High-resolution mapping of reentrant atrial tachycardias: Relevance of low bipolar voltage.

BACKGROUND: Bipolar voltage is widely used to characterize the atrial substrate but has been poorly validated, particularly during clinical tachycardias. OBJECTIVE: The purpose of this study was to evaluate the diagnostic performance of voltage thresholds for identifying regions of slow conduction during reentrant atrial tachycardias (ATs). METHODS: Thirty bipolar voltage and activation maps created during reentrant ATs were analyzed to (1) examine the relationship between voltage amplitude and conduction velocity (CV), (2) measure the diagnostic ability of voltage thresholds to predict CV, and (3) identify determinants of AT circuit dimensions. Voltage amplitude was categorized as "normal" (>0.50 mV), "abnormal" (0.05-0.50 mV), or "scar" (<0.05 mV); slow conduction was defined as <30 cm/s. RESULTS: A total of 266,457 corresponding voltage and CV data points were included for analysis. Voltage and CV were moderately correlated (r = 0.407; P < .001). Bipolar voltage predicted regions of slow conduction with an area under the receiver operating characteristic curve of 0.733 (95% confidence interval 0.731-0.735). A threshold of 0.50 mV had 91% sensitivity and 35% specificity for identifying slow conduction, whereas 0.05 mV had 36% sensitivity and 87% specificity, with an optimal voltage threshold of 0.15 mV. Analyses restricted to the AT circuits identified weaker associations between voltage and CV and an optimal voltage threshold of 0.25 mV. CONCLUSION: Widely used bipolar voltage amplitude thresholds to define "abnormal" and "scar" tissue in the atria are, respectively, sensitive and specific for identifying regions of slow conduction during reentrant ATs. However, overall, the association of voltage with CV is modest. No clinical predictors of AT circuit dimensions were identified.

Effect of Activation Wavefront on Electrogram Characteristics During Ventricular Tachycardia Ablation.

Background Catheter ablation of ventricular tachycardia (VT) in structural heart disease is challenging because of noninducibility or hemodynamic compromise. Ablation often depends on elimination of local abnormal ventricular activities (LAVAs) but which may be hidden in far-field signal. We investigated whether altering activation wavefront affects activation timing and LAVA characterization and allows a better understanding of isthmus anatomy. Methods Patients with ischemic cardiomyopathy underwent mapping using the ultra-high density Rhythmia system (Boston Scientific). Maps were generated for all stable VTs and with pacing from the atrium, right ventricular apex, and an left ventricular branch of the coronary sinus. Results Fifty-six paced maps and 23 VT circuits were mapped in 22 patients. In 79% of activation maps, there was ≥1 line of block in the paced conduction wavefront, with 93% having fixed block and 32% showing functional partial block. Bipolar scar was larger with atrial than right ventricular (31.7±18.5 versus 27.6±16.3 cm2, P=0.003) or left ventricular pacing (31.7±18.5 versus 27.0±19.2 cm2, P=0.009); LAVA areas were smaller with atrial than right ventricular (12.3±10.5 versus 18.4±11.0 cm2, P<0.001) or left ventricular pacing (12.3±10.5 versus 17.1±10.7 cm2, P<0.001). LAVA areas were larger with wavefront propagation perpendicular versus parallel to the line of block along isthmus boundaries (19.3±7.1 versus 13.6±7.4 cm2, P=0.01). All patients had successful VT isthmus ablation. In 11±8 months follow-up, 2 patients had a recurrence. Conclusions Wavefronts of conduction slowing/block may aid identification of critical isthmuses in unmappable VTs. Altering the activation wavefront leads to significant differences in conduction properties of myocardial tissue, along with scar and LAVA characterization. In patients where few LAVAs are identified during substrate mapping, using an alternate activation wavefront running perpendicular to the VT isthmus may increase sensitivity to detect arrhythmogenic substrate and critical sites for reentry.

Cardiac Propagation Pattern Mapping With Vector Field for Helping Tachyarrhythmias Diagnosis With Clinical Tridimensional Electro-Anatomical Mapping Tools.

Ventricular (VT) and atrial (AT) tachycardias are some of the most common clinical cardiac arrhythmias. For ablation of tachycardia substrates, two clinical diagnosis methods are used: invasive electroanatomical mapping for an accurate diagnosis using electrograms (EGMs) acquired with intracardiac catheters, and localized on the surface mesh of the studied cavities; and noninvasive electrocardiographic imaging (ECGi) for a global view of the arrhythmia, with EGMs mathematically reconstructed from body surface electrocardiograms using 3-D cardio-thoracic surface meshes obtained from CT-scans. In clinics, VT and AT are diagnosed by studying activation time maps that depict the propagation of the activation wavefront on the cardiac mesh. Nevertheless, slow conduction areas-a well-known proarrhythmic feature for tachycardias-and tachycardia specific propagation patterns are not easily identifiable with these maps. Therefore, local characterization of the activation wavefront propagation can be helpful for improving VT and AT diagnoses. The purpose of this study is to develop a method to locally characterize the activation wavefront propagation for clinical data. For this, a conduction velocity vector field is estimated and analyzed using divergence and curl mathematical operators. The workflow was first validated on a simulated database from computer models, and then applied to a clinical database obtained from ECGi to improve AT diagnosis. The results show the relevancy and the efficacy of the proposed method to guide ablation of tachyarrhythmias.

Characterizing localized reentry with high-resolution mapping: Evidence for multiple slow conducting isthmuses within the circuit.

BACKGROUND: Reentrant circuits are considered to be critically dependent on a single protected slow conducting isthmus. OBJECTIVE: The purpose of this study was to investigate conduction properties and electrogram (EGM) characteristics of the entire circuit in localized atrial reentrant circuits using high-resolution mapping. METHODS: Fifteen localized reentrant atrial tachycardias were studied with high-resolution mapping (Rhythmia). EGMs along the entire circuit were analyzed offline for fractionation, duration, and amplitude. Maps were exported to MATLAB (MathWorks) to measure bipolar voltage and conduction velocities (CVs) within the circuit. Slow conduction was defined as <30 cm/s. RESULTS: Fifteen localized re-entrant circuits (12 left atrial, 3 right atrial) with mean cycle length 273 ± 40 ms were analyzed using high-resolution maps (22,389 ± 13,375 EGMs). A mean of 4.5 ± 1.6 slow conduction corridors were identified per circuit. Although the entire circuit was of low voltage, the bipolar voltage in slow conducting corridors was significantly lower than the rest of the circuit (0.22 ± 0.20 mV vs 0.50 ± 0.48 mV; P <.001). The mean conduction velocity of the circuit, excluding slow conduction areas, was 90.3 ± 34.3 cm/s vs 13.9 ± 3.5 cm/s (P <.001) in the slow conduction corridors. EGM analysis at the slowest conduction corridors demonstrated fractionation (100%) with longer EGM duration compared to the other slow conduction corridors along the circuit (99 ± 9 ms vs 74 ± 11 ms; P = .003). CONCLUSION: In contrast to current understanding, localized atrial reentrant circuits have multiple sequential "corridors" of very slow conduction (2-7) that contribute to maintenance of arrhythmia. The localized reentry occurs in low-voltage areas, with voltage further reduced in these multiple slow conducting corridors.

Characteristics of Scar-Related Ventricular Tachycardia Circuits Using Ultra-High-Density Mapping: A Multi-Center Study.

BACKGROUND: Ventricular tachycardia (VT) with structural heart disease is dependent on reentry within scar regions. We set out to assess the VT circuit in greater detail than has hitherto been possible, using ultra-high-density mapping. METHODS: All ultra-high-density mapping guided VT ablation cases from 6 high-volume European centers were assessed. Maps were analyzed offline to generate activation maps of tachycardia circuits. Topography, conduction velocity, and voltage of the VT circuit were analyzed in complete maps. RESULTS: Thirty-six tachycardias in 31 patients were identified, 29 male and 27 ischemic. VT circuits and isthmuses were complex, 11 were single loop and 25 double loop; 3 had 2 entrances, 5 had 2 exits, and 15 had dead ends of activation. Isthmuses were defined by barriers, which included anatomic obstacles, lines of complete block, and slow conduction (in 27/36 isthmuses). Median conduction velocity was 0.08 m/s in entrance zones, 0.29 m/s in isthmus regions ( P<0.001), and 0.11 m/s in exit regions ( P=0.002). Median local voltage in the isthmus was 0.12 mV during tachycardia and 0.06 mV in paced/sinus rhythm. Two circuits were identifiable in 5 patients. The median timing of activation was 16% of diastole in entrances, 47% in the mid isthmus, and 77% in exits. CONCLUSIONS: VT circuits identified were complex, some of them having multiple entrances, exits, and dead ends. The barriers to conduction in the isthmus seem to be partly functional in 75% of circuits. Conduction velocity in the VT isthmus slowed at isthmus entrances and exits when compared with the mid isthmus. Isthmus voltage is often higher in VT than in sinus or paced rhythms.

Localized Structural Alterations Underlying a Subset of Unexplained Sudden Cardiac Death.

BACKGROUND: Sudden cardiac death because of ventricular fibrillation (VF) is commonly unexplained in younger victims. Detailed electrophysiological mapping in such patients has not been reported. METHODS: We evaluated 24 patients (29±13 years) who survived idiopathic VF. First, we used multielectrode body surface recordings to identify the drivers maintaining VF. Then, we analyzed electrograms in the driver regions using endocardial and epicardial catheter mapping during sinus rhythm. Established electrogram criteria were used to identify the presence of structural alterations. RESULTS: VF occurred spontaneously in 3 patients and was induced in 16, whereas VF was noninducible in 5. VF mapping demonstrated reentrant and focal activities (87% versus 13%, respectively) in all. The activities were dominant in one ventricle in 9 patients, whereas they had biventricular distribution in others. During sinus rhythm areas of abnormal electrograms were identified in 15/24 patients (62.5%) revealing localized structural alterations: in the right ventricle in 11, the left ventricle in 1, and both in 3. They covered a limited surface (13±6 cm2) representing 5±3% of the total surface and were recorded predominantly on the epicardium. Seventy-six percent of these areas were colocated with VF drivers (P<0.001). In the 9 patients without structural alteration, we observed a high incidence of Purkinje triggers (7/9 versus 4/15, P=0.033). Catheter ablation resulted in arrhythmia-free outcome in 15/18 patients at 17±11 months follow-up. CONCLUSIONS: This study shows that localized structural alterations underlie a significant subset of previously unexplained sudden cardiac death. In the other subset, Purkinje electrical pathology seems as a dominant mechanism.