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.
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.
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 The aim of the study was to define the epicardial substrate and ablation outcome in patients with left ventricular nonischemic cardiomyopathy (NICM) and suspected epicardial ventricular ...tachycardia (VT). Background Ventricular tachycardia in NICM often originates from the epicardium. Methods Twenty-two patients with NICM underwent detailed endocardial and epicardial bipolar voltage maps and VT ablation for suspected epicardial VT. Eight patients with normal hearts and idiopathic VT served to define normal epicardial electrograms. Low-voltage regions were also assessed for wide (>80 ms), split, or late electrograms. Results Normal epicardial bipolar voltage was identified as >1.0 mV on the basis of the reference population. Confluent low-voltage areas were present in 18 epicardial (82%) and 12 endocardial (54%) maps and were typically over basal lateral LV. In the 18 patients with epicardial VT on the basis of activation/pacemapping, the mean epicardial area was greater than the endocardial low-voltage area (55.3 ± 33.5 cm2 vs. 22.9 ± 32.4 cm2 , p < 0.01). Epicardial low-voltage areas showed 49.7% wide (>80 ms), split, and/or late electrograms rarely seen in the reference patients (2.3%). During follow-up of 18 ± 7 months, ablation resulted in VT elimination in 15 of 21 patients (71%) including 14 of 18 patients (78%) with epicardial VT. Conclusions In patients with NICM and VT of epicardial origin, the substrate is characterized by areas of basal LV epicardial > endocardial bipolar low voltage. The electrograms in these areas are not only small (<1.0 mV) but wide (>80 ms), split, and/or late, and help identify the substrate targeted for successful ablation.
Frequent ventricular premature depolarizations (VPDs) can cause reversible left ventricular (LV) dysfunction. However, not all patients normalize their LV function after VPD elimination.
To evaluate ...predictors of recovery of LV function following the elimination of frequent VPDs.
We identified patients with ≥10% VPDs/24 h and an LV ejection fraction of <50% who underwent successful ablation between 2007 and 2011. Subjects were classified as having reversible (≥10% increase to a final LV ejection fraction of ≥50%) or irreversible (≤10% increase or final LV ejection fraction <50%) LV dysfunction on the basis of echocardiographic follow-up. A reference group with ≥10% VPDs but normal LV function was identified.
One hundred fourteen patients with ≥10% VPDs were identified; 66 had preserved and 48 had impaired LV function. Over a median follow-up of 10.6 months, 24 of 48 were classified as reversible and 13 of 48 as irreversible and 11 of 44 were excluded. There was a gradient of VPD QRS duration between the control, reversible, and irreversible groups (mean VPD QRS 135, 158, and 173 ms, respectively; P < .001). This gradient persisted even for the same site of origin. In multivariate analysis, the only independent predictor of irreversible LV function was VPD QRS duration (odds ratio 5.07 95% confidence interval 1.22-21.01 per 10-ms increase).
In patients with LV dysfunction and frequent VPDs, we identified VPD QRS duration as the only independent predictor for the recovery of LV function after ablation. This suggests that VPD QRS duration may be a marker for the severity of underlying substrate abnormality.
Monomorphic ventricular premature depolarizations (VPDs) have been found to initiate ventricular fibrillation (VF) or polymorphic ventricular tachycardia (PMVT) in patients with and without ...structural heart disease.
The purpose of this study was to describe and characterize sites of origin of VPDs triggering VF and PMVT.
The distribution of mapping-confirmed VPDs, electrophysiology laboratory findings, and results of radiofrequency catheter ablation were analyzed.
Among 1132 consecutive patients who underwent ablation for ventricular arrhythmias, 30 patients (2.7%) with documented VF/PMVT initiation were identified. In 21 patients, VF/PMVT occurred in the setting of cardiomyopathy; in 9 patients, VF/PMVT was idiopathic. The origin of VPD trigger was from the Purkinje network in 9, papillary muscles in 8, left ventricular outflow tract in 9, and other low-voltage areas unrelated to Purkinje activity in 4. Each distinct anatomic area of origin was associated with VF/PMVT triggers in patients with and without heart disease. Acute VPD elimination was achieved in 26 patients (87%), with a decrease in VPDs in another 3 patients (97%). During median follow-up of 418 days (interquartile range IQR 144-866), 5 patients developed a VF/PMVT recurrence after a median of 34 days (IQR 1-259). Rare recurrence was noted in patients with and without structural disease and from each distinct anatomic origin. The total burden of VF/PMVT episodes/shocks was reduced from a median of 9 (IQR 2.5-22.5) in the 3 months before ablation to 0 (IQR 0-0, total range 0-2) during follow-up (P <.0001).
Catheter ablation of VPD-triggered VF/PMVT is highly successful. Left ventricular outflow tract and papillary muscles are common and are previously unrecognized sites of origin of these triggers in patients with and without structural heart disease.
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.
Outflow tract ventricular premature depolarizations (VPDs) can be associated with reversible left ventricular cardiomyopathy (LVCM). Limited data exist regarding the outcome after ablation of outflow ...tract VPDs from the LV and the impact of residual VPDs or preexisting LVCM prior to the diagnosis of VPDs on recovery of LV function.
To examine the safety, efficacy, and long-term effect of radiofrequency ablation on LV function in patients with LVCM and frequent outflow tract VPDs and examine the effect of ablation in patients with LVCM known to precede the onset of VPDs and the impact of residual VPD frequency on recovery of LV function.
Sixty-nine patients (43 men; age 51 ± 16 years) with nonischemic LVCM (left ventricular ejection fraction LVEF 35% ± 9%, left ventricular diastolic diameter LVDD 5.8 ± 0.7 cm) were referred for ablation of frequent outflow tract VPDs (29% ± 13%).
VPDs originated in the right ventricular outflow tract in 27 (39%) patients and the left ventricular outflow tract in 42 (61%) patients. After follow-up of 11 ± 6 months, 44 (66%) patients had rare (<2%) VPDs, 15 (22%) had decreased VPD burden (>80% reduction and always <5000 VPDs), and 8 (12%) had no clinical improvement with persistent (5 patients) or recurrent (3 patients) VPDs. Only patients with either rare or decreased VPD burden had a significant improvement in LVEF (ΔLVEF 14% ± 9% vs 13% ± 7% vs -3% ± 6%, respectively, P <.001) and LVDD (ΔLVDD -4 ± 5 vs -2 ± 4 vs 0 ± 4, respectively, P = .038), regardless of chamber of origin. The magnitude of LVEF improvement correlated with the decline in residual VPD burden (r = 0.475, P = .007). Patients with preexisting LVCM had a more modest but still significant improvement in LV function compared to patients without preexisting LVCM (ΔLVEF 8% vs 13%, P = .046). Multivariate analysis revealed ablation outcome, higher LVEF, and absence of preexisting LVCM were independently associated with LVEF improvement.
Frequent outflow tract VPDs are associated with LVCM regardless of ventricle of origin. Significant (>80%) reduction in VPD burden has comparable improvement in LV function to complete VPD elimination. Successful VPD ablation may be beneficial even in patients with preexisting LVCM.
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.
The substrate for ventricular tachycardia (VT) in nonischemic cardiomyopathy (NICM) has a predilection for the basolateral left ventricle with right bundle branch block VT morphology.
The purpose of ...this study was to describe a unique group of NICM patients with septal VT substrate.
Between 1999 and 2010, 31 (11.6%) of 266 patients with NICM undergoing VT ablation had septal substrate and no lateral involvement. Mean age was 59 ± 12 years, and ejection fraction was 30% ± 14%. Eight patients had heart block.
Cardiac magnetic resonance showed septal delayed enhancement in 8 of 9 patients. Electroanatomic mapping demonstrated bipolar low voltage (<1.5 mV) extending from the basal septum in 22 of 31 patients. The remaining 9 patients had normal endocardial bipolar voltage but abnormal unipolar septal voltage (<8.3 mV) consistent with intramural abnormalities. Epicardial mapping in 14 patients showed no scar in 9 and patchy basal left ventricular summit scar in 5. VTs were mapped to the septal substrate, with 62% having right bundle branch block morphology and V(2) precordial transition pattern break in 17% suggesting periseptal exit. After substrate and targeted VT ablation, no VT was inducible in 66% and no "clinical targeted" VT in 86%. Over a mean follow-up of 20 ± 28 months, VT recurred in 10 (32%) patients.
Isolated septal VT substrate is uncommon in NICM. Biventricular low-voltage zones extending from the basal septum are characteristic, but septal scarring can be entirely intramural as evidenced by unipolar/bipolar electrograms and imaging. Multiple unmappable morphologies are the rule, often requiring several procedures aggressively targeting the septal substrate to achieve moderate long-term VT control.
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