Visualization of acute edema in the left atrial myocardium after radiofrequency ablation: Application of a novel high-resolution 3-dimensional magnetic resonance imaging sequence.

BACKGROUND: Ablation-induced left atrial (LA) edema may result in procedural failure due to reversible pulmonary vein isolation. Conventional T2-weighted magnetic resonance edema imaging is limited by low spatial resolution. OBJECTIVE: The purpose of this pilot study was to optimize and validate a 3-dimensional (3D) sampling perfection with application-optimized contrasts using different flip-angle evolution (SPACE) sequence for quantification of T2 signal in the LA, and to apply it in recently ablated patients, comparing myocardial edema on T2-SPACE to tissue damage on late gadolinium enhancement (LGE) imaging. METHODS: Phantom studies were performed to identify 3D-SPACE parameters for optimal contrast between normal and edematous myocardium. Fourteen AF patients were imaged with both 3D-SPACE and dark-blood turbo-spin echo (DB-TSE) to compare image quality and signal intensity between the 2 techniques. Eight patients underwent pre- and postablation 3D-SPACE and 3D-LGE imaging. Ablation points were co-registered with corresponding myocardial sectors, and ablation-induced changes in T2 and LGE signal intensities were measured. RESULTS: Signal-to-noise ratio and contrast-to-noise ratio were higher on SPACE vs DB-TSE (65.5 ± 33.9 vs 35.7 ± 17.9; P = .01; and 59.4 ± 33.0 vs 32.9 ± 17.7; P = .04, respectively). T2-signal correlated well on 3D-SPACE and DB-TSE, such that each unit increase in TSE intensity correlated with a 0.69-unit increase in SPACE intensity (95% confidence interval 0.56-0.82; P <.001). T2 and LGE signal intensities were acutely increased at ablation sites. The extent of postablation edema was higher compared to LGE, although the spatial distribution of hyperenhancement around pulmonary veins seemed similar in both modalities. CONCLUSION: T2-SPACE can be used to map the extent of acute postablation edema in the thin LA myocardium, with improved resolution and lower artifact compared to traditional DB-TSE.

Relation of Electrocardiographic Left Atrial Abnormalities to Risk of Stroke in Patients with Atrial Fibrillation.

The P-wave terminal force in lead V1 (PTFV1) on the 12-lead electrocardiogram (ECG) quantifies left atrial (LA) structural and electrophysiologic abnormalities. We aimed to evaluate the association between PTFV1 and cerebrovascular accident (CVA) as well as LA structure and function in patients with atrial fibrillation (AF). We conducted a cross-sectional study of 229 patients with AF (60 ± 10years, 72% men) with (n = 21) and without (n = 208) a history of CVA, who underwent preablation ECG and cardiac magnetic resonance in sinus rhythm. PTFV1 was defined as the duration (in milliseconds) of the downward deflection of the P wave in lead V1 multiplied by the absolute value of its amplitude (in microvolts) on ECG. PTFV1 is associated with LA minimum volume (Vmin) and left ventricular ejection fraction but not associated with the extent of LA fibrosis quantified by cardiac magnetic resonance late gadolinium enhancement. In addition, PTFV1 is associated with CVA independent of the CHA2DS2-VASc score and LA Vmin (odds ratio 1.23; 95% confidence interval 1.08 to 1.40; p = 0.002). Furthermore, PTFV1 has an incremental value over the CHA2DS2-VASc score as a marker of CVA (p <0.001). In conclusion, ECG-defined PTFV1 is independent marker of stroke in patients with AF and reflects the underlying LA remodeling. Our findings suggest that evaluation of PTFV1 can improve the current risk stratification of stroke.

The Fibrotic Substrate in Persistent Atrial Fibrillation Patients: Comparison Between Predictions From Computational Modeling and Measurements From Focal Impulse and Rotor Mapping.

Focal impulse and rotor mapping (FIRM) involves intracardiac detection and catheter ablation of re-entrant drivers (RDs), some of which may contribute to arrhythmia perpetuation in persistent atrial fibrillation (PsAF). Patient-specific computational models derived from late gadolinium-enhanced magnetic resonance imaging (LGE-MRI) has the potential to non-invasively identify all areas of the fibrotic substrate where RDs could potentially be sustained, including locations where RDs may not manifest during mapped AF episodes. The objective of this study was to carry out multi-modal assessment of the arrhythmogenic propensity of the fibrotic substrate in PsAF patients by comparing locations of RD-harboring regions found in simulations and detected by FIRM (RDsim and RDFIRM) and analyze implications for ablation strategies predicated on targeting RDs. For 11 PsAF patients who underwent pre-procedure LGE-MRI and FIRM-guided ablation, we retrospectively simulated AF in individualized atrial models, with geometry and fibrosis distribution reconstructed from pre-ablation LGE-MRI scans, and identified RDsim sites. Regions harboring RDsim and RDFIRM were compared. RDsim were found in 38 atrial regions (median [inter-quartile range (IQR)] = 4 [3; 4] per model). RDFIRM were identified and subsequently ablated in 24 atrial regions (2 [1; 3] per patient), which was significantly fewer than the number of RDsim-harboring regions in corresponding models (p < 0.05). Computational modeling predicted RDsim in 20 of 24 (83%) atrial regions identified as RDFIRM-harboring during clinical mapping. In a large number of cases, we uncovered RDsim-harboring regions in which RDFIRM were never observed (18/22 regions that differed between the two modalities; 82%); we termed such cases "latent" RDsim sites. During follow-up (230 [180; 326] days), AF recurrence occurred in 7/11 (64%) individuals. Interestingly, latent RDsim sites were observed in all seven computational models corresponding to patients who experienced recurrent AF (2 [2; 2] per patient); in contrast, latent RDsim sites were only discovered in two of four patients who were free from AF during follow-up (0.5 [0; 1.5] per patient; p < 0.05 vs. patients with AF recurrence). We conclude that substrate-based ablation based on computational modeling could improve outcomes.

Feasibility of using patient-specific models and the "minimum cut" algorithm to predict optimal ablation targets for left atrial flutter.

BACKGROUND: Left atrial flutter (LAFL) occurs in patients after atrial fibrillation ablation. Identification of optimal ablation targets to terminate LAFL remains challenging. OBJECTIVE: The purpose of this study was to use patient-specific models to simulate LAFL and predict optimal ablation targets using a novel approach based on flow network theory. METHODS: Late gadolinium-enhanced cardiac magnetic resonance scans from 10 patients with LAFL were used to construct atrial models incorporating fibrosis by investigators blinded to procedural findings. Rapid pacing was applied in silico to induce LAFL. In each LAFL, we represented reentrant wave propagation as an electric flow network and identified the "minimum cut" (MC), which was the smallest amount of tissue that separated the flow into 2 discontinuous components. In silico ablation was applied at MCs, and targets were compared to those that terminated LAFL during catheter ablation. RESULTS: Patient-specific atrial models were successfully generated from patient scans. LAFL was induced in 7 of 10 models. Ablation of MCs terminated LAFL in 4 models and produced new, slower LAFL morphologies in the other 3. For the latter cases, flow analysis was repeated to identify MCs of emergent LAFLs. Ablation of these MCs terminated emergent LAFLs. The MC-based ablation lesions in simulations were similar in length and location to ablation targets that terminated LAFL during catheter ablation for these 7 patients. CONCLUSION: Personalized atrial simulations can predict ablation targets for LAFL. These simulations provide a powerful tool for planning ablation procedures and may reduce procedural times and complications.