Wearables are a viable digital health tool for older Indigenous adults living remotely in Australia (research).

Objective: Health programs for Indigenous people are most effective, acceptable, and sustainable when Indigenous perspectives are prioritized. Codesign builds on Indigenous people's creativity and propensity to experiment with new technologies and ensures research is designed and implemented in a culturally safe and respectful manner. Limited research has focused on older Indigenous people as partners in digital health. No research has focused on the acceptability and feasibility of older Indigenous people using wearables for heart health monitoring. This study provides insights into the acceptability and feasibility for ≥55-year-old Indigenous people living in remote locations to use wearables (watches and patches) to detect atrial fibrillation (AF) and high blood pressure. Methods: This mixed methods study was codesigned and coimplemented with the local Aboriginal Controlled Health Service in a remote area of New South Wales, Australia. It included active involvement and codesign with the participants. The devices used in this study included a Withings Scan watch and a Biobeat patch. Results: Despite challenging conditions (>36°C) and variable internet connectivity, 11 Indigenous older adults participated in a five-day wearables program in a remote location. Participants indicated that using digital health devices was acceptable and feasible for older Indigenous users. They described high levels of comfort, safety and convenience when using wearables (patches and watches) to detect AF. They were active participants in codesigning the program. Conclusion: Older Indigenous Australians are motivated to use wearable health devices. They are keen to participate in codesign innovative health tech programs to ensure new health technologies are acceptable to Indigenous people and feasible for remote locations.

Improved outcomes of conduction system pacing in heart failure with reduced ejection fraction: A systematic review and meta-analysis.

Conduction system pacing (CSP)-His bundle pacing (HBP) and left bundle branch area pacing (LBBAP)-are emerging alternatives to biventricular pacing (BVP) for cardiac resynchronization therapy (CRT) in heart failure. However, evidence is largely limited to small and observational studies. We conducted a meta-analysis including a total of 15 randomized controlled trials (RCTs) and non-RCTs that compare CSP (HBP and LBBAP) with BVP in patients with CRT indications. We assessed the mean differences in QRS duration (QRSd), pacing threshold, left ventricular ejection fraction (LVEF), and New York Heart Association (NYHA) class score. CSP resulted in a pooled mean QRSd improvement of -20.3 ms (95% confidence interval [CI] -26.1 to -14.5 ms; P < .05; I2= 87.1%) vs BVP. For LVEF, a weighted mean increase of 5.2% (95% CI 3.5%-6.9%; P < .05; I2 = 55.6) was observed after CSP vs BVP. The mean NYHA score was reduced by -0.40 (95% CI -0.6 to -0.2; P < .05; I2 = 61.7) after CSP vs BVP. A subgroup analysis of outcomes stratified by LBBAP and HBP demonstrated statistically significant weighted mean improvements of QRSd and LVEF with both CSP modalities compared with BVP. LBBAP resulted in NYHA improvement compared with BVP, without differences between CSP subgroups. LBBAP is associated with a significantly lowered mean pacing threshold of -0.51 V (95% CI -0.68 to -0.38 V) while HBP had increased the mean threshold (0.62 V; 95% CI -0.03 to 1.26 V) compared with BVP; however, this was associated with significant heterogeneity. Overall, both CSP techniques are feasible and effective CRT alternatives for heart failure. Further RCTs are needed to establish long-term efficacy and safety.

Finding a cause in sudden cardiac arrest survivors: Getting the testing right.

Sudden cardiac arrest (SCA) survivors are optimally managed by a multidisciplinary team with expertise in cardiac electrophysiology and cardiac genetics with the capacity to deal with both the medical and psychological needs of patients and their families. Consideration is given to an appropriate selection of second-line investigation, genetic testing, and cascade testing.

Comparison of the arrhythmogenic substrate for ventricular tachycardia in patients with ischemic vs non-ischemic cardiomyopathy - insights from high-density, multi-electrode catheter mapping.

PURPOSE: The purpose of this study was to compare the differences of arrhythmogenic substrate using high-density mapping in ventricular tachycardia (VT) patients with ischemic (ICM) vs non-ischemic cardiomyopathy (NICM). METHODS: Data from patients presenting for VT ablation from December 2016 to December 2020 at Westmead Hospital were reviewed. RESULTS: Sixty consecutive patients with structural heart disease (ICM 57%, NICM 43%, mean age 66 years) having catheter ablation of scar-related VT with pre-dominant left ventricular involvement were included. ICM was associated with larger proportion of dense scar area (bipolar; 19 [12-29]% vs 6 [3-10]%, P < 0.001, unipolar; 20 [12-32]% vs 11 [7-19]%, P = 0.01) compared with NICM. However, the scar ratio (unipolar dense scar [%]/bipolar dense scar [%]) was significantly higher in NICM patients (1.2 [0.8-1.7] vs 1.7 [1.3-2.3], P = 0.003). Larger scar area in ICM was paralleled by higher proportion of complex electrograms (6 [2-13] % vs 3 [1-5] %, P = 0.01), longer and wider voltage based conducting channels, higher incidence of late potential-based conducting channels, longer VT cycle-length (399 ± 80 ms vs 359 ± 68 ms, P = 0.04) and greater maximal stimulation-QRS interval among sites with good pace-map correlation (75 [51-99]ms vs 48 [31-73]ms, P = 0.02). Ventricular arrhythmia (VA) storm was more highly prevalent in ICM than NICM (50% vs 23%, P = 0.03). During the follow-up period, NICM had a significantly higher cumulative incidence for the VA recurrence than ICM (P = 0.03). CONCLUSIONS: High-density multi-electrode catheter mapping of left ventricular arrhythmogenic substrate of NICM tends to show smaller dense scar area and higher scar ratio, compared with ICM, suggestive the extent of epicardial/intramural substrate, with paucity of substrate targets for ablation, which results in the worse outcomes with ablation.

Impact of CPAP on the Atrial Fibrillation Substrate in Obstructive Sleep Apnea: The SLEEP-AF Study.

BACKGROUND: Observational studies report that obstructive sleep apnea (OSA) is associated with an increasingly remodeled atrial substrate in atrial fibrillation (AF). However, the impact of OSA management on the electrophysiologic substrate has not been evaluated. OBJECTIVES: In this study, the authors sought to determine the impact of OSA management on the atrial substrate in AF. METHODS: We recruited 24 consecutive patients referred for AF management with at least moderate OSA (apnea-hypopnea index [AHI] ≥15). Participants were randomized in a 1:1 ratio to commence continuous positive airway pressure (CPAP) or no therapy (n = 12 CPAP; n = 12 no CPAP). All participants underwent invasive electrophysiologic study (high-density right atrial mapping) at baseline and after a minimum of 6 months. Outcome variables were atrial voltage (mV), conduction velocity (m/s), atrial surface area <0.5 mV (%), proportion of complex points (%), and atrial effective refractory periods (ms). Change between groups over time was compared. RESULTS: Clinical characteristics and electrophysiologic parameters were similar between groups at baseline. Compliance with CPAP therapy was high (device usage: 79% ± 19%; mean usage/day: 268 ± 91 min) and resulted in significant AHI reduction (mean reduction: 31 ± 23 events/h). There were no differences in blood pressure or body mass index between groups over time. At follow-up, the CPAP group had faster conduction velocity (0.86 ± 0.16 m/s vs 0.69 ± 0.12 m/s; P (time × group) = 0.034), significantly higher voltages (2.30 ± 0.57 mV vs 1.94 ± 0.72 mV; P < 0.05), and lower proportion of complex points (8.87% ± 3.61% vs 11.93% ± 4.94%; P = 0.011) compared with the control group. CPAP therapy also resulted in a trend toward lower proportion of atrial surface area <0.5 mV (1.04% ± 1.41% vs 4.80% ± 5.12%; P = 0.065). CONCLUSIONS: CPAP therapy results in reversal of atrial remodeling in AF and provides mechanistic evidence advocating for management of OSA in AF.

Sex-Related Differences in Atrial Remodeling in Patients With Atrial Fibrillation: Relationship to Ablation Outcomes.

BACKGROUND: Population studies have demonstrated a range of sex differences including a higher prevalence of atrial fibrillation (AF) in men and a higher risk of AF recurrence in women. However, the underlying reasons for this higher recurrence are unknown. This study evaluated whether sex-based electrophysiological substrate differences exist to account for worse AF ablation outcomes in women. METHODS: High-density electroanatomic mapping of the left atrium was performed in 116 consecutive patients with AF. Regional analysis was performed across 6 left atrium segments. High-density maps were created using a multipolar catheter (Biosense Webster) during distal coronary sinus pacing at 600 and 300 ms. Mean voltage and conduction velocity was determined. Complex fractionated signals and double potentials were manually annotated. RESULTS: Overall, 42 (36%) were female, mean age was 61±8 years and AF was persistent in 52%. Global mean voltage was significantly lower in females compared with males at 600 ms (1.46±0.17 versus 1.84±0.15 mV, P<0.001) and 300 ms (1.27±0.18 versus 1.57±0.18 mV, P=0.013) pacing. These differences were seen uniformly across the left atrium. Females demonstrated significant conduction velocity slowing (34.9±6.1 versus 44.1±6.9 cm/s, P=0.002) and greater proportion of complex fractionated signals (9.9±1.7% versus 6.0±1.7%, P=0.014). After a median follow-up of 22 months (Q1-Q3: 15-29), females had significantly lower single-procedure (22 [54%] versus 54 [75%], P=0.029) and multiprocedure (24 [59%] versus 60 [83%], P=0.005) arrhythmia-free survival. Female sex and persistent AF were independent predictors of single and multiprocedure arrhythmia recurrence. CONCLUSIONS: Female patients demonstrated more advanced atrial remodeling on high-density electroanatomic mapping and greater post-AF ablation arrhythmia recurrence compared with males. These changes may contribute to sex-based differences in the clinical course of females with AF and in part explain the higher risk of recurrence. Graphic Abstract: A graphic abstract is available for this article.

Epicardial-Endocardial Reentry in Ischemic Cardiomyopathy.

In ischemic cardiomyopathy, endocardial reentry has traditionally been the mechanistic paradigm for understanding ventricular tachycardia (VT). However, recognition is growing that epicardial myocardium is a critical component for VT substrate, even in patients with ischemic cardiomyopathy. In this report, we present a novel case of a three-dimensional VT reentry involving epicardial components and an endocardial exit.

Sleep apnoea has a dose-dependent effect on atrial remodelling in paroxysmal but not persistent atrial fibrillation: a high-density mapping study.

AIMS: Obstructive sleep apnoea (OSA) associates with atrial fibrillation (AF), but the relationship of OSA severity and AF phenotype with the atrial substrate remains poorly defined. We sought to define the atrial substrate across the spectrum of OSA severity utilizing high-density mapping. METHODS AND RESULTS: Sixty-six consecutive patients (male 71%, age 61 ± 9) having AF ablation (paroxysmal AF 36, persistent AF 30) were recruited. All patents underwent formal overnight polysomnography and high-density left atrial (LA) mapping (mean 2351 ± 1244 points) in paced rhythm. Apnoea-hypopnoea index (AHI) (mean 21 ± 18) associated with lower voltage (-0.34, P = 0.005), increased complex points (r = 0.43, P < 0.001), more low-voltage areas (r = 0.42, P < 0.001), and greater voltage heterogeneity (r = 0.39, P = 0.001), and persisted after multivariable adjustment. Atrial conduction heterogeneity (r = 0.24, P = 0.025) but not conduction velocity (r = -0.09, P = 0.50) associated with AHI. Patchy regions of low voltage that co-localized with slowed conduction defined the atrial substrate in paroxysmal AF, while a diffuse atrial substrate predominated in persistent AF. The association of AHI with remodelling was most apparent among paroxysmal AF [LA voltage: paroxysmal AF -0.015 (-0.025, -0.005), P = 0.004 vs. persistent AF -0.006 (-0.017, 0.005), P = 0.30]. Furthermore, in paroxysmal AF an AHI ≥ 30 defined a threshold at which atrial remodelling became most evident (nil-mild vs. moderate vs. severe: 1.92 ± 0.42 mV vs. 1.84 ± 0.28 mV vs. 1.34 ± 0.41 mV, P = 0.006). In contrast, significant remodelling was observed across all OSA categories in persistent AF (1.67 ± 0.55 mV vs. 1.50 ± 0.66 mV vs. 1.55 ± 0.67 mV, P = 0.82). CONCLUSION: High-density mapping observed that OSA associates with marked atrial remodelling, predominantly among paroxysmal AF cohorts with severe OSA. This may facilitate the identification of AF patients that stand to derive the greatest benefit from OSA management.

Rapid Access Arrhythmia Clinics (RAACs) Versus Usual Care: Improving Efficiency and Safety of Arrhythmia Management.

BACKGROUND: Rapid access cardiology services have been proposed for assessment of acute cardiac conditions via an outpatient model-of-care that potentially could reduce hospitalisations. We describe a new Rapid Access Arrhythmia Clinic (RAAC) and compare major safety endpoints to usual care. METHODS: We matched 312 adult patients with suspected arrhythmia in RAAC to historical age and sex-matched controls discharged from hospital within Western Sydney Local Health District with suspected arrhythmia. The primary endpoint was a composite of time to first unplanned cardiovascular hospitalisation or cardiac death over 12 months. RESULTS: The average age of RAAC patients was 52.2±18.8 years and 51.6±18.8 years for controls, and 48.4% were female in both groups. Mean time from referral to first attended RAAC appointment was 10.5 days. Most were referred from emergency (177, 56.7%) and cardiologists at time of discharge (65, 20.8%). The most common reason for referral was palpitations (180, 57.7%). In total, 155 (49.7%) had a documented arrhythmia, with the most common being atrial fibrillation/flutter (88, 28.2%). The primary endpoint occurred in 35 (11.2%) patients in the RAAC pathway (97.1[95% CI 70-131.3] per 1,000 person-years), compared to 72 (23.1%) patients for usual care controls (229.5[95% CI 180.2-288.1] per 1,000 person-years). Using a propensity score analysis, RAAC pathway significantly reduced the primary endpoint by 59% compared to usual care (HR 0.41, 95% CI 0.27-0.62; p<0.001). CONCLUSIONS: RAACs for the early investigation and management of suspected arrhythmia is superior to usual care in terms of reduction in unplanned cardiovascular hospitalisation and death.

Genetic Susceptibility to Atrial Fibrillation Is Associated With Atrial Electrical Remodeling and Adverse Post-Ablation Outcome.

OBJECTIVES: This study sought to assess the atrial electrophysiological properties and post-ablation outcomes in patients with atrial fibrillation (AF) with and without the rs2200733 single nucleotide variant. BACKGROUND: The phenotype associated with chromosome 4q25 of the AF-susceptibility locus remains unknown. METHODS: In this study, 102 consecutive patients (ages 61 ± 9 years, 64% male) with paroxysmal or persistent AF were prospectively recruited prior to ablation. Patients were genotyped for rs2200733 and high-density left atrial (LA) electroanatomic maps were created using a multipolar catheter during distal coronary sinus (CS) pacing at 600 ms. Voltage, conduction velocity (CV), CV heterogeneity, and fractionated signals of 6 LA segments were determined. Arrhythmia recurrence was assessed by continuous device (51%) and Holter monitoring. RESULTS: Overall, 41 patients (40%) were single nucleotide variant carriers (38 heterozygous, 3 homozygous). A mean of 2,239 ± 852 points per patient were collected. Carriers had relatively increased CV heterogeneity (45.7 ± 7.5% vs. 35.9 ± 2.3%; p < 0.001), complex signals (9.4 ± 2.9% vs 6.0 ± 1.2%; p = 0.008), regional LA slowing, or conduction block (31.7 ± 8.2% vs. 17.9 ± 1.9%; p = 0.013) particularly in the posterior and lateral walls. There were no differences in CV, voltage, atrial refractoriness, or sinus node function. At follow-up (median: 27 months; range 19 to 31 months), carriers had lower arrhythmia-free survival (51% vs. 80%; p = 0.003). On multivariable analysis, carrier status was independently associated with CV heterogeneity (p = 0.001), complex signals (p = 0.002), and arrhythmia recurrence (p = 0.019). CONCLUSIONS: These data provide the first evidence that the rs2200733-tagged haplotype alters LA electrical remodeling and is a determinant of long-term outcome following AF ablation. The molecular mechanisms underpinning these changes warrant further investigation.

Epicardial Adipose Tissue Accumulation Confers Atrial Conduction Abnormality.

BACKGROUND: Clinical studies have reported that epicardial adipose tissue (EpAT) accumulation associates with the progression of atrial fibrillation (AF) pathology and adversely affects AF management. The role of local cardiac EpAT deposition in disease progression is unclear, and the electrophysiological, cellular, and molecular mechanisms involved remain poorly defined. OBJECTIVES: The purpose of this study was to identify the underlying mechanisms by which EpAT influences the atrial substrate for AF. METHODS: Patients without AF undergoing coronary artery bypass surgery were recruited. Computed tomography and high-density epicardial electrophysiological mapping of the anterior right atrium were utilized to quantify EpAT volumes and to assess association with the electrophysiological substrate in situ. Excised right atrial appendages were analyzed histologically to characterize EpAT infiltration, fibrosis, and gap junction localization. Co-culture experiments were used to evaluate the paracrine effects of EpAT on cardiomyocyte electrophysiology. Proteomic analyses were applied to identify molecular mediators of cellular electrophysiological disturbance. RESULTS: Higher local EpAT volume clinically correlated with slowed conduction, greater electrogram fractionation, increased fibrosis, and lateralization of cardiomyocyte connexin-40. In addition, atrial conduction heterogeneity was increased with more extensive myocardial EpAT infiltration. Cardiomyocyte culture studies using multielectrode arrays showed that cardiac adipose tissue-secreted factors slowed conduction velocity and contained proteins with capacity to disrupt intermyocyte electromechanical integrity. CONCLUSIONS: These findings indicate that atrial pathophysiology is critically dependent on local EpAT accumulation and infiltration. In addition to myocardial architecture disruption, this effect can be attributed to an EpAT-cardiomyocyte paracrine axis. The focal adhesion group proteins are identified as new disease candidates potentially contributing to arrhythmogenic atrial substrate.

Simultaneous epicardial-endocardial mapping of the sinus node in humans with structural heart disease: Impact of overdrive suppression on sinoatrial exits.

BACKGROUND: The 3-dimensional (3D) nature of sinoatrial node (SAN) function has not been characterized in the intact human heart. OBJECTIVE: The purpose of this study was to characterize the 3D nature of SAN function in patients with structural heart disease (SHD) using simultaneous endocardial-epicardial (endo-epi) phase mapping. METHODS: Simultaneous intraoperative endo-epi SAN mapping was performed during sinus rhythm at baseline (SRbaseline) and postoverdrive suppression at 600 ms (SRpost-pace600) and 400 ms (SRpost-pace400) using 2 Abbott Advisor HD Grid Mapping Catheters. Unipolar and bipolar electrograms (EGMs) were exported for phase analysis to determine (1) activation exits; (2) wavefront propagation sequence; (3) endo-epi dissociation; and (4) fractionation. Comparison of these variables was made among the 3 rhythms from an endo-epi perspective. RESULTS: Sixteen patients with SHD were included. SRbaseline activations were unicentric and predominantly exited cranially (87.5%) with endo-epi synchrony. However, with overdrive suppression, a tendency for caudal exit shift and endo-epi asynchrony was observed: SRpost-pace600 vs SRbaseline: cranial endo 75% vs 87.5% (P = .046); cranial epi 68.8% vs 87.5% (P = 0.002); caudal endo 12.5% vs 6.2% (P = 0.215); caudal epi 25% vs 6.2% (P = .0003); and SRpost-pace400 vs SRbaseline: cranial endo 81.3% vs 87.5% (P = 0.335); cranial epi 68.7% vs 87.5% (P = 0.0034; caudal endo 12.5% vs 6.2% (P = .148); caudal epi 31.2% vs 6.2% (P = 0.0017), consistent with multicentricity. EGM fractionation was more prevalent with overdrive suppression. CONCLUSION: During mapping of the intact human heart, SAN demonstrated redundancy of sinoatrial exits with postoverdrive shift in sites of earliest activation and epi-endo dissociation of sinoatrial exits.

Endocardial-Epicardial Phase Mapping of Prolonged Persistent Atrial Fibrillation Recordings: High Prevalence of Dissociated Activation Patterns.

BACKGROUND: Endocardial-epicardial dissociation and focal breakthroughs in humans with atrial fibrillation (AF) have been recently demonstrated using activation mapping of short 10-second AF segments. In the current study, we used simultaneous endo-epi phase mapping to characterize endo-epi activation patterns on long segments of human persistent AF. METHODS: Simultaneous intraoperative mapping of endo- and epicardial lateral right atrium wall was performed in patients with persistent AF using 2 high-density grid catheters (16 electrodes, 3 mm spacing). Filtered unipolar and bipolar electrograms of continuous 2-minute AF recordings and electrodes locations were exported for phase analyses. We defined endocardial-epicardial dissociation as phase difference of ≥20 ms between paired endo-epi electrodes. Wavefronts were classified as rotations, single wavefronts, focal waves, or disorganized activity as per standard criteria. Endo-Epi wavefront patterns were simultaneously compared on dynamic phase maps. Complex fractionated electrograms were defined as bipolar electrograms with ≥5 directional changes occupying at least 70% of sample duration. RESULTS: Fourteen patients with persistent AF undergoing cardiac surgery were included. Endocardial-epicardial dissociation was seen in 50.3% of phase maps with significant temporal heterogeneity. Disorganized activity (Endo: 41.3% versus Epi: 46.8%, P=0.0194) and single wavefronts (Endo: 31.3% versus Epi: 28.1%, P=0.129) were the dominant patterns. Transient rotations (Endo: 22% versus Epi: 19.2%, P=0.169; mean duration: 590±140 ms) and nonsustained focal waves (Endo: 1.2% versus Epi: 1.6%, P=0.669) were also observed. Apparent transmural migration of rotational activations (n=6) from the epi- to the endocardium was seen in 2 patients. Electrogram fractionation was significantly higher in the epicardium than endocardium (61.2% versus 51.6%, P<0.0001). CONCLUSIONS: Simultaneous endo-epi phase mapping of prolonged human persistent AF recordings shows significant Endocardial-epicardial dissociation marked temporal heterogeneity, discordant and transitioning wavefronts patterns and complex fractionations. No sustained focal activity was observed. Such complex 3-dimensional interactions provide insight into why endocardial mapping alone may not fully characterize the AF mechanism and why endocardial ablation may not be sufficient. Graphic Abstract: A graphic abstract is available for this article.

Functional Atrial Endocardial-Epicardial Dissociation in Patients With Structural Heart Disease Undergoing Cardiac Surgery.

OBJECTIVES: The goal of this study was to describe functional endocardial-epicardial dissociation (FEED), signal complexities, and three-dimensional activation dynamics of the human atrium with structural heart disease (SHD). BACKGROUND: SHD commonly predisposes to arrhythmias. Although progressive remodeling is implicated, direct demonstration of FEED in the human atrium has not been reported previously. METHODS: Simultaneous intraoperative mapping of the endocardial and epicardial lateral right atrial wall was performed by using 2 high-density grid catheters during sinus rhythm, pacing drive (600 ms and 400 ms cycle length), and premature extrastimulation (PES). Unipolar electrograms (EGMs) were exported into custom-made software for activation and phase mapping. Difference of ≥20 ms between paired endocardial and epicardial electrodes defined dissociation. EGMs with ≥3 deflections were classified as fractionated. RESULTS: Sixteen patients (mean age 60.5 ± 4.1 years; 18.7% with a history of atrial fibrillation) with SHD (43% ischemia, 57% valvular disease) were included. A total of 9,218 EGMs were analyzed. Compared with sinus rhythm, phase and activation analyses showed significant FEED during pacing at 600 ms and 400 ms (phase mapping 22.4% vs. 10% [p < 0.0001] and 25.8% vs. 10% [p < 0.0001], respectively; activation mapping 25.4% vs. 7.8% [p < 0.0001] and 27.7% vs. 7.8% [p < 0.0001]) and PES (phase mapping 34% vs. 10% [p < 0.0001]; activation mapping 29.5% vs. 7.8% [p < 0.0001]). Fractionated EGMs occurred significantly more during PES compared with sinus rhythm (50.2% vs. 39.5%; p < 0.0001). Activation patterns differed significantly during pacing drive and PES, with preferential epicardial exit during the latter (15.9% vs. 13.8%; p = 0.046). CONCLUSIONS: Simultaneous endocardial-epicardial mapping revealed significant FEED with signal fractionation and preferential epicardial breakthroughs with PES. Such complex three-dimensional interaction in electrical activation provides mechanistic insights into atrial arrhythmogenesis with SHD.

Focal Ventricular Tachycardias in Structural Heart Disease: Prevalence, Characteristics, and Clinical Outcomes After Catheter Ablation.

OBJECTIVES: This study sought to summarize the procedural characteristics and outcomes of patients with structural heart disease (SHD) who have focal ventricular tachycardia (VT). BACKGROUND: Scar-mediated re-entry is the predominant mechanism of VT in SHD. Some SHD patients may have a focal VT mechanism that remains poorly described. METHODS: An extended induction protocol incorporating programmed electrical stimulation, right ventricular burst pacing and isoprenaline was used to elucidate both re-entrant and focal VT mechanisms. RESULTS: Eighteen of 112 patients (16%) with SHD undergoing VT ablation over 2 years had a focal VT mechanism elucidated (mean age 66±13 years; ejection fraction 46±14%; nonischemic cardiomyopathy 10). Repetitive failure of termination with antitachycardia pacing (ATP) (69% of patients) or defibrillator shocks (56%) was a common feature of focal VTs. A median of 3 VTs per patient were inducible (28 focal VTs, 34 re-entrant VTs; 53% of patients had both focal and re-entrant VT mechanism). Focal VTs more commonly originated from the right ventricle (RV) than the left ventricle (LV) (67% vs. 33%, respectively). In the RV, the RV outflow tract was the most common site (33% of all focal VTs), followed by the RV moderator band (22%), apical septal RV (6%), and lateral tricuspid annulus (6%). The lateral LV (non-Purkinje) was the most common LV focal VT site (16%), followed by the papillary muscles (17%). After median follow-up of 289 days, 78% of patients remained arrhythmia-free; no patients had recurrence of focal VT at repeat procedure. In patients with recurrence, defibrillator therapies were significantly reduced from a median of 53 ATP episodes pre-ablation to 10 ATP episodes post-ablation. During follow-up, 2 patients (11%) underwent repeat VT ablation; none had recurrence of focal VT. CONCLUSIONS: Focal VTs are common in patients with SHD and often coexist with re-entrant forms of VT. High failure rate of defibrillator therapies was a common feature of focal VT mechanisms. Uncovering and abolishing focal VT may further improve outcomes of catheter ablation in SHD.