Reentry Circuit Research Articles

Alternative Approaches for Ablation of Resistant Ventricular Tachycardia.

Ventricular tachycardia (VT) ablation is usually performed with an ablation catheter that delivers unipolar radiofrequency (RF) energy to eliminate the re-entry circuit responsible for VT. However, there are some instances when unipolar RF ablation fails, notably in VTs with a deep intramural origin, or cases in which epicardial access is not attainable due to prior cardiac surgery. To overcome these limitations, several alternative approaches have been used in clinical practice, including alcohol ablation or coil embolization, simultaneous unipolar or bipolar RF ablation, surgical ablation, or noninvasive ablation with stereotactic radiosurgery. This review article describes some of these alternative techniques.

Circuits Regulating Pleasure and Happiness-Mechanisms of Depression.

According to our model of the regulation of appetitive-searching vs. distress-avoiding behaviors, the motivation to display these essential conducts is regulated by two parallel cortico-striato-thalamo-cortical, re-entry circuits, including the core and the shell parts of the nucleus accumbens, respectively. An entire series of basal ganglia, running from the caudate nucleus on one side, to the centromedial amygdala on the other side, controls the intensity of these reward-seeking and misery-fleeing behaviors by stimulating the activity of the (pre)frontal and limbic cortices. Hyperactive motivation to display behavior that potentially results in reward induces feelings of hankering (relief leads to pleasure). Hyperactive motivation to exhibit behavior related to avoidance of misery results in dysphoria (relief leads to happiness). These two systems collaborate in a reciprocal fashion. In clinical depression, a mismatch exists between the activities of these two circuits: the balance is shifted to the misery-avoiding side. Five theories have been developed to explain the mechanism of depressive mood disorders, including the monoamine, biorhythm, neuro-endocrine, neuro-immune, and kindling/neuroplasticity theories. This paper describes these theories in relationship to the model (described above) of the regulation of reward-seeking vs. misery-avoiding behaviors. Chronic stress that leads to structural changes may induce the mismatch between the two systems. This mismatch leads to lack of pleasure, low energy, and indecisiveness, on one hand, and dysphoria, continuous worrying, and negative expectations on the other hand. The neuroplastic effects of monoamines, cortisol, and cytokines may mediate the induction of these structural alterations. Long-term exposure to stressful situations (particularly experienced during childhood) may lead to increased susceptibility for developing this condition. This hypothesis opens up the possibility of treating depression with psychotherapy. Genetic and other biological factors (toxic, infectious, or traumatic) may increase sensitivity to the induction of relevant neuroplastic changes. Reversal or compensation of these neuroplastic adjustments may explain the effects of biological therapies in treating depression.

Panoramic characterization of endocardial left atrial activation during human persistent AF: Insights from non-contact mapping

BackgroundThe relative importance of focal drivers, multiple wavelets, rotors and endocardial–epicardial circuits in the maintenance of persistent AF remains unclear. Our objective was to characterize AF wavefront (WF) dynamics during persistent AF. MethodsThe Ensite 3000 (St Jude Medical) non-contact mapping system was used to map the LA of 15 patients with persistent AF. Wavefronts were classified into planar WFs, rotors or focal WFs. For each new WF the site of origin, the unipolar electrogram, and propagation patterns were determined. ResultsAF was characterized by highly unstable patterns of activation with random combinations of 1–2 propagating planar wavefronts alternating with focal activations in a dynamic process. Stable reentry circuits and rotors were never seen. A total of 499 wavefront patterns were analyzed in this study (416 planar wavefronts and 83 focal wavefronts). In an individual patient planar WFs accounted for 67±35% of activations with lifespans of 98±86ms. Focal activations accounted for 29.7±33.5% of activations with lifespans of 76±95ms. The most common sites for new WF generation were the PVs (33%), LA roof (23%), anterior LA (15%), LAA (11%), and posterior LA (8%). The most common unipolar electrogram morphologies observed were QS pattern (34%), rS (29%), CFAE (26%), QR (7%) and Rs (4%), suggesting that WFs may originate from both the endocardial and epicardial surfaces. ConclusionHuman persistent AF is characterized by the formation of highly unstable WFs consisting of various combinations of one to two planar WFs and brief focal activations without any evidence of rotors or sustained focal sources.

Maintenance of Atrial Fibrillation: Are Reentrant Drivers With Spatial Stability the Key?

Presented in the following review are the insights on atrial fibrillation (AF) gained from our recent simultaneous endo-epicardial transmural and panoramic optical mapping studies of the human atria that may begin to resolve the controversy about AF maintenance mechanisms.1–3 It is still hotly debated whether the sustaining mechanism of AF involves multiwavelets self-replicating across the entire atrial myocardium4 or if fibrillatory conduction in the atria is maintained by localized AF drivers.1 Even the term “AF driver,” which is widely used in the current literature,1–3,5–15 is not well defined. In this review, AF drivers are defined as one or several patient-specific localized sources of fast, repetitive activity from which activation propagates and breaks down into fibrillatory conduction in the rest of the atria, targeted ablation of drivers would slow AF, organize AF to atrial tachycardia, or terminate AF (Figure 1). Figure 1. Defining atrial fibrillation (AF) drivers. AF drivers are defined as localized sources of fast, repetitive activity from which activation propagates and breaks down into fibrillatory conduction in the rest of the atria. One or few patient-specific AF drivers may exist simultaneously or sequentially, and targeted ablation (orange stars) of AF drivers would slow, organize to atrial tachycardia (AT), or terminate AF. Light purple ovals, black arrows, and gray arrows represent the AF driver region, path of reentry, and fibrillatory conduction, respectively. IVC indicates inferior vena cava; LA, left atria; RA, right atria; and SVC, superior vena cava. Even if one is convinced that AF drivers exist, there is no clear consensus on the specific electrophysiological mechanism of AF drivers. AF drivers have been hypothesized to represent reentry circuits, rotors, focal sources, or a complex mixture of all these mechanisms. We hypothesize that human AF is maintained by a …

Macroreentrant Loop in Ventricular Tachycardia From the Left Posterior Fascicle: New Implications for Mapping and Ablation.

The underlying mechanisms of reentry during left posterior fascicular ventricular tachycardia (LPF-VT) remain unclear. The purpose of this study is to describe the components of LPF-VT reentry circuit and their electrophysiological properties. Fourteen consecutive patients with LPF-VT underwent electrophysiology study and radiofrequency ablation. Via a multipolar electrode catheter placed from a retrograde aortic approach, a sharp inflection, high-frequency potential (P1) was detected in 9 patients (64%). The ranges of length and velocity of recorded P1 were 9 to 30 mm and 0.5 to 1.2 mm/ms, respectively. Macroreentry involving the ventricular myocardium was confirmed to be the mechanism in all patients by premature ventricular stimuli delivery or entrainment of LPF-VT with progressive fusion, or both. During LPF-VT, the earliest left posterior fascicle (LPF, P2) was considered to be the site of connection between P1 and P2, and the site of the earliest P2 along the left posterior ventricular septum correlated well with the His-ventricular interval during tachycardia. Radiofrequency ablation focused on the P1 potentials (9 patients with a recorded P1) or earliest P2 (5 patients without a recorded P1) was successful in all 14 patients. After 4.5±3.0 months of follow-up, no patients had recurrence of LPF-VT. The LPF-VT macroreentrant loop involves the ventricular myocardium, a part of the LPF, a slow conduction zone, and in certain cases, a specially conducting P1 fiber. The His-ventricular interval during LPF-VT correlates with multiple electrophysiological measures and is a useful marker for identification of the optimal ablation site.

Noninvasive epicardial and endocardial electrocardiographic imaging of scar-related ventricular tachycardia

BackgroundThe majority of life-threatening ventricular tachycardias (VTs) are sustained by heterogeneous scar substrates with narrow strands of surviving tissue. An effective treatment for scar-related VT is to modify the underlying scar substrate by catheter ablation. If activation sequence and entrainment mapping can be performed during sustained VT, the exit and isthmus of the circuit can often be identified. However, with invasive catheter mapping, only monomorphic VT that is hemodynamically stable can be mapped in this manner. For the majority of patients with poorly tolerated VTs or multiple VTs, a close inspection of the re-entry circuit is not possible. A noninvasive approach to fast mapping of unstable VTs can potentially allow an improved identification of critical ablation sites. MethodsFor patients who underwent catheter ablation of scar-related VT, CT scan was obtained prior to the ablation procedure and 120-lead body-surface electrocardiograms (ECGs) were acquired during induced VTs. These data were used for noninvasive ECG imaging to computationally reconstruct electrical potentials on the epicardium and on the endocardium of both ventricles. Activation time and phase maps of the VT circuit were extracted from the reconstructed electrograms. They were analyzed with respect to scar substrate obtained from catheter mapping, as well as VT exits confirmed through ablation sites that successfully terminated the VT. ResultsThe reconstructed re-entry circuits correctly revealed both epicardial and endocardial origins of activation, consistent with locations of exit sites confirmed from the ablation procedure. The temporal dynamics of the re-entry circuits, particularly the slowing of conduction as indicated by the crowding and zig-zag conducting of the activation isochrones, collocated well with scar substrate obtained by catheter voltage maps. Furthermore, the results indicated that some re-entry circuits involve both the epicardial and endocardial layers, and can only be properly interpreted by mapping both layers simultaneously. ConclusionsThis study investigated the potential of ECG-imaging for beat-to-beat mapping of unstable reentrant circuits. It shows that simultaneous epicardial and endocardial mapping may improve the delineation of the 3D spatial construct of a re-entry circuit and its exit. It also shows that the use of phase mapping can reveal regions of slow conduction that collocate well with suspected heterogeneous regions within and around the scar.

Flúter auricular en paciente con isomerismo izquierdo y vena cava inferior izquierda interrumpida

Se comunica la ablación de un flúter auricular con una longitud de ciclo de 260 ms en un paciente de 28 años con isomerismo izquierdo y vena cava inferior izquierda interrumpida. Mediante encarrilamiento, demostramos la participación del istmo suprahepáticotricuspídeo en el circuito de macroreentrada. Realizamos líneas de ablación con radiofrecuencia que detuvieron la arritmia primaria y culminó en ritmo de escape nodal.

Long Postpacing Interval After Entrainment of Tachycardia Including a Slow Conduction Zone Within the Circuit.

Postpacing interval (PPI) measured after entrainment pacing describes the distance between pacing site and reentrant circuit. However, the influential features to PPI remain to be elucidated. This study included 22 cases with slow/fast atrioventricular (AV) nodal reentrant tachycardia (AVNRT), 14 orthodromic AV reciprocating tachycardia (AVRT) using an accessary pathway, 22 typical atrial flutter (AFL), and 18 other macroreentrant atrial tachycardia (atypical AFL). Rapid pacing at a pacing cycle length (PCL) 5% shorter than tachycardia cycle length (TCL) was done from a site on or close to the reentry circuit. Pacing sites included the coronary sinus ostium in AVNRT, earliest atrial activation site in AVRT, and cavotricuspid isthmus in typical AFL. In atypical AFL, tachycardia circuit was determined on the basis of CARTO mapping, and then the pacing site was. TCL was significantly longer in AVNRT and AVRT than in typical AFL and atypical AFL (both P < 0.05). PCL minus TCL value was similar among the 4 groups. PPI minus TCL value (milliseconds) was significantly longer in AVNRT (median, 40 [IQR, 29-60.8]) and AVRT (34 [20-47]) than in typical AFL (0 [0-4]) and atypical AFL (3.5 [0-8]) (both P < 0.05). Furthermore, PPI minus TCL was prolonged with shortening of PCL in AVNRT and AVRT (both P < 0.05), whereas it was unchanged in typical AFL (P = 0.50). PPI after concealed entrainment is prolonged compared with TCL when the reentry circuit involves a slow conduction zone with a decremental conduction property such as the AV node.

Electrophysiologic Scar Substrate in Relation to VT: Noninvasive High-Resolution Mapping and Risk Assessment with ECGI.

Ischemic cardiomyopathy (ICM) can provide the substrate for ventricular tachycardia (VT). To map noninvasively with high resolution the electrophysiologic (EP) scar substrate, identify its relationship to reentry circuits during VT, and stratify VT risk in ICM patients. Noninvasive high-resolution epicardial mapping with electrocardiographic imaging (ECGI) was performed in 32 ICM patients (17 with clinical VT, 15 without VT). Abnormal scar EP substrate was determined based on electrogram (EGM) amplitude (as percentage of maximal peak-to-peak voltage over the entire ventricular epicardium; total scar [TS] < 30%; dense scar [DS] < 15%), fractionation, and presence of late potentials (LPs). Scar burden was defined as the ratio of the scar size to the total epicardial surface area. The VT activation pattern was mapped and correlated with the EP substrate to identify components of the reentry circuit. Patients with VT had higher scar burden (TS: 51.0 ± 9.3% vs 36.5 ± 5.4%, P < 0.05; DS: 29.5 ± 7.3% vs 16.8 ± 6.8%, P < 0.05) with lower normalized unipolar EGM voltage (TS: 0.107 ± 0.027 vs 0.153 ± 0.031, P < 0.05; DS: 0.073 ± 0.023 vs 0.098 ± 0.026, P < 0.05), greater prevalence of fractionated EGMs (TS: 44.1 ± 10.6% vs 26.8 ± 6.3%, P < 0.05; DS: 50.8 ± 10.8% vs 30.9 ± 7.0%, P < 0.05), and LPs (TS: 26.8 ± 10.7% vs 15.8 ± 5.3, P < 0.05). VTs were mapped in eight patients; the reentry circuits were closely related to the EP substrate. ECGI noninvasively identified scar EP substrate that underlies abnormal conduction in ICM patients. It identified regions within the scar that aligned with critical elements of the reentry circuit during VT. ECGI can potentially be used for VT risk stratification in ICM patients.

A Historical Perspective on the Role of Functional Lines of Block in the Re-entrant Circuit of Ventricular Tachycardia.

The ablation strategy for ventricular tachycardia (VT) rapidly evolved from an entrainment mapping approach for identification of the critical isthmus of the re-entrant circuit during monomorphic VT, toward a substrate-based approach aiming to ablate surrogate markers of the circuit during sinus rhythm in hemodynamically nontolerated and polymorphic VT. The latter approach implies an assumption that the circuits responsible for the arrhythmia are anatomical or fixed, and present during sinus rhythm. Accordingly, the lines of block delimiting the channels of the circuits are often considered fixed, although there is evidence that they are functional or more frequently a combination of fixed and functional. The electroanatomical substrate-based approach to VT ablation performed during sinus rhythm is increasingly adopted in clinical practice and often described as scar homogenization, scar dechanneling, or core isolation. However, whether the surrogate markers of the VT circuit during sinus rhythm match the circuit during arrhythmias remains to be fully demonstrated. The myocardial scar is a heterogeneous electrophysiological milieu with complex arrhythmogenic mechanisms that potentially coexist simultaneously. Moreover, the scar consists of different areas of diverse refractoriness and conduction. It can be misleading to limit the arrhythmogenic perspective of the myocardial scar to fixed or anatomical barriers held responsible for the re-entry circuit. Greater understanding of the role of functional lines of block in VT and the validity of the surrogate targets being ablated is necessary to further improve the technique and outcome of VT ablation.

Perpetuation of torsade de pointes in heterogeneous hearts: competing foci or re‐entry?

The underlying mechanism of torsade de pointes (TdP) remains of debate: perpetuation may be due to (1) focal activity or (2) re-entrant activity. The onset of TdP correlates with action potential heterogeneities in different regions of the heart. We studied the mechanism of perpetuation of TdP in silico using a 2D model of human cardiac tissue and an anatomically accurate model of the ventricles of the human heart. We found that the mechanism of perpetuation TdP depends on the degree of heterogeneity. If the degree of heterogeneity is large, focal activity alone can sustain a TdP, otherwise re-entrant activity emerges. This result can help to understand the relationship between the mechanisms of TdP and tissue properties and may help in developing new drugs against it. Torsade de pointes (TdP) can be the consequence of cardiac remodelling, drug effects or a combination of both. The mechanism underlying TdP is unclear, and may involve triggered focal activity or re-entry. Recent work by our group has indicated that both cases may exist, i.e. TdPs induced in the chronic atrioventricular block (CAVB) dog model may have a focal origin or are due to re-entry. Also it was found that heterogeneities might play an important role. In the current study we have used computational modelling to further investigate the mechanisms involved in TdP initiation and perpetuation, especially in the CAVB dog model, by the addition of heterogeneities with reduced repolarization reserve in comparison with the surrounding tissue. For this, the TNNP computer model was used for computations. We demonstrated in 2D and 3D simulations that ECGs with the typical TdP morphology can be caused by both multiple competing foci and re-entry circuits as a result of introduction of heterogeneities, depending on whether the heterogeneities have a large or a smaller reduced repolarization reserve in comparison with the surrounding tissue. Large heterogeneities can produce ectopic TdP, while smaller heterogeneities will produce re-entry-type TdP.

Model assisted biosignal analysis of atrial electrograms

Abstract Cardiologists measure electric signals inside the human heart aiming at a better diagnosis and optimized therapy of atrial arrhythmias like atrial flutter and atrial fibrillation. The catheters that are used for this purpose are improving: now they are able to pick up the electric signals at up to 64 positions inside the heart simultaneously. The patterns of electric depolarization are sometimes very simple, comparable to plane waves. But in case of patients with severe atrial arrhythmias they can be quite complex: U-turns around a line of block, ectopic centres, break throughs, reentry circuits, rotors, fractionated signals and chaotic patterns are often observed. Methods of biosignal analysis can support the cardiologists in classifying the signals and extract information of high diagnostic relevance. Computer models of the electrophysiology of the human heart can serve to design better algorithms for data analysis and to test algorithms, because the “ground truth” is known.

Fascicular Ventricular Tachycardia

Fascicular ventricular tachycardia (fascicular VT) is the most common idiopathic VT of the left ventricle. It presents with a right bundle branch block morphology and predominantly left axis deviation. Most of the available evidence supports the origin of fascicular VT as localized reentry circuits located close to the fascicle of the left bundle branch. During VT, the antegrade limb of the reentry circuit is the abnormal tissue in the left ventricular septum that is associated with slow and decremental conduction with verapamil sensitivity while the retrograde limb is usually the posterior fascicle forming the fast conduction zone. Catheter ablation is a highly effective therapy with long-term success rates of 90% and a low incidence of complications. Most of the fascicular VTs can be ablated during tachycardia by targeting the pre-Purkinje potential or Purkinje potential sites. Key words: Fascicular; Ventricular Tachycardia; Catheter Ablation; Verapamil

Circuits regulating pleasure and happiness in major depression

The introduction of selective serotonin reuptake inhibitors has gradually changed the borders of the major depression disease class. Anhedonia was considered a cardinal symptom of endogenous depression, but the potential of selective serotonin reuptake inhibitors to treat anxiety disorders has increased the relevance of stress-induced morbidity. This shift has led to an important heterogeneity of current major depressive disorder. The complexity can be disentangled by postulating the existence of two different but mutually interacting neuronal circuits regulating the intensity of anhedonia (lack of pleasure) and dysphoria (lack of happiness). These circuits are functionally dominated by partly closed limbic (regulating misery-fleeing behaviour) and extrapyramidal (regulating reward-seeking behaviour) cortico-striato-thalamo-cortical (CSTC) circuits. The re-entry circuits include the shell and core parts of the accumbens nucleus, respectively. Pleasure can be considered to result from finding relief from the hypermotivation to exhibit rewarding behaviour, and happiness from finding relief from negative or conflicting circumstances. Hyperactivity of the extrapyramidal CSTC circuit results in craving, whereas hyperactivity of the limbic system results in dysphoria.

Transbaffle catheter ablation of atrial re-entrant tachycardia within the pulmonary venous atrium in adult patients with congenital heart disease.

Catheter ablation of atrial re-entrant tachycardia in patients after atrial switch procedure for transposition of the great arteries or with a Fontan circulation is technically challenging if the critical part of the re-entry circuit is located within the pulmonary venous atrium (PVA). We report our experience in transbaffle access (TBA) to the PVA for ablation of atrial re-entrant tachycardia focusing on technical details. In eight patients, six after Mustard procedure and two with a Fontan circulation, endocardial mapping of atrial re-entrant tachycardia revealed the critical part of the re-entry circuit within the PVA. A total of 10 ablation procedures were performed. Detailed angiographic assessment of the anatomy of the systemic and pulmonary venous atria was performed prior to baffle puncture. Transbaffle access was successfully established with a standard transseptal needle in 9 of 10 procedures. No major complications occurred. At the end of the procedure and the removal of the transseptal sheath, there was no residual shunt in any patient. Transbaffle access to the PVA for ablation of atrial re-entrant tachycardia is feasible, less invasive than alternative approaches and can be safely applied in patients after Mustard procedure or with a Fontan circulation. However, the rigidity of prosthetic material may preclude baffle puncture at least in a subset of those patients.

Flecainide-induced Torsades de Pointes: Case Report and Review of Literature.

Several antiarrhythmic drugs are prone to cause QT interval prolongation and torsades de pointes (TDP). Predisposing risk factors include congenital channelopathies, severe bradycardia, drugs, and hypokalemia. Individual genetic variation and drug metabolism exaggerate susceptibility to adverse reactions. These proarrhythmic effects create a deficit in the repolarization reserve and prolong action potential duration, resulting in early afterdepolarizations, which promote a reentry circuit. Flecainide, a class IC drug, also exhibits inhibitory actions on the K(+) channels, causing QT interval prolongation. We identified six cases of flecainide-induced TDP in the literature. Most patients had other predisposing factors. Bradycardia was present in all cases. Our case demonstrates two arrhythmias caused by flecainide: atrial flutter with 1:1 atrioventricular conduction and TDP. Both arrhythmias developed in the absence of hypokalemia, with the use of other drugs that prolong QT interval, or genetic predisposition. Therefore, this is purely a drug effect. This case report illustrates a rare but serious proarrhythmic property of flecainide observed particularly in women.

Slow conduction in mixed cultured strands of primary ventricular cells and stem cell-derived cardiomyocytes.

Modern concepts for the treatment of myocardial diseases focus on novel cell therapeutic strategies involving stem cell-derived cardiomyocytes (SCMs). However, functional integration of SCMs requires similar electrophysiological properties as primary cardiomyocytes (PCMs) and the ability to establish intercellular connections with host myocytes in order to contribute to the electrical and mechanical activity of the heart. The aim of this project was to investigate the properties of cardiac conduction in a co-culture approach using SCMs and PCMs in cultured cell strands. Murine embryonic SCMs were pooled with fetal ventricular cells and seeded in predefined proportions on microelectrode arrays to form patterned strands of mixed cells. Conduction velocity (CV) was measured during steady state pacing. SCM excitability was estimated from action potentials measured in single cells using the patch clamp technique. Experiments were complemented with computer simulations of conduction using a detailed model of cellular architecture in mixed cell strands. CV was significantly lower in strands composed purely of SCMs (5.5 ± 1.5 cm/s, n = 11) as compared to PCMs (34.9 ± 2.9 cm/s, n = 21) at similar refractoriness (100% SCMs: 122 ± 25 ms, n = 9; 100% PCMs: 139 ± 67 ms, n = 14). In mixed strands combining both cell types, CV was higher than in pure SCMs strands, but always lower than in 100% PCM strands. Computer simulations demonstrated that both intercellular coupling and electrical excitability limit CV. These data provide evidence that in cultures of murine ventricular cardiomyocytes, SCMs cannot restore CV to control levels resulting in slow conduction, which may lead to reentry circuits and arrhythmias.

Utility of a Novel Rapid High-Resolution Mapping System in the Catheter Ablation of Arrhythmias: An Initial Human Experience of Mapping the Atria and the Left Ventricle

ObjectivesThis study sought to assess the clinical efficacy, safety, and clinical utility of a novel electroanatomical mapping system. BackgroundA new mapping system capable of rapidly acquiring detailed maps based on automatic annotation of thousands of points was recently released for clinical use. This is the first description of its utility in humans. MethodsThe first consecutive 20 cases (7 atrial tachycardia, 8 atrial fibrillation, 3 ventricular tachycardia, and 2 ventricular ectopic beat ablations) were analyzed. The system uses a bidirectional deflectable basket catheter with 64 closely spaced mini-electrodes. It automatically accepts and annotates electrograms when a number of predefined criteria are met. ResultsThirty right atrial maps were acquired in 11 (4 to 15) min, consisting of 7,220 (3,467 to 10,947) points, 22 left atrial maps in 11 (6 to 19) min, consisting of 7,818 (4,379 to 12,262) points and 10 left ventricular maps in 37 (14 to 43) min, consisting of 8,709 (2,605 to 15,514) points. The mini-basket catheter could reach all areas of interest without deflectable sheaths. No embolic events, bleeding complications, or endocardial structure damage were observed. Correction of the automatic annotation was performed in 0.02% of points in 4 of 62 maps. The system revealed re-entry circuits of atrial tachyarrhythmias, identified gaps on linear lesions, and identified and correctly annotated the clinical ventricular ectopic beats and channels of slow conduction within ventricular scar. ConclusionsThe novel automatic mapping system was rapid, safe, and efficacious in mapping a variety of cardiac arrhythmias in humans. Further clinical research is needed to optimize its use in the ablation of complex arrhythmias.

Atrioventricular nodal block with atrioventricular nodal reentrant tachycardia ablation.

The initial model of atrioventricular nodal tachycardia (AVNRT) as a small circuit of reentry within the AV node precluded a catheter-based cure for this arrhythmia without the occurrence of AV conduction block. Landmark observations that the atria were part of the circuit of AVNRT1 and that the arrhythmia could be reset with paced beats placed at sites anatomically distant from the compact AV node2 set the stage for the present expectation of curative ablation without AV block. Despite this understanding of the AVNRT mechanism and the large accrued operator experience during the past 3 decades when ablating this arrhythmia, AV block still occurs in ≈1% to 2.3% as a complication of ablation.3 See Article p 739 In this installment of teaching rounds, Chen et al4 share with us what we can learn from a series of patients with permanent or transient AV block noted during and soon after radiofrequency energy delivery. The authors provide an honest, transparent, and instructive view of their 5 cases. The fact that we are successful ≈99% of the time without complication suggests that the present methods for maintaining safety, including monitoring junctional rhythm during ablation and relating catheter position to the fluoroscopic anatomic approximation of the AV node location are mostly successful. The student of electrophysiology must, however, be aware of how these precautions can fail us. Even closely spaced bipolar electrodes placed over the compact AV node are not able to record electrograms from the node itself. Because we cannot map the structure we need to avoid, we must estimate anatomically its location and correlate this information with our standard fluoroscopic views. ### Utility The compact AV node is located within Koch’s triangle, approximately in its mid and central position. Using the His bundle as a surrogate for the superior vertex and …

Electrogram analysis and pacing are complimentary for recognition of abnormal conduction and far-field potentials during substrate mapping of infarct-related ventricular tachycardia.

Mapping to identify scar-related ventricular tachycardia re-entry circuits during sinus rhythm focuses on sites with abnormal electrograms or pace-mapping findings of QRS morphology and long stimulus to QRS intervals. We hypothesized that (1) these methods do not necessarily identify the same sites and (2) some electrograms are far-field potentials that can be recognized by pacing. From 12 patients with coronary disease and recurrent ventricular tachycardia undergoing catheter ablation, we retrospectively analyzed electrograms and pacing at 546 separate low bipolar voltage (<1.5 mV) sites. Electrograms were characterized as showing evidence of slow conduction if late potentials (56%) or fractionated potentials (76%) were present. Neither was present at (13%) sites. Pacing from the ablation catheter captured 70% of all electrograms. Higher bipolar voltage and fractionation were independent predictors for pace capture. There was a linear correlation between the stimulus to QRS duration during pacing and the lateness of a capturing electrogram (P<0.001), but electrogram and pacing markers of slow conduction were discordant at 40% of sites. Sites with far-field potentials, defined as those that remained visible and not captured by pacing stimuli, were identified at 48% of all pacing sites, especially in areas of low bipolar voltage and late potentials. Initial radiofrequency energy application rendered 74% of targeted sites electrically unexcitable. Far-field potentials are common in scar areas. Combining analysis of electrogram characteristics and assessment of pace capture may refine identification of substrate targets for radiofrequency ablation.