Focal Arrhythmias Research Articles

The Fourth Dimension

Radiofrequency ablation is now a cornerstone in the management of ventricular tachycardia (VT). VT ablation plays a palliative role in decreasing shocks and improving the quality of life in patients with structural heart disease and is often curative in treating VT in patients with normal hearts.1,2 When compared with other types of ablation, however, VT procedures have lower success rates, have a propensity for complications, and are technically challenging. A recognized cause for difficulty is the need to address the 3-dimensional pathological substrate (endocardial, midmyocardial, epicardial). At present, combined endocardial and epicardial approaches3 have largely addressed this problem and, along with a larger electrode and irrigation-based ablation, may allow success for the midmyocardial substrate as well. See article p 324 Recently, a novel syndrome of VT arising from the papillary muscles (PMs) has been described.4,–,6 This arrhythmia, along with VT arising from other endocavitary structures (moderator band, false tendon),7 has brought to light a fourth dimension that the interventional electrophysiologist has to appreciate and navigate during ablation. In this issue of Circulation: Arrhythmia and Electrophysiology , Yamada et al8 report electrophysiological findings in 19 patients who underwent successful ablation of PM VT. We learn from their study the problems related to pace mapping the potential for multiple morphologies arising from a single substrate and the unique mapping and ablation-related difficulty with this entity. When analyzing their findings, we are compelled to address important issues related to the specific mechanism of this novel syndrome, as well as assessing our present general limitations of how we map and ablate VT. The premise that pacing at the site of a focal arrhythmia origin will reproduce the QRS morphology of the tachycardia is a commonly used strategy with ablation.9,10 Yamada …

Septal Ventricular Tachycardia with Alternating LBBB–RBBB Morphology in Isolated Ventricular Noncompaction

Knowledge on ventricular tachycardia (VT) in isolated ventricular noncompaction (IVNC) is limited. We report on a patient with IVNC who presented with cardiogenic shock due to an incessant drug-resistant VT that was cured by radiofrequency ablation. The VT had characteristics of a deep septal focal arrhythmia, which was distinctive by ablation-induced alternation of the rightward and leftward exits, and was difficult to ablate from either side of the ventricular septum.

The Pathophysiologic Basis of Fractionated and Complex Electrograms and the Impact of Recording Techniques on Their Detection and Interpretation

Extracellular electrograms, recorded directly from the heart, are the hallmarks of invasive cardiac electrophysiology and provide information about the electric status of the underlying myocardium. These electrograms are generated by depolarization of cardiomyocytes that generates transmembrane currents in extracellular space and potential differences due to electric resistance of the extracellular medium. In healthy myocardium, the basic configuration of the extracellular electrogram is simple. Under pathological conditions, however, electrograms may consist of multiple components and long duration, which have been attributed to abnormal conduction and arrhythmogenicity. Although complex and fractionated electrograms are presently considered to be a real phenomenon, this was not the case some 20 years ago. Debates about the “fact or artifact” of complex and fractionated electrograms were common.1 At that time, electrograms consisting of multiple “high frequency” components with low amplitudes and long duration, termed “fractionated,” were recorded in patients with healed myocardial infarction during endocardial mapping. Several investigators presumed that fractionated electrograms were artifacts, resulting from movements between electrode and myocardium, filter characteristics of amplifiers, or represented far field effects. A classic example to support the “artifact theory” was the recording of continuous activity from the jello brain.2 In those days, much attention had been paid to fractionated electrograms in healed myocardial infarction to guide catheter ablation or antiarrhythmic surgery.3–5 Although artifacts indeed may cause complex electrograms, most of the complex and fractionated electrograms are a “fact” and caused by the peculiar behavior of activation fronts, due to structural and electric complexity of the underlying myocardium. This article delineates the origin of the unipolar extracellular electrogram, reviews the circumstances that cause fractionated and complex electrograms, and discusses the impact of the recording technique on detection and interpretation of multifaceted electrograms. Extracellular electrograms arise because of transmembrane currents that occur due to differences in the …

Cardiac Arrhythmia Management using a Noncontact Mapping Multielectrode Array

The multielectrode array (MEA) enables noncontact mapping of cardiac arrhythmias; our experience is reviewed and reported. The MEA has a role as first line therapy in multiple arrhythmias. Retrospective and prospective analysis of all consecutive cases performed using the MEA over a 6 year period. Electrophysiological study and catheter ablation, 46% under general anaesthesia, using radiofrequency (RF), cryothermal and low energy direct current (DC) was performed in 66 procedures on 31 females and 29 males, average age 50.2 yrs (19.3-81.6); 8 patients underwent multiple procedures. 24 patients (36%) had undergone past ablation for the same arrhythmia. A wide variety of arrhythmias from all chambers were treated, majority right atrial (56%) and right ventricular (29%). Procedural success was complete in 77.4% and partial/indeterminate in 11.3%, highest in right atrial tachycardia, right ventricular outflow tract ectopy and typical atrial flutter (79, 82 and 100%). RF energy was most commonly used (67%) and DC carried 100% success. Ablation was delivered at 'early activation' and 'breakout' in focal arrhythmias. In re-entrant circuits linear ablation transecting path of activation extending to regions of functional/anatomic block was performed. Two of 7 complications were attributed to the MEA: groin haematomas. At mean 12.4 mo follow up 56% were arrhythmia free, 15% asymptomatic or minimally symptomatic and 12 patients had new arrhythmias. The MEA is effective, safe and suitable for first line therapy in multiple cardiac arrhythmias particularly in the right heart. Further study is warranted comparing it to other mapping techniques.

Wt1 and Retinoic Acid Signaling in the Subcoelomic Mesenchyme Control the Development of the Pleuropericardial Membranes and the Sinus Horns

The cardiac venous pole is a common focus of congenital malformations and atrial arrhythmias, yet little is known about the cellular and molecular mechanisms that regulate its development. The systemic venous return myocardium (sinus node and sinus horns) forms only late in cardiogenesis from a pool of pericardial mesenchymal precursor cells. To analyze the cellular and molecular mechanisms directing the formation of the fetal sinus horns. We analyzed embryos deficient for the Wt1 (Wilms tumor 1) gene and observed a failure to form myocardialized sinus horns. Instead, the cardinal veins become embedded laterally in the pleuropericardial membranes that remain tethered to the lateral body wall by the persisting subcoelomic mesenchyme, a finding that correlates with decreased apoptosis in this region. We show by expression analysis and lineage tracing studies that Wt1 is expressed in the subcoelomic mesenchyme surrounding the cardinal veins, but that this Wt1-positive mesenchyme does not contribute cells to the sinus horn myocardium. Expression of the Raldh2 (aldehyde dehydrogenase family 1, subfamily A2) gene was lost from this mesenchyme in Wt1(-/-) embryos. Phenotypic analysis of Raldh2 mutant mice rescued from early cardiac defects by retinoic acid food supply revealed defects of the venous pole and pericardium highly similar to those of Wt1(-/-) mice. Pericardium and sinus horn formation are coupled and depend on the expansion and correct temporal release of pleuropericardial membranes from the underlying subcoelomic mesenchyme. Wt1 and downstream Raldh2/retinoic acid signaling are crucial regulators of this process. Thus, our results provide novel insight into the genetic and cellular pathways regulating the posterior extension of the mammalian heart and the formation of its coelomic lining.

Mechanoelectrical remodeling and arrhythmias during progression of hypertrophy

Despite a clear association between left ventricular (LV) mechanical dysfunction in end-stage heart failure and the incidence of arrhythmias, the majority of sudden cardiac deaths occur at earlier stages of disease development. The mechanisms by which structural, mechanical, and molecular alterations predispose to arrhythmias at the tissue level before the onset of LV dysfunction remain unclear. In a rat model of pressure overload hypertrophy (PoH) produced by ascending aortic banding, we correlated mechanical and structural changes measured in vivo with key electrophysiological changes measured ex vivo in the same animals. We found that action potential prolongation, a hallmark of electrical remodeling at the tissue level, is highly correlated with changes in LV wall thickness but not mechanical function. In contrast, conduction delays are not predicted by either mechanical or structural changes during disease development. Moreover, disrupted Cx43 phosphorylation at intermediate (increased) and late (decreased) stages of PoH are associated with moderate and severe conduction delays, respectively. Interestingly, the level of interaction between Cx43 and the cytoskeletal protein ZO-1 is exclusively decreased at the late stage of PoH. Closely coupled action potentials consistent with afterdepolarization-mediated triggered beats were readily observed in 6 of 15 PoH hearts but never in controls. Similarly, PoH (8/15) but not control hearts exhibited sustained episodes of ventricular tachycardia after rapid stimulation. The initiation and early maintenance of arrhythmias in PoH were formed by rapid and highly uniform activation wavefronts emanating from sites distal to the former site of stimulation. In conclusion, repolarization but not conduction delays are predicted by structural remodeling in PoH. Cx43 phosphorylation is disrupted at intermediate (increased) and late (decreased) stages, which are associated with conduction delays. Dephosphorylation of Cx43 is associated with loss of interaction with ZO-1 and severe conduction delays. Remodeling at all stages of PoH predisposes to triggers and focal arrhythmias.

Mechanisms of focal ventricular tachycardia in humans

In classifying ventricular arrhythmias, a fundamental distinction is made between focal and macroreentrant mechanisms. Focal arrhythmias demonstrate early activation at a particular site with centrifugal spread of the impulse from this site of origin. In contrast, macroreentrant rhythms involve contiguous but spatially distributed areas of activation. Despite advances in multielectrode and electroanatomical mapping, the distinction of a focal from a macroreentrant mechanism is sometimes problematic.

Feasibility of probabilistic neural networks, Kohonen self‐organizing maps and fuzzy clustering for source localization of ventricular focal arrhythmias from intravenous catheter measurements

Abstract: An important goal of clinical electrophysiological studies is estimation of the source of rhythm disturbances (arrhythmia) in the heart. 15% of ventricular arrhythmias are known to originate from the outer surface of the heart (epicardium). One localization approach targeting the epicardium uses multielectrode catheters placed in the coronary veins. However, epicardial measurement sites from these catheters are limited to locations reached via the coronary veins. This study investigates the feasibility of several pattern classification and neural network approaches for localization of the source of ventricular arrhythmias from sparse measurements acquired from within coronary veins. Specifically, we studied Kohonen self‐organizing maps and fuzzy C‐means clustering methods for the construction of the target vector in neural networks from experimental high‐resolution activation‐time patterns. We also studied two neural network techniques, probabilistic neural networks and backpropagation networks, for the training and test procedures. The results of this study showed that it was possible to localize the arrhythmia source in a relatively small region for approximately 70% of cases. This study, in general, showed that the combination of probabilistic neural networks, Kohonen self‐organizing maps and fuzzy C‐means clustering approaches is feasible in catheter‐based epicardial arrhythmia source localization.

Rewiring the Heart: Stem Cell Therapy to Restore Normal Cardiac Excitability and Conduction

The regenerative capacity of the mammalian heart is insufficient to recover from myocardial infarction. Stem cells are currently considered as a promising and valuable tool to replace the, often large, loss of contractile tissue. One of the bottlenecks hampering fast clinical application is the large amount of cells required to replace a single damaged region combined with an appropriate strategy to succeed in homogeneous repair. A second class of major cardiac disorders for which stem cell therapy might be fruitful and would require less cells for repair, are chronic rhythm disorders. In this area, most research has been focused on stem-cell based biological pacemakers, but increasing amounts of data on AV nodal repair appear in literature. Both therapies, in principle, could eventually replace current instrumentation with electronic pacemakers. Finally, an emerging field of interest explores transplantation of stem cells expressing specific ion channels aiming at suppression of focal arrhythmias, providing an alternative strategy for surgical and catheter-mediated ablation. Since in this second class of applications the number of transplanted cells required may be relatively low, effective clinical therapy may be within close range. Here, we will review recent achievements in the fields of stem-cell based biological pacemakers, AV nodal repair and biological ablation.

Arritmia focal de Vena Pulmonar: desde Bigeminia Oculta hasta Fibrilación Auricular. Tratamiento mediante Ablación

Paroxysmal atrial fibrillation (AF) initiation often occurs from pulmonary vein (PV) ectopy. We describe the case of a young patient with multiple episodes of refractory AF who had, almost permanently, left inferior PV extrasystoles in a pattern of bigeminy. At the beginning this focal arrhythmia was concealed due to exit block, going unnoticed on the electrocardiogram. Subsequently PV couplets were expressed as atrial extrasystoles and finally disorganization of this phenomenon led to AF. PV isolation was performed and after 4 months of follow-up the patient remains free from AF and supraventricular extrasystoles on Holter monitoring.

Combination of Computer Simulations and Experimental Measurements as the Training Dataset for Statistical Estimation of Epicardial Activation Maps From Venous Catheter Recordings

One of the epicardial mapping techniques requires the insertion of multiple multi-electrode catheters into the coronary vessels. The recordings from the intracoronary catheters reflect the electrical activity on the nearby epicardial sites; however, most of epicardial surface is still inaccessible. In order to overcome this limited access problem, a method called the linear least squares estimation was proposed for the reconstruction of high-resolution maps using sparse measurements. In this technique, the relationship between catheter measurements and the remaining sites on the epicardium is created from previously obtained high-resolution maps (training dataset). Even though open-chest surgery is still a relatively frequent occurrence, an additional burden on the patient to obtain epicardial maps might impose an important risk on the patient. In this study, we hypothesize that epicardial maps created from computer simulations might be used in combination with the experimental data. In order to test this hypothesis, we used high-resolution epicardial activation maps acquired from 13 experiments performed on canine hearts that were stimulated via unipolar pacing from sites distributed all over the epicardium. We investigated the feasibility of the Aliev-Panfilov model that generated focal epicardial arrhythmias on Auckland heart. We started the simulations from the sites that corresponded to the pacing sites on the experimental geometry after a registration procedure between the experimental and simulation geometries. We then compared the simulation results with the corresponding experimental activation maps. Finally, we included simulated activation maps alone (100%) and in combination (simulated maps constituted 90%, 75%, 50%, 25%, 10%, and 0% of the training dataset) with experimental maps in the training set, performed the statistical estimation, and obtained the error statistics. The mean correlation coefficient (CC) between the simulated epicardial activation maps with the experimental maps was 0.88. The results of the estimation indicated that only 2.6 mm localization error and 0.05 CC value degradation occurred on average for the replacement of 75% of the experimental maps with the simulated counterparts. This indicated that including an important percentage from simulations may lead to decreased need for open-chest procedures and less burden on the patients.

Intracoronary Infusion of Catecholamines Causes Focal Arrhythmias in Pigs

Acute ischemia causes myriad changes including increased catecholamines. We tested the hypothesis that elevated catecholamines alone are arrhythmogenic. A 504 electrode sock was placed over both ventricles in six open-chest pigs. During control infusion of saline through a catheter in the left anterior descending coronary artery (LAD), no sustained arrhythmias occurred, and the refractory period estimated by the activation recovery interval (ARI) was 175 +/- 14 ms in the LAD bed below the catheter. After infusion of isoproterenol at 0.1 microg/kg/min through the catheter, the ARI in this bed was significantly reduced to 109 +/- 10 ms. A sharp gradient of refractoriness of 43 +/- 10 ms was at the border of the perfused bed. Sustained monomorphic ventricular tachycardia occurred after drug infusion in the perfused bed or near its boundary in all animals with a cycle length of 329 +/- 26 ms and a focal origin. The maximum slope of the ARI restitution curve at the focal origins of the tachyarrhythmias was always <1 (0.62 +/- 0.15). Similar results with a focal arrhythmia origin occurred in two additional pigs in which intramural mapping was performed with 36 plunge needle electrodes in the left ventricular perfused bed. Regional elevation of a catecholamine, which is one of the alterations produced by acute ischemia, can by itself cause tachyarrhythmias. These arrhythmias are closely associated with a shortened refractory period and a large gradient of the spatial distribution of refractoriness but not with a steep restitution curve.

Distinguishing Properties of Cells From the Myocardial Sleeves of the Pulmonary Veins

Background— A common source of arrhythmogenic spontaneous activity instigating atrial fibrillation is the myocardial tissue, or sleeves, at the base of the pulmonary veins. This study compared the properties of cells from the myocardial sleeves of the pulmonary veins (PV m ) with cells from the normal cardiac pacemaker (the sinoatrial node) and regions of the atria. Our objective was to identify key features of these cells that predispose them to becoming the focus of cardiac arrhythmias. Methods and Results— Single cells were isolated from samples of rabbit PV m , central and peripheral sinoatrial node, crista terminalis, and left and right atria. Detailed morphology of cells was assessed and intracellular calcium concentrations measured with the use of Fluo-3. Cells from the PV m were smaller than atrial cells and showed large elevations in diastolic calcium during activation at physiological rates, a feature the PV m cells shared with cells from the sinoatrial node. Unstimulated spontaneous activity was observed in a minority of cells from the PV m , but numerous cells from this region showed spontaneous activity for a brief period immediately subsequent to stimulation at physiological rates. This was not observed in atrial cells. Assessment of calcium removal pathways showed sarcolemmal calcium extrusion in cells from the PV m to have a high reliance on “slow” extrusion pathways to maintain intracellular calcium homeostasis because of a low expression of sodium–calcium exchanger. Conclusions— We conclude that cells from the PV m share some features with cells from the sinoatrial node but also have distinctly unique features that predispose them to the development of spontaneous activity.

Focal Arrhythmia Confined Within the Coronary Sinus and Maintaining Atrial Fibrillation

The coronary sinus (CS) is a complex structure comprising a mesh of circumferential muscular fibers with oblique connections to both atria. We describe further evidence for the clinical importance of CS arrhythmogenicity in maintaining atrial fibrillation (AF) in humans. Since January 2004, following a sequential approach, the CS and the inferior left atrium were ablated in 144 patients with symptomatic drug refractory AF. Patients were included for analysis when this step resulted in the electrical dissociation of the CS from both atria with restoration of sinus rhythm, but with continued arrhythmic activity in the CS. The electrophysiologic mechanism of the confined arrhythmia was considered as focal activity (automaticity or triggered activity) by the presence of electrograms spanning less than 75% of the cycle length in the CS. After restoration of sinus rhythm, four male patients (3% of the patients, three persistent and one permanent AF) were identified in whom arrhythmia continued within the CS. Repetitive activity confined to the disconnected CS was inconsistent in occurrence, as well as in duration (1 sec to 15 min) and cycle length (from 158 to 380 ms). For all four patients, electrogram mapping of the entire CS was compatible with a focal mechanism. In two patients, bursts alternating with slow dissociated activity suggested automaticity. In one patient, local activity consistently coupled to the previous sinus beat favored triggered activity. This study provides evidence that the CS may be a potential source of focal rapid activity maintaining AF.

Arrhythmogenic Mechanisms in a Mouse Model of Catecholaminergic Polymorphic Ventricular Tachycardia

Catecholaminergic polymorphic ventricular tachycardia (VT) is a lethal familial disease characterized by bidirectional VT, polymorphic VT, and ventricular fibrillation. Catecholaminergic polymorphic VT is caused by enhanced Ca2+ release through defective ryanodine receptor (RyR2) channels. We used epicardial and endocardial optical mapping, chemical subendocardial ablation with Lugol's solution, and patch clamping in a knockin (RyR2/RyR2(R4496C)) mouse model to investigate the arrhythmogenic mechanisms in catecholaminergic polymorphic VT. In isolated hearts, spontaneous ventricular arrhythmias occurred in 54% of 13 RyR2/RyR2(R4496C) and in 9% of 11 wild-type (P=0.03) littermates perfused with Ca2+and isoproterenol; 66% of 12 RyR2/RyR2(R4496C) and 20% of 10 wild-type hearts perfused with caffeine and epinephrine showed arrhythmias (P=0.04). Epicardial mapping showed that monomorphic VT, bidirectional VT, and polymorphic VT manifested as concentric epicardial breakthrough patterns, suggesting a focal origin in the His-Purkinje networks of either or both ventricles. Monomorphic VT was clearly unifocal, whereas bidirectional VT was bifocal. Polymorphic VT was initially multifocal but eventually became reentrant and degenerated into ventricular fibrillation. Endocardial mapping confirmed the Purkinje fiber origin of the focal arrhythmias. Chemical ablation of the right ventricular endocardial cavity with Lugol's solution induced complete right bundle branch block and converted the bidirectional VT into monomorphic VT in 4 anesthetized RyR2/RyR2(R4496C) mice. Under current clamp, single Purkinje cells from RyR2/RyR2(R4496C) mouse hearts generated delayed afterdepolarization-induced triggered activity at lower frequencies and level of adrenergic stimulation than wild-type. Overall, the data demonstrate that the His-Purkinje system is an important source of focal arrhythmias in catecholaminergic polymorphic VT.

Source localization of focal ventricular arrhythmias using linear estimation, correlation, and back propagation networks

Catheter-based approaches used in the localization and treatment of the source of heart rhythm disturbances (arrhythmias) have become popular, because they do not require highly invasive and risky open-chest operations. In most of the existing approaches, mapping of the outer surface (epicardium) is not possible even though arrhythmic substrates involving epicardial and subepicardial layers account for about 15% of the ventricular tachycardias. In this study, we report a feasibility study of a novel mapping approach targeting the epicardium which is based on the measurements of multielectrode catheters placed in the coronary veins. We investigated three methods in determining the most probable region of early activation, i.e., the region that contains the source of the abnormal activation on the heart, using only a set of sparse venous catheter recordings. The methods we proposed here were the linear estimation, correlation, and the back propagation networks. The linear estimation technique hypothesized the relationship between venous catheter measurements and unmeasured epicardial sites based on a previously recorded training data set. The correlation method included a comparative analysis between test and training epicardial activation time maps based on the measured values from the venous sites. In the back propagation method, the input layer consisted of the source data in the form of 42 nodes which were the activation time values from the intravenous catheter leads. We used two hidden layers with 600 and 500 nodes, respectively. The output layer consisted of 28 nodes in the output layer that corresponded to the manually selected early activation regions on the epicardium. The results of the linear estimation and the correlation methods showed that they could be used as a good predictor for the region of early activation, and thus, these approaches may be employed to direct a subsequent more focused electrophysiological study and curative radiofrequency (RF) ablation. The back propagation network approach performed relatively well for the right ventricularly paced beats and the results demonstrated its potential as a supporting technique to the estimation and correlation methods. The results of this study encourage further investigation and provides evidence that an epicardial mapping approach based on the venous catheter recordings is feasible and can provide adequate accuracy for clinical applications.

Ablation ektoper rechtsatrialer Tachykardien unter Verwendung eines 20-poligen Mapping-Katheters

Ectopic atrial tachycardia (EAT) are frequently unresponsive to pharmacological antiarrhythmic therapy. Radiofrequency ablation seems to be a safe approach to treat those arrhythmias. In the present study we report our results of radiofrequency ablation of EAT with a new mapping system (Stablemapr, Medtronic). Thirty consecutive patients with right atrial tachycardia were included in the study. In 15 patients (G1) the 20-polar Stablemapr was used for localization of the arrhythmia foci. Data were compared with a control group (G2, n=15), in which mapping was performed conventionally. The demographic characteristics and the distribution of the different cardiac diseases were comparable in both groups. In group 1 the identification of the EAT was facilitated by the placement of the 20-pole mapping catheter in the right atrium. In group 2 point by point measurements were performed to find the earliest local atrial activation compared to a reference electrode in the high right atrium (activation mapping), or foci were identified by analysis of the P-wave morphology during stimulation (pacemapping). It was possible to successfully ablate all atrial tachycardias. The distribution of the foci was similar in both groups (G1/G2): near to the superior (3/5) and inferior (1/0) caval vene ostium, on the free wall (3/3), at the coronary sinus ostium (3/3) and on the interatrial septum (5/4). The mean procedure (G1: 88+/-33 vs G2: 151+/-61 min; p= or <0.05) and fluoroscopic times (G1: 19+/-9 vs G2: 38+/-28 min; p= or <0.05) were significantly shorter in group 1. Moreover, the mean number of radiofrequency applications was reduced significantly by using the new mapping system (G1: 10+/-10 vs G2: 16+/-13; p= or <0.05). Radiofrequency ablation of EAT with right atrial focus can be performed safely and successfully using a 20-pole mapping catheter. The greatest advantages compared to conventional mapping and ablation strategies lies in the shortened investigation and fluoroscopic time.

Arrhyyhmogenic right ventricular dysplasia; radiologic findings of the left ventricle: A case report and review of the literature

Abstract Arrhythmogenic right ventricular dysplasia (ARVD) is characterized by progressive fibro fatty replacement of the right ventricular myocardium which constitutes a substrate for electrical instability and a focus of ventricular arrhythmias. Most of the patients have some degree of left ventricular involvement which also affects the right ventricle by the same disease process. From thirty percent to 50% of patients with ARVD have a family history of the disease. The most common pattern of inheritance is autosomal dominant. Clinically, ARVD usually presents with ventricular arrhythmias, and there is approving evidence that this is the underlying disease in a substantial number of sudden deaths among young, especially healthy individuals. The diagnosis of ARVD relies on the presence of structural and functional abnormalities of the right ventricle, electrophysiological abnormalities, and family history. The imaging modalities are conventional angiography, echocardiography (ECO), radionuclide angiography, ultra fast computed tomography, and magnetic resonance imaging. (MRI). We are presenting a case of ARVD with ECO, computed tomography (CT), and MRI findings.

Recording Techniques for Clinical Electrophysiology

The precise techniques employed in the electrophysiology laboratory influence the nature of the electrograms that are recorded during mapping procedures. Unipolar recordings that are minimally filtered can be useful for mapping focal arrhythmia sources, but have substantial far-field signal that can obscure low-amplitude signals of interest in abnormal regions. Bipolar recordings are standard in most laboratories because rejection of far-field signal facilitates identification of local potentials in abnormal areas, but the signal of interest can be beneath either recording electrode and far-field signals do occur. Simultaneously obtained unipolar recordings are a useful adjunct to bipolar recordings in some situations. High pass filtering and digital sampling also influence electrogram characteristics. High pass filtering of unipolar recordings can be useful to reduce far-field components, but limits inferences from electrogram morphology.

780 Mapping and ablation of recurrent arrhythmias after MAZE III surgery for lone atrial fibrillation

Purpose: Maze III surgery for lone paroxysmal atrial fibrillation (PAF) shows freedom of arrhythmias in over 80% of patients. The mechanisms of late recurrences of arrhythmias are unclear. Methods: 11 of 139 pts who underwent classical MAZE III surgery were evaluated by electrophysiological study (EPS) for arrhythmia recurrence. Multipolar catheters in both atria were used to induce and map tachycardia. LocaLisaTM or NavXTM were used for 3-D mapping of the atrial anatomy and activation. RFCA was performed with a standard 4-mm RF catheter. Results: During ECG follow-up after MAZE III surgery, continuous atrial ectopy was seen in 1 pt, atypical flutter (FL) was present in 2, PAF in 5, typical FL and PAF in 1, AVNRT in 1 and AVNRT with PAF in the remaining pt. In 4 pts EPS showed persisting conduction from the pulmonary vein (PV) button to the remaining atrium. Conduction over the mitral isthmus (MI) persisted in 5, and over the tricuspid isthmus (TI) in 2 pts. The surgical lines were thus incomplete in a total of 7 pts. Three pts with an incomplete PV button line had PAF and PV potentials, and a successful ostial RFCA isolation of all 4 PVs was performed. One pt with an incomplete TI line had typical FL, successfully treated with RFCA of the isthmus. This pt also had PAF, but a remaining left atrial focus could not be abolished. One pt with an incomplete MI line had atypical FL, but RFCA failed to close the isthmus gap. In the remaining 6 pts, incomplete surgery did not correlate with arrhythmias. After successful RFCA of AVNRT in 2 pts, atrial arrhythmias persisted in one. In the pt with atrial ectopy, a septal focus could not be ablated. In the remaining 3 pts, atypical FL, ectopy or PAF were also found to be focal, in one of them possibly due to an epicardial remnant of surgical material. In only 1 pt RFCA could abolish a right septal focus. So far, 7 pts have become asymptomatic after successful RFCA. Conclusion: Arrhythmia recurrence after classical MAZE III surgery is related to incomplete surgical lines around the PVs and AV annulus, or focal atrial activation. Localization and ablation of surgical gaps and focal arrhythmias in these postoperative atria remains difficult despite sophisticated mapping.