High Dominant Frequencies and Fractionated Potentials Do Not Indicate Focal or Rotational Activation During AF.

BACKGROUND: Dominant frequencies (DFs) or complex fractionated atrial electrograms (CFAEs), indicative of focal sources or rotational activation, are used to identify target sites for atrial fibrillation (AF) ablation in clinical studies, although the relationship among DF, CFAE, and activation patterns remains unclear. OBJECTIVES: This study sought to investigate the relationship between patterns of activation underlying DF and CFAE sites during AF. METHODS: Epicardial high-resolution mapping of the right and left atrium including Bachmann's bundle was performed in 71 participants. We identified the highest dominant frequency (DFmax) and highest degree of CFAE (CFAEmax) with the use of existing clinical criteria and classified patterns of activation as focal or rotational activation and smooth propagation, conduction block (CB), collision and remnant activity, and fibrillation potentials as single, double, or fractionated potentials containing, respectively, 1, 2, or 3 or more negative deflections. Relationships among activation patterns, DFmax, and potential types were investigated. RESULTS: DFmax were primarily located at the left atrioventricular groove and did not harbor focal activation (proportion focal waves: 0% [IQR: 0%-2%]). Compared with non-DFmax sites, DFmax were characterized by more frequent smooth propagation (22% [IQR: 7%-48%] vs 17% [IQR: 11%-24%]; P = 0.001), less frequent conduction block (69% [IQR: 51%-81%] vs 74% [IQR: 69%-78%]; P = 0.006), a higher proportion of single potentials (72% [IQR: 55%-84%] vs 6%1 [IQR: 55%-65%]; P = 0.003), and a lower proportion of fractionated potentials (4% [IQR: 1%-11%] vs 12% [IQR: 9%-15%]; P = 0.004). CFAEmax were mainly found at the pulmonary veins area, and only 1% [IQR: 0%-2%] of all CFAEmax contained focal activation. Compared with non-CFAEmax sites, CFAEmax sites were characterized by less frequent smooth propagation (1% [IQR: 0%-1%] vs 17% [IQR: 12%-24%]; P < 0.001) and more frequent remnant activity (20% [IQR: 12%-29%] vs 8% [IQR: 5%-10%]; P < 0.001), and harbored predominantly fractionated potentials (52% [IQR: 43%-66%] vs 12% [IQR: 9%-14%]; P < 0.001). CONCLUSIONS: Focal or rotational patterns of activation were not consistently detected at DFmax domains and CFAEmax sites. These findings do not support the concept of targeting DFmax or CFAEmax according to existing criteria for AF ablation.

Atrial extrasystoles enhance low-voltage fractionation electrograms in patients with atrial fibrillation.

BACKGROUND AND AIMS: Atrial extrasystoles (AES) provoke conduction disorders and may trigger episodes of atrial fibrillation (AF). However, the direction- and rate-dependency of electrophysiological tissue properties on epicardial unipolar electrogram (EGM) morphology is unknown. Therefore, this study examined the impact of spontaneous AES on potential amplitude, -fractionation, -duration, and low-voltage areas (LVAs), and correlated these differences with various degrees of prematurity and aberrancy. METHODS AND RESULTS: Intra-operative high-resolution epicardial mapping of the right and left atrium, Bachmann's Bundle, and pulmonary vein area was performed during sinus rhythm (SR) in 287 patients (60 with AF). AES were categorized according to their prematurity index (>25% shortening) and degree of aberrancy (none, mild/opposite, moderate and severe). In total, 837 unique AES (457 premature; 58 mild/opposite, 355 moderate, and 154 severe aberrant) were included. The average prematurity index was 28% [12-45]. Comparing SR and AES, average voltage decreased (-1.1 [-1.2, -0.9] mV, P < 0.001) at all atrial regions, whereas the amount of LVAs and fractionation increased (respectively, +3.4 [2.7, 4.1] % and +3.2 [2.6, 3.7] %, P < 0.001). Only weak or moderate correlations were found between EGM morphology parameters and prematurity indices (R2 < 0.299, P < 0.001). All parameters were, however, most severely affected by either mild/opposite or severely aberrant AES, in which the effect was more pronounced in AF patients. Also, there were considerable regional differences in effects provoked by AES. CONCLUSION: Unipolar EGM characteristics during spontaneous AES are mainly directional-dependent and not rate-dependent. AF patients have more direction-dependent conduction disorders, indicating enhanced non-uniform anisotropy that is uncovered by spontaneous AES.

Unipolar atrial electrogram morphology is affected by age: evidence from high-resolution epicardial mapping.

BACKGROUND: It is unknown which features of unipolar atrial electrogram (U-AEGM) morphology are affected by ageing and whether age-related changes in U-AEGM morphology are equally distributed throughout the right and left atria. PATIENTS AND METHODS: Epicardial high-resolution mapping was performed in patients undergoing coronary artery bypass grafting surgery during sinus rhythm (SR). Mapping areas include the right atrium (RA), left atrium (LA), pulmonary vein area (PVA) and Bachmann's bundle (BB). Patients were categorized into a young (age < 60) and aged (age ≥ 60) group. U-AEGM were classified as single potentials (SPs, one deflection), short double potentials (SDPs, deflection interval ≤ 15ms), long double potentials (LDPs, deflection interval > 15ms) and fractionated potentials (FPs, ≥3 deflections). RESULTS: A total of 213 patients (age: 67 (59-73) years; young group N = 58, aged group N = 155) were included. Only at BB, the proportion of SPs (p = 0.007) was significantly higher in the young group, while the proportion of SDPs (p = 0.051), LDPs (p = 0.004) and FPs (p = 0.006) was higher in the aged group. After adjusting for potential confounders, older age was associated with a reduction in SPs [regression coefficient (ß): -6.33, 95% confident interval (CI): -10.37 to -2.30] at the expense of an increased proportion of SDPs (ß: 2.49, 95% CI: 0.09 to 4.89), LDPs (ß: 1.94, 95% CI: 0.21 to 3.68) and FPs (ß: 1.90, 95% CI: 0.62 to 3.18). CONCLUSIONS: Age-related remodeling particularly affects BB as indicated by the decreased amount of non-SP at this location in the elderly.Key MessagesAgeing preferentially affects the morphology of unipolar atrial electrograms recorded at Bachmann's bundle.At Bachmann's bundle, the proportion of short double-, long double- and fractionated potentials increase during ageing at the expense of a decrease in the proportion of single potentials, reflecting aggravation of abnormalities in conduction.The increase in abnormal unipolar atrial electrograms at Bachmann's bundle during ageing supports the concept that Bachmann's bundle may play an important role in development of age-related arrhythmias such as atrial fibrillation.

'Vanishing' fragmented potential at the epicardium in a patient with Brugada syndrome.

A man in his 40s with Brugada syndrome underwent catheter ablation for ventricular fibrillation. When we performed epicardial mapping again to check for residual ablation sites after ablation, a remarkable reproducible fragmented potential was observed at the anterior aspect of the right ventricle using an Advisor HD Grid (Abbott), which had not been detected during the initial mapping before ablation, and which was invisible to the ablation catheter. Fluoroscopic imaging demonstrated a shiny area anterior to the heart, suggesting trapped air, presumed to have arisen when the sheath was inserted into the pericardial space. The air trapped between the heart and pericardium prevented the HD grid from contacting the epicardium, resulting in the recording of a fragmented potential. The trapped air was removed manually via the sheath, and the potential vanished. When fragmented potentials are observed at the anterior right ventricle (RV) in the epicardium, air trapping should be ruled out by fluoroscopy.

Electrogram fractionation during sinus rhythm occurs in normal voltage atrial tissue in patients with atrial fibrillation.

INTRODUCTION: Electrogram (EGM) fractionation is often associated with diseased atrial tissue; however, mechanisms for fractionation occurring above an established threshold of 0.5 mV have never been characterized. We sought to investigate during sinus rhythm (SR) the mechanisms underlying bipolar EGM fractionation with high-density mapping in patients with atrial fibrillation (AF). METHODS: Forty-five patients undergoing AF ablation (73% paroxysmal, 27% persistent) were mapped at high density (18562 ± 2551 points) during SR (Rhythmia). Only bipolar EGMs with voltages above 0.5 mV were considered for analysis. When fractionation (> 40 ms and >4 deflections) was detected, we classified the mechanisms as slow conduction, wave-front collision, or a pivot point. The relationship between EGM duration and amplitude, and tissue anisotropy and slow conduction, was then studied using a computational model. RESULTS: Of the 45 left atria analyzed, 133 sites of EGM fragmentation were identified with voltages above 0.5 mV. The most frequent mechanism (64%) was slow conduction (velocity 0.45 m/s ± 0.2) with mean EGM voltage of 1.1 ± 0.5 mV and duration of 54.9 ± 9.4 ms. Wavefront collision was the second most frequent (19%), characterized by higher voltage (1.6 ± 0.9 mV) and shorter duration (51.3 ± 11.3 ms). Pivot points (9%) were associated with the highest degree of fractionation with 70.7 ± 6.6 ms and 1.8 ± 1 mV. In 10 sites (8%) fractionation was unexplained. The EGM duration was significantly different among the 3 mechanisms (p = .0351). CONCLUSION: In patients with a history of AF, EGM fractionation can occur at amplitudes > 0.5 mV when in SR in areas often considered not to be diseased tissue. The main mechanism of EGM fractionation is slow conduction, followed by wavefront collision and pivot sites.

An improved procedure for isolating adult mouse cardiomyocytes for epicardial activation mapping.

Cardiovascular disease is a leading cause of death and disability worldwide. Although genetically modified mouse models offer great potential for robust research in vivo, in vitro studies using isolated cardiomyocytes also provide an important approach for investigating the mechanisms underlying cardiovascular disease pathogenesis and drug actions. Currently, isolation of mouse adult cardiomyocytes often relies on aortic retrograde intubation under a stereoscopic microscope, which poses considerable technical barriers and requires extensive training. Although a simplified, Langendorff-free method has been used to isolate viable cardiomyocytes from the adult mouse heart, the system requires enzymatic digestions and continuous manual technical operation. This study established an optimized approach that allows isolation of adult mouse cardiomyocytes and epicardial activation mapping of mouse hearts using a Langendorff device. We used retrograde puncture through the abdominal aorta in vivo and enzymatic digestion on the Langendorff perfusion device to isolate adult mouse cardiomyocytes without using a microscope. The yields of isolated cardiomyocytes were amenable to patch clamp techniques. Furthermore, this approach allowed epicardial activation mapping. We used a novel, simplified method to isolate viable cardiomyocytes from adult mouse hearts and to map epicardial activation. This novel approach could be beneficial in more extensive research in the cardiac field.

Electrophysiological characteristics of epicardial to endocardial breakthrough in intractable cavotricuspid isthmus-dependent atrial flutter.

BACKGROUND: Epicardial to endocardial breakthrough (EEB) exists widely in atrial arrhythmia and is a cause for intractable cavotricuspid isthmus (CTI)-dependent atrial flutter (AFL). This study aimed to investigate the electrophysiological features of EEB in EEB-related CTI dependent AFL. METHODS: Six patients with EEB-related CTI-dependent AFL were identified among 142 consecutive patients who underwent CTI-dependent AFL catheter ablation with an ultra-high-density, high-resolution mapping system in three institutions. Activation maps and ablation procedure were analyzed. RESULTS: A total of seven EEBs were found in six patients. Four EEBs (including three at the right atrial septum and one in paraseptal isthmus) were recorded in three patients during tachycardia. The other three EEBs were identified at the inferolateral right atrium (RA) during pacing from the coronary sinus. The conduction characteristics through the EEB-mediated structures were evaluated in three patients. Two patients only showed unidirectional conduction. Activation maps indicated that CTI-dependent AFL with EEB at the atrial septum was actually bi-atrial macro-reentrant atrial tachycardia (BiAT). Intensive ablation at the central isthmus could block CTI bidirectionally in four cases. However, ablation targeted at the inferolateral RA EEB was required in two cases. Meanwhile, local potentials at the EEB location gradually split into two components with a change in activation sequence. CONCLUSIONS: EEB is an underlying cause for intractable CTI-dependent AFL. EEB-mediated structure might show unidirectional conduction. CTI-dependent AFL with EEB at the atrial septum may represent BiAT. Intensive ablation targeting the central isthmus or EEB at the inferolateral RA could block the CTI bidirectionally.

Epicardial Conduction Speed, Electrogram Abnormality, and Computed Tomography Attenuation Associations in Arrhythmogenic Right Ventricular Cardiomyopathy.

OBJECTIVES: This study sought to evaluate the association between contrast-enhanced multidetector computed tomography (CE-MDCT) attenuation and local epicardial conduction speed (ECS) and electrographic abnormalities in patients with arrhythmogenic right ventricular cardiomyopathy (ARVC) and ventricular tachycardia (VT). BACKGROUND: CE-MDCT is a widely available and fast imaging technology with high spatial resolution that is less prone to defibrillator generator-related safety issues and image artifacts. However, the association between hypoattenuation on MDCT and VT substrates in ARVC remains unknown. METHODS: Patients with ARVC who underwent CE-MDCT followed by endocardial (n = 30) and epicardial (n = 21) electroanatomical mapping (EAM) and VT ablation were prospectively enrolled. Right ventricular (RV) mid-myocardial attenuation was calculated from 3-dimensional MDCT images and registered to EAM. Local ECS was calculated by averaging the ECS between each point and 5 adjacent points with concordant wave front direction. RESULTS: A total of 17,311 epicardial and 5,204 endocardial points were included. In multivariable regression analysis clustered by patient, RV myocardial attenuation was associated with epicardial bipolar voltage amplitude (2.5% decrease in amplitude per 10 HU decrease in attenuation; p < 0.001), with endocardial unipolar voltage amplitude (0.9% decrease in amplitude per 10 HU decrease in attenuation; p < 0.001), and with ECS (0.4% decrease in ECS per 10 HU decrease in attenuation; p = 0.001). CONCLUSIONS: CE-MDCT attenuation distribution is associated with regional ECS and electrographic amplitude in ARVC. Regions with low attenuation likely reflect fibro-fatty involvement in the RV and may serve as important VT substrates in patients with ARVC who are undergoing VT ablation.

Mapping and Ablation of Ventricular Fibrillation Associated With Early Repolarization Syndrome.

BACKGROUND: We conducted a multicenter study to evaluate mapping and ablation of ventricular fibrillation (VF) substrates or VF triggers in early repolarization syndromes (ERS) or J-wave syndrome (JWS). METHODS: We studied 52 patients with ERS (4 women; median age, 35 years) with recurrent VF episodes. Body surface electrocardiographic imaging and endocardial and epicardial electroanatomical mapping of both ventricles were performed during sinus rhythm and VF for localization of triggers, substrates, and drivers. Ablations were performed on VF substrates, defined as areas that had late depolarization abnormalities characterized by low-voltage fractionated late potentials, and VF triggers. RESULTS: Fifty-one of the 52 patients had detailed mapping that revealed 2 phenotypes: group 1 had late depolarization abnormalities predominantly at the right ventricular (RV) epicardium (n=40), and group 2 had no depolarization abnormalities (n=11). Group 1 can be subcategorized into 2 groups: Group 1A included 33 patients with ERS with Brugada electrocardiographic pattern, and group 1B included 7 patients with ERS without Brugada electrocardiographic pattern. Late depolarization areas colocalize with VF driver areas. The anterior RV outflow tract/RV epicardium and the RV inferior epicardium are the major substrate sites for group 1. The Purkinje network is the leading underlying VF trigger in group 2 that had no substrates. Ablations were performed in 43 patients: 31 and 5 group 1 patients had only VF substrate ablation and VF substrates plus VF trigger, respectively (mean, 1.4±0.6 sessions); 6 group 2 patients and 1 patient without group classification had only Purkinje VF trigger ablation (mean, 1.2±0.4 sessions). Ablations were successful in reducing VF recurrences (P<0.0001). After follow-up of 31±26 months, 39 (91%) had no VF recurrences. CONCLUSIONS: There are 2 phenotypes of ERS/J-wave syndrome: one with late depolarization abnormality as the underlying mechanism of high-amplitude J-wave elevation that predominantly resides in the RV outflow tract and RV inferolateral epicardium, serving as an excellent target for ablation, and the other with pure ERS devoid of VF substrates but with VF triggers that are associated with Purkinje sites. Ablation is effective in treating symptomatic patients with ERS/J-wave syndrome with frequent VF episodes.

A rule-based method for predicting the electrical activation of the heart with cardiac resynchronization therapy from non-invasive clinical data.

BACKGROUND: Cardiac Resynchronization Therapy (CRT) is one of the few effective treatments for heart failure patients with ventricular dyssynchrony. The pacing location of the left ventricle is indicated as a determinant of CRT outcome. OBJECTIVE: Patient specific computational models allow the activation pattern following CRT implant to be predicted and this may be used to optimize CRT lead placement. METHODS: In this study, the effects of heterogeneous cardiac substrate (scar, fast endocardial conduction, slow septal conduction, functional block) on accurately predicting the electrical activation of the LV epicardium were tested to determine the minimal detail required to create a rule based model of cardiac electrophysiology. Non-invasive clinical data (CT or CMR images and 12 lead ECG) from eighteen patients from two centers were used to investigate the models. RESULTS: Validation with invasive electro-anatomical mapping data identified that computer models with fast endocardial conduction were able to predict the electrical activation with a mean distance errors of 9.2 ±â€¯0.5 mm (CMR data) or (CT data) 7.5 ±â€¯0.7 mm. CONCLUSION: This study identified a simple rule-based fast endocardial conduction model, built using non-invasive clinical data that can be used to rapidly and robustly predict the electrical activation of the heart. Pre-procedural prediction of the latest electrically activating region to identify the optimal LV pacing site could potentially be a useful clinical planning tool for CRT procedures.

Changes in atrial electrophysiological and structural substrate and their relationship to histology in a long-term chronic canine atrial fibrillation model.

BACKGROUND: Atrial fibrillation (AF) is related to numerous electrophysiological changes; however, the extent of structural and electrophysiological remodeling with long-term AF is not well characterized. METHODS: Dogs (n = 6) were implanted with a neurostimulator in the right atrium (AF group). No implantation was done in the Control group (n = 3). Electroanatomical mapping was done prior to and following more than 6 months of AF. Magnetic resonance imaging was also done to assess structural remodeling. Animals were euthanized and tissue samples were acquired for histological analysis. RESULTS: A significant increase was seen in the left atrial (LA) volume among all AF animals (22.25 ± 12.60 cm3 vs 34.00 ± 12.23 cm3 , P = .01). Also, mean bipolar amplitude in the LA significantly decreased from 5.96 ± 2.17 mV at baseline to 3.23 ± 1.51 mV (P < .01) after chronic AF. Those significant changes occurred in each anterior, lateral, posterior, septal, and roof regions as well. Additionally, the dominant frequency (DF) in the LA increased from 7.02 ± 0.37 Hz to 10.12 ± 0.28 Hz at chronic AF (P < .01). Moreover, the percentage of fibrosis in chronic AF animals was significantly larger than that of control animals in each location (P < .01). CONCLUSIONS: Canine chronic AF is accompanied by a significant decrease in intracardiac bipolar amplitudes. These decreased electrogram amplitude values are still higher than traditional cut-off values used for diseased myocardial tissue. Despite these "normal" bipolar amplitudes, there is a significant increase in DF and tissue fibrosis.

Mastering the art of epicardial access in cardiac electrophysiology.

Access to the epicardial space is fundamental to several cardiac procedures. While traditional indications include catheter ablation of ventricular arrhythmias and accessory pathways, novel indications include left atrial appendage occlusion, esophageal protection, mapping and ablation during atrial fibrillation procedures, implantation of epicardial pacing leads, and phrenic nerve displacement to facilitate safe ablation of atrial and ventricular arrhythmias. Accessing the epicardial space safely is a major challenge requiring intimate knowledge of cardiac anatomy, extensive training, and expertise. Over the past years, multiple technological advances have led to significant improvements in epicardial access success and safety. Important examples of such advances include CO2 insufflation through the coronary sinus or the right atrial appendage, pressure sensor needle, computed tomography, cardiac magnetic resonance, and electroanatomic mapping-guided epicardial access. In addition, we provide special maneuvers to minimize inadvertent right ventricular perforation.

Impact of low-voltage zones on the left atrial anterior wall on the reduction in the left atrial appendage flow velocity in persistent atrial fibrillation patients.

BACKGROUND: The reduction in the left atrial appendage (LAA) flow velocity is related to the presence of emboli in atrial fibrillation (AF) patients. The LAA is located on the left superior side of the left atrial (LA) anterior wall, and we investigated the relationship between the reduction in the LAA flow velocity (LAAFV) and low voltage zones (LVZs < 0.5 mV) on the LA anterior wall. METHODS: In 146 persistent AF patients, LAAFV measurements, by transesophageal echocardiography, and catheter ablation were performed. LA mapping was performed before ablation during sinus rhythm, and the locations of any anterior-LVZs were documented. RESULTS: Eighty-one patients had a documented LVZ on the LA anterior wall, and those with an LVZ had a significantly lower LAAFV compared to those without (anterior-LVZ(+) vs. anterior-LVZ(-) = 26 ± 11 vs. 34 ± 10 cm/s, p < 0.001), while no significant difference was observed when compared to the other LVZ regions. A low-LAAFV (≦ 20 cm/s) was observed in 36 patients, and the CHADS2-vasc score and existence of an anterior-LVZ were associated with a low-LAAFV. In patients with anterior-LVZs, the distance between the anterior-LVZ and LAA orifice correlated with a low LAAFV (r = 0.534, p < 0.001) as compared to the surface area of the anterior-LVZ (r = - 0.288, p = 0.009). CONCLUSIONS: In persistent AF patients, an LVZ on the LA anterior wall was associated with a low LAAFV. In addition, an anterior-LVZ located near the LAA orifice was further related to a reduction in the LAAFV.

Prolonged action potential duration and dynamic transmural action potential duration heterogeneity underlie vulnerability to ventricular tachycardia in patients undergoing ventricular tachycardia ablation.

AIMS: Differences of action potential duration (APD) in regions of myocardial scar and their borderzones are poorly defined in the intact human heart. Heterogeneities in APD may play an important role in the generation of ventricular tachycardia (VT) by creating regions of functional block. We aimed to investigate the transmural and planar differences of APD in patients admitted for VT ablation. METHODS AND RESULTS: Six patients (median age 53 years, five male); (median ejection fraction 35%), were studied. Endocardial (Endo) and epicardial (Epi) 3D electroanatomic mapping was performed. A bipolar voltage of <0.5 mV was defined as dense scar, 0.5-1.5 mV as scar borderzone, and >1.5 mV as normal. Decapolar catheters were positioned transmurally across the scar borderzone to assess differences of APD and repolarization time (RT) during restitution pacing from Endo and Epi. Epi APD was 173 ms in normal tissue vs. 187 ms at scar borderzone and 210 ms in dense scar (P < 0.001). Endocardial APD was 210 ms in normal tissue vs. 222 ms in the scar borderzone and 238 ms in dense scar (P < 0.01). This resulted in significant transmural RT dispersion (ΔRT 22 ms across dense transmural scar vs. 5 ms in normal transmural tissue, P < 0.001), dependent on the scar characteristics in the Endo and Epi, and the pacing site. CONCLUSION: Areas of myocardial scar have prolonged APD compared with normal tissue. Heterogeneity of regional transmural and planar APD result in localized dispersion of repolarization, which may play an important role in initiating VT.

The relationship between obstructive sleep apnea and recurrence of atrial fibrillation after pulmonary vein isolation using a contact force-sensing catheter.

PURPOSE: Our aim was to elucidate the relationship between obstructive sleep apnea (OSA) and atrial fibrillation (AF) recurrence after repeated pulmonary vein isolation (PVI). METHODS: We conducted a non-randomized observational study, with the data prospectively collected. One hundred patients (paroxysmal AF, n = 89) underwent PVI using a contact force-sensing catheter. All patients underwent an electrophysiological study and additional ablation for left atrium-pulmonary vein (PV) reconnection and non-PV foci, 6 months after the first treatment session, regardless of AF recurrence. Those with an apnea-hypopnea index ≥ 15 were diagnosed with OSA. Continuous positive air pressure (CPAP) therapy was initiated after the second treatment session, based on results of a sleep study. For analysis, patients were classified into the non-OSA (n = 66), treated OSA (OSA patients undergoing CPAP; n = 11), and untreated OSA (n = 23) groups, and between-group differences evaluated. RESULTS: After the first session, AF recurrence was observed in 18.2% (12/66) and 14.7% (5/34) of patients without and with OSA, respectively (P = 0.678). After the second procedure, the rate of AF recurrence was 12.1% (8/66) in the non-OSA group, 9.1% (1/11) in the treated OSA group, and 8.7% (2/23) in the untreated OSA group (log-rank P = 0.944). CONCLUSIONS: The rate of AF recurrence might not be greater in patients with untreated OSA than in those without OSA and those with treated OSA after repeated PVI, using a contact force-sensing catheter, for patients with paroxysmal or short-term persistent AF.

Characterizing left ventricular mechanical and electrical activation in patients with normal and impaired systolic function using a non-fluoroscopic cardiovascular navigation system.

PURPOSE: Cardiac disease frequently has a degenerative effect on cardiac pump function and regional myocardial contraction. Therefore, an accurate assessment of regional wall motion is a measure of the extent and severity of the disease. We sought to further validate an intra-operative, sensor-based technology for measuring wall motion and strain by characterizing left ventricular (LV) mechanical and electrical activation patterns in patients with normal (NSF) and impaired systolic function (ISF). METHODS: NSF (n = 10; ejection fraction = 62.9 ± 6.1%) and ISF (n = 18; ejection fraction = 35.1 ± 13.6%) patients underwent simultaneous electrical and motion mapping of the LV endocardium using electroanatomical mapping and navigational systems (EnSite™ NavX™ and MediGuide™, Abbott). Motion trajectories, strain profiles, and activation times were calculated over the six standard LV walls. RESULTS: NSF patients had significantly greater motion and systolic strains across all LV walls than ISF patients. LV walls with low-voltage areas showed less motion and systolic strain than walls with normal voltage. LV electrical dyssynchrony was significantly smaller in NSF and ISF patients with narrow-QRS complexes than ISF patients with wide-QRS complexes, but mechanical dyssynchrony was larger in all ISF patients than NSF patients. The latest mechanical activation was most often the lateral/posterior walls in NSF and wide-QRS ISF patients but varied in narrow-QRS ISF patients. CONCLUSIONS: This intra-operative technique can be used to characterize LV wall motion and strain in patients with impaired systolic function. This technique may be utilized clinically to provide individually tailored LV lead positioning at the region of latest mechanical activation for patients undergoing cardiac resynchronization therapy. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov . Unique identifier: NCT01629160.

Mapping of ventricular arrhythmias using a novel noninvasive epicardial and endocardial electrophysiology system.

INTRODUCTION: The aim of this study was to assess the use of a novel noninvasive epicardial and endocardial electrophysiology system (NEEES) for mapping of ventricular arrhythmias. METHODS: Eight patients (2 females, mean age 50±17 years) with ischemic (n=3) and nonischemic (n=5) cardiomyopathy and inducible ventricular arrhythmias during electrophysiology study were enrolled. Noninvasive mapping of ventricular arrhythmias was performed using the NEEES based on body-surface electrocardiograms and computed tomography imaging data. Arrhythmia patterns were analyzed using noninvasive phase mapping. RESULTS: Macro-reentrant VT circuits were observed in 3 ischemic and 1 nonischemic cardiomyopathy patient, respectively. In the remaining 4 patients, phase mapping revealed relatively stable rotor activity and multiple wavelets. CONCLUSIONS: Noninvasive cardiac mapping was able to visualize the macro-reentrant circuits in patients with scar-related VT. In patients without myocardial scar only polymorphic VT or VF was inducible, and rotor activity and multiple wavelets were observed.

Distinctive Left Ventricular Activations Associated With ECG Pattern in Heart Failure Patients.

BACKGROUND: In contrast to patients with left bundle branch block (LBBB), heart failure patients with narrow QRS and nonspecific intraventricular conduction delay (NICD) display a relatively limited response to cardiac resynchronization therapy. We sought to compare left ventricular (LV) activation patterns in heart failure patients with narrow QRS and NICD to patients with LBBB using high-density electroanatomic activation maps. METHODS AND RESULTS: Fifty-two heart failure patients (narrow QRS [n=18], LBBB [n=11], NICD [n=23]) underwent 3-dimensional electroanatomic mapping with a high density of mapping points (387±349 LV). Adjunctive scar imaging was available in 37 (71%) patients and was analyzed in relation to activation maps. LBBB patients typically demonstrated (1) a single LV breakthrough at the septum (38±15 ms post-QRS onset); (2) prolonged right-to-left transseptal activation with absence of direct LV Purkinje activity; (3) homogeneous propagation within the LV cavity; and (4) latest activation at the basal lateral LV. In comparison, both NICD and narrow QRS patients demonstrated (1) multiple LV breakthroughs along the posterior or anterior fascicles: narrow QRS versus LBBB, 5±2 versus 1±1; P=0.0004; NICD versus LBBB, 4±2 versus 1±1; P=0.001); (2) evidence of early/pre-QRS LV electrograms with Purkinje potentials; (3) rapid propagation in narrow QRS patients and more heterogeneous propagation in NICD patients; and (4) presence of limited areas of late activation associated with LV scar with high interindividual heterogeneity. CONCLUSIONS: In contrast to LBBB patients, narrow QRS and NICD patients are characterized by distinct mechanisms of LV activation, which may predict poor response to cardiac resynchronization therapy.

A novel method to enhance phenotype, epicardial functional substrates, and ventricular tachyarrhythmias in Brugada syndrome.

BACKGROUND: Fever is associated with the manifestation of Brugada phenotype and ventricular tachycardia/ventricular fibrillation (VT/VF) in patients with Brugada syndrome (BrS). The thermal effect on the pathogenesis of functional substrates in BrS remains unknown. OBJECTIVE: This study aimed to elucidate the thermal effect on BrS phenotype, VT/VF, and electrophysiological characteristics of epicardial functional substrates in BrS. METHODS: We consecutively studied 15 patients with BrS receiving radiofrequency catheter ablation for drug-refractory ventricular tachyarrhythmias. Baseline characteristics, electrocardiographic features, and changes in epicardial functional substrates before and after epicardial warm water instillation (n = 6) were recorded and analyzed. RESULTS: A total of 15 male patients (mean age 41.3 ± 10.3 years) with type 1 BrS presenting with ventricular tachyarrhythmias were consecutively enrolled. Epicardial mapping in 11 patients demonstrated a significantly larger epicardial scar/low-voltage zone (LVZ) area within the right ventricular outflow tract and anterior right ventricular free wall than within the endocardium (6.32 ± 12.74 cm2 vs 52.91 ± 45.25 cm2; P = .007). Epicardial warm water instillation in 6 patients led to a significant enlargement of the functional scar/LVZ area (123.83 ± 35.26 cm2 vs 63.53 ± 40.57 cm2; P = .03), accelerated conduction velocity of the endocardium and epicardium without scar/LVZ area, and increased VT/VF inducibility (16.7% vs 100%; P = .02). Ablation by targeting premature ventricular complexes and/or epicardial abnormal substrates rendered noninducibility of VT/VF and prevented the recurrences of VT/VF. CONCLUSION: Epicardial warm water instillation enhanced functional epicardial substrates, which contributed to the increased inducibility of ventricular tachyarrhythmias in BrS. Ablation by targeting the triggers and abnormal epicardial substrates provided an effective strategy for preventing ventricular tachyarrhythmia recurrences in BrS.