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We reviewed the different approaches used for central vein access during insertion of cardiac implantable electronic devices. The benefits and hazards of each approach (cephalic vein cutdown, axillary vein cannulation using venography and ultrasound) are discussed. Each approach has its advantages and hazards that need to be considered for the individual patient and balanced against the skills of the operator. The benefits of ultrasound guided venous access in reducing radiation exposure to the patient and implanter, avoiding the need for angiographic contrast and in minimizing the risk of pneumothorax and inadvertent arterial puncture are highlighted. Trainees should be taught each approach to deal with patient variability. Ultrasound guidance should be considered as a mainstream option for most patients. [ABSTRACT FROM AUTHOR]

Background: Post-myocardial infarction (MI) remodeling contributes to increased electrophysiological and structural heterogeneity and arrhythmogenesis. Utilising the post-infarct ovine model our aim was to determine unipolar electrogram frequency characteristics consequent to this remodeling and the development of Ventricular Tachycardia (VT). Methods and results: Mapping studies were performed on 14 sheep at >1 month post-MI induction. Sheep were divided into VT inducible (n = 7) and non-inducible (n = 7) groups. Multielectrode needles (n = 20) were deployed within and surrounding ventricular scar for electrophysiological assessment of electrogram amplitude and width. Spectral analysis of electrograms was undertaken using wavelet and fast fourier transformations (WFFT) to calculate root mean square (RMS) power intervals spanning 0-300Hz in 20Hz intervals. Quantitative assessment between electrophysiological and histological parameters including collagen density, and structural organization of the myocardium was performed. Increasing myocardial scar density resulted in attenuation of electrogram amplitude and RMS values. (all p<0.01). Between groups there were no differences in electrogram amplitude (p = 0.37), however WFFT analysis revealed significantly higher RMS values in the VT group (p<0.05) in association with high frequency fractional components of the electrogram. As scar density increased, greater between-group differences in RMS were observed spanning this high frequency (200-280Hz) spectrum and which were proportionally dependent on the degree of structural disorganisation of the myocardium (p<0.001) and number of extrastimuli required to induce VT (p<0.05). Conclusion: High frequency unipolar electrogram spectral characteristics were quantitatively co-influenced by the presence of fibrosis and degree of myocardial structural dissorganisation and were associated with the propensity for development of VT. [ABSTRACT FROM AUTHOR]

Aims: Longer procedural time is associated with complications in radiofrequency atrial fibrillation ablation. We sought to reduce ablation time and thereby potentially reduce complications. The aim was to compare the dimensions and complications of 40 W/30 s setting to that of high-power ablations (50-80 W) for 5 s in the in vitro and in vivo models.Methods and Results: In vitro ablations-40 W/30 s were compared with 40-80 W powers for 5 s. In vivo ablations-40 W/30 s were compared with 50-80 W powers for 5 s. All in vivo ablations were performed with 10 g contact force and 30 mL/min irrigation rate. Steam pops and depth of lung lesions identified post-mortem were noted as complications. A total of 72 lesions on the non-trabeculated part of right atrium were performed in 10 Ovine. All in vitro ablations except for the 40 W/5 s setting achieved the critical lesion depth of 2 mm. For in vivo ablations, all lesions were transmural, and the lesion depths for the settings of 40 W/30 s, 50 W/5 s, 60 W/5 s, 70 W/5 s, and 80 W/5 s were 2.2 ± 0.5, 2.3 ± 0.5, 2.1 ± 0.4, 2.0 ± 0.3, and 2.3 ± 0.7 mm, respectively. The lesion depths of short-duration ablations were similar to that of the conventional ablation. Steam pops occurred in the ablation settings of 40 W/30 s and 80 W/5 s in 8 and 11% of ablations, respectively. Complications were absent in short-duration ablations of 50 and 60 W.Conclusion: High-power, short-duration atrial ablation was as safe and effective as the conventional ablation. Compared with the conventional 40 W/30 s setting, 50 and 60 W ablation for 5 s achieved transmurality and had fewer complications. [ABSTRACT FROM AUTHOR]

Background: Atrial arrhythmias may still occur in patients after durable pulmonary vein isolation (PVI).Objective: The purpose of this study was to examine the incidence of patients undergoing ablation for recurrent arrhythmia despite chronic PVI and their clinical outcomes.Methods: Patients undergoing repeat left atrial ablation procedures were selected from a prospective registry. From this population, we identified patients with chronic PVI. Clinical characteristics, ablation strategies, and outcomes were analyzed.Results: Between January 2003 and December 2013, 1045 patients underwent 1298 repeat left atrial procedures. Of these, 900 patients had atrial fibrillation (AF) and 145 had atrial flutter (AFL)/atrial tachycardia (AT). Fifty-two patients (5.0%; 27 with AF and 25 with AFL/AT) had chronic PVI and were included in the study. Patients were followed for 19.7 ± 5.6 months. In patients with AF, 11 (41%) had a non-PV trigger identified. Ablation strategies included non-PV trigger ablation (n = 11), empiric trigger-site ablation (n = 3), provoked arrhythmia ablation (n = 9), complex fractionated atrial electrogram ablation (n = 2), and linear ablation (n = 2). During follow-up, 9 (33%) had no recurrence, 7 (26%) had rare AF (≤2 episodes during follow-up ≥1 year), and 11 (41%) had AF recurrence. In patients with AFL/AT, 12 (48%) had no recurrence, 4 (16%) had rare recurrence (≤2 episodes during follow-up ≥1 year), and 9 (36%) had recurrence.Conclusion: In patients with PVI undergoing a repeat procedure during the time period studied, only a small portion had chronic PVI. A strategy of targeting non-PV triggers for AF and linear/focal ablation for AFL/AT may achieve long-term arrhythmia control in the majority of patients. [ABSTRACT FROM AUTHOR]

Background: 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.Objective: We aimed to examine whether timing or frequency of ERAA after pulmonary vein antral isolation (PVAI) affects long-term ablation success.Methods: 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).Results: 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]).Conclusions: 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. [ABSTRACT FROM AUTHOR]

Background Anatomic studies have reported the presence of shared myocardial fibers between approximately half of ipsilateral pulmonary veins (IPVs). Objective The purpose of this study was to assess the prevalence of electrical connection between IPVs and the impact of antral isolation with or without carina ablation on IPV connection. Methods Thirty consecutive patients undergoing atrial fibrillation (AF) ablation (14 redo) were included. Wide antral pulmonary vein isolation (PVI) was performed with or without carina lesions. For each PV set, IPV electrical connection was assessed before and after PVI by pacing and recording from the ostium of both IPVs using a circular mapping catheter and the ablation catheter. Adenosine was given after PVI to assess for acute PV reconnection. Results Before PVI without preceding AF ablation procedure, all the PVs had ipsilateral connection albeit frequently via the left atrium. After PVI, 65.6% of the IPVs were connected without carina ablation vs 17.7% if prior carina ablation ( P = .001). Left vs right IPVs were connected in 57.1% and 72.2% of the cases without carina ablation, respectively, vs 30% and 0% of cases with carina ablation ( P = .19 and P = .001). When transient PV reconnection was demonstrated during adenosine challenge, connected IPVs uniformly demonstrated simultaneous reconnection. Conclusion Electrical connection between IPVs is uniformly demonstrated before any ablation. Two-thirds of the IPVs are connected after antral PVI, and carina ablation decreases IPV connection. Connected IPVs consistently show the same response to adenosine challenge; therefore, a single catheter positioned in either of the IPVs with electrical connection is sufficient to confirm reconnection in both veins. [ABSTRACT FROM AUTHOR]

Background The moderator band (MB) can be a source of premature ventricular contractions (PVCs), monomorphic ventricular tachycardia (VT), and idiopathic ventricular fibrillation (IVF). Objective The purpose of this study was to define the electrocardiographic (ECG) characteristics and procedural techniques to successfully identify and ablate MB PVCs/VT. Methods 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. Results 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 (>V 4 ), 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. Conclusion 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. [ABSTRACT FROM AUTHOR]

Background Characterization of left atrial scar using bipolar voltage (BiV) mapping is not well defined. We have previously shown that the BiV range of 0.2–0.45 mV can identify chronic scar from prior pulmonary vein isolation (PVI). Objective This study sought to determine a BiV range that can identify atrial inexcitable dense scar (IDS) in patients acutely and chronically after PVI. Methods Thirty consecutive patients undergoing first time (n = 15) or redo (n = 15) PVI were included. A left atrial shell was created using electroanatomic mapping, and IDS was defined by inability to capture at an output of 10 mA and a pulse width of 2 ms in sinus rhythm, circumferentially at the edge of PVI-related scar (≤5 mm). At each pacing site, BiV amplitude and atrial capture were recorded. Results Overall, 837 pacing sites were assessed. BiV predicted IDS (receiver operating characteristic curve area 0.93 for first time PVI and 0.90 for redo PVI). In first time PVI, the best BiV value to predict IDS was 0.45 mV for the left pulmonary vein–left atrial appendage (LAA-LPV) ridge (sensitivity 0.98; specificity 1.0) and 0.2 mV for other localizations (sensitivity 0.91; specificity 0.86). In redo PVI, the best BiV value to predict IDS was 0.2 mV for the LAA-LPV ridge (sensitivity 0.77; specificity 1.0) and 0.15 mV for other localizations (sensitivity 0.81; specificity 0.82). Conclusion BiV reproducibly identifies acute and chronic IDS using a cutoff value of 0.2 mV (0.45 mV for the LAA-LPV ridge) in patients undergoing first time PVI and 0.15 mV (0.2 mV for the LAA-LPV ridge) in patients undergoing redo PVI. IDS thus identified may be a rigorous tool for validating PVI. [ABSTRACT FROM AUTHOR]

Purpose: Unipolar (UE) and bipolar electrograms (BE) are utilized to identify arrhythmogenic substrate. We quantified the effect of increasing distance from the source of propagation on local electrogram amplitude; and determined if transmural electrophysiological gradients exist with respect to propagation and stimulation depth. Methods: Mapping was performed on 5 sheep. Deployment of >50 quadripolar transmural needles in the LV were located in Cartesian space using Ensite. Contact electrograms from all needles were recorded during multisite bipolar pacing from epicardial then endocardial electrodes. Analysis was performed to determine stimulus distance to local activation time, peak negative amplitude (V-P), and peak-peak amplitude (VP-P) for (1) unfiltered UE, and (2) unfiltered and 30 Hz high-pass filtered BEs. Each sheep was analysed using repeated ANOVA. Results: Increasing distance from the pacing sites led to significant (p<0.01) attenuation of UEs (V-P = 7.0±0.5%; VP-P = 5.4±0.3% per cm). Attenuation of BE with distance was insignificant (Vp-p unfiltered  = 2.2±0.5%; filtered  = 1.7±1.4% per cm). Independent of pacing depth, significant (p<0.01) transmural electrophysiological gradients were observed, with highest amplitude occurring at epicardial layers for UE and endocardial layers for BE. Furthermore, during pacing, propagation was earlier at the epicardium than endocardial layer by 1.6±2.0 ms (UE) and 1.4±2.8 ms (BE) (all p>0.01) during endocardial stimulation, and 2.3±2.4 ms (UE) and 1.8±3.7 ms (BE) during epicardal stimulation (all p<0.01). Conclusions: Electrogram amplitude is inversely proportional to propagation distance for unipolar modalities only, which affected V-P>VP-P. Conduction propagates preferentially via the epicardium during stimulation and is believed to contribute to a transmural amplitude gradient. [ABSTRACT FROM AUTHOR]

Background Pacemaker (PM) interrogation requires correct manufacturer identification. However, an unidentified PM is a frequent occurrence, requiring time-consuming steps to identify the device. Objective The purpose of this study was to develop and validate a novel algorithm for PM manufacturer identification, using the ECG response to magnet application. Methods Data on the magnet responses of all recent PM models (↜15 years) from the 5 major manufacturers were collected. An algorithm based on the ECG response to magnet application to identify the PM manufacturer was subsequently developed. Patients undergoing ECG during magnet application in various clinical situations were prospectively recruited in 7 centers. The algorithm was applied in the analysis of every ECG by a cardiologist blinded to PM information. A second blinded cardiologist analyzed a sample of randomly selected ECGs in order to assess the reproducibility of the results. Results A total of 250 ECGs were analyzed during magnet application. The algorithm led to the correct single manufacturer choice in 242 ECGs (96.8%), whereas 7 (2.8%) could only be narrowed to either 1 of 2 manufacturer possibilities. Only 2 (0.4%) incorrect manufacturer identifications occurred. The algorithm identified Medtronic and Sorin Group PMs with 100% sensitivity and specificity, Biotronik PMs with 100% sensitivity and 99.5% specificity, and St. Jude and Boston Scientific PMs with 92% sensitivity and 100% specificity. The results were reproducible between the 2 blinded cardiologists with 92% concordant findings. Conclusion Unknown PM manufacturers can be accurately identified by analyzing the ECG magnet response using this newly developed algorithm. [ABSTRACT FROM AUTHOR]

Background: Frequent ventricular premature depolarizations (VPDs) can cause cardiomyopathy (CMP). The mechanisms underlying its development remain unclear, with VPD burden being only a weak predictor of risk.Objective: To determine whether VPD QRS duration at the time of initial presentation could predict risk for the subsequent development of CMP in patients with normal left ventricular ejection fraction (LVEF).Methods: From consecutive patients referred for ablation between January 1, 2006, and April 2, 2013, with ≥10% VPDs on 24-hour Holter monitoring, we identified 45 patients with normal LVEF and an electrocardiogram of the targeted VPD, who were then followed for at least 6 months (median 14 months; interquartile range [IQR] 8-32 months) before intervention. We excluded patients with structural or genetic heart disease.Results: Of the 45 patients, 28 (62%) maintained normal LVEF and 17(38%) developed VPD-induced CMP. VPD burden was similar (26.5% [IQR 19.3%-39.5%] vs 26.0% [IQR 16.4%-41.0%]; P = 0.4) between the 2 groups. Patients who developed VPD-induced CMP had significantly longer VPD QRS duration (159 ms vs 142 ms; P < .001) and a longer sinus QRS duration (97 ms vs 89 ms; P = .04). A VPD QRS duration of ≥153 ms best predicted development of VPD CMP (82% sensitivity and 75% specificity). Longer VPD QRS duration and a non-outflow tract site of VPD origin were independent risk factors for left ventricular dysfunction after multivariate analysis.Conclusion: VPD QRS duration longer than 153 ms and a non-outflow tract site of origin might be useful predictors of the subsequent development of VPD-induced CMP. [ABSTRACT FROM AUTHOR]

Background--Collagen has been attributed as the principal structural substrate of ventricular tachycardia (VT) after myocardial infarction (MI), even though adiposity of myocardium after MI is well recognized histologically. We investigated the effects of intramyocardial adiposity compared with collagen on electrophysiological properties, connexin43 expression, and VT induction after MI. Methods and Results--Simultaneous left ventricular plunge-needle, noncontact mapping was performed in sheep without MI (MI-; n=5), with MI and inducible VT (MI+VT+; n=7), and with MI and no inducible VT (MI+VT-; n=8). Histological intramyocardial quantity of adipose and collagen and degree of discontinuity were coregistered with electrophysiological parameters (MI+; 290 specimens). Additional assessment of connexin43 expression was performed. Left ventricular scar contained a body mass-independent abundance of adipocytes (adipose:collagen=0.8). Increased adipose density and discontinuity contributed to a greater inverse correlation (r) with conduction velocity (r for adipose=0.39, r for discontinuity=0.45, r for collagen=0.26) and electrogram amplitude (r for adipose=0.73, r for contiguity=0.77, r for collagen=0.68) compared with collagen. Collagen density was similar between the MI+ groups (P>0.29). However, the MI+VT+ group demonstrated a significant (all P≤0.01) increase in adipose (8%) and discontinuity (qualitative) and decrease in conduction velocity (13%) and electrogram amplitude (21%) at MI borders compared with the MI+VT-group. In scar, myocytes adjacent to fibrofatty interfaces demonstrated increased connexin43 lateralization. A gradient increase in adipose was observed at sites that supported preferential presystolic VT activation and exhibited attenuation of excitation wavelength (P<0.001). Conclusions--Intramyocardial adiposity, in association with myocardial discontinuity within left ventricular scar borders, is a significant factor associated with altered electrophysiological properties, aberrant connexin43 expression, and increased propensity for VT after MI. [ABSTRACT FROM AUTHOR]