Three-Dimensional Late Gadolinium Enhancement Cardiovascular Magnetic Resonance Predicts Inducibility of Ventricular Tachycardia in Adults With Repaired Tetralogy of Fallot.

BACKGROUND: Adults with repaired tetralogy of Fallot die prematurely from ventricular tachycardia (VT) and sudden cardiac death. Inducible VT predicts mortality. Ventricular scar, the key substrate for VT, can be noninvasively defined with late gadolinium enhancement (LGE) cardiovascular magnetic resonance but whether this relates to inducible VT is unknown. METHODS: Sixty-nine consecutive repaired tetralogy of Fallot patients (43 male, mean 40±15 years) clinically scheduled for invasive programmed VT-stimulation were prospectively recruited for prior 3-dimensional LGE cardiovascular magnetic resonance. Ventricular LGE was segmented and merged with reconstructed cardiac chambers and LGE volume measured. RESULTS: VT was induced in 22 (31%) patients. Univariable predictors of inducible VT included increased RV LGE (odds ratio [OR], 1.15; P=0.001 per cm3), increased nonapical vent LV LGE (OR, 1.09; P=0.008 per cm3), older age (OR, 1.6; P=0.01 per decile), QRS duration ≥180 ms (OR, 3.5; P=0.02), history of nonsustained VT (OR, 3.5; P=0.02), and previous clinical sustained VT (OR, 12.8; P=0.003); only prior sustained VT (OR, 8.02; P=0.02) remained independent in bivariable analyses after controlling for RV LGE volume (OR, 1.14; P=0.003). An RV LGE volume of 25 cm3 had 72% sensitivity and 81% specificity for predicting inducible VT (area under the curve, 0.81; P<0.001). At the extreme cutoffs for ruling-out and ruling-in inducible VT, RV LGE >10 cm3 was 100% sensitive and >36 cm3 was 100% specific for predicting inducible VT. CONCLUSIONS: Three-dimensional LGE cardiovascular magnetic resonance-defined scar burden is independently associated with inducible VT and may help refine patient selection for programmed VT-stimulation when applied to an at least intermediate clinical risk cohort.

Peri-mitral atrial flutter: personalized ablation strategy based on arrhythmogenic substrate.

Aims: The aim of this study is to characterize the arrhythmogenic substrate for peri-mitral atrial flutter (PMAFL), thereby determining a personalized ablation strategy to treat PMAFL. Methods and results: Thirty-six consecutive PMAFL patients (mean age: 63.8 ± 11.3, 23 males) underwent detailed three-dimensional electroanatomic mapping in left atrium (LA). The LA was divided into septal-anterior wall (SAW), posterior inferior wall (PIW), and mitral isthmus (MI) region, respectively. Ablation strategy was determined based on the endocardial bipolar voltage map. Based on electrophysiological substrates, 10, 17, and 9 cases were classified into iatrogenic, spontaneous, and no-substrate PMAFL, respectively. The mean voltage in SAW was significantly lower in spontaneous PMAFL (iatrogenic: 1.07 ± 0.66 mV; spontaneous: 0.65 ± 0.44 mV; no-substrate: 1.60 ± 0.53 mV, P <0.001), while iatrogenic PMAFL patients had the lowest voltage in MI (0.51 ± 0.23 mV vs. 1.55 ± 0.78 mV, 1.61 ± 0.56 mV, P <0.001). No low-voltage or slow conduction zone was found in the no-substrate PMAFL group. Fifteen spontaneous PMAFLs were successfully terminated by modified septal-anterior (9/10) or conventional anterior ablation line (6/7). Eight iatrogenic PMAFLs (8/10) were terminated by reinforcing the previous ablation areas. Cardioversion without PMAFL ablation was done in no-substrate PMAFL patients. After a median follow-up of 12 (7-39) months, two spontaneous PMAFL patients received redo procedures for recurrence due to "gap" conduction. Conclusions: The ablation strategy for PMAFL patients should be based on the arrhythmogenic substrate, but not the indiscriminate MI ablation. No-substrate PMAFLs during AF ablation could be monitored after cardioversion and might not need further ablation.

Standardized review of atrial anatomy for cardiac electrophysiologists.

Catheter ablation of cardiac arrhythmias has rapidly evolved from a highly experimental procedure to a standard form of therapy for various tachyarrhythmias. The advances in this field have included, first, the development of techniques of catheter ablation that often requires the precise destruction of minute amounts of arrhythmogenic tissues and, second, techniques of resynchronization therapy that require pacing different parts of the ventricles. A detailed prepocedural knowledge of cardiac anatomy can improve the safety of the procedure and its rate success. It helps the electrophysiologist to choose the appropiate region for ablation, shortening the procedural time. The atrial anatomy structures are usually localized before ablation by different imaging techniques such as fluoroscopy, electroanatomic mapping, intracardiac echocardiography or multidetector computed tomography. In this review, we describe the normal anatomy of the atria, highlighting the landmarks of interest to intervencional cardiologist, stressing their relationship to other structures. This article is part of a JCTR special issue on Cardiac Anatomy.

Right ventricular outflow tract imaging with CT and MRI: Part 2, Function.

OBJECTIVE: MRI and CT have become the ideal methods for assessing the complex function of the conotruncal region, including the right ventricular outflow tract (RVOT). In this review, we focus on the role of CT and MRI to evaluate RVOT function in relation to developmental malformations. CONCLUSION: We discuss the role of imaging pertinent to electrophysiologic assessment for cardiac arrhythmias. The RVOT is an important ablation target for radiofrequency ablation of ventricular tachycardia. Architectural changes of the myocardial strands in the RVOT, scar, and fibrofatty tissue may play a role in the development of RVOT ventricular arrhythmias. With CT and MRI, some of these changes can be revealed.

Focal atrial tachycardia originating from the non-coronary aortic sinus: electrophysiological characteristics and catheter ablation.

OBJECTIVES: We sought to investigate electrophysiological characteristics and catheter ablation in patients with focal atrial tachycardia (AT) originating from the non-coronary aortic sinus (AS). BACKGROUND: In patients with failed ablation of focal AT near the His bundle (HB) region, an origin from the non-coronary AS should be considered because of the close anatomical relationship. METHODS: This study included 9 patients with focal AT, in 6 of whom attempted radiofrequency (RF) ablation had previously failed. Activation mapping was performed during tachycardia to identify an earliest activation in the atria and the AS. The aortic root angiography was performed to identify the origin in the AS before RF ablation. RESULTS: Focal AT was reproducibly induced by atrial pacing. Mapping in atria demonstrated that the earliest atrial activation was located at the HB region, whereas mapping in the non-coronary AS demonstrated that an earliest atrial activation preceded the atrial activation at the HB by 12.2 +/- 6.9 ms and was anatomically located superoposterior to the HB in all 9 patients. Also, His potentials were not found at the successful site in the non-coronary AS in all 9 patients. The focal AT was terminated in <8 s in all 9 patients. Junctional beats and PR prolongation did not occur during RF application in all 9 patients. No complications occurred in any of the nine patients. All 9 patients were free of arrhythmias without antiarrhythmic drugs during a follow-up of 9 +/- 3 months. CONCLUSIONS: In patients with focal AT near the HB region, mapping in the non-coronary AS can improve clinical outcome.

A model for in vivo validation of linear lesions in the right atrium.

UNLABELLED: Linear lesions have been proposed for treatment of complex atrial arrhythmias including atrial macroreentry tachycardia and compartmentalization in atrial fibrillation. AIM: To judge the effectiveness of a given lesion design, definite endpoints are necessary to ascertain the completeness of the line of block produced. METHODS AND RESULTS: We report validation criteria for long linear lesions in the right atrium in 42 pts, that combine both conventional and 3D mapping information (CARTO). Transferring from the validation of bi-directional block of the cavotricuspid isthmus line for atrial flutter, we validated 2 additional long linear lesions in the right atrium (anterior line and intercaval line). In addition to a complete isthmus line in all 42 pts, in 28 pts a complete anterior line was achieved and validated by both conventional and CARTO criteria. A complete intercaval line was deployed in 11 pts with complete anterior and isthmus lines (with a characteristic shift for the intercaval line) and in 5 pts without a complete anterior line (without characteristic shift). CONCLUSIONS: Conventional catheters placed at strategic locations on opposite sides of the intended ablation line, can depict a sudden characteristic change in the activation sequence. Using a combination of both techniques, deployment and validation of long linear lesion can be facilitated.

Reentrant circuits in the canine atrioventricular node during atrial and ventricular echoes: electrophysiological and histological correlation.

BACKGROUND: The anatomic-electrophysiological correlation of AV nodal reentry is unclear. To localize reentrant circuits during atrial and ventricular echoes and to characterize sites of slow conduction and block, we correlated histology with electrophysiology of the AV node. METHODS AND RESULTS: In 10 isolated dog hearts, extracellular electrical activity was recorded in Koch's triangle at 208 or 247 sites (interelectrode distance, 0.5 and 0.3 mm) after removal of 0.7 to 1.5 mm of overlying atrial tissue. Resection did not affect refractory periods. Five hearts were subjected to histology. Complete atrial echoes were induced in 1 heart, incomplete atrial echoes in 5 hearts. Unidirectional conduction block occurred at the atrial-transitional cell junction in the superior area. Zones of slow conduction arose at the atrial-transitional or the transitional-compact node junction in the inferior area. Complete reentrant circuits of ventricular echoes were obtained in 5 hearts. Unidirectional conduction block occurred at the compact node-transitional cell junction in the superior area. Localized zones of slow conduction arose at the junctions between the different types of tissue in the inferior area. CONCLUSIONS: In the dog heart, tissue architecture and functional dissociation between the inferior and the superior region of the AV node enable dual physiology and reentry. Slow conduction and functional conduction block occur at the junctions between the different types of tissue in the AV nodal area. Atrial echoes were enabled by conduction block at the atrial-transitional cell junction, whereas during ventricular echoes conduction block occurred at the compact node-transitional cell junction.

High density endocardial mapping of shifts in the site of earliest depolarization during sinus rhythm and sinus tachycardia.

Previous mapping studies of sinus rhythm suggest faster rates arise from more cranial sites within the lateral right atrium. In the intact, beating heart, mapping has been limited to epicardial plaques or single endocardial catheters. The present study was designed to examine shifts in the site of the earliest endocardial depolarization during sinus rhythm and sinus tachycardia using high density activation mapping. Noncontact mapping of the right atrium during sinus rhythm was performed on ten anesthetized swine. Recordings were made during sinus rhythm, phenylephrine infusion, and isoproterenol infusion. The hearts were then excised and the histological sinus node identified. The mean minimum and maximum cycle lengths recorded were 355 +/- 43 and 717 +/- 108 ms. A median of three (range two to five) sites of earliest endocardial depolarization were documented in each animal. With increasing heart rate the site of earliest endocardial depolarization remained stationary until a sudden shift in a cranial or caudal direction, often to sites beyond the histological sinoatrial node. The endocardial shift was unpredictable with considerable variation between animals; however, faster rates arose from more cranial sites (r = 0.46, P = 0.023). There was no difference in the mean cycle length of sinus rhythm originating from specific positions on the terminal crest (r = 0.44, P = 0.17). Cranial sites displayed a more diffuse pattern of early depolarization than caudal sites. In the porcine heart the relationship between heart rate and site of earliest endocardial depolarization shows considerable variation between individual animals. These findings may have implications for clinical mapping and ablation procedures.

Characterization of left atrial activation in the intact human heart.

BACKGROUND: The patterns of activation of the human left atrium (LA), how they relate to atrial myocardial architecture, and their role in arrhythmogenesis remain largely unknown. METHODS AND RESULTS: Left atrial endocardial activation was mapped in 19 patients with a percutaneous noncontact mapping system. Earliest endocardial breakthrough during sinus rhythm (SR) occurred more frequently in the septal (63%, principally posteroseptal) than anterosuperior (37%) LA and varied little with isoproterenol or high right atrial pacing rate. Regardless of site of breakthrough, LA activation was characterized in all patients by propagation around a variably complete line of functional conduction block, descending on the posterior wall from the roof, passing between the ostia of the superior and then inferior pulmonary veins (PVs) before turning septally, passing below the oval fossa, and merging further anteriorly with the septal mitral annulus. Examination of the myocardial architecture in 10 normal adult postmortem hearts revealed an abrupt change in subendocardial fiber orientation along a line following the same course. During episodes of focal initiation of atrial fibrillation (AF), interaction was observed between wavefronts entering the LA from PVs and this functional line of conduction block that resulted in LA macroreentry or formation of daughter wavefronts. CONCLUSIONS: The LA endocardium has complex but characteristic patterns of activation during sinus rhythm, pacing, and AF initiation by PV ectopy that are determined largely by the functional properties of atrial musculature. These findings have important implications for both pacing and ablative strategies for the prevention of initiation of AF.

Characteristics of right atrial activation during coronary sinus pacing.

INTRODUCTION: Anatomic and electrical connections between the left atrium and right atrium (RA) have been described. The relationship between coronary sinus (CS) pacing site and RA activation has not been examined. METHODS AND RESULTS: Fifteen anesthetized swine underwent high-density noncontact mapping of the RA during pacing from up to five different sites within the CS. Isopotential mapping identified the site of earliest RA depolarization and the pattern of subsequent activation. Hearts were excised and endocardial dissection performed. Earliest RA activation occurred at the CS os with proximal CS pacing sites and at Bachmann's bundle at distal pacing sites. The mean depth at which a shift in earliest RA activation site occurred was 46 +/- 13 mm (range 21 to 63 mm). RA activation times following earliest activation at the CS and Bachmann's bundle were 40 +/- 4 msec and 51 +/- 6 msec (P < 0.002). Conduction delay or block was recorded at the lateral cavotricuspid isthmus, terminal crest, and tendon of Todaro. Latest RA activation always occurred in the high anterolateral atrium after ascending the anterolateral wall. The lateral RA was activated by the wavefront that traversed the posterior wall rather than by the wavefront crossing the cavotricuspid isthmus, even with earliest RA activation at the CS os. CONCLUSION: The site of earliest RA activation during CS pacing is dependent upon the pacing depth within the CS. In the porcine heart, areas of conduction delay influence RA activation patterns and timings. These findings may have implications for patients undergoing assessment of radiofrequency ablation of atrial flutter.