The relevance of focal triggers in persistent atrial fibrillation (PerAF) and long-standing persistent atrial fibrillation (LSPAF) has not been previously investigated.
We prospectively evaluated the ...prevalence and distribution of AF triggers in patients referred for catheter ablation of PerAF and LSPAF.
We analyzed consecutive patients undergoing first time AF ablation who underwent a standardized trigger protocol including cardioversion of induced or spontaneous AF and infusion of up to 20 μg of isoproterenol for 15-20 minutes either before or after pulmonary vein (PV) isolation accomplished. Triggers were defined as AF/sustained atrial tachyarrhythmia or repetitive atrial premature depolarizations.
A total of 2168 patients were included (mean age 57 ± 11 years; 1636 75% men), with 1531 patients having paroxysmal AF (PAF) (71%), 496 having PerAF (23%), and 141 having LSPAF (7%). PV triggers were found in 1398 patients with PAF (91%), 449 patients with PerAF (91%), and 129 patients with LSPAF (91%) (P = .856 for comparison across groups). Non-PV triggers were elicited in a total of 234 patients (11%), and the prevalence was similar across the different types of AF (PAF, 165 11%; PerAF, 54 11%; LSPAF, 15 11%; P = .996 for comparison across groups).
PVs are the main AF trigger site in patients with PerAF and LSPAF, with an overall prevalence similar to that found in patients with PAF. These results support the current recommendations for PV isolation as the cornerstone of catheter ablation to eliminate AF triggers in PerAF and LSPAF.
Frequent right ventricular (RV) pacing can lead to a decline in left ventricular ejection fraction (LVEF).
This study aimed to identify incidence and predictors of RV pacing-induced cardiomyopathy ...(PICM).
We retrospectively studied 1750 consecutive patients undergoing pacemaker implantation between 2003 and 2012. Patients were included if baseline LVEF was normal, single-chamber ventricular or dual-chamber pacemaker (but not implantable cardioverter-defibrillator or biventricular pacemaker) was implanted, frequent (≥20%) RV pacing was present, and repeat echocardiogram was available ≥1 year after implantation. PICM was defined as ≥10% decrease in LVEF, resulting in LVEF <50%. Patients with alternative causes of cardiomyopathy were excluded. Predictors of the development of PICM were identified using multivariate Cox proportional hazards modeling.
Of 257 patients meeting study criteria, 50 (19.5%) developed PICM, with a decrease in mean LVEF from 62.1% to 36.2% over a mean follow-up period of 3.3 years. Those who developed PICM were more likely to be men, with lower baseline LVEF and wider native QRS duration (bundle branch blocks excluded; P = .005, P = .03, and P = .001, respectively). In multivariate analysis, male gender (hazard ratio 2.15; 95% confidence interval 1.17-3.94; P = .01) and wider native QRS duration (hazard ratio 1.03 per 1 ms increase; 95% confidence interval 1.01-1.05; P < .001) were independently associated with the development of PICM. Native QRS duration >115 ms was 90% specific for the development of PICM.
PICM may be more common than previously reported, and risk for its occurrence begins below the commonly accepted threshold of 40% pacing burden. Men with wider native QRS duration (particularly >115 ms) are at increased risk. These patients warrant closer follow-up with a lower threshold for biventricular pacing.
The moderator band (MB) can be a source of premature ventricular contractions (PVCs), monomorphic ventricular tachycardia (VT), and idiopathic ventricular fibrillation (IVF).
The purpose of this ...study was to define the electrocardiographic (ECG) characteristics and procedural techniques to successfully identify and ablate MB PVCs/VT.
In 10 patients with left bundle branch block morphology PVCs/VT, electroanatomic mapping in conjunction with intracardiac echocardiography (ICE) localized the site of origin of the PVCs to the MB. Clinical characteristics of the patients, ECG features, and procedural data were collected and analyzed.
Seven patients presented with IVF and 3 presented with monomorphic VT. In all patients, the ventricular arrhythmias (VAs) had a left bundle branch block QRS with a late precordial transition (>V4), a rapid downstroke of the QRS in the precordial leads, and a left superior frontal plane axis. Mean QRS duration was 152.7 ± 15.2 ms. Six patients required a repeat procedure. After mean follow-up of 21.5 ± 11.6 months, all patients were free of sustained VAs, with only 1 patient requiring antiarrhythmic drug therapy and 1 patient having isolated PVCs no longer inducing VF. There were no procedural complications.
VAs originating from the MB have a distinctive morphology and often are associated with PVC-induced ventricular fibrillation. Catheter ablation can be safely performed and is facilitated by ICE imaging.
Treatment strategies to prevent ventricular tachycardia (VT) in patients with an implantable cardioverter-defibrillator (ICD) include antiarrhythmic drugs (AADs) and catheter ablation (CA).
The ...purpose of this study was to systematically compare the efficacy of AADs and CA for the prevention of VT in patients with ICDs.
Major databases were searched (October 2015) for randomized trials evaluating AADs or CA vs standard medical therapy to prevent VT in ICD patients. Primary outcome was the number of VT episodes leading to appropriate ICD interventions.
Eight trials (n = 2268, follow-up 15 ± 6 months) evaluated AADs, and 6 trials (n = 427, follow-up 14 ± 8 months) evaluated CA. A significant reduction in appropriate ICD interventions was found with both CA (odds ratio OR 0.45, 95% confidence interval CI 0.28-0.71, P = .001) and AADs (OR 0.66, 95% CI 0.44-0.97, P = .037), with no significant difference between the 2 treatment strategies. The benefit of AADs was driven by amiodarone and not confirmed with other AADs. A reduction of inappropriate ICD interventions was found with AADs (OR 0.30, P = .001) but not with CA. Both CA and AADs were not associated with decreased mortality over follow-up. Amiodarone appeared to increase the risk of death (OR 3.36, 95% CI 1.36-8.30, P = .009).
In patients with an ICD, both AADs (amiodarone) and CA reduce the risk of recurrent VT compared to control medical therapy, with no significant difference between the 2 treatments. AADs are also associated with a reduction of inappropriate ICD therapies. The significant reduction of recurrent VT episodes does not appear to result in a mortality benefit, with a potential for increased mortality with amiodarone.
Objectives The goal of this study was to determine the relationship of the ventricular tachycardia (VT) isthmus to channels of preserved voltage on an electroanatomic voltage map in postinfarction ...cardiomyopathy. Background Substrate mapping in patients with postinfarction cardiomyopathy and VT may involve lowering the voltage cutoff that defines the scar (<1.5 mV) to identify “channels” of relative higher voltage within the scar. However, the prevalence of channels within the scar identified by using electroanatomic mapping and the relationship to the protected VT isthmus identified by entrainment mapping is unknown. Methods Detailed bipolar endocardial voltage maps (398 ± 152 points) from 24 patients (mean age 69 ± 9 years) with postinfarction cardiomyopathy (ejection fraction 33 ± 9%) and tolerated VT were reviewed. Endocardial scar was defined according to voltage <1.5 mV. Isolated late potentials (ILPs) were identified and tagged on the electroanatomic voltage map. The baseline voltage cutoffs were then adjusted until all channels were identified. The VT isthmus was identified using entrainment mapping. Results Inferior and anterior/lateral infarction was present by voltage mapping in 18 and 6 patients, respectively (scar area 44 ± 24 cm2 ). By adjusting voltage cutoffs, 37 channels were identified in 21 (88%) of 24 patients. The presence of ILPs within a channel was seen in 11 (46%) of 24 patients and 17 (46%) of 37 channels. A VT isthmus site was contained within a channel in only 11 of 24 patients or 11 of 37 channels. No difference in voltage characteristics was identified between clinical and nonclinical channels. Voltage channels with ILPs harbored the clinical isthmus with a sensitivity and specificity of 78% and 85%, respectively. Conclusions Channels were identified in 88% of patients with VT by adjusting the voltage limits of bipolar maps; however, the specificity of those channels in predicting the location of VT isthmus sites was only 30%. The presence of ILPs inside the voltage channel significantly increases the specificity for identifying the clinical VT isthmus.
Early recurrence of atrial arrhythmia (ERAA) is common after atrial fibrillation (AF) ablation and is associated with long-term recurrence. However, the association between timing or frequency of ...ERAA and long-term ablation success remains unclear.
We aimed to examine whether timing or frequency of ERAA after pulmonary vein antral isolation (PVAI) affects long-term ablation success.
Three hundred AF patients (100 paroxysmal, 100 persistent, 100 long-standing persistent; mean age 59.5 ± 9.6 years, 79% male) undergoing PVAI were included. All patients underwent 30-day monitoring with mobile continuous outpatient telemetry after PVAI and were followed for >1 year. ERAA was defined as AF or organized atrial tachycardia (OAT) in the first 6 weeks, and was categorized as early (weeks 1-2), intermediate (weeks 3-4), or late (weeks 5-6). Long-term ablation success was defined as the absence of AF/OAT lasting >30 seconds off antiarrhythmic drugs 1 year after a single ablation (excluding first 6 weeks).
ERAA occurred in 169 patients (53%); of those, 79 (46.7%) had single ERAA and 90 (53.3%) had multiple ERAAs. ERAA occurred less commonly with paroxysmal versus persistent or long-standing persistent AF (46% vs 57% and 66%; P = .017). ERAA was associated with worse ablation success at 1 year (38.1% vs 79.5% no ERAA; P < .001). Multiple (vs single) ERAA more strongly predicted long-term ablation failure (OR: 4.5; 95% CI 2.3-8.8).
ERAA after PVAI is associated with decreased long-term ablation success. Patients experiencing multiple ERAA events are at greatest risk for long-term arrhythmia recurrence and represent a subgroup in whom early reablation may be considered.
Objectives The goal of this study was to evaluate the ability of noninvasive programmed stimulation (NIPS) after ventricular tachycardia (VT) ablation to identify patients at high risk of recurrence. ...Background Optimal endpoints for VT ablation are not well defined. Methods Of 200 consecutive patients with VT and structural heart disease undergoing ablation, 11 had clinical VT inducible at the end of ablation and 11 recurred spontaneously. Of the remaining 178 patients, 132 underwent NIPS through their implantable cardioverter-defibrillator 3.1 ± 2.1 days after ablation. At 2 drive cycle lengths, single, double, and triple right ventricular extrastimuli were delivered to refractoriness. Clinical VT was defined by comparison with 12-lead electrocardiograms and stored implantable cardioverter-defibrillator electrograms from spontaneous VT episodes. Patients were followed for 1 year. Results Fifty-nine patients (44.7%) had no VT inducible at NIPS; 49 (37.1%) had inducible nonclinical VT only; and 24 (18.2%) had inducible clinical VT. Patients with inducible clinical VT at NIPS had markedly decreased 1-year VT-free survival compared to those in whom no VT was inducible (<30% vs. >80%; p = 0.001), including 33% recurring with VT storm. Patients with inducible nonclinical VT only, had intermediate 1-year VT-free survival (65%). Conclusions When patients with VT and structural heart disease have no VT or nonclinical VT only inducible at the end of ablation or their condition is too unstable to undergo final programmed stimulation, NIPS should be considered in the following days to further define risk of recurrence. If clinical VT is inducible at NIPS, repeat ablation may be considered because recurrence over the following year is high.
Objectives This study sought to assess the value of left ventricular (LV) endocardial unipolar electroanatomical mapping (EAM) in identifying irreversibility of LV systolic dysfunction in patients ...with left ventricular nonischemic cardiomyopathy (LVCM). Background Identifying irreversibility of LVCM would be helpful but cannot be reliably accomplished by bipolar EAM or cardiac magnetic resonance identification of macroscopic scar. Methods Detailed endocardial LV EAM was performed in 3 groups: 1) 24 patients with irreversible LVCM (I-LVCM) but with no or minimal macroscopic scar (<15% LV surface) evidenced on bipolar voltage EAM and/or cardiac magnetic resonance; 2) 14 patients with reversible ventricular premature depolarization–mediated LVCM (R-LVCM); and 3) 17 patients with structurally normal hearts. LV endocardial unipolar electrogram amplitude and area of unipolar amplitude abnormality were defined after excluding macroscopic scar. Results Unipolar amplitude differed in the 3 groups: median of 7.6 (interquartile range IQR: 5.5 to 9.7) mV in I-LVCM group, 13.2 (IQR: 10.4 to 16.2) mV in R-LVCM group, and 16.3 (IQR: 13.6 to 19.8) mV in structurally normal hearts group (p < 0.001). Areas of unipolar abnormality represented a large proportion of total LV surface in I-LVCM, 64.7% (IQR: 47.5% to 75.9%) compared with R-LVCM, 5.2% (IQR: 0.0% to 19.1%) and structurally normal hearts, 0.1% (IQR: 0.0% to 0.9%), groups (p < 0.001). A unipolar abnormality area cutoff of 32% of total LV surface was 96% sensitive and 100% specific in identifying irreversible cardiomyopathy among patients with LV dysfunction (I-LVCM and R-LVCM), p < 0.001. Conclusions Detailed unipolar voltage mapping can identify irreversible myocardial dysfunction consistent with fibrosis, even in the absence of bipolar EAM or cardiac magnetic resonance abnormalities, and may serve as valuable prognostic tool in patients presenting with LVCM to facilitate clinical decision making.
Abstract Background In patients referred for radiofrequency catheter ablation (RFCA) of ventricular tachycardia (VT) in the setting of structural heart disease, early post-procedural mortality (EM) ...has not been previously investigated. Objectives The purpose of this study was to evaluate EM after catheter ablation of scar-related VT. Methods Associations between clinical and procedural variables and EM (within 31 days of the procedure) were tested in patients with structural heart disease undergoing RFCA of VT at 12 international centers. Results Of 2,061 patients (mean age 62 ± 13 years; left ventricular ejection fraction LVEF 34 ± 13%; 53% ischemic etiology), EM occurred in 100 (5%; 95% confidence interval CI: 4% to 6%). A total of 54 (3%) patients died before hospital discharge (median 9 days after the procedure; 25% for refractory VT), including 12 (0.6%) after a major procedure-related complication. In multivariable analysis, the following factors were found to be significantly associated with EM: LVEF (odds ratio OR per percent decrease: 1.12; 95% CI: 1.05 to 1.20; p < 0.001), chronic kidney disease (OR: 2.73; 95% CI: 1.10 to 6.80; p = 0.030), presentation with VT storm (OR: 3.61; 95% CI: 1.37 to 9.48; p = 0.009), and presence of unmappable VTs (OR: 5.69; 95% CI: 1.37 to 23.69; p = 0.017). Recurrent VT was also associated with an increased risk of subsequent death (hazard ratio: 7.19; 95% CI: 5.57 to 9.28; p < 0.001) and EM (hazard ratio: 11.45; 95% CI: 7.47 to 17.59; p < 0.001). Conclusions In a contemporary cohort of patients with scar-related VT undergoing RFCA, EM occurred in 5% of cases. Clinical and procedural variables indicating poorer clinical status (low LVEF, chronic kidney disease, VT storm, and unmappable VTs) and post-procedural VT recurrence may predict EM. Identification of such features may prompt early consideration for hemodynamic support or other care to help mitigate later potential complications.
Most postinfarct ventricular tachycardias (VTs) are sustained by a reentrant mechanism. The "protected isthmus" of the reentrant circuit is critical for the maintenance of VTs and the target for ...catheter ablation. Various techniques based on conventional electrophysiology and/or detailed three-dimensional (3D) reconstruction of the VT circuit are used to unmask this isthmus.
The purpose of this study was to assess pace-maps (PMs) to identify postinfarct VT isthmuses. We hypothesized that an abrupt change in paced QRS morphology may be used to identify a VT isthmus and be targeted for successful ablation.
High-density 3D PMs were matched to the subsequent 3D endocardial reentrant VT activation mapping in 10 patients (8 men; age 70.7 ± 10.8 years) who underwent successful postinfarct VT ablation. At each pacing site in a given patient, the 12-lead ECG recorded during pacing was compared to that of VT, with the resulting matching percentage (up to 100% for perfect matches) allocated to this point to generate color-coded PMs.
With respect to VT isthmuses, the best percentages of matching were found in the exit zones and isthmus exit part (89% ± 8% and 84% ± 7%, respectively) and the poorest adjacent to scar border in the outer entrance zones (23% ± 28%), in the entrance zones (39% ± 34%), and in the entrance part of the isthmus (32% ± 26%). The color-coded sequence (from the best to the poorest matching sites) on the PMs revealed figure-of-eight pictures matching the VT activation time maps and identifying VT isthmuses.
Pace-mapping is useful for unmasking VT isthmuses in patients with well-tolerated postinfarct endocardial reentrant VTs.
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