Search

Background: It is not clear if antiarrhythmic drug therapy (AAD) after catheter ablation (CA) of atrial fibrillation (AF) increases mortality.Objective: To determine whether there is an association between AAD therapy and mortality after CA of AF.Methods: There were 3624 consecutive patients with AF (mean age: 59 ± 11 years, women: 27%, paroxysmal AF: 58%). An AAD was used in 2253 patients (62%, AAD group) for a mean duration of 1.3 ± 0.8 years, during a mean follow-up of 6.7 ± 2.2 years after CA of AF. Using propensity score matching, with every 2 patients using an AAD matched to 1 patient who did not use AAD (NO-AAD group), Cox regression models were utilized to assess the association between AAD use (as a time-variable covariate) and all-cause mortality.Results: There were a total of 50 deaths (2.2%) in the AAD and 62 deaths (4.5%) in the NO-AAD groups, respectively (P = .02). At the time of death, 46 of 50 patients (92%) who died in the AAD cohort were still using an AAD (P = .21, compared to baseline use). On multivariate analysis, although the risk of death was not statistically significant between the AAD and NO-AAD cohorts, there was a trend towards mortality benefit with AAD therapy (hazard ratio [HR]: 0.66, 95% confidence interval [CI]: 0.43-1.00, P = .05), regardless of the rhythm or anticoagulation status.Conclusion: AAD use after CA of AF is not associated with an increased risk of mortality, suggesting that when carefully chosen and monitored, AADs appear to be safe after CA of AF. [ABSTRACT FROM AUTHOR]

Background: The role of cryoballoon ablation (CBA) for antral pulmonary vein isolation (APVI) has not been well established in persistent atrial fibrillation (PerAF). Isolation of the left atrial posterior wall (BOX) after APVI has been suggested to improve the efficacy of radiofrequency catheter ablation (RFA) in PerAF.Objective: The purpose of this study was to compare characteristics and clinical outcomes of APVI by CBA vs APVI + BOX by contact force-guided RFA (CF-RFA) in patients with PerAF.Methods: APVI was performed in 167 consecutive patients with PerAF (mean age 64 ± 9 years; left atrial diameter 46 ± 6 mm) using CBA (n = 90) or CF-RFA (n = 77). After APVI, a roofline was created in 33 of 90 patients (37%) in the CBA group and BOX was performed in all 77 patients in the CF-RFA group.Results: During 21 ± 10 months of follow-up after a single ablation procedure, 37 of 90 patients (41%) in the CBA group (APVI) and 39 of 77 (51%) in the CF-RFA group (APVI + BOX) remained in sinus rhythm without antiarrhythmic drugs (AADs) (P = .22). During repeat ablation, APVI + BOX using CF-RFA was performed in 20 of 90 patients (22%) and in 18 of 77 patients (23%) who initially underwent CBA or CF-RFA, respectively. At 19 ± 10 months after repeat ablation, sinus rhythm was maintained in 55 of 90 patients (61%) and 52 of 77 patients (68%) in the CBA and CF-RFA groups without AADs, respectively (P = .39).Conclusion: In PerAF, an initial approach of APVI by CBA or APVI + BOX by CF-RFA has a similar efficacy of 40%-50% without AADs. After repeat ablation for APVI + BOX by CF-RFA in ∼25%, sinus rhythm is maintained in 60%-70% of patients without AADs. [ABSTRACT FROM AUTHOR]

Background: There are no randomized controlled studies of the efficacy and safety of protamine to reverse anticoagulant effects of heparin after catheter ablation (CA) of atrial fibrillation (AF).Objective: The purpose of this study was to determine the efficacy and safety of protamine to expedite vascular hemostasis and ambulation after CA of AF.Methods: CA to eliminate AF (n = 139) or left atrial flutter (n = 11) was performed in 150 patients using radiofrequency catheter ablation (n = 112) or cryoballoon ablation (n = 38). CA was performed under uninterrupted anticoagulation with warfarin in 28 patients or after skipping a single dose of a novel oral anticoagulant in 122 patients who were randomized to receive protamine (n = 77) or to the control group (n = 73). Baseline and procedural characteristics were similar between the 2 groups. Hemostasis was achieved manually once the activated clotting time returned to preprocedural values.Results: The maximum activated clotting time during CA was 359 ± 31 and 359 ± 29 seconds in the protamine and control groups, respectively (P = .91). The time to hemostasis was 123 ± 95 minutes in the protamine group and 260 ± 70 minutes in the control group (P < .001). The time to ambulation was 316 ± 80 and 480 ± 92 minutes in the protamine and control groups, respectively (P < .001). There were no differences in the rates of major or minor vascular access complications or thromboembolic events (P > .05).Conclusion: Protamine expedites vascular hemostasis and time to ambulation by ∼3 hours after CA of AF without an increase in the risk of vascular or thromboembolic complications. [ABSTRACT FROM AUTHOR]

Background: The role of obstructive sleep apnea (OSA) on the response to cardiac resynchronization therapy (CRT) and all-cause mortality in patients with advanced heart failure (HF) is unknown.Objective: We assessed the association between OSA, response to CRT, and all-cause mortality in patients with HF.Methods: We analyzed records of 548 consecutive patients (mean age 65 ± 13 years; 216 (39%) women; mean follow-up period 76 ± 17 months) who received a CRT-defibrillator device from January 15, 2007 to March 30, 2016 at our tertiary care referral center.Results: A total of 180 patients (33%) had OSA. Fewer patients in the OSA group (109 [61%]) had improvement in left ventricular ejection fraction (EF) than did those in the non-OSA group (253 [69%]) (P = .001). A total of 144 patients (27%) died by the end of follow-up (OSA group: 61 [33%]; non-OSA group 83 [23%]; P < .001). OSA diagnosis was associated with a lower chance of improvement in EF (hazard ratio 0.71; 95% confidence interval 0.60-0.89) and a higher risk of all-cause mortality (hazard ratio 3.7; 95% confidence interval 2.5-6.8). This was true in continuous positive airway pressure-compliant patients and in patients with nonischemic cardiomyopathy. However, among patients with ischemic cardiomyopathy, the chance of improvement in EF and all-cause mortality was similar in patients with OSA and those without OSA.Conclusion: OSA is associated with a decreased response to CRT and an increase in all-cause mortality in patients with HF. The differential effect of OSA on CRT response in patients with ischemic cardiomyopathy and nonischemic cardiomyopathy needs further study. [ABSTRACT FROM AUTHOR]

Background: Frequent premature ventricular complexes (PVCs) have been associated with increased mortality. However, the optimal approach to the risk stratification of these patients is unclear.Objective: The purpose of this study was to prospectively assess the use of cardiac magnetic resonance imaging (MRI) and programmed ventricular stimulation to identify patients with PVCs undergoing radiofrequency ablation at risk for adverse long-term outcomes.Methods: A total of 321 consecutive patients (52 ± 15 years; 157 men [49%]; left ventricular ejection fraction 51% ± 12%) underwent PVC ablation between 2004 and 2015, preceded by cardiac MRI to assess for structural heart disease (SHD). Programmed stimulation was performed at the time of the ablation procedure. If ventricular tachycardia (VT) was induced in the presence of SHD, an implantable cardioverter-defibrillator (ICD) was implanted.Results: SHD was identified by MRI in 64 patients (20%), and sustained monomorphic VT was inducible in 15 patients (5%). Fourteen patients had both SHD and inducible VT, and received an ICD after the procedure. The primary endpoint of VT/ventricular fibrillation or death was met in 15 patients after a median 20 months of follow-up. The combination of SHD by MRI and VT inducibility conferred independently an increased risk of adverse outcome (multivariate hazard ratio 25.73, 95% confidence interval 6.74-98.20; P <.001).Conclusion: Preablation cardiac MRI and programmed stimulation can be useful for risk stratification in patients with frequent PVCs. Patients with inducible VT in the setting of SHD may benefit from ICD implantation after ablation regardless of left ventricular ejection fraction. [ABSTRACT FROM AUTHOR]

Background: Left atrial (LA) circumferential ablation has been reported to eliminate atrial fibrillation (AF). Whether an ablation without encirclement of the pulmonary veins (PVs) is as effective as LA circumferential ablation is not clear.Objectives: The purpose of this study was to compare the efficacy of LA circumferential ablation and nonencircling linear ablation in patients with chronic AF.Methods: Eighty patients with chronic AF were randomized to undergo LA circumferential ablation (n = 40) or nonencircling linear ablation (n = 40). In LA circumferential ablation, the PVs were encircled, with additional lines made in the mitral isthmus and posterior wall or roof. In nonencircling linear ablation, 4 +/- 1 ablation lines were created through areas of complex electrograms, with lines in the roof (38), anterior wall (36), septum (40), mitral isthmus (32), and posterior annulus (6). The endpoint of LA circumferential ablation and nonencircling linear ablation was voltage abatement.Results: LA flutter occurred in 15% after LA circumferential ablation and in 18% after nonencircling linear ablation (P = .8). A repeat ablation procedure was performed for recurrent AF in 7 and 11 patients or for atrial flutter in 6 and 4 patients after LA circumferential ablation and nonencircling linear ablation, respectively (P = .8). At 9 +/- 4 months, the prevalence of AF was 28% in the LA circumferential ablation and 25% in the nonencircling linear ablation group (P = .8). Sixty-eight percent and 60% of patients were in sinus rhythm and free of AF and atrial flutter in the absence of antiarrhythmic drug therapy after LA circumferential ablation and nonencircling linear ablation, respectively (P = .5). There were no complications.Conclusion: Nonencircling linear ablation and LA circumferential ablation are equally efficacious in eliminating chronic AF. However, the advantage of nonencircling linear ablation is that it eliminates the need for ablation along the posterior wall of the LA. Therefore, nonencircling linear ablation may avoid the small but real risk of atrioesophageal fistula formation associated with LA circumferential ablation. [ABSTRACT FROM AUTHOR]

Background: The effects of left atrial (LA) circumferential ablation on LA function in patients with atrial fibrillation (AF) have not been well described. Objectives: The purpose of this study was to determine the effect of LA circumferential ablation on LA function. Methods: Gated, multiphase, dynamic contrast-enhanced computed tomographic (CT) scans of the chest with three-dimensional reconstructions of the heart were used to calculate the LA ejection fraction (EF) in 36 patients with paroxysmal (n = 27) or chronic (n = 9) AF (mean age 55 +/- 11 years) and in 10 control subjects with no history of AF. Because CT scans had to be acquired during sinus rhythm, a CT scan was available both before and after (mean 5 +/- 1 months) LA circumferential ablation (LACA) in only 10 patients. A single CT scan was acquired in 8 patients before and in 18 patients after LACA ablation. Radiofrequency catheter ablation was performed using an 8-mm-tip catheter to encircle the pulmonary veins, with additional lines along the mitral isthmus and the roof. Results: In patients with paroxysmal AF, LA EF was lower after than before LACA (21% +/- 8% vs 32 +/- 13%, P = .003). LA EF after LA catheter ablation was similar among patients with paroxysmal AF and those with chronic AF (21% +/- 8% vs 23 +/- 13%, P = .7). However, LA EF after LA catheter ablation was lower in all patients with AF than in control subjects (21% +/- 10% vs 47% +/- 5%, P < .001). Conclusion: During medium-term follow-up, restoration of sinus rhythm by LACA results in partial return of LA function in patients with chronic AF. However, in patients with paroxysmal AF, LA catheter ablation results in decreased LA function. Whether the impairment in LA function is severe enough to predispose to LA thrombi despite elimination of AF remains to be determined. [ABSTRACT FROM AUTHOR]

Background: The coronary sinus (CS) and its branches may play a role in the genesis of various arrhythmias. Applications of radiofrequency energy within the CS may be necessary. Atrio-esophageal fistula has been recognized as a complication of ablation along the posterior left atrial wall. Objectives: The purpose of this study was to describe the in vivo topographic anatomy of the CS, esophagus, and coronary arteries using computed tomography (CT). Methods: Helical contrast CT of the heart with three-dimensional and endoscopic reconstructions was performed in 50 patients (28 men and 22 women; mean age 54 +/- 10 years). The images were reformatted to determine the relationships among the CS, adjacent blood vessels, and esophagus and to determine the nature and thickness of surrounding tissue layers. Results: Mean CS ostium diameter was 12 +/- 4 mm, and mean thickness of the periosteal fat layer was 3 +/- 2 mm. In 40 of the 50 patients (80%), the esophagus was adjacent to the CS, starting 24 +/- 9 mm from the ostium, and remained in contact for a mean length of 7 +/- 5 mm. Mean thickness of the fat layer between the esophagus and CS was 1 +/- 1 mm, and mean thickness of the anterior wall of the esophagus was 3 +/- 2 mm. In 10 patients (20%), there was no contact between the esophagus and CS. In 40 patients (80%), the right coronary artery was less than 5 mm from the CS (minimum distance 1 +/- 1 mm) over a mean length of 17 +/- 11 mm. In all patients, the circumflex artery was less than 5 mm from the CS (minimum distance 1 +/- 0.4 mm) over a mean length of 16 +/- 9 mm in patients with right-dominant coronary circulation and over a mean length of 86 +/- 11 mm in patients with left-dominant coronary circulation. Conclusion: The CS often lies very close to the esophagus and coronary arteries. During radiofrequency energy ablation in the CS, caution should be exercised to prevent injury to surrounding structures. [ABSTRACT FROM AUTHOR]

Objectives: The purpose of this study was to determine the prevalence and clinical significance of macroreentrant atrial tachycardia (AT) after left atrial (LA) circumferential ablation for atrial fibrillation (AF).Background: Linear ablation for AF may result in macroreentrant AT.Methods: Three hundred forty-nine patients (age 54 +/- 11 years) underwent LA circumferential ablation for AF (paroxysmal in 227). Ablation lines were created around the left-sided and right-sided pulmonary veins, with additional ablation lines in the posterior LA and mitral isthmus. If macroreentrant AT was observed acutely in the electrophysiology laboratory, it was not ablated. If an organized AT occurred during follow-up, the initial strategy was rate control. If AT persisted for > 3 to 4 months, catheter ablation was performed.Results: Seventy-one patients (20%) had spontaneous or induced macroreentrant AT (cycle length 244 +/- 31 ms) in the electrophysiology laboratory following LA circumferential ablation. During follow-up, 85 patients (24%) experienced spontaneous AT (cycle length 238 +/- 35 ms) at a mean of 44 +/- 62 days following LA circumferential ablation. Among the 71 patients with macroreentrant AT acutely following LA circumferential ablation, 39 (55%) developed AT during follow-up. Among the 85 patients with AT during follow-up, the tachycardia remitted without a repeat ablation procedure in 28 patients (33%), most commonly within 5 months. Twenty-eight of the 349 patients (8%) underwent a repeat ablation procedure for AT. The critical isthmus was localized to the mitral isthmus in 17 of 28 patients (61%).Conclusions: Macroreentrant AT is a common form of proarrhythmia after LA circumferential ablation for AF. Because it may resolve spontaneously, ablation of AT should be deferred for several months. [ABSTRACT FROM AUTHOR]

Objectives: The purpose of this study was to determine the effect of left atrial circumferential ablation on the size of the left atrium and pulmonary veins (PVs). Background: The long-term effects of left atrial circumferential ablation on left atrial and PV size and anatomy have not been analyzed in quantitative fashion. Methods: PV and left atrial sizes were analyzed in 41 consecutive patients (mean age 54 +/- 12 years) with paroxysmal (n = 25) or chronic (n = 16) atrial fibrillation. Computed tomography of the chest with three-dimensional reconstruction was performed before and 4 +/- 2 months after left atrial circumferential ablation. Left atrial circumferential ablation was performed to encircle the PVs 1 to 2 cm from the ostia, using a power output of 70 W. Additional ablation lines were created in the posterior left atrium and mitral isthmus. Radiofrequency energy also was delivered within the circles and at the PV ostia in 51% of patients at a reduced power output of 35 W. Results: At 6 months, 36 patients (88%) were in sinus rhythm without antiarrhythmic drug therapy, including 3 patients (7%) who developed persistent left atrial flutter and underwent subsequent successful ablation of atrial flutter. There was a 15 +/- 16% decrease in left atrial volume (P < .01) and 10 +/- 35% decrease in PV ostial area (P < .01), without focal narrowing, in patients with a successful outcome. Focal PV stenosis did not occur in any of the 41 patients. Conclusions: Maintenance of sinus rhythm after left atrial circumferential ablation is associated with reduced left atrial and PV ostial size. Left atrial circumferential ablation for atrial fibrillation does not cause PV stenosis. [ABSTRACT FROM AUTHOR]

Background Frequent idiopathic premature ventricular complexes (PVCs) can result in PVC-induced cardiomyopathy. Frequent PVCs can also aggravate ischemic cardiomyopathy. Objective The purpose of this study was to investigate the impact of frequent PVCs on nonischemic cardiomyopathy. Methods This was a consecutive series of 30 patients (mean age 59.1 ± 12.1; 18 men; mean ejection fraction [EF] 38% ± 15%) with structurally abnormal hearts based on the presence of scar on cardiac magnetic resonance imaging and/or a history of cardiomyopathy before the presence of frequent PVCs who were referred for ablation of frequent PVCs. Results Ablation was successful in 18 of 30 patients (60%), resulting in an increase of mean EF from 33.9% ± 14.5% to 45.7% ± 17% ( P < .0001) during mean follow-up of 30 ± 28 months. The PVC burden in these patients was reduced from 23.1% ± 8.8% to 1.0% ± 0.9% ( P < .0001). Mean EF did not change in patients with a failed ablation procedure (44.4 ± 16 vs 43.5 ± 21, P = .85). The PVC site of origin was in scar tissue in 14 of 18 patients with a successful ablation procedure. Mean New York Heart Association functional class improved from 2.3 ± 0.6 to 1.1 ± 0.2 ( P < .0001) in patients with a successful outcome and remained unchanged in patients with an unsuccessful outcome (1.9 ± 0.9 vs 1.9 ± 0.7, P = 1). Conclusion In patients with frequent PVCs and nonischemic cardiomyopathy, EF and functional class can be improved but not always normalized by successful PVC ablation. In most patients with an effective ablation, the arrhythmogenic substrate was located in scar tissue. [ABSTRACT FROM AUTHOR]

Background Atrial fibrillation (AF) is associated with a significant increase in the risk of stroke and mortality. It is unclear whether maintaining sinus rhythm (SR) after radiofrequency ablation (RFA) is associated with an improvement in stroke risk and survival. Objective The purpose of this study was to determine whether SR after RFA of AF is associated with an improvement in the risk of cerebrovascular events (CVEs) and mortality during an extended 10-year follow-up. Methods RFA was performed in 3058 patients (age 58 ± 10 years) with paroxysmal (n = 1888) or persistent AF (n = 1170). The effects of time-dependent rhythm status on CVEs and cardiac and all-cause mortality were assessed using multivariable Cox models adjusted for baseline and time-dependent variables during 11,347 patient-years of follow-up. Results Independent predictors of a higher arrhythmia burden after RFA were age (estimated beta coefficient [β] = 0.017 per 10 years, 95% confidence interval [CI] 0.006-0.029, P = .003), left atrial (LA) diameter (β = 0.044 per 5-mm increase in LA diameter, 95% CI 0.034-0.055, P <.0001), and persistent AF (β = 0.174, 95% CI 0.147-0.201, P <.0001). CVEs and cardiac and all-cause mortality occurred in 71 (2.3%), 33 (1.1%), and 111 (3.6%), respectively. SR after RFA was associated with a significantly lower risk of cardiac mortality (hazard ratio [HR] 0.41, 95% CI 0.20-0.84, P = .015). There was not a significant reduction in all-cause mortality (HR 0.86, 95% CI 0.58-1.29, P = .48) or CVEs (HR 0.79, 95% CI 0.48-1.29, P = .34) in patients who remained in SR after RFA. Conclusion Maintenance of SR after RFA is associated with a reduction in cardiovascular mortality in patients with AF. [ABSTRACT FROM AUTHOR]

Background: The prevalence and clinical consequences of coronary arterial injury in a large series of patients undergoing radiofrequency ablation (RFA) of atrial fibrillation (AF) are unknown. Objective: The purpose of this study was to describe the frequency and clinical consequences of coronary arterial injury in a large series of patients undergoing catheter ablation of AF and postablation atrial tachycardia. Methods: The medical records of 5,709 consecutive patients undergoing RFA of AF were reviewed. Heart specimens were also dissected to analyze the course of the coronary arteries. Results: Arterial injury occurred in 8 patients (0.14%). Three patients developed ventricular fibrillation (VF) due to occlusion of the distal or proximal circumflex (Cx) artery related to RFA in the distal coronary sinus (CS) or base of the LA appendage, respectively. Two VF patients underwent stenting. Five patients developed acute sinus node (SN) dysfunction. In 4/5 patients, the culprit site was subjacent to the SN artery (per computed tomography) coursing over the anterior LA (n = 3) or the septal RA (n = 1). Two patients required a permanent pacemaker. In the heart specimens, the SN artery, after its origin from the proximal Cx artery, coursed along the anterior LA. Also, the proximal Cx artery was found in the atrioventricular groove underneath the base of the LA appendage. Conclusion: Clinically apparent injury to the coronary arteries during LA ablation for AF is rare. However, it may be associated with potentially life-threatening ventricular arrhythmias and acute SN dysfunction requiring permanent pacing. The culprit sites seem to be in the distal coronary sinus and the anterior LA, and correlate well with the course of the coronary arteries in pathologic specimens. Vigilance and low-power settings are important in minimizing the risk of arterial injury. [Copyright &y& Elsevier]

Background: The right ventricular outflow tract (RVOT) is the most common site of origin of ventricular arrhythmias (VAs) in patients with idiopathic VAs. A left bundle branch block, inferior axis morphology arrhythmia is the hallmark of RVOT arrhythmias. VAs from other sites of origin can mimic RVOT VAs, and ablation in the RVOT typically fails for these VAs. Objective: To analyze reasons for failed ablations of RVOT-like VAs. Methods: Among a consecutive series of 197 patients with an RVOT-like electrocardiographic (ECG) morphology who were referred for ablation, 38 patients (13 men; age 46 ± 14 years; left ventricular ejection fraction 47% ± 14%) in whom a prior procedure failed within the RVOT underwent a second ablation procedure. ECG characteristics of the VA were compared to a consecutive series of 50 patients with RVOT VAs. Results: The origin of the VA was identified in 95% of the patients. In 28 of 38 (74%) patients, the arrhythmia origin was not in the RVOT. The VA originated from intramural sites (n = 8, 21%), the pulmonary arteries (n = 7, 18%), the aortic cusps (n = 6, 16%), and the epicardium (n = 5, 13%). The origin was within the RVOT in 10 (26%) patients. In 2 (5%) patients, the origin could not be identified despite biventricular, aortic, and epicardial mapping. The VA was eliminated in 34 of 38 (89%) patients with repeat procedures. The ECG features of patients with failed RVOT-like arrhythmias were different from the characteristics of RVOT arrhythmias. Conclusions: In patients in whom ablation of a VA with an RVOT-like appearance fails, mapping of the pulmonary artery, the aortic cusps, the epicardium, the left ventricular outflow tract, and the aortic cusps will help identify the correct site of origin. The 12-lead ECG is helpful in differentiating these VAs from RVOT VAs. [Copyright &y& Elsevier]

Abstract: Objectives: To determine whether risk for implantable cardioverter-defibrillator (ICD) therapy varies by body mass index (BMI) in systolic heart failure (HF). Background: It is unknown whether obesity increases sudden death risk in patients with systolic HF. Methods: Secondary analysis of patients with HF, left ventricular ejection fraction ≤0.40 and ICD (N = 464) was performed using Cox regression modeling to assess risk for first delivered ICD therapy, with patients grouped by BMI (kg/m2): normal (18.5 to <25), overweight (25 to <30), and obese (≥30). Results: Overweight patients, compared with patients with normal BMI, had greater adjusted risk for first ICD therapy (HR 1.66; 95% CI 1.02–2.71; P = 0.04), whereas obese BMI was not associated with risk for first ICD therapy. Conclusions: There was an inverted U-shaped relationship between BMI and risk for first ICD therapy among systolic HF patients, with highest risk in overweight BMI. [Copyright &y& Elsevier]

Background: Most infarct-related ventricular tachycardias (VTs) have an exit site that can be targeted by endocardial ablation. However, some VT reentry circuits have an exit site that is intramural or epicardial. Even these circuits may have an endocardial component that can be endocardially ablated. Objective: To assess the prevalence of postinfarction VTs with a nonendocardial exit site that can be successfully eliminated by endocardial ablation. Methods: Twenty-eight consecutive patients with postinfarction VT (27 men, age 69±8 years, ejection fraction 0.25%±0.15%) were referred for VT ablation. A total of 213 VTs were inducible (cycle length 378±100 ms). Pace mapping was performed throughout the scar, and critical sites were identified for 137 VTs (64.5%). Critical sites identified by entrainment mapping and/or pace mapping were divided into exit and nonexit sites depending on the stimulus-QRS/VT cycle length ratio (S-QRS/VT CL≤0.3 vs>0.3). Results: Endocardial exit sites (S-QRS/VTCL≤0.3) were identified for 100 of 137 VTs. Only critical nonexit sites were identified for 37 of 137 (27%) VTs. Nonexit sites were confined to a smaller area within the endocardium (1.81±1.7 cm2) and were located within dense scar (0.28±0.24 mV) further away from the border zone (2.05±2.79 cm) than did the VT exit sites. Exit sites had a larger area of matching pace maps (3.86±1.9 cm2; P<.01) and were at a closer distance to the border zone (0.93±1.06 cm; P<.01). A total of 133 of 137 VTs were ablated. The success rate was similar for VTs in which exit sites were targeted (n = 90 of 100) and VTs in which only nonexit sites were targeted (n = 36 of 37) (P = .83). Conclusions: In about one-third of postinfarction VTs for which critical sites were identified, the exit site was not endocardial. Critical nonexit sites that are effective for ablation are often within dense scar at a distance from the border zone and can be missed if only the border zone is targeted. [Copyright &y& Elsevier]

Background: It is not clear whether dabigatran is as safe and effective as uninterrupted anticoagulation with warfarin during radiofrequency catheter ablation (RFA) of atrial fibrillation (AF). Objective: To compare the safety and efficacy of dabigatran by using a novel administration protocol and uninterrupted anticoagulation with warfarin for periprocedural anticoagulation in patients undergoing RFA of AF. Methods: In this case-control analysis, 763 consecutive patients (mean age 61±10 years) underwent RFA of AF using dabigatran (N = 191) or uninterrupted warfarin (N = 572) for periprocedural anticoagulation. In all patients, anticoagulation was started≥4 weeks before RFA. Dabigatran was held after the morning dose on the day before the procedure and resumed 4 hours after vascular hemostasis was achieved. Results: A transesophageal echocardiogram performed in all patients receiving dabigatran did not demonstrate an intracardiac thrombus. There were no thromboembolic complications in either group. The prevalence of major (4 of 191, 2.1%) and minor (5 of 191, 2.6%) bleeding complications in the dabigatran group were similar to those in the warfarin group (12 of 572, 2.1%; P = 1.0 and 19 of 572, 3.3%; P = .8, respectively). Pericardial tamponade occurred in 2 of 191 (1%) patients in the dabigatran group and in 7 of 572 (1.2%) patients in the warfarin group (P = 1.0). All patients who had a pericardial tamponade, including 2 in the dabigatran group, had uneventful recovery after perdicardiocentesis. On multivariate analysis, international normalized ratio (odds ratio [OR] 4.0; 95% confidence interval [CI] 1.1–15.0; P = .04), clopidogrel use (OR 4.2; 95% CI 1.5–12.3; P = .01), and CHA2DS2-VASc score (OR 1.4; 95% CI 1.1–1.8; P = .01) were the independent risk factors of bleeding complications only in the warfarin group. Conclusions: When held for approximately 24 hours before the procedure and resumed 4 hours after vascular hemostasis, dabigatran appears to be as safe and effective as uninterrupted warfarin for periprocedural anticoagulation in patients undergoing RFA of AF. [Copyright &y& Elsevier]

Background: While macroreentrant atrial tachycardias (ATs) have been reasonably well described, little is known about small reentrant circuits. Objective: To compare characteristics of large and small reentrant circuits after ablation of persistent atrial fibrillation. Methods: Seventy-seven patients (age 61±10 years; left atrium 46±6 mm; ejection fraction 0.52±0.13) underwent a procedure for postablation AT. The p-wave duration, circuit size, electrogram characteristics, and conduction velocity were determined. Results: AT was due to macroreentry in 62 (80%) patients, a small reentrant circuit in 13 (17%), and a focal mechanism in 2 (3%). The p-wave duration during small reentrant ATs was shorter than that during macroreentry (174±12 ms vs 226±22 ms; P<.0001). The duration of fractionated electrograms at the critical site was longer in small vs large circuits (167±43 ms vs 98±38 ms, respectively; P<.0001) and accounted for a greater percentage of the tachycardia cycle length (59%±18% vs 38%±14%, respectively; P<.0001). The mean diameters of macroreentrant and small reentrant circuits were 44±7 and 26±11 mm, respectively (P<.0001). The mean conduction velocity along the small circuits was lower (0.5±0.2 m/s vs 1.2±0.3 m/s; P<.0001). Catheter ablation eliminated the AT in all 77 patients. Conclusions: AT due to a small reentrant circuit after ablation of atrial fibrillation may be distinguished from macroreentry by a shorter p-wave duration and the presence of long-duration electrograms at the critical site owing to extremely slow conduction. These features may aid the clinician in the mapping of postablation ATs. [ABSTRACT FROM AUTHOR]

Background: Patients with frequent premature ventricular complexes (PVCs) and PVC-induced cardiomyopathy usually have recovery of left ventricular (LV) dysfunction postablation. The time course of recovery of LV function has not been described. Objective: To describe the time course and predictors of recovery from LV dysfunction after effective ablation of PVCs in patients with PVC-induced cardiomyopathy. Methods: In a consecutive series of 264 patients with frequent idiopathic PVCs referred for PVC ablation, LV dysfunction was present in 87 patients (mean ejection fraction 40%±10%). The PVC burden was reduced to<20% of the initial PVC burden in 75 patients. In these patients, echocardiography was repeated 3–4 months postablation. If LV function did not normalize after 3–4 months, a repeat echocardiogram was performed every 3 months until there was normalization or stabilization of LV function. Results: The ejection fraction normalized at a mean of 5±6 months postablation. The majority of patients (51 of 75, 68%) with PVC-induced LV dysfunction had a recovery of LV function within 4 months. In 24 (32%) patients, recovery of LV function took more than 4 months (mean 12±9 months; range 5–45 months). An epicardial origin of PVCs was more often present (13 of 24, 54%) in patients with delayed recovery of LV function than in patients with early recovery of LV function (2 of 51, 4%; P<.0001). The PVC-QRS width was significantly longer in patients with delayed recovery than in patients with recovery within 4 months (170±21 ms vs 159±16 ms; P = .02). In multivariate analysis, only an epicardial PVC origin was predictive of delayed recovery of LV function in patients with PVC-induced cardiomyopathy. Conclusions: PVC-induced cardiomyopathy resolves within 4 months of successful ablation in most patients. In about one-third of the patients, recovery is delayed and can take up to 45 months. An epicardial origin predicts delayed recovery of LV function. [Copyright &y& Elsevier]

BACKGROUND: Radiation therapy’s (RT’s) effects on cardiac implantable electronic devices (CIEDs) such as implantable cardioverter-defibrillators (ICDs) and pacemakers (PMs) are not well established, leading to device removal or relocation in preparation for RT. OBJECTIVE: To determine the effect of scattered RT on CIED performance. METHODS: We analyzed 69 patients—50 (72%) with PMs and 19 (28%) with ICDs—receiving RT at the University of Michigan. Collected data included device model, anatomic location, and treatment beam energies, treatment type, and estimated dose to the device. Patients were treated with either high-energy (16-MV) and/or low-energy (6 MV) photon beams with or without electron beams (6–16 MeV). The devices were interrogated with pre- and post-RT and/or weekly with either in-treatment or home interrogation, depending on the patient’s dependence on the device and the estimated or measured delivered dose. Outcomes analyzed were inappropriate ICD therapies, device malfunctions, or device-related clinical events. RESULTS: The PMs were exposed to 84.4±99.7 cGy of radiation, and the ICDs were exposed to 92.1±72.6 cGy of radiation. Two patients with ICDs experienced a partial reset of the ICD with the loss of historic diagnostic data after receiving 123 and 4 cGy, respectively. No device malfunction or premature battery depletion was observed at 6-month follow-up from RT completion. CONCLUSIONS: CIED malfunction due to indirect RT exposure is uncommon. Regular in-treatment or home interrogation should be done to detect and treat these events and to ensure that diagnostic data are preserved. [Copyright &y& Elsevier]

Background: Patients with frequent premature ventricular complexes (PVCs) are at risk of developing reversible PVC-induced cardiomyopathy (rPVC-CMP). Not all determinants of rPVC-CMP are known. Objective: To assess the impact of the QRS duration of PVCs on the development of rPVC-CMP. Methods: In a consecutive series of 294 patients with frequent idiopathic PVCs referred for PVC ablation, the width of the PVC-QRS complex was assessed. The QRS width was correlated with the presence of rPVC-CMP. Results: The PVC-QRS width was significantly greater in patients with rPVC-CMP than in patients without rPVC-CMP (164 ± 20 ms vs 149 ± 17 ms; P < .0001). The site of origin of the PVC had an impact on the PVC-QRS width, with epicardial PVCs having the broadest QRS complexes. Patients with PVCs originating from the right ventricular outflow tract or the fascicles had the narrowest QRS complexes. After adjusting for PVC burden, symptom duration, and PVC site of origin, PVC-QRS width and an epicardial PVC origin were independently associated with rPVC-CMP. Based on receiver operator characteristics analysis, a QRS duration of >150 ms best differentiated patients with and without rPVC-CMP (area under the curve 0.66; sensitivity 80%; specificity 52%). The PVC burden for developing rPVC-CMP is significantly lower in patients with a PVC-QRS width of ≥150 ms than in patients with a narrower PVC-QRS complex (22% ± 13% vs 28% ± 12%; P < .0001). Conclusion: Broader PVCs and an epicardial PVC origin are associated with the development of rPVC-CMP independent of the PVC burden. [Copyright &y& Elsevier]

Background: Postinfarction ventricular tachycardia (VT) typically involves the left ventricular endocardium. Right ventricular involvement in the arrhythmogenic substrate of postinfarction VT is considered unusual. Objective: To assess the role of right ventricular mapping and ablation in patients with prior septal myocardial infarction. Methods: From among 37 consecutive patients with recurrent postinfarction VT, 18 patients with evidence of left ventricular septal involvement of myocardial infarction were identified; these patients were the subjects of this report. In these 18 patients, 166 VTs (cycle length 372 ± 117 ms) were induced. Right ventricular voltage mapping was performed in all 18 patients with left ventricular septal myocardial infarction. Results: Right ventricular voltage mapping showed areas of low voltage in 11 patients; pace mapping from these areas revealed matching pace maps for 17 VTs, and radiofrequency ablation from the right ventricular endocardium but not the left ventricular endocardium eliminated 14 of 17 VTs. VTs with critical components in the right ventricle had a left bundle branch block morphology that had similar characteristics as left bundle branch block VTs with critical areas involving the left ventricular septum. Patients with right ventricular VT breakthrough sites had a lower ejection fraction than did patients without VT breaking out on the right ventricular septum (18% ± 5% vs 33% ± 15%; P = .01). Conclusions: Right ventricular mapping and ablation may be necessary in order to eliminate all inducible VTs in patients with postinfarction VT. More than half the patients with septal myocardial infarction have right ventricular septal areas that are critical for postinfarction VT and that cannot be eliminated by left ventricular ablation alone. [ABSTRACT FROM AUTHOR]

Post-infarction arrhythmias are most often confined to scar tissue. Scar can be detected by delayed-enhanced cardiac magnetic resonance. The purpose of this study was to assess the feasibility of pre-procedural scar identification and intraprocedural real-time image registration with an electroanatomical map in 23 patients with previous infarction and ventricular arrhythmias (VAs). Registration accuracy and cardiac magnetic resonance/electroanatomical map correlations were assessed, and critical areas for VA were correlated with the presence of scar. With a positional registration error of 3.8 ± 0.8 mm, 86% of low-voltage points of the electroanatomical map projected onto the registered scar. The delayed-enhanced cardiac magnetic resonance–defined scar correlated with the area of low voltage (R = 0.82, p < 0.001). All sites critical to VAs projected on the registered scar. Selective identification and extraction of delayed-enhanced cardiac magnetic resonance defined scar followed by registration into a real-time mapping system are feasible and help to identify and display the arrhythmogenic substrate in post-infarction patients with VAs. [Copyright &y& Elsevier]

Background: Frequent idiopathic premature ventricular complexes (PVCs) can result in a reversible form of cardiomyopathy. In this study, the determinants of PVC-induced left ventricular (LV) dysfunction were assessed. Methods: The subjects of this study were 241 consecutive patients (115 men [48%], mean age 48 ± 14 years) referred for ablation of frequent PVCs. One hundred eighty patients (75%) experienced palpitations and 61 (25%) did not. The PVC burden was determined by 24-hour Holter monitoring, and echocardiograms were performed to assess LV function. An LV ejection fraction of <50% was considered abnormal. Results: LV ejection fraction (mean 0.36 ± 0.09) was present in 76 of 241 patients (32%). There was a higher prevalence of males among the patients with PVC cardiomyopathy compared to patients with normal LV function (51/76 [67%] vs 64/165 [39%]; P <.0001). The mean PVC burden was significantly higher in patients with PVC cardiomyopathy than in patients with normal LV function (28% ± 12% vs 15% ± 13%; P <.0001). Among symptomatic patients, those with cardiomyopathy had a significantly longer duration of palpitations (135 ± 118 months) compared with patients with normal LV function (35 ± 52 months; P <.0001). The proportion of asymptomatic patients was significantly higher in the presence of cardiomyopathy (36/76, 47%) than in normal LV function (25/165, 15%; P <.0001). Symptom duration of 30 to 60 months, symptom duration >60 months, the absence of symptoms, and the PVC burden in asymptomatic patients were independent predictors of impaired LV function (adjusted odds ratio [95% confidence interval]: 4.0 [1.1-14.4], 20.1 [6.3-64.1], 13.1 [4.1-37.8], and 2.1 [1.2-3.6], respectively). Conclusions: The duration of palpitations and the absence of symptoms are independently associated with PVC-induced cardiomyopathy. [ABSTRACT FROM AUTHOR]

Background: Frequent idiopathic premature ventricular complexes (PVCs) can result in a reversible form of cardiomyopathy. In this study, the determinants of PVC-induced left ventricular (LV) dysfunction were assessed. Methods: The subjects of this study were 241 consecutive patients (115 men [48%], mean age 48 ± 14 years) referred for ablation of frequent PVCs. One hundred eighty patients (75%) experienced palpitations and 61 (25%) did not. The PVC burden was determined by 24-hour Holter monitoring, and echocardiograms were performed to assess LV function. An LV ejection fraction of <50% was considered abnormal. Results: LV ejection fraction (mean 0.36 ± 0.09) was present in 76 of 241 patients (32%). There was a higher prevalence of males among the patients with PVC cardiomyopathy compared to patients with normal LV function (51/76 [67%] vs 64/165 [39%]; P <.0001). The mean PVC burden was significantly higher in patients with PVC cardiomyopathy than in patients with normal LV function (28% ± 12% vs 15% ± 13%; P <.0001). Among symptomatic patients, those with cardiomyopathy had a significantly longer duration of palpitations (135 ± 118 months) compared with patients with normal LV function (35 ± 52 months; P <.0001). The proportion of asymptomatic patients was significantly higher in the presence of cardiomyopathy (36/76, 47%) than in normal LV function (25/165, 15%; P <.0001). Symptom duration of 30 to 60 months, symptom duration >60 months, the absence of symptoms, and the PVC burden in asymptomatic patients were independent predictors of impaired LV function (adjusted odds ratio [95% confidence interval]: 4.0 [1.1–14.4], 20.1 [6.3–64.1], 13.1 [4.1–37.8], and 2.1 [1.2–3.6], respectively). Conclusions: The duration of palpitations and the absence of symptoms are independently associated with PVC-induced cardiomyopathy. [ABSTRACT FROM AUTHOR]

Background: Idiopathic epicardial ventricular arrhythmias can be targeted from the coronary venous system or the pericardial space, the endocardium, or the aortic sinus cusps. Objective: The purpose of this study was to analyze systematically the contribution of ablation at sites other than the epicardium to eliminate an arrhythmia originating in the epicardium. Methods: In a consecutive patient series of 33 patients (14 women, age 51 ± 14 years, ejection fraction 51% ± 9%) with epicardial ventricular arrhythmias, mapping and ablation was performed via the cardiac venous system/pericardial space, the aortic sinus cusp, and the left ventricular endocardium. An arrhythmia was defined as epicardial if the earliest onset of activation and a matching pace-map (≥10/12 leads) were identified in the epicardium. Results: In 12/33 patients (36%), either an endocardial approach alone (n = 3) or a combined endocardial/epicardial (n = 6), cusp/endocardial (n = 1), or cusp/epicardial (n = 2) approach was required to eliminate the ventricular arrhythmias. In 10 of 33 patients (30%), epicardial ablation alone was effective in eliminating epicardial ventricular arrhythmias. Ablation was ineffective due to failure to reach the site of origin with the ablation catheter in 5 of 33 patients (15%), the site of origin was too close to an epicardial artery or the phrenic nerve in 3 patients (6%), and power delivery was insufficient in 3 patients (9%). Conclusion: About one-third of epicardial arrhythmias require ablation from sites other than the epicardium to eliminate the arrhythmia focus. [ABSTRACT FROM AUTHOR]

Background: Frequent premature ventricular complexes (PVCs) can cause cardiomyopathy. The mechanism is not known and may be multifactorial. Objective: This study assessed the role of PVC interpolation in PVC-induced cardiomyopathy. Methods: In 51 consecutive patients (14 women, age 49 ± 15 years, ejection fraction (EF) 0.49 ± 0.14) with frequent PVCs, 24-hour Holter recordings were performed. The amount of interpolation was determined and correlated with the presence of PVC-induced cardiomyopathy. In addition, parameters measured during an electrophysiology study were correlated with the Holter findings. Results: Fourteen of the 21 patients (67%) with cardiomyopathy had interpolated PVCs, compared with only 6 of 30 patients (20%) without PVC-induced cardiomyopathy (P <.001). Patients with interpolated PVCs had a higher PVC burden than patients without interpolation (28% ± 12% vs. 15% ± 15%; P = .002). The burden of interpolated PVCs correlated with the presence of PVC cardiomyopathy (21% ± 30% vs. 4% ± 13%; P = .008). Both PVC burden and interpolation independently predicted PVC-induced cardiomyopathy (odds ratio 1.07, 95% confidence interval 1.01 to 1.13, P = .02; and odds ratio 4.43, 95% confidence interval 1.06 to 18.48, P = .04, respectively). The presence of ventriculoatrial block at a ventricular pacing cycle length of 600 ms correlated with the presence of interpolation (P = .004). Patients with interpolation had a longer mean ventriculoatrial block cycle length than patients without interpolated PVCs (520 ± 110 ms vs. 394 ± 92 ms; P = .01). Conclusion: The presence of interpolated PVCs was predictive of the presence of PVC cardiomyopathy. Interpolation may play an important role in the generation of PVC-induced cardiomyopathy. [ABSTRACT FROM AUTHOR]

Background: Ventricular tachycardia (VT) in patients with idiopathic dilated cardiomyopathy often originates from the basal left ventricular myocardium and also can originate from the conduction system. The basal left ventricular myocardium reaches to the base of the aortic sinus cusps. Objective: The purpose of this study was to assess the prevalence of VT originating from the aortic sinus cusps in patients with idiopathic dilated cardiomyopathy. Methods: Thirty-three consecutive patients with nonischemic cardiomyopathy (24 men, age: 59 ± 11 years, ejection fraction: 29% ± 14%) were referred for ablation. Results: VTs originating from the aortic sinus cusps were identified in 8 of 33 patients (24%). The presence of low voltage in the basal left ventricle correlated with the inducibility of aortic sinus cusp VTs. All but 1 aortic sinus cusp VTs were effectively ablated. In 1 patient, the site of origin of the VT was <10 mm from the ostium of the left main coronary artery and ablation was not attempted. Conclusion: In patients with idiopathic dilated cardiomyopathy, VT often originates from the aortic sinus cusps. The large majority of these VTs can be successfully ablated. [ABSTRACT FROM AUTHOR]

Background: Atrial stretch is thought to play a role in the development of atrial fibrillation (AF). However, the precise mechanism by which stretch contributes to AF maintenance in humans is unknown. Objective: The purpose of this study was to determine the impact of left atrial (LA) pressure on AF frequency in patients undergoing catheter ablation of AF. Methods: The subjects of this study were 58 consecutive patients with persistent AF (n = 40) or paroxysmal AF (n = 18) undergoing LA ablation. LA pressure was measured before ablation. Both atria and the coronary sinus were mapped, and regional dominant frequency (DF) was determined. Results: Mean LA pressure in the persistent AF group was significantly higher than in the paroxysmal AF group (18 ± 5 vs 10 ± 4 mmHg, P <.0001). Mean DF in the persistent AF group was also higher than in the paroxysmal AF group (6.36 ± 0.51 Hz and 5.83 ± 0.54 Hz, P = .0006). In patients with persistent AF, there was a significant correlation between LA pressure and DF at the LA appendage (r = 0.55, P = .0002). DFmax was found at the LA appendage region in 24 (60%) of the 40 patients with persistent AF (P = .0006). In multivariate analysis, LA pressure was the only independent predictor of DFmax in the LA appendage (P = .04, odds ratio 1.41, 95% confidence interval 1.02–1.94). Conclusion: Higher LA pressure in patients with persistent AF implies that these patients are more vulnerable to stretch-related remodeling than are patients with paroxysmal AF. The DF of AF was directly related to LA pressure in patients with persistent AF. This finding suggests that atrial stretch may contribute to the maintenance of AF in humans by stabilizing high-frequency sources. [ABSTRACT FROM AUTHOR]

Background: Structural factors contributing to the development of postinfarction ventricular tachycardia (VT) are unclear. The purpose of this study was to analyze infarct architecture and electrogram characteristics in patients with and without inducible VT and to identify correlates of postinfarction VT.Methods and Results: Twenty-four postinfarction patients (median age, 64 [53, 70] years) were referred for radiofrequency catheter ablation of VT (n = 12) or frequent symptomatic premature ventricular contractions (PVCs) (n = 12). Delayed-enhanced (DE) MRI was obtained before ablation. Electroanatomical mapping was performed and scar area and electrogram characteristics of the scar tissue compared in patients with and without inducible VT. The median ejection fraction in patients with and without inducible VT was 27% (22%, 43%) and 43% (40%, 47%), respectively (P = 0.085). Subendocardial infarct area determined by DE-MRI was larger in patients with inducible VT (43 [38, 62] cm(2)) than in those with noninducible VT (8 [4, 11] cm(2); P = 0.002), and unipolar and bipolar voltages on electroanatomical maps were significantly lower in patients with inducible VT (both P<0.05). An infarct volume of >14% identified 11 of 12 patients with inducible VT (area under the curve, 0.94; P = 0.007). On electroanatomical mapping, distinct sites with isolated potentials (IPs) were more prevalent in patients with inducible VT than in those without (13.2% versus 1.1% of points within scar; P < 0.001). The number of inducible VTs correlated with the number of distinct sites with IPs (R = 0.87; P<0.0001).Conclusions: Scar tissue in postinfarction patients with inducible VT shows quantitative and qualitative differences from scars in patients without inducible VT. Scar size and IPs are correlated with VT inducibility. [ABSTRACT FROM AUTHOR]

Background: Ablation of arrhythmias arising from the papillary muscles (PAPs) is challenging. Objective: The purpose of this study was to assess the predictors of successful catheter ablation in patients with ventricular arrhythmias arising from the PAPs. Methods: Forty consecutive patients (15 women, mean age 51 ± 14 years, left ventricular ejection fraction 0.46 ± 0.13) with refractory PAP arrhythmias underwent mapping and ablation. Catheter stability was assessed with intracardiac echocardiography. Activation mapping and/or pace mapping were performed to identify the site of origin. Electrophysiological data and anatomic characteristics were assessed in patients with effective versus ineffective ablation. Catheter stability was assessed with intracardiac echocardiography. Results: Radiofrequency ablation was acutely effective in eliminating the targeted arrhythmia in 31 patients (78%). The presence of Purkinje potentials at the site of origin of the targeted arrhythmia was associated with an effective outcome (48% vs. 0%; P = .01). The mass of the arrhythmogenic PAPs in the left ventricle was significantly larger in patients with failed versus effective ablation (4.7 ± 2.2 g vs. 2.3 ± 0.6 g; P < .0001). Also, the presence of a matching pace map at the earliest endocardial activation time was associated with an effective procedure (71% vs. 22%; P = .02) Conclusion: The presence of Purkinje potentials at the site of origin and a smaller size of the PAP are associated with successful ablation of PAP arrhythmias. [ABSTRACT FROM AUTHOR]

Background: Frequent idiopathic premature ventricular complexes (PVCs) can result in a reversible form of left ventricular dysfunction. The factors resulting in impaired left ventricular function are unclear. Whether a critical burden of PVCs can result in cardiomyopathy has not been determined. Objective: The objective of this study was to determine a cutoff PVC burden that can result in PVC-induced cardiomyopathy. Methods: In a consecutive group of 174 patients referred for ablation of frequent idiopathic PVCs, the PVC burden was determined by 24-hour Holter monitoring, and transthoracic echocardiograms were used to assess left ventricular function. Receiver-operator characteristic curves were constructed based on the PVC burden and on the presence or absence of reversible left ventricular dysfunction to determine a cutoff PVC burden that is associated with left ventricular dysfunction. Results: A reduced left ventricular ejection fraction (mean 0.37 ± 0.10) was present in 57 of 174 patients (33%). Patients with a decreased ejection fraction had a mean PVC burden of 33% ± 13% as compared with those with normal left ventricular function 13% ± 12% (P <.0001). A PVC burden of >24% best separated the patient population with impaired as compared with preserved left ventricular function (sensitivity 79%, specificity 78%, area under curve 0.89) The lowest PVC burden resulting in a reversible cardiomyopathy was 10%. In multivariate analysis, PVC burden (hazard ratio 1.12, 95% confidence interval 1.08 to 1.16; P <.01) was independently associated with PVC-induced cardiomyopathy. Conclusion: A PVC burden of >24% was independently associated with PVC-induced cardiomyopathy. [Copyright &y& Elsevier]

Background: Premature ventricular complexes (PVCs) and ventricular tachycardia (VT) with origin in the left ventricular papillary muscle have recently been described. There are no prior studies describing the characteristics of the ventricular arrhythmias (VAs) arising from the right ventricular papillary muscles (RV PAPs). Methods: Among 169 consecutive patients who underwent a catheter ablation of a VA, eight patients with RV PAPs were identified (seven men, mean PVC burden 17.0% ± 20%). A control group consisted of 10 consecutive patients with arrhythmias originating from the right ventricle (10 women, mean PVC burden 13.9% ± 12.8%). All patients underwent cardiac magnetic resonance imaging (MRI). Intracardiac echocardiography was used to identify the site of origin of the RV PAP arrhythmias. The site of origin of a total of 15 distinct PAP arrhythmias was mapped to the following papillary muscles: posterior (n = 3), anterior (n = 4), or septal (n = 8). Results: Postablation echocardiograms did not reveal new tricuspid regurgitation. During a mean follow-up of 8 ± 9 months, there were no adverse outcomes. The PVC burden was reduced from 17% ± 20% preablation to 0.6% ± 0.8% postablation in the RV PAP group and from 13.9% ± 12.8% to 0.3% ± 0.4% in the control group. The QRS complex was broader in the RV PAP group compared with in the control group (163 ± 21 ms vs. 141 ± 22 ms; P = .02). RV PAP arrhythmias originating from the posterior or anterior RV PAPs more often had a superior axis with late R-wave transition (>V4) compared with septal RV RAP arrhythmias, which more often had an inferior axis with an earlier R-wave transition in the precordial leads (≤V4; P <.05). Conclusion: PVCs and VT may originate in the RV PAPs. Radiofrequency ablation is effective in eliminating these arrhythmias. [Copyright &y& Elsevier]

Background: Termination of persistent atrial fibrillation (AF) by radiofrequency ablation (RFA) is associated with a high probability of freedom from AF but requires extensive ablation and long procedure times. Objective: The purpose of this study was to determine whether a critical decrease in the dominant frequency (DF) of AF is a sufficient endpoint for RFA of persistent AF. Methods: Antral pulmonary vein isolation (APVI) followed by RFA of complex fractionated atrial electrograms (CFAEs) in the atria and coronary sinus was performed in 100 consecutive patients with persistent AF. The DF of AF in lead V1 and in the coronary sinus was determined by fast Fourier transform (FFT) analysis at baseline and before termination of AF to identify a critical decrease in DF predictive of sinus rhythm after RFA. Results: A ≥11% decrease in DF had the highest accuracy in predicting freedom from atrial arrhythmias, with a sensitivity of 0.71 and a specificity of 0.82 (P <.001). At a mean follow-up of 14 ± 3 months after one ablation procedure, sinus rhythm was maintained off antiarrhythmic drugs in 8/35 (23%) and 20/26 (77%) of patients with a <11% and ≥11% decrease in DF, respectively (P <.001). Sinus rhythm was maintained in 24/39 patients (62%) in whom RFA terminated AF. The duration of RFA and total procedure time were longer in patients with AF termination (95 ± 23 and 358 ± 87 minutes) than in patients with a <11% decrease in the DF (77 ± 16 and 293 ± 70 minutes) or ≥11% decrease in DF (80 ± 17 and 289 ± 73 minutes), respectively (P <.01). Among the variables of age, gender, left atrial diameter, duration of AF, left ventricular ejection fraction, duration of RFA, a ≥11% decrease in DF, and termination of AF, a ≥11% decrease in DF (odds ratio = 9.89, 95% confidence interval [CI] 2.84–34.47) and termination during RFA (OR = 4.38, 95% CI 1.50–12.80) were the only independent predictors of freedom from recurrent atrial arrhythmias. Conclusion: In a retrospective analysis of consecutive patients with persistent AF, a decrease in the DF of AF by 11% in response to APVI and ablation of CFAEs was associated with a probability of maintaining sinus rhythm that was similar to that when RFA terminates AF. [Copyright &y& Elsevier]

Objectives: To identify and characterize ablation lesions after radiofrequency (RF) catheter ablation of ventricular arrhythmias in patients without prior myocardial infarction and to correlate the ablation lesions with the amount of RF energy delivered and the clinical outcome. Background: Visualization of RF energy lesions after ablation of ventricular arrhythmias might help to identify reasons for ablation failure. Methods: In a consecutive series of 35 patients (19 women, age: 48 ± 15 years, ejection fraction: 0.56 ± 0.12) without structural heart disease who were referred for ablation of ventricular arrhythmias, cardiac magnetic resonance imaging with delayed enhancement was performed before and after ablation. Ablation lesions were sought in the post-ablation cardiac magnetic resonance images. The endocardial area, depth, and volume of the lesions were measured. Lesion size was correlated with the type of ablation catheter used and the duration of RF energy delivered. Results: In 25 of 35 patients (71%), ablation lesions were identified by delayed enhancement a mean of 22 ± 12 months after the initial ablation procedure. The mean lesion volume was 1.4 ± 1.4 cm3, with a mean endocardial area of 3.5 ± 3.0 cm2. The largest lesions (mean volume of 2.9 ± 2.1 cm3 with an endocardial area of 6.4 ± 3.4 cm2) were identified in patients in whom the arrhythmias originated in the papillary muscles. Ablation duration correlated with lesion size (r = 0.67, p < 0.001). There was no difference in lesion volume with irrigated versus nonirrigated ablation catheters (1.0 ± 0.73 vs. 2.0 ± 2.1 cm3, p = 0.09). Identification of ablation lesions in patients with a failed procedure identified the sites where ineffective RF energy lesions were created. Conclusions: RF ablation lesions can be detected long term after an ablation procedure targeting ventricular arrhythmias in patients without previous infarction. Lesion size correlates with the amount of RF energy delivered and is largest when a targeted arrhythmia originates in a papillary muscle. [Copyright &y& Elsevier]

Background: Inappropriate implantable cardioverter-defibrillator (ICD) therapy of atrial tachycardia (AT) with 1:1 atrioventricular (AV) conduction is common because it is difficult to discriminate from ventricular tachycardia (VT) with 1:1 retrograde conduction. Tachycardia cycle length (CL) variability and the relationship between atrial and ventricular CLs may be useful in discriminating AT from VT with 1:1 retrograde conduction. Objective: The purpose of this study was to evaluate the usefulness of the relationship between the atrial and ventricular CLs in differentiating AT with 1:1 conduction from VT with 1:1 retrograde conduction. Methods: We studied 71 patients who had a tachycardia with a 1:1 AV relationship and significant CL variability. Thirty-nine patients had AT (21 inducible and 18 simulated), and 32 patients had VT (11 inducible and 21 simulated). The relationship between atrial and ventricular CLs was examined. Results: A change in atrial CL predicted the change in subsequent ventricular CL in 37 (95%) of 39 patients with AT and in none of the patients with VT. A change in preceding ventricular CL predicted the change in atrial CL in 31 (97%) of 32 patients with VT and in only one (3%) of 39 patients with AT. The sensitivity, specificity, and positive and negative predictive values of a change in atrial CL predicting the change in ventricular CL for AT with significant CL variability were 95%, 100%, 100%, and 94%, respectively. The corresponding values for the change in preceding ventricular CL predicting the change in atrial CL for AT with significant CL variability were 97%. Conclusion: The relationship between atrial and ventricular CL is useful in differentiating AT from VT with retrograde conduction. A change in atrial CL that predicts the change in subsequent ventricular CL rules in AT and excludes VT. [Copyright &y& Elsevier]

Background: Left atrial appendage (LAA) isolation is rare and may be associated with impaired transport function and thromboembolism. Objective: The purpose of this study was to determine the mechanisms of inadvertent isolation of the LAA during atrial fibrillation (AF) ablation. Methods: This study consisted of 11 patients (ejection fraction 0.43 ± 0.18, left atrial diameter 51 ± 8 mm) with persistent AF who had LAA conduction block during a procedure for AF (n = 8) or atrial tachycardia (AT) (n = 3). Results: LAA conduction block occurred during ablation at the Bachmann bundle region in 6 patients, mitral isthmus in 3, LAA base in 2, and coronary sinus in 1. The mean distance from the ablation site to the LAA base was 5.0 ± 1.9 cm. LAA isolation was transient in all 6 patients in whom LAA conduction was monitored and was permanent in the 4 patients in whom conduction was not monitored during energy delivery. The remaining patient was noted to have LAA isolation during a redo procedure before any ablation. Nine of (82%) the 11 patients have remained arrhythmia-free without antiarrhythmic drugs at mean follow-up of 6 ± 7 months, and all have continued taking warfarin. Conclusion: Electrical isolation of the LAA may occur during ablation of persistent AF and AT even when the ablation site is remote from the LAA. This likely is due to disruption of the Bachmann bundle and its leftward extension, which courses along the anterior left atrium and bifurcates to surround the LAA. Monitoring of LAA conduction during ablation of persistent AF or AT is important in avoiding permanent LAA isolation. [Copyright &y& Elsevier]

Background: Frequent idiopathic premature ventricular complexes (PVC) are associated with a reversible form of cardiomyopathy. The effect of frequent PVCs on left ventricular function has not been evaluated in post-infarction patients. Objective: This study sought to evaluate the value of post-infarction PVC ablation and possible determinants of a reversible cardiomyopathy. Methods: Thirty consecutive patients (24 men, age 61 ± 12, left ventricular ejection fraction [LVEF] 0.36 ± 0.12) with remote myocardial infarction referred for implantable cardioverter-defibrillator (ICD) implantation for primary prevention of sudden death or for management of symptomatic ventricular tachycardia or PVCs were evaluated. Fifteen patients with a high PVC burden (≥5% of all QRS complexes on 24-h Holter monitor) underwent mapping and ablation of PVCs before ICD implantation. The remaining 15 patients served as a control group. LVEF was assessed by echocardiography, and scar burden was assessed by cardiac magnetic resonance imaging with delayed enhancement (DE-MRI) in both groups. Results: PVC ablation was successful in 15 of 15 patients and reduced the mean PVC burden from 22 ± 12% to 2.6 ± 5.0% (P <.001). After the procedure, LVEF increased significantly from 0.38 ± 0.11 to 0.51 ± 0.09 in the PVC ablation group (P = .0001). In the control group, LVEF remained unchanged within the same time frame (0.34 ± 0.14 vs. 0.33 ± 0.15; P = .6). Patients with frequent PVCs had a significantly smaller scar burden by DE-MRI compared with control patients. Five of the patients with frequent PVCs underwent ICD implantation. Conclusion: Post-infarction patients with frequent PVCs may have a reversible form of cardiomyopathy. DE-MRI may identify patients in whom the LVEF may improve after ablation of frequent PVCs. [Copyright &y& Elsevier]

Background: Delayed enhanced magnetic resonance imaging (DE-MRI) can be used for the exact assessment of myocardial infarct scar. Electroanatomic (EA) mapping can identify the subendocardial extension of infarcts and is used to identify and eliminate areas critical for postinfarction ventricular arrhythmias. Objectives: The purpose of this study was to correlate DE-MRI with EA mapping in postinfarction patients with ventricular arrhythmias to assess myocardial infarct architecture and its relationship to postinfarction ventricular arrhythmias. Methods: EA mapping during sinus rhythm was performed in 14 postinfarction patients (10 men; age 64 ± 10 years; ejection fraction 0.33 ± 0.12) referred for ablation of ventricular arrhythmias. All patients underwent prior DE-MRI. Both DE-MRI and EA mapping data were registered in three-dimensional space. Presence of scar and its transmurality as well as scar core versus gray zone were assessed on DE-MRI and correlated with EA maps; furthermore, the electrogram characteristics of the EA map were correlated with the DE-MRI. Results: Scar areas as assessed by bipolar and unipolar voltages in the EA map both correlated well with the scar as defined by DE-MRI. The best cutoff value to differentiate subendocardial scar from normal myocardium was 1.0 mV for bipolar voltage and 5.8 mV for unipolar voltage. Areas with DE had distinct electrophysiologic characteristics compared with nonenhancing sites. All identified sites that were critical for postinfarction ventricular tachycardia (31/31) and premature ventricular complexes (5/5) were located within areas of DE, with most (71%) being located in the core area of the scar. Conclusions: DE-MRI can accurately predict the EA characteristics of corresponding subendocardial locations. Critical sites of postinfarction arrhythmias were confined to areas of DE. The scar information on MRI can be selectively imported into an EA mapping system to facilitate the mapping and ablation procedure. [Copyright &y& Elsevier]

Background: Left atrial (LA) ablation of atrial fibrillation (AF) may rarely be complicated by an atrio-esophageal fistula. Objective: The purpose of this study was to determine the feasibility of mechanical displacement of the esophagus in patients undergoing LA ablation. Methods: Twelve patients underwent mechanical displacement of the esophagus performed by an endoscopist during an LA ablation procedure under conscious sedation. Results: The intrinsic course of the esophagus was near the left pulmonary veins (PVs) in 6 patients, the right PVs in 5 patients, and the mid-LA in 1 patient. In 10 (83%) of the 12 patients, the esophagus could be displaced with the endoscope. The maximal displacement toward the left-sided and right-sided PVs was 2.4 and 2.1 cm, respectively. In 2 (22%) of the 9 patients in whom a prior procedure was unsuccessful because of an unfavorable esophageal course, the esophagus remained at the same location to which it was displaced after removal of the endoscope, facilitating energy delivery at the target site. In the remaining 7 patients, the esophagus returned to its original location after the endoscope was removed. There were no complications related to the endoscopic procedure. Conclusion: The esophagus can be mechanically displaced with an endoscope during an LA ablation procedure under conscious sedation. However, in most patients, the esophagus assumes its original course after removal of the endoscope. In some patients in whom PV isolation is problematic because of an unfavorable esophageal course, endoscopic displacement may facilitate safe energy delivery over the posterior LA. [Copyright &y& Elsevier]

Background: During catheter ablation of complex fractionated atrial electrograms, persistent atrial fibrillation (AF) may convert to an atrial tachycardia (AT). Objective: The purpose of this study was to investigate the possible mechanisms of AT by examining the spectral and electrophysiologic characteristics of AF and ATs that occur after catheter ablation of AF. Methods: The subjects of this study were 33 consecutive patients with persistent AF who had conversion of AF to AT during ablation of AF (group I) and 20 consecutive patients who underwent ablation of persistent AT that developed more than 1 month after AF ablation (group II). Spectral analysis of the coronary sinus (CS) electrograms and lead V1 was performed during AF at baseline, before conversion, and during AT. The spatial relationship between the AT mechanism and ablation sites was examined. Results: A spectral component with a frequency that matched the frequency of AT was present in the baseline periodogram of AF more often in group I (52%) than in group II (20%, P = .02). Ablation resulted in a decrease in the dominant frequency of AF but not in the frequency of the spectral component that matched the AT. There was a significant direct relationship between the baseline dominant frequency of AF and the frequency of AT in the CS in group I (r = 0.76, P <.0001) but not in group II (r = 0.38, P = .09). ATs were macroreentrant in 64% and 60% of patients in groups I and II, respectively (P = .8). The AT site was more likely to be distant (>1 cm) from AF ablation sites in group I (70%) than in group II (35%, P = .007). Conclusion: The findings of this study suggest that ATs observed during ablation of AF often may be drivers of AF that become manifest after elimination of higher-frequency sources and fibrillatory conduction. [Copyright &y& Elsevier]

Background: Pace mapping is used to identify critical areas for postinfarction ventricular tachycardia (VT). Unexcitable scar during pacing with standard output can identify borders of the reentry circuit. Unexcitable scar is not thought to contain surviving muscle fibers critical to the circuit. Due to current-to-load mismatch or a deep seated isthmus, higher power might be required in order to obtain capture. Objective: The purpose of this study was to evaluate the value of high-output pacing in patients with postinfarction VT. Methods: In a consecutive series of 18 patients (15 men, age 62 ± 9, EF 0.29 ± 0.15) with postinfarction VT, a voltage map was obtained and bipolar pace mapping was performed in areas with low voltage (<1.5 mV) at an output of 10 mA and 2 ms pulse width (PW). High-output capture was defined as capture that failed at these settings but succeeded at higher pacing output. The pacing output was increased to 20 mA at 2 ms, and the PW was increased to 10 ms as required to achieve capture. Results: Seventy-seven VTs were induced. Thirty-nine isthmus sites were identified. Focal areas with high-output capture were observed in 12/18 patients (output: 20 mA; mean PW: 7.3 ± 3.5 ms). In 9/18 patients, this area was critical for the reentry circuit of 10 clinical VTs (23% of isthmus sites). In one third of patients, isthmus sites were identified only by high-output pacing. Conclusion: High-output pacing can be helpful in identifying critical areas of postinfarction VT that otherwise may be missed. [Copyright &y& Elsevier]

Background: The papillary muscles (PAP) have been implicated in arrhythmogenesis, largely based on theoretical considerations and experimental studies. Few clinical studies have described papillary muscle arrhythmias. Objective: This study sought to describe ventricular arrhythmias arising from the left ventricular PAPs in a consecutive series of patients without prior myocardial infarction and to compare these arrhythmias with fascicular arrhythmias. Methods: Nine of 122 consecutive patients (7%) presenting with symptomatic premature ventricular complexes (PVCs) or nonsustained ventricular tachycardia (VT) were found to have a site of origin in the anterolateral or posteromedial left ventricular PAP. Their mean age was 57 ± 9 years, and the mean ejection fraction was 0.49 ± 13. Four of 9 patients had idiopathic cardiomyopathy. The PAP involvement was established by intracardiac echocardiography. Eight of the 122 patients (6.5%) had idiopathic VT originating in the left anterior or posterior fascicle, and these patients served as a control group. Results: Compared with patients with fascicular arrhythmias, the QRS width was significantly greater in patients with PAP arrhythmias (150 ± 15 ms vs. 127 ± 11 ms; P = .001). Presystolic Purkinje potentials were identified at all effective ablation sites for fascicular arrhythmias, but in arrhythmias originating from PAPs, more distal Purkinje potentials often were recorded from the Purkinje–myocardial interface located at the PAP. All arrhythmias originating from the PAPs and the fascicles were effectively ablated. Echocardiography before and after radiofrequency ablation did not show new or worsened mitral insufficiency. Conclusion: The PAPs can give rise to ventricular arrhythmias in normal and structurally abnormal hearts without prior infarcts. Intracardiac echocardiography seems helpful in recognizing and guiding radiofrequency ablation of PAP arrhythmias. [Copyright &y& Elsevier]

Background: Postinfarction reentrant ventricular tachycardia (VT) is usually scar-related. However, the sites of origin of premature ventricular complexes (PVCs) in the setting of healed myocardial infarction have not been well characterized. Objective: The purpose of this study was to determine the site of origin of frequent PVCs in postinfarction patients with VT and to determine the relationship to VT exit sites. Methods: Mapping and catheter ablation were performed in 13 consecutive patients (12 men, mean age 62 ± 8 years, mean ejection fraction 0.32 ± 0.12) with prior myocardial infarction, sustained monomorphic VT, and >10 PVCs/h. The mean PVC burden was 12% ± 11% on a 24-hour Holter monitor. Electroanatomical left ventricular voltage maps were constructed during sinus rhythm to identify scars. Endocardial activation maps of the PVCs were correlated with the voltage maps, and the most prevalent PVCs were ablated. The effect of PVC ablation on the inducibility of VT was determined. Results: Seventeen sustained monomorphic VTs were reproducibly inducible. There were a total of 34 different PVC morphologies. The site of origin was identified for 18 of the 34 PVC morphologies in 12 of 13 patients. The 18 PVCs for which the site of origin could be identified accounted for 89% of the PVC burden in these patients. The site of PVC origin was in the infarct scar in 11 patients, the border zone in 1 patient, and unidentifiable in 1 patient. The site of PVC origin corresponded to the VT exit site for 14 of 17 reproducibly inducible VTs. The PVCs that were successfully mapped were ablated, and this rendered VT no longer inducible. Conclusion: Postinfarction PVCs usually arise from the infarct scar, and their site of origin often corresponds to the exit site of a reentrant VT. Therefore, catheter ablation of the PVCs often is associated with the loss of inducible VT. [Copyright &y& Elsevier]

Background: Pace mapping has been used to identify the site of origin of focal ventricular arrhythmias. The spatial resolution of pace mapping has not been adequately quantified using currently available three-dimensional mapping systems. Objective: The purpose of this study was to determine the spatial resolution of pace mapping in patients with idiopathic ventricular tachycardia or premature ventricular contractions originating in the right ventricular outflow tract. Methods: In 16 patients with idiopathic ventricular tachycardia/ectopy from the right ventricular outflow tract, comparisons and classifications of pace maps were performed by two observers (good pace map: match >10/12 leads; inadequate pace map: match ≤10/12 leads) and a customized MATLAB 6.0 program (assessing correlation coefficient and normalized root mean square of the difference (nRMSd) between test and template signals). With an electroanatomic mapping system, the correlation coefficient of each pace map was correlated with the distance between the pacing site and the effective ablation site. The endocardial area within the 10-ms activation isochrone was measured. Results: The ablation procedure was effective in all patients. Sites with good pace maps had a higher correlation coefficient and lower nRMSd than sites with inadequate pace maps (correlation coefficient: 0.96 ± 0.03 vs 0.76 ± 0.18, P <.0001; nRMSd: 0.41 ± 0.16 vs 0.89 ± 0.39, P <.0001). Using receiver operating characteristic curves, appropriate cutoff values were >0.94 for correlation coefficient (sensitivity 81%, specificity 89%) and ≤0.54 for nRMSd (sensitivity 76%, specificity 80%). Good pace maps were located a mean of 7.3 ± 5.0 mm from the effective ablation site and had a mean activation time of −24 ± 7 ms. However, in 3 (18%) of 16 patients, the best pace map was inadequate at the effective ablation site, with an endocardial activation time at these sites of −25 ± 12 ms. Pace maps with correlation coefficient ≥0.94 were confined to an area of 1.8 ± 0.6 cm2. The 10-ms isochrone measured 1.2 ± 0.7 cm2. Conclusion: The spatial resolution of a good pace map for targeting ventricular tachycardia/ectopy is 1.8 cm2 in the right ventricular outflow tract and therefore is inferior to the spatial resolution of activation mapping as assessed by isochronal activation. In approximately 20% of patients, pace mapping is unreliable in identifying the site of origin, possibly due a deeper site of origin and preferential conduction via fibers connecting the focus to the endocardial surface. [Copyright &y& Elsevier]