrequency (RF) catheter ablation of an atrial tachycardia. According to reports, during the previous two electrophysiologic (EP) studies both a typical atrial flutter and a left atrial reentrant tachycardia (cycle length 190 ms) could be induced with burst pacing. Nevertheless, RF catheter ablation had failed in both cases, either because it was not possible to attain bidirectional block across the cavotricuspid isthmus (despite a large number of RF applications), or due to transformation of left reentrant tachycardia into atrial fibrillation during entrainment mapping and the impossibility of reinducing the same tachycardia after DC cardioversion. The patient continued to have frequent, prolonged episodes of palpitations despite several antiarrhythmic drug trials. Twelve-lead ECG documented an atrial tachycardia with a p-p interval of 240-280 ms and a variable degree of AV block as well as atrial fibrillation. The patient underwent several successful DC cardioversions for both arrhythmias. Transthoracic echocardiography revealed left atrial and ventricular enlargement, left ventricular systolic and diastolic dysfunction, and mild mitral and moderate tricuspid regurgitation.At the time of the third EP study, a decapolar catheter was placed in the coronary sinus (CS) and a bipolar catheter was positioned in the right ventricle. An 8-French deflectable quadripolar irrigated-tip catheter  was used for mapping and ablation. Mapping was performed using the Carto system . RF current was delivered through a Cordis Stockert generator between the 4-mm tip of the catheter and an adhesive patch on the posterior chest wall. Ablation was performed in temperature-controlled mode with a target temperature of 50°C and a power limit of 50 W. Saline was infused at a rate of 3 ml/min between ablations and 30 ml/min during RF current delivery. After obtaining a right atrial activation map with an electroanatomical reconstruction of the right atrium during proximal CS pacing, a regular tachycardia, with ECG morphology similar to the clinically documented tachycardia, was induced with burst pacing . The CS Sequential mapping of the right atrium during tachycardia revealed a nonreentrant activation pattern with an early septal area. Mapping of the left atrium was performed through transeptal catheterization. Two discrete scars (areas with bipolar voltage ≤0.05 mV) (1-3) along with adjacent points displaying fragmented or double potentials were located on the left anterior wall. They were confined to a larger region of low voltage (≤0.5 mV). The entire cycle length of the tachycardia was recorded within this region and the activation map was consistent with a figure-8 circuit. We hypothesized that activation propagated craniocaudally, through a common channel bordered by two lines of double potentials in its upper portion . In its Ablation targeted the common isthmus (isolated RF applications) and both the common channel and the medial turnaround of the circuit . Both attempts failed due to poor catheter stability. With the aim of continuing the ablation procedure under coronary sinus pacing, we attempted to interrupt the tachycardia by overdrive pacing, but this maneuver led to transformation into a second tachycardia with a CL of 190 ms (not shown in this paper). This tachycardia was DC-converted to sinus rhythm and the procedure continued afterwards under CS pacing. Nevertheless, the same technical difficulties further precluded the successful ablation of the circuit. Remapping the ablation points confirmed persistence of electrograms with the same configuration and the procedure was interrupted (long procedure time).Tachycardias with figure-8 activation pattern have been described both in the right and left atrium, most frequently in patients who have undergone surgery for congenital heart defects and valve disease -7. As wiIt is conceivable that a figure-8 activation pattern may be encountered in both reentrant and focal tachycardias . The latWe have found in the literature 5 patients with atrial tachycardias and a remote history of isolated aortic valve replacement  ,5-7. AllIn this report we describe a figure-8 tachycardia originating in the left anterior atrial wall in another patient with previous aortic valve replacement. The full cycle length of the tachycardia was mapped inside a low voltage zone containing electrically silent areas and multiple sites exhibiting  double- or fragmented potentials. This fact suggests a severely affected anatomical substrate. In order to avoid terminating or transforming the tachycardia, as reported during the previous two EP studies in this patient, we did not perform entrainment. Ablation targeted what was regarded as the common and medial channels  and, presumably, in order to avoid other secondary circuits, it should have been continued in the lateral channel as well. Tachycardia interruption along with its noninducibility after severance of these channels would have supported our hypothesis concerning the electrophysiological mechanism and the configuration of the circuit. However the instability and difficult maneuverability of the catheter, probably explained by the anatomical position of the targeted area, precluded a transmural ablation. Additional factors contributing to this outcome might be the structural changes of the anatomical substrate and the fact that we targeted first the common and medial channels. Shah et al. . noted tThis report confirms that patients with previous aortic valve replacement may have areas with abnormal electrophysiology in the left atrium that favor complex atrial tachycardias.  Participation of the left anterior atrial wall in such tachycardias  may be related to mechanical trauma during surgery (due to the proximity of this region to aortic root) as well as to intra- and postoperative atrial ischemia. In cases of figure-8 activation patterns, confirmation of the tachycardia mechanism and geometry of the circuit requires detailed activation mapping combined with entrainment and/or a successful ablation strategy .


Observation of Coincident arrhythmias is not uncommon but the co-existence of idiopathic verapamil sensitive left ventricular tachycardia (ILVT) with other arrhythmias is very rare. We hereby presented a 30 year old male patient with a history of frequent episodes of palpitations and sustained narrow complex tachycardia. During electrophysiologic study two arrhythmias, one with narrow complexes which was shown to be typical atrioventricular nodal re-entrant tachycardia and the other with wide QRS complexes and right bundle branch block and left axis morphology, compatible with ILVT, were inducible. Radiofrequency catheter ablation of both arrhythmias was done at two consecutive sessions. The patient has remained asymptomatic without antiarrhythmic therapy for the past six months. Idiopathic sustained ventricular tachycardia (VT) accounts for 10-20% of patients with sustained monomorphic VT , but coeWe hereby presented a 30 year old male patient with three years history of frequent episodes of palpitation. He had no structural heart disease. His previous medical records revealed several ECGs during arrhythmia all showing regular narrow complex tachycardia with a rate of 180beat/min. There was no documented wide complex tachycardia. During initial EP study a narrow complex tachycardia was reproducibly induced  which waearliest PP recording site  were introduced via left femoral vein and positioned at RV apex (and right ventricular outflow tract), His bundle and high right atrium. A 7F steerable decapolar catheter (2-5-2 mm) was introduced via left femoral artery  and positioned in LV on interventricular septum for recording intracardiac signals during sinus rhythm and tachycardia. This catheter was used as a guide for localization of earliest purkinje potential (PP) recording site by ablation catheter. A 7F ablation catheter  was introduced via right femoral artery and positioned in LV on septum for mapping and subsequent RF ablation. The ILVT was terminated by mechanical pressure at ing site . RF enerThis case describes the coincidence of AVNRT and ILVT. Occurrence of AVNRT in combination with idiopathic VT has been previously described. In patients with RVOT tachycardia the incidence of AVNRT has been reported to be as high as 15% . Our finearliest PP during tachycardia should be targeted.Wagshal AB, et al.  also repThis case represents the co-incidence of ILVT and AVNRT and underscores the importance of searching for dual AV node physiology and AVNRT in patients with ILVT.


A 25 year old man underwent electrophysiology study for recurrent symptomatic paroxysmal palpitations. There were no documented episodes of supraventricular tachycardia on surface ECG.  Delta waves were absent on baseline ECG.A decapolar catheter was placed in the coronary sinus with the distal and proximal pair of electrodes configured as CS 1-2 and CS 9-10 respectively. Quadripolar catheters were positioned in the high right atrium, His-bundle region and right ventricular apex. During straight atrial pacing with a drive-cycle length of 340ms, the following arrhythmia was induced . The corThe surface ECG revealed a narrow complex supraventricular tachycardia with alternating R-R intervals at 310ms and 360ms . The int On close inspection of the intracardiac electrogram, two different alternating A-H intervals were observed, which presented as alternating R-R intervals on the surface ECG.The A-H intervals were 110ms and 160ms consecutively. We deduced that the antegrade limb of this macro-reentrant circuit involved both the fast and slow AV nodal pathways alternating with each other.Radiofrequency ablation of the left lateral pathway via a retrograde aortic approach was performed. The tachycardia was successfully terminated. Further electrophysiology studies confirmed the presence of dual AV nodal pathways. There were no further inducible arrhythmias even with isoproterenol infusion. The slow pathway was thus not ablated.The mechanism for this supraventricular tachycardia with alternating R-R intervals involved two alternating antegrade limbs  with different conduction times and a common retrograde concealed left sided accessory pathway. This electrophysiological mechanism had been postulated previously based on appearance of the surface ECG without intracardiac recordings .


Idiopathic fascicular ventricular tachycardia is an important cardiac arrhythmia with specific electrocardiographic features and therapeutic options. It is characterized by relatively narrow QRS complex and right bundle branch block pattern. The QRS axis depends on which fascicle is involved in the re-entry. Left axis deviation is noted with left posterior fascicular tachycardia and right axis deviation with left anterior fascicular tachycardia. A left septal fascicular tachycardia with normal axis has also been described. Fascicular tachycardia is usually seen in individuals without structural heart disease. Response to verapamil is an important feature of fascicular tachycardia.  Rare instances of termination with intravenous adenosine have also been noted. A presystolic or diastolic potential preceding the QRS, presumed to originate from the Purkinje fibers can be recorded during sinus rhythm and ventricular tachycardia in many patients with fascicular tachycardia. This potential  has been used as a guide to catheter ablation. Prompt recognition of fascicular tachycardia especially in the emergency department is very important. It is one of the eminently ablatable ventricular tachycardias. Primary ablation has been reported to have a higher success, lesser procedure time and fluoroscopy time. In general ventricular tachycardias have wide QRS complexes.  One of the earliest descriptions of ventricular tachycardia (VT) with a narrow QRS complex was by Cohen et al in 1972  This obsZipes et al postulated that the origin of the tachycardia was localized to a small region of reentry or triggered automaticity located in the posteroinferior left ventricle, close to the posterior fascicle of the left bundle branch.2Response to verapamil suggested a role for the slow inward calcium channel in the genesis of the arrhythmia. Endocardial mapping during tachycardia revealed the earliest activation at the ventricular apex and mid septum . The tacRecently Kuo et al has questioned the involvement of the fascicle of the left bundle branch in ILVT . They stFascicular tachycardia has been classified into three subtypes: (1) left posterior fascicular VT  with a rEndocardial activation mapping during VT identifies the earliest site in the region of the infero-posterior left ventricular septum. This finding, along with VT morphology and short retrograde VH interval suggests a left posterior fascicular origin. Nakagawa and colleagues  recordedSome date suggest that the tachycardia may originate from a false tendon or fibro- muscular band that extends from the posteroinferior left ventricle to the basal septum . HistoloFascicular tachycardia can be induced by programmed atrial or ventricular stimulation in most cases. Isoprenaline infusion may be required in certain cases; rarely there may be difficulty in induction despite isoprenaline infusion. Endocardial mapping identifies the earliest activation in the posteroapical left ventricular septum in patients with posterior fascicular tachycardia.A high frequency potential with short duration, preceding the QRS has been described as the Purkinje potential . This haIntravenous verapamil is effective in terminating the tachycardia. However the efficacy of oral verapamil in preventing tachycardia relapse is variable. Good response and resolution of tachycardiomyopathy with verapamil treatment was noted by Toivonen et al , while CThe young age of most patients with need for long-term antiarrhythmic treatment and attendant side effects prompted the search for curative therapies. Fontaine et al (1987) described successful treatment of ILVT by application of a high-energy DC shock (fulguration) between the catheter tip and a neutral plate placed under the patient's back . Klein eDifferent approaches for radiofrequency ablation have been described by various authors. Nakagawa et al preferred careful localization of the Purkinje potential in guiding ablation. They selected the area where a Purkinje potential precedes the QRS complex during tachycardia . WellensSince fascicular VT is sometimes difficult to induce despite pharmacological provocation, some workers  prefer primary ablation. In a recent report, seven cases of incessant fascicular VT were successfully ablated with no recurrence . They re


Double tachycardia is a relatively rare condition. We describe a 21 year old woman with history of frequent palpitations. In one of these episodes, she had wide complex tachycardia with right bundle branch and inferior axis morphology. A typical atrioventricular nodal tachycardia was induced during electrophysiologic study, aimed at induction of clinically documented tachycardia. Initially no ventricular tachycardia was inducible. After successful ablation of slow pathway, a wide complex tachycardia was induced by programmed stimulation from right ventricular outflow tract. Mapping localized the focus of tachycardia in left ventricular outflow tract and successfully ablated via retrograde aortic approach. During 7 month's follow-up, she has been symptom free with no recurrence. This work describes successful ablation of rare combination of typical atrioventricular nodal tachycardia and left ventricular outflow tract tachycardia in the same patient during one session. Double tachycardia, defined as the simultaneous occurrence of atrial and ventricular ,2 or junA 21 year old woman with no evidence of structural heart disease referred to our center for evaluation of palpitation and dizziness. The structural heart disease was excluded by physical examination and transthoracic echocardiography. Transthoracic echocardiography showed normal cardiac chambers (including right ventricle), normal valvular function and ejection fraction (EF) without any wall motion abnormalities. During an episode of palpitation, the standard 12-lead electrocardiogram (ECG) showed documented wide complex tachycardia with a heart rate of 125 beats /min. The tachycardia was refractory to two intravenous antiarrhythmics . The wide complex tachycardia had inferior axis and right bundle branch block morphology compatible with LVOT-tachycardia . The basAfter obtaining written informed consent, electrophysiologic study was done in the postabsorptive and nonsedated state. During programmed electrical stimulation from atrium and ventricle, dual AV nodal physiology with nonsustained AVNRT was induced. Then programmed ventricular stimulation was performed with standard protocol at three cycle length  and three extrastimuli up to coupling interval of 200 ms from two sites . No ventricular tachycardia was induced with and without isoproterenol infusion. Repeat programmed atrial stimulation resulted in induction of sustained AVNRT under isoproterenol infusion . RadiofrDouble tachycardia was a relatively uncommon type of tachycardia in previous reports ,3,5. In Idiopathic VT most commonly arises from RV than LV (70% versus 30%) . IdiopatIn this patient, clinically documented arrhythmia was ventricular tachycardia arising from the LVOT area whereas AVNRT was the first tachycardia induced by programmed stimulation in the electrophysiologic laboratory, although this had not been documented clinically. Slow pathway ablation was done because of patient request and report of future recurrence of AVNRT in such patients . Then LVCo existence of AVNRT and LVOT-tachycardia may be a no more than chance association. This suggestion appears to be supported by presence of different mechanisms for both each type of tachycardia. On the other hand, some debate was made for this hypothesis in Kautzner study explaining this combination by presence of common trigger in patients with combination of AVNRT and RVOT-tachycardia .Our case demonstrated: 1) Presence of rare coexistence of AVNRT and LVOT-tachycardia 2) Feasibility of successful ablation of combination of AVNRT and LVOT-tachycardia in the same patient during one session.


A 21-year old man with history of 8 year palpitation was referred for electrophysiologic study and possible radiofrequency ablation. Physical examination and transthoracic echocardiographic study did not disclose any abnormality. Baseline ECG showed normal sinus rhythm with normal PR and QRS intervals and no evidence of preexcitation. Antiarrhythmic drugs (propranolol and verapamil) were discontinued two days before the procedure. Baseline intervals in sinus rhythm were as follows: sinus cycle length=690 msec, AH=74 msec, HV=37 msec, QRS=90 msec, PR=133 msec. The minimal pacing cycle length maintaining 1:1 antegrade conduction (AVWP) was 320 msec and the minimal pacing cycle length maintaining 1:1 retrograde conduction (VAWP) was 400 msec. Single extrastimulus testing in the right atrium and the right ventricular apex leaded to a sustained narrow complex tachycardia. The arrhythmia was a short PR- long RP tachycardia with following characteristics: cycle length=376 msec, AH=141 msec, HV=42 msec, VA=200 msec, HA (HRA) =236 msec, HA (His) =243 msec and eccentric atrial activation during the arrhythmia . The arrA ventricular extrastimulus delivered at RV septum in the inflow region synchronous with His activation during the arrhythmia neither advanced nor delayed the subsequent atrial activation. Earlier ventricular premature beat at the RV septum terminated the arrhythmia (the His was not refractory) without conduction to the atrium. Right ventricular apical pacing at a cycle length just shorter than the tachycardia cycle length showed the same retrograde atrial activation sequence as during the arrhythmia.Subsequently, the right atrioventricular annulus was mapped in the tachycardia and the shortest VA interval was noted at the posterolateral of tricuspid annulus. The radiofrequency current was delivered to this site at the ventricular aspect of tricuspid annulus and resulted in termination of the arrhythmia within 5 seconds. The successful ablation site had a VA interval of 109 msec .Following this ablation, programmed atrial and ventricular stimulation failed to induce any arrhythmia and retrograde atrial activity sequence during burst ventricular pacing was concentric. Comparing retrograde atrial activity sequence before ablation with retrograde atrial activity sequence after ablation in the same pacing cycle length showed a significant decrease in VA interval after ablation of the accessory pathway . What isThe differential diagnosis of a short PR- long RP tachycardia should include atypical AVNRT, orthdromic AVRT involving a slowly conducting retrograde accessory pathway and atrial tachycardia.There are a variety of pacing maneuvers which can be useful in differentiating these arrhythmias. One of the most important methods of diagnosing the presence and participation of retrogradely conducting bypass tracts during SVT is the ability of a ventricular extrastimulus to depolarize the atrium, with the same atrial activation sequence as supraventricular tachycardia when the His bundle is refractory. The site of stimulation relative to the site of the bypass tract and the rate of the tachycardia are the main determinants of the ability to preexcite the atrium.  Because the slowly conducting bypass tracts have decremental conduction property, the response to premature ventricular stimuli results in slowing of VA conduction which can retard the return cycle .Burst pacing from the right ventricle at a cycle length just shorter than the tachycardia cycle length is another maneuver. If ventricular pacing produces the same retrograde activation sequence, a bypass tract can be diagnosed.  Also, measuring the delta H- A interval  can distinguish tachycardia that is due to AVNRT from septal bypass tract .Based on the electrophysiologic findings, the patient had a slowly conducting right posterolateral accessory pathway and the arrhythmia was an orthdromic AVRT. The concealed accessory pathway that conducts in retrograde fashion with a decremental property usually is located in posterior region near the posterior interatrial septum. In our case, the accessory pathway was located at posterolateral region of tricuspid annulus. Ticho et al reported four patients with the permanent form of junctional tachycardia in whom slowly conducting retrograde accessory pathways were located in sites other than the posteroseptal area. It was in the right free wall in two patients, in the right anterior septum in one patient and in the left free wall in one patient .In our case, eccentric atrial activation both during the arrhythmia and during ventricular pacing was diagnostic of a concealed bypass tract.The ventricular extrastimulus could not advance or delay the subsequent atrial activation. It might be due to the location or slow conduction property of the accessory pathway.Before ablation of the accessory pathway, retrograde atrial activation sequence had been eccentric and conduction had been via the accessory pathway with slowly conducting property but after that, retrograde atrial activation sequence was concentric with short VA interval. Since the retrograde His signal could not be seen, HA interval during RV pacing could not be determined. According to post-ablation study, VA conduction was decremental and no arrhythmia was inducible so the presence of another accessory pathway is unlikely and it seems that retrograde atrial conduction was via fast pathway. But, what is the reason that retrograde atrial conduction had been predominantly via the accessory pathway before we ablated it?We reviewed the intracardiac electrograms. During the procedure, we had to sedate the patient. Before sedation of the patient, retrograde atrial activation had been concentric with short VA interval but after that, retrograde atrial activation was eccentric. It could be related to the decrease of sympathetic activity and catecholamine release after sedation of the patient. Because sympathetic stimulation could enhance AV node conduction and shorten its effective refractory period, the impulses had been conducted to atrium via fast pathway. Although slowly conducting accessory pathways behave like AV node in many respects, they have quantitatively differing response to autonomic and pharmacologic manipulation. It is similar to different responses of slow and fast pathways to autonomic stimulation in patients with AVNRT. For example, adrenergic stimulation tends to shorten ERP of fast pathway (both antegrade and retrograde) to a greater extent that of the slow pathway .The persistence of conduction via the accessory pathway can be explained with repetitive concealed antegrade penetration of AV node by the impulse reaching the atrium, after being conducted retrogradely via the accessory pathway.In conclusion, post-ablation retrograde atrial activation sequence was concentric and conduction was via AV node (fast pathway) so after ablation of the accessory pathway, VA interval was shortened and it seems that atrial and ventricular electrograms were fused.


Atrial flutter (AFL) is a common arrhythmia in clinical practice. Several experimental models such as tricuspid regurgitation model, tricuspid ring model, sterile pericarditis model and atrial crush injury model have provided important information about reentrant circuit and can test the effect of antiarrhythmic drugs. Human atrial flutter has typical and atypical forms. Typical atrial flutter rotates around tricuspid annulus and uses the crista terminalis and sometimes sinus venosa as the boundary. The IVC-tricuspid isthmus is a slow conduction zone and the target of radiofrequency ablation. Atypical atrial flutter may arise from the right or left atrium. Right atrial flutter includes upper loop reentry, free wall reentry and figure of eight reentry. Left atrial flutter includes mitral annular atrial flutter, pulmonary vein-related atrial flutter and left septal atrial flutter. Radiofrequency ablation of the isthmus between the boundaries can eliminate these arrhythmias. Atrial flutter (AFL) is a frequent arrhythmia second only to atrial fibrillation in clinical practice. Since Jolly and Ritchie first recorded AFL in 1910, over the next several decades there was surprisingly little progress in understanding its mechanisms . Using aBoyden et al cut the chorda tendineae of the anterior and septal leaflets of the tricuspid valve using a knife and produced some degree of tricuspid insufficiency and volume overload induced enlargement of the right atrium . From thFrame et al made an intercaval incision connected with a second incision in the right atrial free wall to create a Y-shaped lesion . The atrAfter pericardiotomy, the atrial surfaces were then generously dusted with sterile talcum powder, a single layer of gauze is then put on the right and left atrial free walls, and the pericardiotomy is repaired . The atrAtrial crush injury was created with a surgical clamp placed on the right atrial free wall, producing a lesion parallel to and 1.5 cm above the atrioventricular ring, extending from the base of the right atrial appendage 1.5 to 2.5 cm posteriorly toward the intercaval zone and 3 to 4 cm wide . Atrial Human AFL is defined by the undulating P wave in the ECG with saw-tooth appearance. Typical AFL has positive P waves in lead V1, negative P waves in lead V6, and negative P waves in lead II, III, and aVF. Activation mapping using the Halo catheter and 3-D mapping system showed the activation wave front goes downward in the free wall , travels through the cavotricuspid isthmus, spread upward in the septal wall, and crosses the crista terminalis to complete the reentrant circuit. Reverse typical FL has negative P waves in lead V1, positive P wave in lead V6, and positive P waves in lead II, III, and aVF. The action sequence was the reverse of typical AFL.In this laboratory, we have studied the electrophysiologic properties of typical AFL circuit. It was consistent with previous findings that the low right atrial isthmus, defined as a path bounded by the orifice of inferior vena cava, eustachian valve/ridge, coronary sinus ostium, and tricuspid annulus, is a zone of slow conduction during AFL -11. FurtUsing activation and entrainment mapping from closely spaced sites around the tricuspid annulus during typical AFL, Kalman et al confirmed that all sites around the circumference of the tricuspid annulus were a part of the flutter reentrant circuit, since the postpacing interval was equal to the flutter cycle length. Thus, tA flat resetting response was observed in most cases of typical AFL, signifying a fully excitable gap ,23. The Using the noncontact mapping system, we could demonstrate that some patients had a single incomplete line of block in the crista terminalis during typical atrial flutter. This resulted in double loop reentry during typical atrial flutter, one circulating around the tricuspid annulus, and the other rotating around a part of crista terminalis through the conduction gap . RF ablaAtypical AFL may arise from the right or left atrium. There are no consistent ECG characteristics. However, using three criteria  can differentiate left from right AFL .Using a noncontact, 3D mapping technique, we have demonstrated a macroreentrant circuit localized to the upper portion of the right atrium . The wavUsually there is a low voltage zone in the anterior free wall, which may be due to spontaneous scar formation. The activation wave front circulates around this low voltage zone and the electrograms at this zone show double potentials . RF ablaThe type I figure-of-eight reentry (n = 4) demonstrated simultaneous upper and lower loop reentry sharing a common pathway through conduction gap in the crista terminalis . The twoThis macroreentrant circuit rotates around the mitral annulus, either counterclockwise or clockwise . The bouMacroreentrant circuits can rotate around one or more pulmonary veins and a scar in the posterior wall or roof of the left atrium . These cThe macroreentrant circuit rotates around the left septum primum, either counterclockwise or clockwise ,30. The AFL is a reentrant arrhythmia and needs anatomic or functional barriers to maintain its activation. Typical AFL rotates around the tricuspid annulus with the crista terminalis and tricuspid annulus as barriers. Atypical AFL may originate from the right or left atrium without involving the cavotricuspid isthmus. The barriers may be scars, crista terminalis, mitral annulus, pulmonary veins, or septum primum. RF ablation of the isthmus between the boundaries can cure this arrhythmia.


Supraventricular tachycardias are quite common in clinical practice. Medical treatment of supraventricular tachycardia often involves regular intake of drugs for several years. Problems of drug therapy include poor efficacy and bothersome side effects including proarrhythmia. This has lead to the development of non-pharmacological therapies. Arrhythmia surgery initially demonstrated that many types of supraventricular arrhythmias could be cured. However during the past decade arrhythmia surgery has been largely replaced by catheter ablation. Catheter ablation can be defined as the use of an electrode catheter to destroy small areas of myocardial tissue or conduction system, or both, that are critical to the initiation or maintenance of cardiac arrhythmias. Arrhythmias most likely to be amenable to cure with catheter ablation are those which have a focal origin or involve a narrow, anatomically defined isthmus . This reSupraventricular tachyarrhythmias have been classified into regular and irregular  . Atrial 1. Atrioventricular re-entry tachycardias (AVRT), using the ventricle as part of the circuit; these tachycardias are dependent on the presence of an accessory atrioventricular (AV) pathway.2. Atrioventricular nodal re-entry tachycardia (AVNRT), where the re-entry circuit is within the AV node and the ventricle plays no part in maintaining the arrhythmia.3. Atrial tachycardia, where the re-entry circuit does not involve any part of the AV junction e.g. atrial flutter, ectopic atrial tachycardia.Catheter ablations are performed in cardiac electrophysiology laboratories specially equipped with recorders, programmed stimulators and ablators. Ever since 1989, radiofrequency current has been used for ablation, while earlier attempts were with direct current. The procedure is typically performed using conscious sedation. Two to five multipolar electrode catheters are inserted percutaneously under local anaesthesia into a femoral, brachial, subclavian, or internal jugular veins and positioned in the heart under fluoroscopic guidance. Each electrode catheter has four or more electrodes. The most distal electrode pair is usually used for pacing and the delivery of critically timed extra stimuli, while all of the electrodes are used to record electrograms from localised regions within the heart. Up to 50 W of radiofrequency energy is delivered for 30-60 seconds as a continuous, unmodulated, sinusoidal waveform with a frequency of approximately 500,000 Hz, between the 4 mm tip of a deflectable ablation catheter and a ground plate positioned on the patient's back or chest. The temperature of the ablation electrode can be monitored and the power output automatically adjusted to achieve a targeted electrode temperature of between 60-70°C. Knowledge of the electrode temperature at a particular ablation site is useful in determining whether an unsuccessful application of radiofrequency energy failed because of inaccurate mapping or inadequate heating [AVRT utilizes accessory pathways which are anomalous extra nodal connections between the epicardial surface of the atrium and ventricle along the atrioventricular groove. Accessory pathways can be classified based on their location along the mitral or tricuspid annulus, type of conduction , and whether they are capable of antegrade conduction, retrograde conduction, or both. Accessory pathways which are capable only of retrograde conduction are concealed while those capable of antegrade conduction are manifest, demonstrating pre-excitation on a standard ECG. AVRT is the most common arrhythmia in patients with a manifest accessory pathway, occurring in 75% of cases.An electrophysiological study is performed to localise the accessory pathway and determine its conduction characteristics prior to ablation. Accurate localisation of an accessory pathway is critical to the success of catheter ablation procedures. Preliminary localisation of the accessory pathway can be determined based on the delta wave and QRS morphology on the surface ECG in patients with manifest pre-excitation. Mapping of concealed accessory pathways and more accurate localisation of manifest accessory pathways require analysis of the retrograde atrial activation sequence and/or antegrade ventricular activation sequence. Right sided and posteroseptal accessory pathways are typically localised and ablated using a steerable electrode catheter with a 4 mm distal electrode positioned along the tricuspid annulus or in the coronary sinus os from the inferior vena cava. The location of left sided accessory pathways can be determined using a multipolar electrode catheter positioned in the coronary sinus, which runs parallel to the left atrioventricular groove or with a steerable catheter positioned in the left atrium or ventricle. Once localised to a region of the heart, precise mapping and ablation is performed using a steerable 4 mm tipped electrode catheter positioned along the mitral annulus using either the transeptal or retrograde aortic approach. These two approaches for ablation of left sided accessory pathways are associated with a similar rate of success and incidence of complications . The decAppropriate sites for radiofrequency energy delivery during ablation of manifest accessory pathways are characterised by early ventricular activation, the presence of an accessory pathway potential, and stability of the local electrogram . ApproprEfficacy of catheter ablation of accessory pathways varies from 89-99% -9. The sAtrioventricular nodal re-entrant tachycardia (AVNRT) occurs in patients with dual AV nodal physiology. They have two functionally distinct pathways known as the slow and fast pathway. The slow pathway has a shorter refractory period. During the common form of AVNRT, an atrial premature beat travels down the slow pathway and gets conducted back by the fast pathway to depolarise the atrium. In the uncommon variety, the reverse pattern occurs. The fast pathway is located anteriorly along the septal portion of the tricuspid annulus, near the compact atrioventricular node, whereas the atrial insertion of the slow pathway is located more posteriorly along the tricuspid annulus, closer to the coronary sinus ostium.AVNRT can be cured by ablating either the fast pathway or the slow pathway. However, it has clearly been shown that catheter ablation of the slow pathway using a "posterior approach" is associated with greater safety and efficacy. For this reason, the "anterior approach" is merely of historical interest. Fast pathway ablation is by an "anterior" approach. Catheter ablation is performed by locating an electrogram with a large His potential and then withdrawing the ablation catheter into the right atrium until the atrial signal is at least twice that of the ventricular signal (A:V ratio > 2) with a His potential no larger than 50 μV. Radiofrequency energy is then applied during sinus rhythm for 30-60 seconds while watching for prolongation in the PR interval. Energy delivery is immediately terminated if atrioventricular block occurs. Successful ablation of AVNRT is characterised by lengthening of the PR interval and the inability to induce the tachycardia. There is elimination or pronounced attenuation of retrograde conduction during ventricular pacing. The atrioventricular block cycle length and the atrioventricular node effective refractory period are not usually altered during ablation by the anterior approach. Anterior approach is successful in about 90% of cases. Inadvertent atrioventricular block occurs in approximately 7% of patients. Recurrence rate is about 9% .Slow pathway ablation is by the "posterior" approach. The ablation catheter is directed into the right ventricle low near the posterior septum and is then withdrawn until an electrogram is recorded with a small atrial electrogram and a large ventricular electrogram (A:V ratio < 0.5). Specific ablation sites along the posterior portion of the tricuspid annulus can be selected based either on the appearance of the local atrial electrogram or based strictly on anatomic factors. While using the electrogram guided approach, fractionated atrial electrograms with a late "slow potential" are targeted. In the anatomic approach, the initial applications are delivered at the level of the coronary sinus ostium and subsequent applications at more superior sites. Junctional beats occurring during the application of radiofrequency energy are a marker for successful ablation. Successful ablation is characterised by an increase in the atrioventricular block cycle length and in the atrioventricular node effective refractory period and elimination of inducible AVNRT. The posterior approach for ablation of AVNRT is effective in greater than 95-97% of patients .  AtriovCatheter ablation of sustained regular atrial tachycardias can also be performed with high safety and efficacy. Focal atrial tachycardia, whether reentrant, automatic, or triggered can be ablated with success rates greater than 90%. The site for ablation is generally chosen based on early activation. Typical atrial flutter is also amenable to cure with catheter ablation. This macroreentrant arrhythmias is localized to the right atrium. Atrial flutter can be cured by creating a continuous, transmural, linear lesion between the tricuspid annulus and the inferior vena cava. This procedure is generally referred to as an "isthmus" ablation. Catheter ablation of atrial flutter can be performed with an efficacy greater than 90% and a < 5% risk of recurrence of atrial flutter. Non-isthmus dependant atrial flutter can also be treated with catheter ablation. These regular atrial tachycardias, with rates between 250 and 350 bpm often involve scars created during prior cardiac surgery. The procedure can be accomplished by defining a critical region of conduction which is necessary for maintenance of the arrhythmia. The creation of a linear lesion in this region can result in cure of the tachycardia. Catheter ablation of non-isthmus dependant atrial flutter can be accomplished with an efficacy of greater than 80% and a < 5% risk of major complications.Because of the remarkable safety and efficacy of catheter ablation, it is now considered as first line therapy for most types of supraventricular arrhythmias. These include AVNRT, AVRT, atrial tachycardia, and atrial flutter. It is anticipated that the dream of curing atrial fibrillation with ablation techniques will also be realized sometime during the next five years.


Tachycardia induced tachycardias are not common in clinical practice, and it is believed that most cases of double tachycardia are coincidental. The existence of two different tachycardias in the same patient almost always poses problems in the electrophysiology laboratory. However, in rare instances, the emergence of a second tachycardia can actually provide invaluable information about the first one. In this report, we describe a 30-year-old woman who presented with palpitations. Electrophysiological study revealed that atrial programmed stimulation at baseline induced right ventricular outflow tract (RVOT) tachycardia and supraventricular tachycardia. The study also showed that each of the tachycardias was able to induce the other. A short run of RVOT tachycardia during supraventricular tachycardia was able to entrain the latter. This finding provided important information about the nature of the supraventricular tachycardia, which proved to be atrioventricular nodal reentrant tachycardia. Both of these tachycardias were successfully ablated, and the patient’s palpitations disappeared. Simultaneous occurrence of supraventricular and ventricular tachycardia in the same patient is very rare. Concomitance of both these forms is usually coincidental, except in cases of digitalis toxicity and catecholaminergic tachycardias ,2. We reA 30-year-old woman was referred to our hospital for evaluation of non-sustained ventricular tachycardia. She complained of palpitations lasting 20 to 30 minutes, and said she had had this problem for 2 years. Episodes of non-sustained ventricular tachycardia were documented during an exercise stress test. She was treated with verapamil and metoprolol with no success. Her physical examination was normal and an echocardiogram revealed no structural abnormalities. Electrocardiography showed frequent monomorphic ventricular premature beats of left bundle-branch block and inferior axis configuration.An electrophysiological study was performed with the patient in postabsorptive, non-sedated state. An EP Tracer electrophysiology system  was used. During the study, sinus rhythm was very frequently interrupted by spontaneous repetitive monomorphic non-sustained ventricular tachycardias (NSVT) with left bundle-branch block and inferior axis configuration. Mapping studies performed using an ablation catheter  revealed that the ectopic activity originated from the RVOT. However, attempts to precisely map these premature depolarizations were frequently interrupted by a supraventricular tachycardia of cycle length 280 ms, which was started by the NSVT. The supraventricular tachycardia had a ventriculoatrial interval of 45 ms, which suggested either AVNRT or atrial tachycardia as the pathophysiologic mechanism.Due to the frequent ventricular premature beats and runs of NSVT, it was not possible to further analyze and identify the exact nature of this supraventricular tachycardia. In order to continue mapping for the ventricular tachycardia, it was necessary to terminate the supraventricular tachycardia by overdrive pacing each time. There were occasions when the supraventricular tachycardia initiated the NSVT and vice versa . An episThe ventricular tachycardia was eliminated after 14 radiofrequency applications  were delivered to the RVOT. Ventricular programmed stimulation after the ablation revealed no inducible ventricular tachycardias and demonstrated that the ventriculoatrial conduction was decremental. Atrial programmed stimulation showed dual atrioventricular nodal physiology and inducible AVNRT. A single radiofrequency application to the right posterior septum eliminated the dual nodal physiology and AVNRT. At a follow-up check 1 month after the procedure, the patient was free of palpitations.Tachycardia induced tachycardia is a rare phenomenon that is only discussed in a few case reports in the literature. Wagshal and colleagues described one patient with idiopathic left ventricular tachycardia and AVNRT . In thatCooklin and McComb recently reported a case in which AVNRT was induced by RVOT tachycardia during infusion of isoprenaline in an electrophysiological study . Our patThe consecutive occurrence of two different tachycardias during electrophysiological testing always presents a major challenge for the electrophysiologist. During our electrophysiological study, we aimed to ablate the RVOT tachycardia first since it was responsible for the patient’s main symptoms. However, our attempts to locate the earliest ventricular activating sites during RVOT tachycardia were frequently interrupted by intervening AVNRT. To address this, we changed our strategy and decided to ablate the supraventricular tachycardia first, but the frequent premature beats and ventricular tachycardias arising from the RVOT prevented analysis of the mechanism of the supraventricular tachycardia. Thus, we had to change our plan again, and finally ablated the RVOT tachycardia after 14 radiofrequency applications.Apart from the problems mentioned above, we observed that double tachycardias actually helped establish the diagnosis during electrophysiological study. In our case, a three-beat run of RVOT tachycardia during the supraventricular tachycardia entrained the latter with an ‡atrial-ventricular’ pattern, and helped us diagnose AVNRT .In conclusion, this case is of particular interest because of the unusual finding of double tachycardia, with each form capable of inducing the other. The case is also noteworthy in that it highlights the advantages and disadvantages of dealing with two different tachycardias in the electrophysiology laboratory.


A 15-year-old girl, previously asymptomatic for palpitations, underwent a successful atrial septal defect (ASD) device closure. Twelve weeks after the procedure, the patient was admitted complaining of dyspnoea on effort and palpitations. The twelve-lead ECG showed a narrow QRS tachycardia with slight heart rate irregularity, with a mean HR of 170bpm. P waves were not clearly identified with a suspicious of negative P-waves in II, III and aVF leads. No clear relationship could be observed between the suspected P waves and QRS complexes .Echocardiographic evaluation showed normal position of ASD Device, with no residual shunts, mild dilatation of right atrium and right ventricle with a moderate biventricular systolic function impairment. Transesophageal electrophysiological study showed an atrial tachycardia with a regular A-A interval of 220ms and an A-V conduction delay with a A-V nodal Wenckebach periodicity, leading to an irregular V-V interval ranging between 375 and 300ms . OverdriThe case represents a rare form of intra-atrial re-entry tachycardia with an A-V nodal Wenckebach periodicity. It has been already shown that in intra-atrial re-entry tachycardia, variables degrees of block may be present throughout the entire episode of sustained tachycardia. Neither the ventricles nor the A-V node are required for this arrhythmia. It is the appearance of AV block with maintenance of the supraventricular tachycardia that strongly suggests a supranodal origin. The presence of persistent termination of the arrhythmia through atrial pacing excluded an automatic origin.


Pacemapping (PM) is an electrophysiologic technique designed to help locating tachycardia sources by stimulating at different endocardial sites in order to reproduce the clinical tachycardia characteristics. A recorded electrocardiogram (ECG) during the clinical tachycardia has been conventionally used as reference. Yet, endocardial activation pattern during tachycardia may be utilized as well to guide the procedure. In focal tachycardia ablation, PM guide has consistently provided remarkable outcomes , while oAn important issue regarding PM is the electrical configuration of the stimulation catheter, bipolar or unipolar. During bipolar pacing, stimulation poles (anode and cathode) are located at the distal tip of the catheter and usually both are contacting the endocardium. Using this configuration, myocardium can be captured at the cathode, anode or both sites simultaneously decreasing mapping accuracy. On the contrary, unipolar pacing captures exclusively local myocardium next to the distal electrode . Thus, uConduction properties of paced stimuli seem to depend on myocardial conditions. Pacing ventricular scar tissue, as in patients with prior myocardial infarction (MI), shows a delay between the electrical stimulus and the QRS onset, suggesting local slow conduction. These impaired conduction zones may represent potential substrates for reentrant circuits involved in ventricular tachycardia (VT).Regarding atrial PM, it is unclear whether the conduction pattern of an atrial stimulus depend on the paced site, electrical voltage or the stimulating rate. This issue was recently addressed by Perez-Castellano el al . Pacing A PM limitation is that pacing at two different points may induce similar surface ECG or endocavitary recordings. An optimal spatial PM resolution requires a short maximum distance between two points generating similar ECG. Usually, the spatial resolution of unipolar stimulation is shorter than 5 mm . SpatialThe highest benefit of PM has been found in focal tachycardia mapping, especially in idiopathic VT. However, PM has been reported in a broad variety of arrhythmias. In the following sections we will review its usefulness and feasibility sorted by type of arrhythmia.Atrial tachycardia (AT) is defined as focal when its source is a precise point at the atria. Focal AT are due to triggered activity, increased automatism or microreentry. The precise origin of a focal AT can be readily determined using PM by pacing at different sites of the atria to emulate the P waveform of the tachycardia  or the aMcLean et al  reportedSippensGroenewegen et al  used a mAnother tool for targeting AT ablation is PM guided by endocavitary recordings. This technique compares the atrial activation sequence during tachycardia, as shown by endocavitary recordings, and the sequence obtained during pacing with a mapping catheter at different atrial sites. Tracy et al reported excellent results using this technique in 10 focal AT ablation procedures [A focal origin has been reported in most patients with paroxysmal atrial fibrillation (AF). These foci are usually located in the pulmonary veins (PV) and its ablation is becoming a curative therapy. Ablation strategies include empirical electric isolation of the four PV or a selective approach ablating only the culprit PV. The latter can be extraordinarily demanding as finding the culprit vein is frequently challenging. Deen et al  reportedActivation patterns at CT and CS differed at every paced PV. In order to measure activation times they considered the CS proximal electrodes (CS 9-10) as a reference, corresponding to time zero. According to their findings they concluded:1.- Pacing of right PVs showed activation of CS was from proximal to distal: reaching CS 9-10 15.8 ms and 24 ms before CS 1-2 in right superior PV (RSPV) and right inferior PV (RIPV), respectively. Pacing of left PVs showed activation of CS from distal to proximal: reaching CS 1-2 23.8 ms and 20.1 ms before CS 9-10 in left superior PV (LSPV) and left inferior PV (LIPV), respectively.2.- Activation of CT was earlier in CT 5-6 and CT 11-12 during pacing of  RSPV and RIPV, respectively. Pacing of left PVs showed earlier activation at CT 3-4 with activation pattern from top to bottom. Total activation time of CT was longer for the LSPV (33.7 ms) than for the LIPV (19.3 ms).An excellent correlation was observed between atrial activation sequence obtained by PM and the location of the focus at the PV under traditional electrophysiological criteria.Conventional strategies for accesory pathway (AcP) mapping face certain limitations, leading to prolonged procedures and the need for multiple RF applications during ablation. Perez-Castellano et al reported a new mapping approach to help localize the atrial insertion of AcP by reproducing the atrial activation sequence during orthodromic tachycardia through atrial pacing at the mapping catheter .This method is based on the relative timing of activation between two stable reference electrograms, used to estimate the atrial activation sequence during tachycardia and during pacing . The autThis method is complementary with traditional mapping criteria  and its In patients with preexcited tachycardia implicating Mahaim fibers underwent attempted catheter ablation of the accessory pathway is possible to locate the accessory pathway ventricular insertion site used the criteria of concordance between paced and spontaneous QRS morphologies during pace mapping . This crThe right ventricular outflow tract (RVOT) tachycardia is the most frequent idiopatic VT, it origin is usually a single and well-limited focus. In the majority of patients this focus is located in RVOT’s anterior septal wall below the pulmonary valve; occasionally, the posterior septal and free walls are involved. These patients do not show overt structural heart disease, thus ventricular excitation and conduction properties are preserved. These conditions, as opposed to scar tissue, facilitate identifying the origin of the VT using PM.Conventionally, ventricular PM is performed in sinus rhythm, pacing at a cycle length similar to the clinical VT, trying to reproduce the QRS morphology during VT . Paced aFar-field capture may interfere with an adequate PM evaluation by distorting the paced QRS morphology. In order to reduce this detrimental effect, unipolar or bipolar with a distance between poles no longer than 5 mm are the recommended pacing configurations . RegardiActivation mapping constitutes an additional tool for idiopathic VT mapping. As an example, in a recently published series of six RVOT tachycardia cases, Timmermans et al using activation mapping located the origin of the tachycardia in the pulmonary artery, followed by successful ablation . PresystSome ECG patterns may suggest the primary location of a VT within the RVOT. The presence of Q waves in DI suggests an anterior septal origin, while R waves in DI suggest a more posterior source. When the R wave transition occurs early in precordial leads suggests an origin in the upper RVOT, a later transition (from V2) points to a lower location, below the pulmonary valve. Digit et al performed PM at the RVOT in healthy individuals in order to define ECG patterns from the different stimulated points to suggest the origin of RVOT tachycardias . The autOther idiopathic VT is the fascicular VT, is usually verapamil-sensible and has been demonstrated to arise from the left posterior or left anterior fascicle, with a right bundle branch block configuration and left-axis deviation or right-axis deviation, respectively. The ablation of a fascicular VT can be guided by activation mapping and/or Purkinje potential preceded the QRS during VT, behind VT exit to be associated with an optimal match between the paced rhythm and the clinical VT . TherefoMyocardial infarction is the leading substrate for monomorphic sustained VT. In hemodinamically tolerated VT, radiofrequency ablation constitutes a major therapeutic option associated or not to implantable cardioverter defibrillators. Percutaneous VT ablation reduces the rate of recurrences, avoids potential toxic effects of antiarrhythmic drugs and it is associated to a lower risk than EP-guided surgical resection procedures. Gonska et al performing a single morphology VT ablation reported an acute success rate close to 75% . AblatioUsefulness of PM in this subset of patients is limited. Scar tissue impairs ventricular conduction properties and favours conduction blockade. Thus, in this context, pacing in sinus rhythm to reproduce an exact VT QRS morphology is usually challenging or unsuccessful.The electrocardiographic VT morphology is determined by the initial activation site (circuit exit), and by the ventricular activation pathway. When PM is performed at or near the exit of a reentrant circuit, the induced QRS morphology may resemble the VT QRS . HoweverAs mentioned before, PM spatial resolution worsens with bipolar stimulation by inducing electrical capture at both electrodes. Kadish and coworkers  demonstrPM also helps to characterize slow conduction zones usually located within scars, manifested as a delay between the stimulus and the QRS onset . In normal hearts the S-QRS interval is shorter than 40 ms, while most of myocardial areas with abnormal fractionated EGM in sinus rhythm show a S-QRS delay longer than 40 ms. Demonstrating the presence of slow conduction zones is not enough to guide an ablation procedure, as they constitute a regular finding in infarcted areas . However


Sudden death might complicate the follow-up of symptomatic patients with the Wolff-Parkinson-White syndrome (WPW) and might be the first event in patients with asymptomatic WPW. The risk of sudden death is increased in some clinical situations. Generally, the noninvasive studies are unable to predict the risk of sudden death correctly . The electrophysiological study is the best means to detect the risk of sudden death and to evaluate the nature of  symptoms. Methods used to define the prognosis of WPW are well-defined. At first the maximal rate of conduction through the accessory pathway  is evaluated; programmed atrial stimulation using 1 and 2 extrastimuli delivered at different cycle lengths is then used to determine the accessory pathway refractory period and to induce a supraventricular tachycardia. These methods should be performed in the control state and repeated in adrenergic situations either during exercise test or more simply during a perfusion of small doses of isoproterenol. The induction of an atrial fibrillation with rapid conduction through the accessory pathway  is the sign of a form of WPW at risk of sudden death. At the time of the curative treatment of Wolff-Parkinson-White syndrome (WPW) by radiofrequency ablation ,2, it isThe exact risk of patients with the WPW syndrome to develop this complication is not known. It was relatively high in old studies in symptomatic patients ,4 1.5%)%5-7]. ThThe pattern of WPW syndrome on 12 lead surface ECG, the permanent or intermittent feature are not specific, although posteroseptal location and permanent forms are more frequently noted in patients at risk of rapid arrhythmias ,10. Several non invasive studies were proposed but their diagnostic value is low :- The abrupt disappearance of WPW syndrome during an exercise stress testing was proposed as a sign of accessory pathway with long refractory period -13; howe- Pharmacological tests  were also proposed : the disappearance of the pattern of WPW syndrome was reported as a sign of accessory pathway with long refractory period ; howeverElectrophysiologic study appears to be the most reliable method to establish the prognosis of WPW syndrome Patients might be studied by transesophageal route ,19 or inIt should be noted that all electrophysiologic studies in WPW syndrome might be dangerous and should be performed with an external defibrillator ready to be used, because a ventricular fibrillation can be induced in asymptomatic or symptomatic patients  Figure .Surface electrocardiograms and esophageal electrogram are simultaneously recorded on paper at speeds of 25 or 100 mm/sec. Cardiac stimulation is performed with a programmable stimulator which is connected to a pulse amplifier that can deliver pulses at width of 16 ms with a 29 mA output in the case of esophageal stimulation. For a simple electrophysiological study, only one catheter is needed : a bipolar silicone esophageal lead or one bipolar intracardiac catheter. A multipolar catheter electrode is  used only for the mapping of left atrium in patients who need a catheter ablation of the accessory pathway.The classical protocol is as follows:- Incremental atrial pacing is performed until second degree atrioventricular block occurs. The maximal rate of 1/1 conduction trough the accessory should be noted.- Programmed atrial stimulation at  basic cycle lengths of 600 ms and 400 ms with the introduction of one and two extrastimuli is performed : the disappearance of WPW syndrome indicates the accessory pathway refractory period. The method  is also used to induce a supraventricular tachycardia, generally an orthodromic tachycardia, rarely an antidromic tachycardia or an atrial tachycardia or fibrillation.- These data should be studied under adrenergic situations, except in patients who have a risk of sudden death in control state. Two methods are used : atrial pacing might be repeated during an exercise testing  ,22 which- Sustained atrial fibrillation or reciprocating tachycardia is defined as a tachycardia that is longer than 1 minute. The exact duration of induced tachycardia to be considered as pathological is still controversed and varies from 30 sec up to 5 minutes .- Conduction over the accessory atrioventricular connection is evaluated by the measurement of the shortest atrial cycle length at which there is 1 to 1 conduction over the accessory connection and the shortest atrial tachycardia cycle length at which there is 1 to 1 conduction over the accessory connection.- The Wolff-Parkinson-White syndrome is considered as representing a risk of sudden death when the following association is observed : sustained atrial fibrillation is induced and the shortest RR interval between preexcited beats is < 250 ms in the control state in adults, < 220 ms in children  Figure .- The exact nature of the prexcitation syndrome is assessed. Most of the WPW syndrome are related to a atrioventricular accessory connection or Kent bundle : the degree of prexcitation increases during premature atrial stimulation until the refractory period of accessory pathway is reached, because the conduction time does not change in accessory pathway with the shortening of atrial cycle length while it increases in the AV node. Rarely the WPW syndrome is related to a nodoventricular accessory pathway or Mahaim bundle and the degree of preexcitation remains unchanged during premature atrial stimulation.- The accessory pathway refractory period depends on the driven cycle length. Refractory period of the accessory pathway decreases as the driven cycle length shortens.- Beta adrenergic stimulation results in shortening of the anterograde refractory period of the accessory pathway  and an increase in ventricular rates during atrial pacing and atrial fibrillation . Isoprot- Atrial fibrillation is easily induced during intracardiac studies by salvos of rapid atrial stimulation and is not specific . The ind- Ventricular tachyarrhythmias also are easily induced in asymptomatic or symptomatic patients by programmed ventricular stimulation and are not specific in patients with WPW syndrome : the induction of a ventricular fibrillation is noted in 4 % of WPW syndrome and the induction of nonsustained multiform ventricular tachycardia in 37 % of them .- Antidromic tachycardia which is a reciprocating tachycardia using the accessory pathway for the anterograde conduction and the normal AV conduction system for retrograde conduction, is a rare finding (5%), more frequently noted in young patients with a good retrograde normal VA conduction or in patients with several accessory pathways and seems more frequent in patients at risk of rapid arrhythmias.- Orthodromic tachycardia which is a reciprocating tachycardia using the normal AV conduction system for the anterograde conduction and the accessory pathway for the retrograde conduction, is rarely induced in asymptomatic patients (< 10%) ,34, but - The incidence of forms considered at risk of rapid arrhythmias is similar in patients with symptomatic and asymptomatic patients and concerns 10 % of the total population with WPW syndrome  ,34, indeMoreover, the presence of syncope does not increase the chance to find a potentially dangerous form in adults ; in youn- The indications of electrophysiological study are now large in symptomatic patients to perform in a second time the catheter ablation of patients complaining frequent sustained tachycardias. The study should be performed by catheterisation.- In patients with syncope, but no documented tachycardia, electrophysiological study is necessary and might be performed by transesophageal route because the role of the accessory pathway in the occurrence of syncope remains rare in adults .- In patients who have a documented rapid or syncopal atrial fibrillation, electrophysiological study is not indicated, because direct catheter ablation of the accessory pathway is recommended. The location of the Kent bundle is easier in sinus rhythm and the induction of an atrial fibrillation should be avoided.- In asymptomatic patients, the indications of electrophysiolgical study are more debatable . At firsSome indications of a systematic electrophysiological are actually recommended :1) most of sudden deaths have the peculiarity to occur during exercise . Because2) the second indication is the detection of a WPW syndrome in a patient with high responsibility profession such as professional pilot While these indications are largely in teenagers and adults less than 40 years of age, the indications in children or elderly are more controversial :- in children, the conduction in accessory pathway and normal AV conduction system are more rapid, probably without  a clinical significance : in the study of Bromberg   a cycle - in elderly, the shortest atrial pacing cycle length with 1:1 anterograde conduction via the bypass tract increased progressively with age -44. HoweTherefore, because of the increase of the sport in all ranges of age and particularly in young children or after 60 years, the risk of occurrence of a potentially severe arrhythmia in an asymptomatic WPW patient should be not underestimated. The reliability and the simplicity of transesophageal study in WPW permits easy detection of forms at risk of severe arrhythmia.In conclusion, electrophysiological study is the best means to define the prognosis of a patient with the WPW syndrome. The study is easily performed by the transesophageal route. The indications should be large to avoid the misdiagnosis of a form at risk of rapid arrhythmias. This dangerous form is relatively rare in  asymptomatic patients or symptomatic patients with unexplained syncope. Most of these patients (>85%) would be allowed to continue their activities, without specific treatment, because they have a benign form of Wolff-Parkinson-White syndrome. In remaining patients, the development of the curative treatment of this disease by radiofrequency application on the accessory pathway  permits


Incisional sustained tachycardias are frequent in patients who have undergone a surgical repair of interatrial defect. A 43-year-old woman with drug refractory, highly symptomatic, persistent atrial tachycardia in the last year, was referred to our unit for catheter ablation. The patient had undergone a cardiac operation for repairing interatrial secundum ostium type defect with a patch five years before. A previous radiofrequency ablation procedure had been performed for common atrial flutter. We describe a case of incisional  atrial tachycardia ablation guided by the new EnSite NavX system equipped with a new electroanatomic mapping system. Incisional sustained tachycardias are frequent in patients who have undergone surgical repair of  an interatrial defects ,2. The mA 43-year-old woman with drug refractory, highly symptomatic, persistent atrial tachycardia in the last year, was referred to our unit for catheter ablation. Five years ago the patient was undergone  a cardiac operation for repairing an interatrial secundum ostium type defect. ECG showed an atrial tachycardia whose features resembled a common atrial flutter. Echocardiography images showed no  significant atrial dilation, no residual interatrial shunt and a normal ventricular systolic function.A quadripolar Josephson diagnostic catheter was inserted into the coronary sinus via left subclavian vein as a reference. A bipolar Cournard diagnostic catheter was inserted into the right ventricular apex. A  20-pole steerable catheter was placed around the tricuspid annulus. An 8 mm tip catheter (Boston Scientific EP Technologies) was used for mapping and ablation. The electrophysiological findings showed a stable atrial tachycardia of 230 ms cycle length which was firstly misunderstood as a common atrial flutter (counter clockwise) showing a caudocranial septal activation and craniocaudal activation along the right lateral atrial wall. The ablation catheter was therefore positioned on the cavo-tricuspid (CT) isthmus, considering this region crucial for the macroreentry circuit. But overdrive pacing at 210 ms cycle length from CT isthmus did not show any concealed entrainment. So we were inclined to believe that it was an incisional tachycardia and therefore we performed a reconstruction of the three-dimensional geometry of the right atrium  using the EnSite NavX system.An activation-voltage map was obtained moving the ablation catheter point by point inside the right atrium while the patient was still in stable atrial tachycardia. The voltage map showed a large no-signal area  on interatrial septum corresponding to a large patch used for repairing an interatrial defect . A largeRF application  in continuous way (70 Watts 55 °C) was then attempted along this isthmus drawing back the ablation catheter from the scar area to the tricuspid valve annulus, trying to connect the two areas of anatomic obstacles. We moved the ablation catheter along this line obtaining local electrogram disappearance or  voltage reduction more than 70%. EnSite NavX mapping system allowed us to move ablation catheter in  the right atrium without using fluoroscopy  during the procedure.After four RF applications along the isthmus between the patch on the atrial septum and the tricuspid valve annulus, atrial tachycardia was not yet interrupted though no significant local electrogram was still detectable along the ablation line we had performed. In order to verify ablation line continuity we performed an electroanatomic and activation remapping of the isthmus region which showed a gap on the ablation line  near theThe patient was followed up monthly after the procedure. Each month history, 12-lead ECG and 24 hour ECG Holter were analyzed. Ten months after the procedure though the patient had not taken any anti-arrhythmic drugs, there was no recurrence of palpitation or documented atrial tachycardia.The case shows that EnSite NavX system provides an excellent electroanatomic and activation map of any cardiac chamber and reliable monitoring of the ablation catheter. This system let us quickly made a diagnosis of incisional tachycardia with an anatomic circuit of macroreentry different from that of a common atrial flutter allowing us to identify a slow conduction isthmus in a place that was not the CT isthmus, though the electrocardiography feature of the atrial tachycardia was similar to a common atrial flutter. The Ensite NavX system rapidly identified a gap in the linear lesion we had performed, and allowed us to terminate the atrial tachycardia. NavX significantly reduces fluoroscopy time during ablation procedures and also allows to successfully perform difficult procedures with complex substrates. NavX supports detection of anatomic isthmus variations, particularly deep pouches or recesses ,14.


Arrhythmogenic right ventricular dysplasia/cardiomyopathy is a disorder characterized by frequent ventricular tachycardia originating from the right ventricle and fibro-fatty replacement of right ventricular myocardium. Though the disorder was originally described during surgical ablation of refractory ventricular tachycardia, catheter ablation of tachycardia is one of the options for patients not responding to anti arrhythmic agents. Direct current fulguration was used in the initial phase followed by radiofrequency catheter ablation. In the present day scenario, all patients with risk for sudden cardiac death should receive an implantable cardioverter defibrillator. Radiofrequency catheter ablation remarkably reduces the frequency of defibrillator therapies. Direct current fulguration can still be considered in cases when radiofrequency ablation fails, though it requires higher expertise, general anesthesia and carries a higher morbidity. Newer mapping techniques have helped in identification of the site of ablation. In general, the success rate of ablation in arrhythmogenic right ventricular dysplasia is less than in other forms of right ventricular tachycardias like right ventricular outflow tract tachycardia. Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD) is a disorder characterized by fibro-fatty replacement of the right ventricular myocardium, frequent ventricular tachycardia originating from the right ventricle and right heart failure. It was originally described by Fontaine et al during surgical ablation of refractory ventricular tachycardia . The firThough historically the original description of ARVD was during surgical ablation, pharmacological therapy was the initial mode of treatment in most cases. Surgical ablation by right ventricular disconnection was resorted to in resistant cases . PeroperThe initial reports on catheter ablation in ARVD were using direct current fulguration -8. One oRadiofrequency catheter ablation for ARVD has been in use since early nineties . It has Entrainment mapping can be used to characterize reentry circuits in ARVD to guide ablation -15. The Endocardial mapping can detect abnormal fragmented electrograms with delayed potentials. Pacemapping confirms the ablation site by producing a QRS morphology identical to the clinical VT . RecentlThree dimensional Real-time Positioning Management System (RPM) has also been used for guiding ablation in ARVD . RPM useO'Donnell et al have highlighted the electrophysiological differences between patients with ARVD and right ventricular outflow tract tachycardia (RVOT VT) . Though Ablation of ventricular tachycardias in ARVD still remains a clinical challenge, though more and more cases are being reported in the literature -23.


Wide complex tachycardia (WCT) refers to a cardiac rhythm of more than 100 beats per minute with a QRS duration of 120 ms or more on the surface electrocardiogram (ECG). It often presents a diagnostic dilemma for the physician particularly in determining its site of origin, which can be ventricular or supraventricular. In one series, only 32% of clinicians correctly diagnosed ventricular tachycardia (VT) in patients who presented with WCT [WCT that is grossly irregular typically represents atrial fibrillation with aberrant conduction or preexcitation. If its rate exceeds 200 beats per minute, the likelihood of atrial fibrillation with conduction over an accessory pathway should be entertained. In this article, we will discuss the approach to the evaluation and management of regular WCT.The differential diagnosis of regular wide complex tachycardia includes three major categories: ventricular tachycardia (VT), supraventricular tachycardia (SVT) with aberrance and preexcited tachycardia.Ventricular tachycardia is the most common etiology accounting for about 80 % of WCT -4. VentrSVT with aberrance accounts for a small portion of WCT. SVT typically originates in atrial tissue and/or AV junction and utilizes the normal atrioventricular (AV) conduction system for ventricular activation. Aberrance occurs when there is delay or block in the His-Purkinje system during antegrade conduction of impulses over the normal AV fascicles. Essentially, all types of SVT with aberrant conduction can present as a WCT. These include atrial tachycardias, atrioventricular nodal reentrant tachycardias, orthodromic reciprocating tachycardias, and other rare forms of SVT.Preexcited tachycardias are conducted antegradely over an accessory pathway (AP). Evidence for the presence of an AP can be manifest of the surface electrocardiogram (ECG) which can show intermittent or continuous presence of a delta wave associated with a short PR interval. The delta wave represents the part of the ventricular myocardium that is depolarized through the AP.An increasingly recognized cause of WCT is electrographic artifact . The cliVentricular paced rhythms represent a small portion of WCT. Sometimes the bipolar ventricular spike is small and difficult to see. The WCT is typically of LBBB pattern and superior leftward axis with right ventricular apical pacing. This pattern can vary significantly with the site of pacing. The tachycardia can be due to any form of SVT where the pacemaker is tracking sensed atrial activity and is pacing the ventricles at a fast rate. It can also represent a pacemaker-mediated tachycardia where the pacemaker is tracking retrogradely conducted atrial activity during ventricular pacing. A history and physical examination revealing the presence of a cardiac implantable device provide important clues to this diagnosis.A history of structural heart disease, particularly of coronary artery disease or prior myocardial infarction, strongly suggests a diagnosis of VT in patients presenting with WCT ,9. The oAlthough the blood pressure and heart rate are not particularly useful in differentiating WCT of ventricular versus supraventricular origin, certain physical signs such as the demonstration of AV dissociation strongly suggest a diagnosis of VT. These signs include the presence of cannon A waves on jugular vein examination, irregular intensity of the first heart sound by auscultation, and varying systolic blood pressure. These physical signs are highly specific and sensitive for the diagnosis of VT . Vagal mAn uncommon but sometimes useful semi-invasive procedure in the evaluation of patients with WCT is the placement of a transesophageal probe to record the atrial electrical activity and establish the diagnosis .The ECG remains a cornerstone in the diagnosis of WCT. A plethora of different diagnostic criteria have been suggested to distinguish between the various etiologies of WCT, each with different sensitivity and specificity -21.The most useful ECG criterion in establishing the diagnosis of VT is the presence of AV dissociation with more ventricular than atrial events. This practically rules out the possibility of the WCT representing an SVT. Fusion beats during WCT also imply the presence of AV dissociation, since they are the result of the simultaneous activation of the ventricular myocardium through both the normal conduction system and from an ectopic ventricular focus. A capture beat, also known as Dressler beat, is a narrow QRS complex resulting from a well-timed P wave capturing the ventricular myocardium through the normal conduction system during VT. A narrow complex beat, however, can also occur during WCT in patients with SVT and underlying bundle branch block (BBB). In this case, a ventricular premature beat originating from or close to the non-conducting bundle branch fuses with the impulses traveling down the contralateral bundle resulting in simultaneous ventricular activation on both sides of the septum and in a narrow QRS complex.The QRS duration has been proposed as a criterion to differentiate between WCT of ventricular and supraventricular origins. Wellens and colleagues found that 69% of VTs had QRS duration greater than 140 ms, whereas no SVT had QRS duration in this range . This crThe cardiac electrical axis during WCT is also useful to determine the origin of the abnormal rhythm. In the presence of a right superior (northwest) axis, the WCT is unlikely to represent an SVT, since this ECG pattern is inconsistent with any type of typical bundle-branch or fascicular block. Also, electrical concordance across the precordium  is rarely consistent with an SVT, and typically represents an anteroapical (negative concordance) or a posterobasal (positive concordance) left ventricular VT.Morphology is also often used to differentiate between WCT of ventricular from supraventricular origins . In the In certain situations, patient can have episodes of WCT that may require invasive electrophysiologic (EP) testing to make a diagnosis. The primary indication for EP testing in patients with WCT is if the correct diagnosis is unclear after analysis of available ECG tracings and the knowledge of the correct diagnosis is necessary for patient care. This is listed by the American College of Cardiology/American Heart Association task force as a class I indication for performing an EP study . Class IMost patients do not have spontaneous episodes of tachycardia during EP testing and have to be induced into the abnormal rhythm by burst pacing or premature stimulation at various sites and cycle lengths, with and without β-adrenergic stimulation. It is important however to make sure that the arrhythmia induced is the clinical arrhythmia responsible for the patient's presentation. This is achieved by careful comparison of the morphology and rate of the induced tachycardia with those of prior recordings obtained by ECG, holter monitors, or event monitors. Complete electrophysiologic testing is usually necessary not only to differentiate between VT and SVT but also to distinguish between the various forms of these arrhythmias.As mentioned before, AV dissociation is the hallmark of ventricular tachycardia. The difficulty arises when patients have retrograde 1:1 VA activation during VT. This can be difficult to distinguish from an SVT. In this situation, recording a His bundle electrogram and analyzing its relationship to the atrial and ventricular electrograms is essential for establishing the diagnosis. Also, performing electrophysiologic and pharmacologic maneuvers to try to dissociate the atria from the ventricles can be of great help.The initial approach to the management of the patient who presents with WCT depends primarily on the patient's hemodynamic status. Patients with low blood pressure, pulmonary edema, severe angina, or other evidence of poor perfusion associated with the WCT should be promptly cardioverted back into normal rhythm, using synchronized electrical direct current. Hitting the patient on the chest, also called "thump version" can sometimes terminate a WCT presumably by mechanically inducing a premature ventricular complex that interrupts the reentrant circuit of the tachycardia.For the hemodynamically stable patient, time should be spent on analyzing data from the history, physical examination, and ECG recordings to reach a diagnosis with a high degree of confidence. As mentioned above, from a statistical standpoint, the most likely diagnosis in patients with WCT is VT. Assuming this diagnosis even in the hemodynamically stable patient until proven otherwise is the safest approach to management.Because it can terminate both SVT and VT, Amiodarone (class III) is the agent of choice for stable WCT particularly if the etiology is uncertain. It is also particularly useful in patients with poor ejection fraction, since it has a favorable hemodynamic profile . ProcainAfter the acute management of an episode of WCT, long-term plans should be made to prevent the recurrence of the episodes, minimize their symptomatic impact, and protect the patient against sudden cardiac death. In general, the therapeutic options include pharmacological treatment with anti-arrhythmic drugs, device treatment with the automatic implantable cardioverter-defibrillator, and catheter ablation procedures. A combination of two or more of these modalities is sometimes necessary.In the patient with SVT, a catheter-based approach to therapy is curative in the overwhelming majority of patients and provides protection against sudden cardiac death in patients with the Wolf-Parkinson-White syndrome who have a rapidly conducting antegrade accessory pathway. In those patients whose ablation procedure fails or who choose not to undergo an invasive test, numerous antiarrhythmic medications can be used to suppress the SVT including b-blockers, calcium channel blockers, or class I and class III anti-arrhythmic drugs.In patients with poor ejection fraction and sustained ventricular tachycardia, device therapy is usually recommended. Pharmacologic therapy is used as an adjunctive therapy to minimize the episodes of VT and prevent defibrillator shocks. Occasionally, catheter ablation is needed as an adjunctive therapy for frequent or incessant VTs that fail to respond to medications.Not all VTs, however, are life-threatening and require device therapy. Idiopathic VTs occur in structurally normal hearts and carry a very good prognosis. These include right and left ventricular outflow tract VTs and left ventricular fascicular (verapamil-sensitive) VTs. Like SVTs, idiopathic VTs can also be cured with catheter ablation with good success rates ,26.Patients who present with WCT constitute a challenge to the diagnostic acumen of physicians. If misdiagnosed, these patients can be mismanaged, which can lead to lethal consequences. In the hemodynamically unstable patient, synchronized electrical cardioversion is the initial therapy. In the stable patient, physicians should use all clues provided by the history, physical examination, and ECG, in reaching the correct diagnosis. Until proven otherwise, any WCT should be managed as if it were VT, in keeping with the consideration of "First, do no harm". This implies that physicians should refrain from using long acting AV nodal blocking agents that can induce hypotension in an otherwise stable patient.


Bundle branch reentrant (BBR) tachycardia is an uncommon form of ventricular tachycardia (VT) incorporating both bundle branches into the reentry circuit. The arrhythmia is usually seen in patients with an acquired heart disease and significant conduction system impairment, although patients with structurally normal heart have been described. Surface ECG in sinus rhythm (SR) characteristically shows intraventricular conduction defects. Patients typically present with presyncope, syncope or sudden death because of VT with fast rates frequently above 200 beats per minute. The QRS morphology during VT is a typical bundle branch block pattern, usually left bundle branch block, and may be identical to that in SR. Prolonged His-ventricular (H-V) interval in SR is found in the majority of patients with BBR VT, although some patients may have the H-V interval within normal limits. The diagnosis of BBR VT is based on electrophysiological findings and pacing maneuvers that prove participation of the His- Purkinje system in the tachycardia mechanism. Radiofrequency catheter ablation of a bundle branch can cure BBR VT and is currently regarded as the first line therapy. The technique of choice is ablation of the right bundle. The reported incidence of clinically significant conduction system impairment requiring implantation of a permanent pacemaker varies from 0% to 30%. Long-term outcome depends on the underlying cardiac disease. Patients with poor systolic left ventricular function are at risk of sudden death or death from progressive heart failure despite successful BBR VT ablation and should be considered for an implantable cardiovertor-defibrillator. Bundle branch reentrant (BBR) tachycardia is a form of ventricular tachycardia (VT) incorporating both bundle branches into the reentry circuit. Another variant of the His-Purkinje macro-reentry utilizing ramifications of the left bundle branch is referred to as interfascicular reentrant tachycardia.Reentry within the His-Purkinje system (HPS) in humans was first documented by Akhtar et al ,2 in stuBBR VT is usually seen in patients with an acquired structural heart disease and significant conduction system impairment -11. DilaSurface ECG in sinus rhythm characteristically shows intraventricular conduction defects with or without PR interval prolongation. The conduction defects are presented by non-specific or typical bundle branch block patterns with prolonged QRS duration-12. AlthPatients usually present with presyncope, syncope or sudden death because of VT with fast rates frequently above 200 beats per minute -12. The Prolonged His-ventricular (H-V) interval in sinus rhythm is found in the majority of patients with BBR VT -12. AlthBBR VT is usually inducible with conventional pacing protocols. Both atrial and ventricular programmed stimulation or burst pacing can be useful. In some patients, the arrhythmia may be inducible only with atrial pacing stressing the importance of using atrial stimulation for evaluation of patients with VT or syncope . Left veThe following electrophysiological features are consistent with the bundle branch reentry mechanism : (1) repRecording from both sides of the septum may help in the identification of the bundle branch reentry mechanism. Documentation of typical H-RB-V-LB (during VT with LBBB morphology) or H-LB-V-RB (during VT with RBBB morphology) activation sequence would further support BBR VT diagnosis. In addition, during VT with LBBB morphology right ventricular excitation must precede the left ventricular excitation. The opposite is true for the VT with RBBB morphology .Pacing maneuvers, if feasible, can be extremely helpful. Ability to dissociate His or, particularly, RB (LB) potential would strongly argue against bundle branch reentry mechanism. The combination of concealed entrainment  by atrial pacing and manifest entrainment (manifest QRS fusion) by ventricular pacing has been recently proposed as a useful diagnostic criterion for BBR VT with LBBB QRS morphology . AnalysiInterfascicular tachycardia has been less commonly reported ,28,32-34The differential diagnosis of BBR VT includes other mechanisms of VT and different types of supraventricular tachycardia with aberrant conduction. All electrophysiological findings and pacing maneuvers described above that prove participation of the HPS in the tachycardia mechanism and exclude passive retrograde activation of the HPS help to differentiate between bundle branch reentry and other mechanisms of VT. The exclusion of supraventricular tachycardia is particularly important because QRS morphology during BBR VT is a typical bundle branch block pattern and also may be similar to that in sinus rhythm. The differential diagnosis should be based on the complimentary use of the diagnostic criteria of bundle branch reentry as well as supraventricular tachycardia . Since APharmacologic antiarrhythmic therapy, both empiric and electrophysiologically guided, is usually ineffective. Radiofrequency catheter ablation of a bundle branch can cure BBR VT and is currently regarded as the first line therapy. The technique of choice is ablation of the RB -10. UsinAblation of interfascicular tachycardia is guided by fascicular potentials. Successful ablation of the arrhythmia can be performed by targeting either the left anterior or posterior fascicle ,19,32-34The available data on long-term outcome of patients with BBR VT treated by catheter ablation come from small retrospective series including predominantly patients with left ventricular dysfunction -11,24,27