Slow Conduction Zone Research Articles

Electroanatomic Characterization and Ablation Outcome of Nonlesion Related Left Atrial Macroreentrant Tachycardia in Patients Without Obvious Structural Heart Disease

Descriptions for left atrial macroreentry tachycardia (LAMRT) in patients without obvious structural heart disease or previous surgery or catheter radiofrequency (RF) ablation have been sparse. Ten of 226 patients (7 women, mean age 57 ± 14) with LAMRT underwent electroanatomic mapping and catheter ablation. None of the 10 patients had structural heart disease or history of previous surgery or catheter ablation. In all patients, the reentry circuits were located within a large low-voltage (bipolar voltage ≤ 0.5 mV) area in left atrium (LA), which contained 2.6 ± 1.2 electrically silent areas (ESAs) and/or lines of double potentials (LDPs). The tachycardia circuit propagated through a narrow isthmus (<5 mm width) bounded by ESAs/LDPs and adjacent anatomical barriers (e.g., mitral annulus). In these isthmus, low amplitude (0.21 ± 0.05 mV), long-duration (123 ± 14 milliseconds) fractionated electrograms were found in 8 tachycardias, accounting for 43 ± 5% of the tachycardia cycle length. In 2 other tachycardias without fractionated electrograms, the electrogram amplitude in the isthmus was extremely low (<0.1 mV). RF energy was delivered at the isthmuses and terminated all 10 tachycardias. After ablation, the original LAMRT was not inducible in all patients. During follow-up (mean 14 ± 10 months), 2 patients developed recurrence of ATs and were successfully ablated. Extensive scarring of the LA formed arrhythmogenic substrates of LAMRT in this group of patients. Ablation targeting these narrow, slow conduction zones eliminated atrial tachycardia in all patients.

Comparison of the Location of Slow Conduction Velocity in Cavotricuspid‐Dependent Atrial Flutter in Patients With and Without Prior Atriotomy: Different Arrhythmogenic Basis and Clinical Implications for Placement of Atriotomy

Slow Zone in CTI-Dependent Flutter After Atriotomy. Earlier studies have shown that the slow conduction zone in patients with cavotriscuspid (CTI)-dependent atrial flutter without prior surgery (NS-AFL) is the CTI. However, the location of this slow zone in patients with CTI-dependent flutter and a prior atriotomy has not been formally studied. Identification of the slow zone in patients with prior atriotomy and CTI-dependent atrial flutter (PA-AFL) and comparison with NS-AFL may have important clinical implications. Seventeen consecutive patients with PA-AFL and 17 consecutive patients with NS-AFL were included. Conduction velocity (CV) was measured using 3-dimensional mapping in 3 areas around the TVA. These regions were defined as the CTI area from lateral inferior vena cava orifice to coronary sinus ostium (region I), mid- to upper-septum (S), and free wall (F). In region F, the CV was much slower in PA-AFL than in NS-AFL patients (0.43 ± 0.13 vs 0.76 ± 0.26 m/s, P < 0.01). However, region I was slower in NS-AFL than PA-AFL (0.57 ± 0.18 m/s vs 0.84 ± 0.24 m/s, P < 0.01). In all PA-AFL patients, the slow zone was in region F. But in most (11/17) NS-AFL patients the slow zone was in region I. There was no significant difference in CV in region S between the 2 groups. Unlike NS-AFL, CTI in PA-AFL displays relatively normal conduction but the slow zone is on the free wall. This arrhythmogenecity of atriotomy may perhaps be avoided if the incisional line were altered to extend to the TV. (J Cardiovasc Electrophysiol, Vol. 23, pp. 988-995, September 2012).

Identification of the Slow Conduction Zone in a Macroreentry Circuit of Verapamil‐Sensitive Idiopathic Left Ventricular Tachycardia Using Electroanatomic Mapping

Although idiopathic left ventricular tachycardia (ILVT) has been shown to possess a slow conduction zone (SCZ), the details of the electrophysiological and anatomic aspects are still not well understood. We hypothesized that the SCZ can be identified using a 3-dimensional electroanatomic (EA) mapping system. Ten patients with ILVT were mapped using a 3-dimensional electroanatomic (EA) mapping system. After a 3-dimensional endocardial geometry of the left ventricular was created, the conduction system with left Purkinje potential (PP) and the SCZ with diastolic potential (DP) in LV were mapped during sinus rhythm (SR) and ventricular tachycardia (VT) and were tagged as special landmarks in the geometry. The electrophysiological and anatomic aspects of it were investigated. EA mapping during SR and VT was successfully performed in 7 patients, during VT in 3 patients. The SCZ with DPs located at the inferoposterior septum was found in 7 patients during SR and all patients during VT. The length of the SCZ was 25.2 ± 2.3 mm with conduction velocity 0.08 ± 0.01 m/s. No differences in these parameters were found between patients during SR and VT (P > 0.05). An area with PP was found within the posterior septum. A crossover junction area with DP and PP was found in 7 patients during SR and VT. This area with DP and PP during SR coincided or were in proximity to such area during VT and radiofrequency ablation targeting the site within the area abolished VT in all patients. The ILVT substrate within the junction area of the SCZ and the posterior fascicular can be identified and can be used to guide the ablation of ILVT.

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A Simultaneous X-Ray/MRI and Noncontact Mapping Study of the Acute Hemodynamic Effect of Left Ventricular Endocardial and Epicardial Cardiac Resynchronization Therapy in Humans

Cardiac resynchronization therapy (CRT) using endocardial left ventricular (LV) pacing may be superior to conventional CRT. We studied the acute hemodynamic response to conventional CRT and LV pacing from different endocardial sites using a combined cardiac MRI and LV noncontact mapping (NCM) protocol to gain insights into the underlying mechanisms. Fifteen patients (age, 63 ± 10 years; 12 men) awaiting CRT were studied in a combined x-ray and MRI laboratory. Delayed-enhancement cardiac magnetic resonance was performed to define areas of myocardial fibrosis. Patients underwent an electrophysiological study incorporating endocardial and epicardial LV pacing. Acute hemodynamic response was measured using a pressure wire within the LV cavity to derive LV dP/dt max. NCM was used to define areas of slow conduction. There was a significant improvement in all LV pacing modes versus baseline (P<0.001). LV endocardial CRT from the best endocardial site was superior to conventional CRT, with a 79.8 ± 49.0% versus 59.6 ± 49.5% increase in LV dP/dt max of from baseline (P<0.05). The hemodynamic benefits of pacing were greater when LV stimulation was performed outside of areas of slow conduction defined by NCM (P<0.001). Delayed-enhancement cardiac magnetic resonance was able to delineate zones of slow conduction seen with NCM in ischemic patients but was unreliable in nonischemic patients. Endocardial LV pacing appears superior to conventional CRT, although the optimal site varies between subjects and is influenced by pacing within areas of slow conduction. Delayed-enhancement cardiac magnetic resonance was a poor predictor of zones of slow conduction in nonischemic patients.

Onset of Reentrant Ventricular Tachycardia Modulated by Variable Impulse Propagation through the Zone of Slow Conduction

We report an 18-year-old woman, who had undergone surgical repair of tetralogy of Fallot, and then underwent successful intracardiac recordings within the zone of slow conduction (ZSC) of the reentry circuit on the initiation of premature ventricular contractions (PVC) and reentrant ventricular tachycardia (VT), obtained with multielectrode basket catheter. PVC a) were caused by wavefronts of sinus cycles entering and exiting the ZSC, and b) were not repetitive because the wavefront of the PVC could not reenter the ZSC. Similarly, VT developed after delayed potentials of sinus cycles, and was sustained because the wavefront following the 1st cycle of VT was able to repetitively reenter and exit the ZSC. Thus, spontaneous changes in the conductivity of the ZSC, like an on-off switch, appeared to determine the onset and sustenance of reentrant VT.

181 Identification of electrophysiological substrate for ventricular arrhythmias in patients with repaired tetralogy of Fallot

Patients with repaired tetralogy of Fallot (TOF) represent a new category of patients referred to electrophysiology laboratory for ventricular arrhythmia (VA) mapping and ablation. Different anatomical regions have been identified as potentially responsible for reentry: ventricular septal defect (VSD) patch, surgical incisions, right ventricular outflow tract (RVOT) patch. We aimed to investigate electrophysiological substrate responsible for potential VA in patients with repaired TOF. All patients with repaired TOF referred to the CHU de Bordeaux for VA evaluation from January 2008 to april 2010 underwent right ventricular (RV) 3D mapping. Sinus activation and voltage mapping was then performed before VA induction ± ablation. 7 patients (4 male, 42,5 ± 12 years old) underwent RV mapping during VA evaluation. Surgical repair of TOF had been realized 36 ± 11 years before the procedure. All patients displayed a right bundle branch block on 12 lead electrocardiogram. Sinus rhythm RV activation begins in all patients in the septum and then activates the RV centrifugally with a zone of slow conduction with a double potential (100 ± 30 ms) going from the tricuspid annulus (TA) to the RVOT. Voltage maps (figure) show systematically the same pattern of a zone of low voltage (< 1.5 mV) due to the VSD repair close to the RVOT scar area. This area fits with the slow conduction area. In the 2 patients with sustained ventricular tachycardia (VT), critical isthmus was located in this area. Specific activation and voltage pattern was found in these Fallot patients. In the 2 patients with sustained VT, the critical isthmus was found between VSD repair patch and RVOT scar.

A case with cardic sarcoidosis which essential slow conduction zone of ventricular tachycardia is present in the left ventricular aneurysm without the low voltage area

A case with cardic sarcoidosis which essential slow conduction zone of ventricular tachycardia is present in the left ventricular aneurysm without the low voltage area

Termination of atrial fibrillation by flecainide: mechanistic insights from spectral analysis

This editorial refers to ‘Increase in organization index predicts atrial fibrillation termination with flecainide post-ablation: spectral analysis of intracardiac electrograms’ by J. Tuan et al ., on page 488. The pathophysiology of atrial fibrillation (AF) is complex and remains incompletely understood. Atrial fibrillation is usually initiated by rapidly discharging foci, often from within the pulmonary veins, which is then maintained by an abnormal left atrial substrate. Experimental evidence suggests that AF is driven by rapidly discharging foci and waves rotating around fixed structures (mother rotors).1 These drivers give rise to daughter wavelets which propagate around the atria giving the appearance of ‘fibrillatory conduction’. Recurrent paroxysms of AF cause structural and electrophysiological remodelling of the left atrium eventually allowing it to persist.2 Within hours, there are changes in ion channel expression which shorten action potential duration (APD) and effective refractory period (ERP).2 Ultrastructural changes beginning within days of onset of AF include left atrial fibrosis, accumulation of extracellular matrix, and reduced expression of connexin 40 reducing conduction velocity.2 Heterogeneity of refractory periods and zones of slow conduction promote re-entry and support wavelets propagating around the atria. Flecainide exerts its effect through blockade of sodium channels ( I Na) and potassium channels ( I K1 and I KAch), which reduces conduction velocity and increases APD and ERP, respectively.3 These changes have opposing effects on wavelength, which is a product of conduction velocity and ERP. An increase in ERP and AF cycle length was demonstrated in response to flecainide in a canine model of AF.4 A concomitant increase in size and decrease in the number of re-entry wavelets was observed on high-density epicardial mapping. The authors assumed that the prolongation of ERP was the predominant effect, and that re-entry was … *Corresponding author. Tel: +44 207 601 8639; fax: +44 207 601 8627, Email: r.schilling{at}qmul.ac.uk

High-Density Substrate Mapping in Brugada Syndrome

Two principal mechanisms are thought to be responsible for Brugada syndrome (BS): (1) right ventricular (RV) conduction delay and (2) RV subepicardial action potential shortening. This in vivo high-density mapping study evaluated the conduction and repolarization properties of the RV in BS subjects. A noncontact mapping array was positioned in the RV of 18 BS patients and 20 controls. Using a standard S(1)-S(2) protocol, restitution curves of local activation time and activation recovery interval were constructed to determine local maximal restitution slopes. Significant regional conduction delays in the anterolateral free wall of the RV outflow tract of BS patients were identified. The mean increase in delay was 3-fold greater in this region than in control (P=0<0.001). Local activation gradient was also maximally reduced in this area: 0.33+/-0.1 (mean+/-SD) mm/ms in BS patients versus 0.51+/-0.15 mm/ms in controls (P<0.0005). The uniformity of wavefront propagation as measured by the square of the correlation coefficient, r(2), was greater in BS patients versus controls (0.94+/-0.04 versus 0.89+/-0.09 [mean+/-SD]; P<0.05). The odds ratio of BS hearts having any RV segment with maximal restitution slope >1 was 3.86 versus controls. Five episodes of provoked ventricular tachycardia arose from wave breaks originating from RV outflow tract slow-conduction zones in 5 BS patients. Marked regional endocardial conduction delay and heterogeneities in repolarization exist in BS. Wave break in areas of maximal conduction delay appears to be critical in the initiation and maintenance of ventricular tachycardia. These data indicate that further studies of mapping BS to identify slow-conduction zones should be considered to determine their role in spontaneous ventricular arrhythmias.

A Deductive Mapping Strategy for Atrial Tachycardia Following Atrial Fibrillation Ablation: Importance of Localized Reentry

Atrial tachycardia (AT) occurring following catheter ablation of persistent atrial fibrillation (AF) may be challenging to map and ablate because their mechanism and location is unpredictable and may be multiple in an individual patient. A prospective cohort of 128 consecutive patients presenting 246 AT in the context of prior AF ablation was investigated. Using activation and entrainment mapping and applying the consensus definition of AT, we evaluated a deductive diagnostic approach based on up to three steps: (1) cycle length regularity, (2) search for macroreentry (i.e., involving >2 separate atrial segments), and (3) if macroreentry excluded, search for focal origin giving a centrifugal activation of the atria. A total of 238/246 (97%) sustained AT (mean cycle length [CL] 284 +/- 87 ms) were successfully mapped (single AT, 51 pts; multiple AT, 77 pts) with a diagnostic time of 10 +/- 8 min per tachycardia. AT were macroreentrant in 109 (46%) and focal in 129 (54%). Of the latter, only 34 focal AT originated from a discrete point site fulfilling the consensus criteria, while a distinct mechanism, localized reentry (AT that was neither macro reentry nor focal), was identified in 95. Localized reentry was defined by (1) electrograms covering >or=75% of the cycle length of AT within an area covering a single or 2 contiguous segments, (2) postpacing interval (PPI) < 30 ms at the site, (3) an identifiable zone of slow conduction, and (4) centrifugal activation of the atrium from the area. This prospective study demonstrates the feasibility of rapid and accurate identification of all types of postablation AT in a large cohort of patients and describes the dominant role of localized reentry as a novel mechanism of AT.

Genesis of complex fractionated atrial electrograms in zones of slow conduction: A computer model of microfibrosis

Complex fractionated atrial electrograms are used as potential targets for catheter ablation therapy of atrial fibrillation. Although fibrosis has been associated with the presence of fractionated electrograms, characterizing the substrate through the inspection of electrograms is challenging. This study sought to determine how progression of microfibrosis and slow conduction affect electrogram morphology. A microstructure computer model representing a monolayer of cardiac cells was developed. Slow conduction was induced by: (1) sodium channel blockade, (2) uniform reduction in cell-to-cell coupling, and (3) microfibrosis incorporated as a set of collagenous septa disconnecting transverse coupling. The density (0 to 30%) and length (30 to 945 microm) of these collagenous septa were varied. Unipolar and bipolar electrograms were computed during paced rhythm for a set of electrodes with different tip sizes. The analysis of unipolar electrograms with realistic temporal and spatial filtering showed that increasing the density and length of collagenous septa decreased conduction velocity by up to 75% and increased the amount of fractionation (up to 14 deflections) and asymmetry of the electrograms. In contrast, slow conduction induced by sodium channel blockade or uniformly reduced coupling did not result in electrogram fractionation. When a larger electrode was used, electrogram amplitude was smaller and fractionation increased in a substrate-dependent way. Microscale obstacles cause significant changes to electrogram waveforms. Conduction velocity and electrogram amplitude and degree of fractionation can be used to discriminate the nature of the substrate and characteristics of fibrosis, giving rise to slow conduction.

A Case of Radiofrequency Catheter Ablation of Ventricular Tachycardia Associated with an Old Myocardial Infarction Guided by a Noncontact Mapping System

We describe here a 72‐year‐old man with ventricular tachycardia (VT) associated with an old myocardial infarction, in whom noncontact mapping guided radiofrequency catheter ablation (RFCA) successfully eliminated the VT. Right ventricular pacing induced 3 VTs with different QRS morphologies and axes, 2 of which were hemodynamically unstable. A dynamic virtual activation map constructed during the VTs superimposed on a virtual voltage map constructed during sinus rhythm demonstrated that all VTs shared a single large myocardial scar in the inferolateral portion of the left ventricle which served as a slow conduction zone. All VTs were eliminated by RFCA at the exit or within the critical slow conduction zone. The patient has been free from any VT recurrences during a follow‐up period of 22 months.

Quantitative Analysis of the Duration of Slow Conduction in the Reentrant Circuit of Ventricular Tachycardia After Myocardial Infarction

Few data are available to define the circuits in ventricular tachycardia (VT) after myocardial infarction and the conduction time (CT) through the zone of slow conduction (SCZ). This study assessed the CT of the SCZ and identified different reentrant circuits. During VTs, concealed entrainment (CE) was attempted. The SCZ was identified by a difference between postpacing interval (PPI) and VT cycle length (VTcl) < or =30 ms. Since the CT in the normally conducting part of the VT circuit is constant during VT and CE, a CE site within the reentrant circuit with (S-QRS)/PPI > or = 50% was classified as an inner reentry in which the entire circuit was within the scar, and a CE site with (S-QRS)/PPI < 50% as a common reentry in which part of the circuit was within the scar and part out of the scar. CE was achieved in 20 VTs (12 patients). Six VTs (30%) with a (S-QRS)/PPI > or =50% were classified as inner reentry and 14 VTs (70%) with a (S-QRS)/PPI <50% during CE mapping as common reentry. The EG-QRS interval (308 +/- 73 ms vs 109 +/- 59 ms, P < 0.0001) was significantly longer and the incidence of systolic potentials higher (4/6 vs 0/12, P < 0.001) in the inner reentry group. For the 14 VTs with a common reetry, the CT of the SCZ was 348 +/- 73 ms, while the CT in the normal area was 135 +/- 50 ms. According to the proposed classification, 30% of VTs after myocardial infarction had an entire reentrant circuit within the scar. In VTs with a common reentrant circuit, the CT of the SCZ is approximately four times longer than the CT in the normal area, accounting for more than 70% of VTcl.

Characterization of Left Atrial Tachyarrhythmias in Patients Following Atrial Fibrillation Ablation:Correlation of surface ECG with Intracardiac Mapping.

With expected success rates in excess of 80% for achieving long term arrhythmia control, catheter based ablation has become a popular treatment strategy in the management of patients with atrial fibrillation (AF). However, the success of AF ablation has been tempered by the occurrence of post procedure left atrial tachycardias and / or flutters, which can be seen in up to 30% of the patients. These arrhythmias are perpetuated either due to abnormalities of impulse formation (abnormal automaticity / triggered activity), or abnormalities of impulse conduction (micro / macroreentry). Regardless of the underlying mechanism, these tachycardias manifest distinct "P" or flutter waves on the surface ECG, recognition of which may facilitate their characterization / localization. However, because of the frequent overlap in the morphology of P waves, intracardiac mapping is often the only way to distinguish them apart. This is accomplished using a combination of activation, entrainment and electroanatomic mapping techniques. Tachycardias resulting from abnormalities of impulse formation and / or microreentry are characteristically focal and usually confined in and around pulmonary vein (PV) segments which have reconnected (septal aspect of right PVs and anterior aspect of left PVs). In contrast, macroreentrant tachycardias manifest a large circuit dimension involving zone(s) of slow conduction. These are most commonly seen to occur around the mitral valve but can develop in any part of the left atrium where "gaps" across prior ablation lesion sets create altered conduction. Successful ablation of focal tachycardias is usually accomplished by isolating the reconnected PV segment(s). In case of macroreentrant arrhythmias however, a more extensive ablation approach is typically required in order to achieve conduction block across isthmus of the circuit. Using these strategies, the majority of left atrial tachycardias occurring post AF ablation can be successfully cured with excellent long term results.

Accessory Atrioventricular Pathways

By definition, accessory atrioventricular pathways are aberrant muscle bundles that connect the atrium to a ventricle outside of the regular atrioventricular conduction system. Clinically, they may manifest as substrates for ventricular preexcitation. The first accessory pathway in a patient who suffered from Wolff-Parkinson-White syndrome was described in 1943 by Wood, Wolferth, and Geckler.1 Shortly after, Ohnell created a reconstruction of an accessory pathway that very elegantly showed the close proximity of the pathway to the fibrous attachment of the mitral valve and its relationship with the sulcus coronarius (Figure, A).2 Subsequent histological studies have demonstrated unequivocally that these pathways are the anatomic substrates for the classical Wolff-Parkinson-White variety of preexcitation. Figure. A, Ohnell’s depiction of an accessory bundle in the left atrioventricular groove.2 Reprinted with permission from Blackwell Publishing. B, Histological section stained with Masson’s trichrome (fibrous tissue in green and myocardium in red) to show an accessory left-sided pathway (arrow) skirting the mitral annulus. C, Histological section showing a broad right-sided accessory pathway (arrow) that is formed by a myocardial pouch extending from the right atrial appendage to the ventricle and ultimately traced to a small right ventricular vein. This pathway is some distance from the fibrous annulus of the tricuspid valve. *Valvar annulus. Article p 1508 Accessory atrioventricular pathways are found most often in the parietal atrioventricular junctional areas, including the paraseptal areas. They breach the insulation provided by the fibrofatty tissues of the atrioventricular groove (sulcus tissue) and the hingelines (fibrous annulus) of the valves. They are rarely found in the area of fibrous continuity between the aortic and mitral valves because in this area, there is usually a wide gap between the atrial myocardium and ventricular myocardium to accommodate the aortic outflow tract. On the left parietal side, the accessory pathways tend …

Refinement of CARTO-guided substrate modification in patients with ventricular tachycardia after myocardial infarction

Substrate modification guided by CARTO system has been introduced to facilitate linear ablation of ventricular tachycardia (VT) after myocardial infarction (MI). However, there is no commonly accepted standard approach available for drawing these ablation lines. Therefore, the aim of the present study was to practically refine this time consuming procedure. Substrate modification was performed in 23 consecutive patients with frequent VTs after MI using the CARTO system. The initial target site (ITS) for ablation was identified by pace mapping (PM) during sinus rhythm and/or entrainment pacing (EM) during VT. According to the initial target site, two approaches were used. The initial target site in approach one has a similar QRS morphology as VT and an interval from the stimulus to the onset of QRS complex (S-QRS) of = 50 ms during PM in sinus rhythm or a difference of the post pacing interval and VT cycle length = 30 ms during concealed entrainment pacing of VT; The initial target site in approach two has an similar QRS morphology as VT and an S-QRS of < 50 ms during PM in sinus rhythm. Overall, 50 lines were performed with a length of (35 +/- 11) mm. Procedure time averaged (232 +/- 56) minutes, fluoroscopy time (10 +/- 8) minutes. Sixteen patients were initially involved into approach one. After completion of 3 +/- 1 ablation lines, no further VT was inducible in 13 patients. The remaining 3 patients were switched to use the alternative approach. However, in none of them the alternative approaches were successful. Approach two was initially used in 7 patients. After completion of 3 +/- 1 ablation lines, no further VT was inducible in only 2 patients. The remaining 5 patients were switched to approach one, which resulted in noninducibility of VT in 4 of them. The initial successful rate was significantly higher in the group of approach one compared to that in the group of approach two (13/16 patients vs 2/7 patients, P = 0.026). The approach for substrate modification of VT after MI can be optimized by identifying the appropriate initial target site with specific characteristics within the zone of slow conduction. The refined approach may facilitate linear ablation of VT, and further reduce the procedure and fluoroscopy time.

Reentrant Ventricular Tachycardia Originating in the Right Ventricular Outflow Tract Slow Conduction Identified by Right Coronary Artery Ostium Pacing

A case of reentrant ventricular tachycardia (VT) originating from the right ventricular outflow tract (RVOT) is described. An electrophysiological study revealed that programmed stimulation from the right ventricle apex induced 2 types of VT with similar left bundle branch block configuration and inferior axis. Yet, VT cycle length (CL) was different; one was stable, sustained VT with a CL of 360 ms and the other was hemodynamically intolerable VT with a CL of 330 ms. Similarly for both VTs, perfect pace mapping was obtained at the anterior septum beneath the pulmonary valve in the RVOT, and exits of both VTs were very close. Entrainment mapping during stable VT was performed and the anterior septum RVOT was designated as the exit for the stable VT. Intriguingly, entrainment pacing from the ostium of the right coronary artery showed that the post-pacing interval was identical to VTCL. The stimulus to QRS interval was very long (340 ms) during entrainment with concealed fusion, and the right coronary artery ostium was therefore consistent with the VT reentry circuit inner loop or the upper portion of the VT reentry circuit exit. These findings suggest that the stable VT reentry circuit had a slow conduction zone from the ostium of the right coronary artery to the exit in the anterior septum RVOT. When radiofrequency catheter ablation was performed at the 2 exits of the anterior septum RVOT, both VTs then could not be induced.

Critical Slow Conduction Zone Located between the Tricuspid Annulus and a Myocardial Infarct Scar in a Patient with Multiple Ventricular Tachycardia Late after Myocardial Infarction

A patient underwent an electrophysiological study (EPS) and catheter ablation (CA) for ventricular tachycardia (VT) that developed 11 years after myocardial infarction.Entrainment mapping (EM) of the left ventricle did not identify the origin of the VT during induction. Electro‐anatomical mapping revealed a low voltage area from the anterior to the inferior left ventricular wall. Another EPS was performed for right ventricular mapping.A basket catheter was placed in the right ventricle to evaluate impulse propagation and we attempted to identify the VT circuit with EM during the same VT (complete left bundle branch block configuration, inferior axis) as the previous EPS.Eight different VT appeared, three of which were sustained during CA. The reentry circuit exit was identified on the tricuspid annulus (TA) at the 9:00 site and radiofrequency (RF) ablation was performed, but the axis transformed from the inferior to the superior and another VT appeared. Despite RF ablation to the VT circuit exit at the 5:00 site, another sustained VT appeared. Finally, it was terminated by ablation to a critical slow conduction zone (SCZ) located near the 7:00 site one year later. Electro‐anatomical voltage mapping detected a critical isthmus between TA and right ventricle infarct scar.Here, we describe a rare SCZ proximal to the TA in a patient with VT late after myocardial infarction.

Gene Transfer of Connexin43 Mutants Attenuates Coupling in Cardiomyocytes

Modification of electrical conduction would be a useful principle to recruit in preventing or treating certain arrhythmias, notably ventricular tachycardia (VT). Here we pursue a novel gene transfer approach to modulate electrical conduction by reducing gap junctional intercellular communication (GJIC) and hence potentially modify the arrhythmia substrate. The ultimate goal is to develop a nondestructive approach to uncouple zones of slow conduction by focal gene transfer. Lentiviral vectors encoding connexin43 (Cx43) internal loop mutants were produced and studied in vitro. Transduction of neonatal rat ventricular myocytes (NRVMs) revealed the expected subcellular localization of the mutant gene product. Fluorescent dye transfer studies showed a significant reduction of GJIC in NRVMs that had been genetically modified. Additionally, adjacent mutant gene-modified NRVMs displayed delayed calcium transients, indicative of electrical uncoupling. Multi-site optical mapping of action potential (AP) propagation in gene-modified NRVM monolayers revealed a 3-fold slowing of conduction velocity (CV) relative to nontransduced NRVMs. In conclusion, lentiviral vector-mediated gene transfer of Cx43 mutants reduced GJIC in NRVMs. Electrical charge transfer was also reduced as evidenced by delayed calcium transients in adjacent NRVMs and reduced CV in NRVM monolayers. These data validate a molecular tool that opens the prospect for gene transfer targeting gap junctions as an approach to modulate cardiac conduction.