Cardiovascular Disease Burden, Mortality, and Sudden Death Risk in Epilepsy: A UK Biobank Study.

BACKGROUND: Sudden death is the leading cause of mortality in medically refractory epilepsy. Middle-aged persons with epilepsy (PWE) are under investigated regarding their mortality risk and burden of cardiovascular disease (CVD). METHODS: Using UK Biobank, we identified 7786 (1.6%) participants with diagnoses of epilepsy and 6,171,803 person-years of follow-up (mean 12.30 years, standard deviation 1.74); 566 patients with previous histories of stroke were excluded. The 7220 PWE comprised the study cohort with the remaining 494,676 without epilepsy as the comparator group. Prevalence of CVD was determined using validated diagnostic codes. Cox proportional hazards regression was used to assess all-cause mortality and sudden death risk. RESULTS: Hypertension, coronary artery disease, heart failure, valvular heart disease, and congenital heart disease were more prevalent in PWE. Arrhythmias including atrial fibrillation/flutter (12.2% vs 6.9%; P < 0.01), bradyarrhythmias (7.7% vs 3.5%; P < 0.01), conduction defects (6.1% vs 2.6%; P < 0.01), and ventricular arrhythmias (2.3% vs 1.0%; P < 0.01), as well as cardiac implantable electric devices (4.6% vs 2.0%; P < 0.01) were more prevalent in PWE. PWE had higher adjusted all-cause mortality (hazard ratio [HR], 3.9; 95% confidence interval [CI], 3.01-3.39), and sudden death-specific mortality (HR, 6.65; 95% CI, 4.53-9.77); and were almost 2 years younger at death (68.1 vs 69.8; P < 0.001). CONCLUSIONS: Middle-aged PWE have increased all-cause and sudden death-specific mortality and higher burden of CVD including arrhythmias and heart failure. Further work is required to elucidate mechanisms underlying all-cause mortality and sudden death risk in PWE of middle age, to identify prognostic biomarkers and develop preventative therapies in PWE.

Genetic mechanisms underlying arrhythmogenic mitral valve prolapse: Current and future perspectives.

Mitral valve prolapse (MVP) is a heart valve disease that is often familial, affecting 2%-3% of the general population. MVP with or without mitral regurgitation can be associated with an increased risk of ventricular arrhythmias and sudden cardiac death (SCD). Research on familial MVP has specifically focused on genetic factors, which may explain the heritable component of the disease estimated to be present in 20%-35%. Furthermore, the structural and electrophysiological substrates underlying SCD/ventricular arrhythmia risk in MVP have been studied postmortem and in the electrophysiology laboratory, respectively. Understanding how familial MVP and rhythm disorders are related may help patients with MVP by individualizing risk and working to develop effective management strategies. This contemporary, state-of-the-art, expert review focuses on genetic factors and familial components that underlie MVP and arrhythmia and encapsulates clinical, genetic, and electrophysiological issues that should be the objectives of future research.

Predicted Deleterious Variants in Cardiomyopathy Genes Prognosticate Mortality and Composite Outcomes in UK Biobank.

BACKGROUND: Inherited cardiomyopathies present with broad variation of phenotype. Data are limited regarding genetic screening strategies and outcomes associated with predicted deleterious variants in cardiomyopathy-associated genes in the general population. OBJECTIVES: The authors aimed to determine the risk of mortality and composite cardiomyopathy-related outcomes associated with predicted deleterious variants in cardiomyopathy-associated genes in the UK Biobank. METHODS: Using whole exome sequencing data, variants in dilated, hypertrophic, and arrhythmogenic right ventricular cardiomyopathy-associated genes with at least moderate evidence of disease causality according to ClinGen Expert Panel curations were annotated using REVEL (≥0.65) and ANNOVAR (predicted loss-of-function) considering gene-disease mechanisms. Genotype-positive and genotype-negative groups were compared using time-to-event analyses for the primary (all-cause mortality) and secondary outcomes (diagnosis of cardiomyopathy; composite outcome of diagnosis of cardiomyopathy, heart failure, arrhythmia, stroke, and death). RESULTS: Among 200,619 participants (age at recruitment 56.46 ± 8.1 years), 5,292 (2.64%) were found to host ≥1 predicted deleterious variants in cardiomyopathy-associated genes (CMP-G+). After adjusting for age and sex, CMP-G+ individuals had higher risk for all-cause mortality (HR: 1.13 [95% CI: 1.01-1.25]; P = 0.027), increased risk for being diagnosed with cardiomyopathy later in life (HR: 5.75 [95% CI: 4.58-7.23]; P < 0.0001), and elevated risk for composite outcome (HR: 1.29 [95% CI: 1.20-1.39]; P < 0.0001) than CMP-G- individuals. The higher risk for being diagnosed with cardiomyopathy and composite outcomes in the genotype-positive subjects remained consistent across all cardiomyopathy subgroups. CONCLUSIONS: Adults with predicted deleterious variants in cardiomyopathy-associated genes exhibited a slightly higher risk of mortality and a significantly increased risk of developing cardiomyopathy, and cardiomyopathy-related composite outcomes, in comparison with genotype-negative controls.

Frequency, Penetrance, and Variable Expressivity of Dilated Cardiomyopathy-Associated Putative Pathogenic Gene Variants in UK Biobank Participants.

BACKGROUND: There is a paucity of data regarding the phenotype of dilated cardiomyopathy (DCM) gene variants in the general population. We aimed to determine the frequency and penetrance of DCM-associated putative pathogenic gene variants in a general adult population, with a focus on the expression of clinical and subclinical phenotype, including structural, functional, and arrhythmic disease features. METHODS: UK Biobank participants who had undergone whole exome sequencing, ECG, and cardiovascular magnetic resonance imaging were selected for study. Three variant-calling strategies (1 primary and 2 secondary) were used to identify participants with putative pathogenic variants in 44 DCM genes. The observed phenotype was graded DCM (clinical or cardiovascular magnetic resonance diagnosis); early DCM features, including arrhythmia or conduction disease, isolated ventricular dilation, and hypokinetic nondilated cardiomyopathy; or phenotype-negative. RESULTS: Among 18 665 individuals included in the study, 1463 (7.8%) possessed ≥1 putative pathogenic variant in 44 DCM genes by the main variant calling strategy. A clinical diagnosis of DCM was present in 0.34% and early DCM features in 5.7% of individuals with putative pathogenic variants. ECG and cardiovascular magnetic resonance analysis revealed evidence of subclinical DCM in an additional 1.6% and early DCM features in an additional 15.9% of individuals with putative pathogenic variants. Arrhythmias or conduction disease (15.2%) were the most common early DCM features, followed by hypokinetic nondilated cardiomyopathy (4%). The combined clinical/subclinical penetrance was ≤30% with all 3 variant filtering strategies. Clinical DCM was slightly more prevalent among participants with putative pathogenic variants in definitive/strong evidence genes as compared with those with variants in moderate/limited evidence genes. CONCLUSIONS: In the UK Biobank, ≈1 of 6 of adults with putative pathogenic variants in DCM genes exhibited early DCM features potentially associated with DCM genotype, most commonly manifesting with arrhythmias in the absence of substantial ventricular dilation or dysfunction.

Diagnosis, significance, and management of ventricular thrombi in patients referred for VT ablation.

INTRODUCTION: In patients with structural heart disease presenting with ventricular tachycardia (VT), detection of ventricular thrombi and subsequent management can be challenging. This study aimed to assess the value of multimodality imaging with cardiac magnetic resonance imaging (CMR), contrast-enhanced transthoracic echocardiography (TTE), and computed tomography (CT) for thrombus detection as well as a management algorithm geared towards anticoagulation and deferred ablation for patients referred for VT ablation. METHODS AND RESULTS: A total of 154 consecutive patients referred for VT ablation underwent preprocedural multimodality imaging with CMR, CT, and TTE. In 9 patients (6%) a new ventricular thrombus was detected and anticoagulation was initiated. Thrombi were detected by CMR in nine patients, by CT in seven patients, and by TTE in two patients. Five patients eventually underwent endocardial VT ablation procedures 6.0 ± 2.0 months after initiation of anticoagulation with one patient also requiring an epicardial approach. Two patients died while on anticoagulation, unrelated to ventricular arrhythmia. Four of five patients were rendered non-inducible and no testing was performed in 1/5 patients. Areas containing left ventricular thrombi were non-excitable with pacing. Six of thirty-two inducible VTs were mapped in close vicinity of ventricular thrombi. No clinical embolic events occurred during the ablation procedures. CONCLUSIONS: Ventricular thrombus was detected in 6% of consecutive patients with structural heart disease undergoing VT ablation. CMR was the most sensitive modality, while contrast-enhanced TTE failed to detect the majority of thrombi. Anticoagulation followed by ablation can be safely and successfully performed in patients with ventricular thrombi.

Factors predictive for delayed enhancement in cardiac resonance imaging in patients undergoing catheter ablation of premature ventricular complexes.

BACKGROUND: Patients undergoing ablation of premature ventricular complexes (PVCs) can have cardiac scar. Risk factors for the presence of scar are not well defined. OBJECTIVES: To determine the prevalence of scarring detected by delayed enhancement cardiac magnetic resonance imaging (DE-CMR) in patients undergoing ablation of PVCs, to create a risk score predictive of scar, and to explore correlations between the scoring system and long-term outcomes. METHODS: DE-CMR imaging was performed in consecutive patients with frequent PVCs referred for ablation. The full sample was used to develop a prediction model for cardiac scar based on demographic and clinical characteristics, and internal validation of the prediction model was done using bootstrap samples. RESULTS: The study consisted of 333 patients (52% male, aged 53.2 ± 14.5 years, preablation ejection fraction 50.9% ± 12.2%, PVC burden 20.7 ± 13.14), of whom 112 (34%) had DE-CMR scarring. Multiple logistic regression analysis showed age (odds ratio [OR] 1.02 [1.01-1.04]/year, P = .019) and preablation ejection fraction (OR 0.92 [0.89-0.94]/%, P < .001) to be predictive of scar. A weighted risk score incorporating age and ejection fraction was used to stratify patients into low-, medium-, and high-risk groups. Scar prevalence was around 86% in the high-risk group and 12% in the low-risk group; high-risk patients had worse survival free of arrhythmia. CONCLUSIONS: Cardiac scar was present in one-third of patients referred for PVC ablation. A weighted risk score based simply on patient age and preprocedural ejection fraction can help discriminate between patients at high and low risk for the presence of cardiac scar and worse arrhythmia outcomes.

The value of cardiac magnetic resonance imaging and programmed ventricular stimulation in patients with ventricular noncompaction and ventricular arrhythmias.

INTRODUCTION: Left ventricular noncompaction (LVNC) is associated with ventricular arrhythmias (VA) including premature ventricular complexes, and ventricular tachycardia (VT). The value of imaging with delayed enhancement cardiac magnetic resonance (DE-CMR) and programmed ventricular stimulation (PVS) for risk stratification in patients with VA and LVNC is unknown. The purpose of this study was to determine whether DE-CMR and PVS are beneficial for risk stratification and whether CMR helps to identify VA target sites. METHODS AND RESULTS: Consecutive patients with LVNC undergoing ablation for VAs were included, all patients had preprocedure DE-CMR. A total of 23 patients (7 women, 46 ± 14 years, ejection fraction 35 ± 14) were included and followed for 2.9 ± 2.2 years. DE-CMR scar was present in 12/23 patients (52%). PVS was performed in 20/23 patients, 8/10 patients (80%) with scar were inducible for VT compared to 0/10 (0%) patients without scar (p < .001). VA target sites in patients with scarring were located adjacent to areas of scarring in all but 1 patient and ablation was successful in 15/23 patients (65%). Patients with scar had worse survival free of VT than those without scar (log rank p = .01) and patients with inducible VT had worse survival free of VT than those who were noninducible (log rank p < .001). CONCLUSIONS: The presence of CMR defined scar in patients with LVNC was associated with inducible VT and worse outcomes. Inducibility for VT was associated with VT recurrence. Furthermore, CMR is beneficial in localizing the arrhythmogenic substrate in LVNC and therefore can aid in procedural planning.

Mapping and Ablation of Intramural Ventricular Arrhythmias: A Stepwise Approach Focused on the Site of Origin.

OBJECTIVES: This study sought to establish a mapping and ablation strategy to target intramural ventricular arrhythmias (VAs) by identifying the precise arrhythmia site of origin (SOO). BACKGROUND: Radiofrequency ablation of intramural VAs is challenging because the arrhythmia origin is difficult to localize. METHODS: In 83 consecutive patients with intramural VAs, a stepwise mapping approach was performed: ablation targeted directly the SOO when possible followed by the closest adjacent anatomical structure when necessary. If the SOO could not be identified, the earliest endocardial breakout sites were ablated. Safety and procedural outcomes between patients in whom the SOO could and could not be identified were compared. RESULTS: The SOO was identified in 19 of 83 (23%) patients, and radiofrequency ablation was effective in eliminating VAs in all 19 (100%) patients by ablation at the SOO alone (n = 3), at the SOO and an anatomically adjacent area (n = 7), or at an anatomically adjacent area alone (n = 9). Breakout site mapping and ablation in the remaining 64 patients in whom the SOO was not identified was effective in 43 of 64 patients, which was significantly less than in patients in whom the SOO was identified (67% vs. 100%; p < 0.05). CONCLUSIONS: Identification of the SOO was associated with a successful ablation procedure by either targeting the SOO directly or targeting an adjacent anatomical structure. Ablation at the breakout sites of intramural VAs has a lower efficacy than when the SOO can be directly targeted.

Risk stratification in patients with nonischemic cardiomyopathy and ventricular arrhythmias based on quantification of intramural delayed enhancement on cardiac magnetic resonance imaging.

INTRODUCTION: Intramural scarring is a risk factor for sudden cardiac death. The objective of this study was to determine the value of scar quantification for risk stratification in patients with nonischemic cardiomyopathy (NICM) undergoing ablation procedures for ventricular arrhythmias (VA). METHODS AND RESULTS: Cardiac late gadolinium-enhanced magnetic resonance imaging was performed in patients with NICM referred for ablation of premature ventricular complexes or ventricular tachycardia (VT). Only patients with intramural delayed enhancement were included. Scar volume was measured and correlated with immediate and long-term outcomes. Receiver operator curves, Wilcoxon signed-rank testing, and logistic regression were used to compare patient characteristics. The study consisted of 99 patients (74 males, mean age: 59.6 [54.0-68.1] years, ejection fraction [EF]: 46.0 [35.0-60.0]%). Patients without clinical VT or inducible VT had smaller total and core scar size compared to patients with a history of VT or inducible VT (total scar 1.12 [0.74-1.79] cm3 vs 7.45 [4.16-12.21] cm3 , P < .001). A total scar volume of greater than or equal to 2.78 cm3 was associated with inducibility of VT (AUC 0.94, 95% CI [0.89-0.98], sensitivity 85%, specificity 90%). Scar volume was associated with VT inducibility independent of a prior history of VT or the preprocedure EF (adjusted OR 1.67 [1.24-2.24]/cm3 , P < .01). CONCLUSION: Quantification of scar size in patients with intramural scarring is useful for risk stratification in patients with NICM and VA independent of the EF or a prior history of VT. Scar characteristics of patients without a history of VT who have inducible VT are similar to patients with a history of VT.

Stepwise Approach for Ventricular Tachycardia Ablation in Patients With Predominantly Intramural Scar.

OBJECTIVES: The goal of this study was to assess the value of a stepwise, image-guided ablation approach in patients with cardiomyopathy and predominantly intramural scar. BACKGROUND: Few reports have focused on catheter-based ventricular tachycardia (VT) ablation strategies in patients with predominantly intramural scar. METHODS: The study included patients with predominantly intramural scar undergoing VT ablation. A stepwise strategy was performed consisting of a localized ablation guided by conventional mapping criteria followed by a more extensive ablation if VT remained inducible. The extensive ablation was guided by the location and extent of intramural scarring on delayed enhanced-cardiac magnetic resonance imaging. A historical cohort who did not undergo additional extensive ablation was identified for comparison. A novel measurement, the scar depth index (SDI), indicating the percent area of the scar at a given depth, was correlated with outcomes. RESULTS: Forty-two patients who underwent stepwise ablation (median age 61 years [interquartile range: 55 to 69 years], 35 male patients, median left ventricular ejection fraction 36.0% [25.0% to 55.0%], ischemic [n = 4] or nonischemic cardiomyopathy [n = 38]) were followed up for a median of 17 months (8 to 36 months). A stepwise approach resulted in a 1-year freedom from VT, death, or cardiac transplantation of 76% (32 of 42). Patients who underwent additional extensive ablation had a lower risk of events than a clinically similar historical cohort (N = 19) (hazard ratio: 0.30; 95% CI: 0.13 to 0.68; p < 0.004). SDI>5mm was associated with worse long-term outcomes (hazard ratio: 1.03; 95% CI: 1.01 to 1.06%; p = 0.03), SDI>5mm >16.5% was associated with failed ablation (area under the curve: 0.84; 95% CI: 0.71 to 0.97). CONCLUSIONS: Stepwise ablation using delayed enhanced-cardiac magnetic resonance guidance is a novel approach to VT ablation in patients with predominantly intramural scarring. The SDI correlates with immediate procedural and long-term outcomes.

Risk stratification in patients with frequent premature ventricular complexes in the absence of known heart disease.

BACKGROUND: Frequent premature ventricular complexes (PVCs) can be an indicator of structural heart disease. OBJECTIVE: The purpose of this study was to determine the prevalence of scarring detected by delayed enhancement cardiac magnetic resonance (DE-CMR) imaging in patients with frequent PVCs without apparent structural heart disease and to determine the value of programmed ventricular stimulation (PVS) for risk stratification in patients with frequent PVCs and myocardial scarring. METHODS: DE-CMR imaging was performed in patients without apparent heart disease who had frequent PVCs and were referred for ablation. In the presence of scarring, scar volume was measured and correlated with outcome variables. All patients underwent PVS and were monitored for the occurrence of ventricular arrhythmias. Logistic regression was used to compare imaging and procedural findings with long-term outcomes, with adjustment for postablation ejection fraction (EF). RESULTS: The study consisted of 272 patients (135 men; mean age 52 ± 15 years; EF 52% ± 12%). DE-CMR scar was found in 67 patients (25%), and 7 (3%) were found to have inducible ventricular tachycardia (VT). The presence and amount of DE-CMR were related to the risk of long-term VT independent of EF (hazard ratio 18.8 [95% confidence interval] [2.0-176.6], P = .01; and hazard ratio 1.4 [1.1-1.7] per cm3 scar, P <.001, respectively). The positive predictive value and negative predictive value of PVS for VT during long-term follow-up were 71% and 100%, respectively. CONCLUSION: Preprocedural cardiac DE-CMR and PVS can be used to identify patients with frequent PVCs without apparent heart disease who are at risk for VT.

Targeting Noninducible Clinical Ventricular Tachycardias in Patients With Prior Myocardial Infarctions Based on Stored Electrograms.

BACKGROUND: Ablation of postinfarction ventricular tachycardia (VT) has been shown to reduce VT recurrence and decrease mortality. However, VT recurrence can occur despite extensive ablation procedures. The lack of inducibility of clinical VTs during ablation procedures remains problematic and may be in part responsible for VT recurrences. In this prospective study, we targeted documented but noninducible clinical VTs based on stored implantable cardioverter-defibrillator (ICD) electrograms. METHODS: Radiofrequency ablation was performed in a consecutive group of 66 postinfarction patients (mean age, 67.5±9.2 years; men, 61; mean left ventricular ejection fraction, 25.1±10.8%) in whom clinical VTs were not inducible during an ablation procedure. In the first 33 patients (control group), only inducible VTs were targeted, and in the second 33 patients, noninducible clinical VTs were also targeted by pace-mapping based on stored ICD-electrograms (ICD-electrogram-guided ablation group). Procedural and clinical outcomes were compared at 24 months post-ablation. RESULTS: VT recurred in 5 patients (15%) in whom the ICD-electrogram-guided approach was performed and in 13 patients (39%) in the control group. Freedom from recurrent VT was higher (log-rank P=0.04) in the ICD-electrogram-guided group, but there was no difference in ventricular fibrillation or in total mortality between both groups. CONCLUSIONS: Ablation guided by pace-mapping of noninducible postinfarction clinical VTs based on ICD-electrograms is feasible and reduces the risk of recurrent VT.

Postinfarction Myocardial Calcifications on Cardiac Computed Tomography: Implications for Mapping and Ablation in Patients With Nontolerated Ventricular Tachycardias.

BACKGROUND: Postinfarction ventricular tachycardia (VT) generally involves myocardial fibers surrounded by scar. Calcification of scar tissue has been described, but the relationship between calcifications within endocardial scar and VTs is unclear. The purpose of this study was to assess the prevalence of myocardial calcifications as detected by cardiac computed tomography (CT) and the benefit for mapping and ablation focusing on nontolerated VTs. METHODS: Fifty-six consecutive postinfarction patients had a cardiac CT performed before a VT ablation procedure. Another 56 consecutive patients with prior infarction without VT who had cardiac CTs served as a control group. RESULTS: Myocardial calcifications were identified in 39 of 56 patients (70%) in the postinfarction group with VT, compared with 6 of 56 patients (11%) in the control group without VT. Calcifications were associated with VT when compared with a control group. A calcification volume of 0.538 cm3 distinguished patients with calcification-associated VT from patients without calcification-associated VTs (area under the curve, 0.87; sensitivity, 0.87; specificity, 0.88). Myocardial calcifications corresponded to areas of electrical nonexcitability and formed a border for reentry circuits for 49 VTs (33% of all VTs for which target sites were identified) in 24 of 39 patients (62%) with myocardial calcifications. A nonconfluent calcification pattern was associated with VT target sites independent of calcification volume ( P=0.01). CONCLUSIONS: Myocardial calcifications detected by cardiac CT in patients with prior infarction are associated with VT. The calcifications correspond to areas of unexcitability and represent a fixed boundary of reentry circuits that can be visualized by CT. Calcifications correspond to effective ablation sites in >1/3 of patients with postinfarction VT.

Significance of clinical ventricular tachycardias induced by antitachycardia pacing in patients with prior myocardial infarction.

BACKGROUND: In patients with implantable cardioverter-defibrillator (ICD), ventricular tachycardia (VT) can occur spontaneously or as a result of antitachycardia pacing (ATP) that changes, rather than terminates, a spontaneous VT to a different VT. The relevance of ATP-induced VTs is uncertain. OBJECTIVE: The purpose of this study was to assess the clinical relevance of ATP-mediated VTs in patients undergoing VT ablation procedures. METHODS: Stored ICD electrograms of 162 consecutive patients with prior myocardial infarction referred for VT ablation (mean age 67.5 ± 9.2 years; 150 men; median ejection fraction 25% [IQR 20%-35%]) were reviewed. Clinical VTs were classified as spontaneous or ATP-induced. All VTs were targeted during the ablation procedures. RESULTS: Of 554 ICD-recorded clinical VTs, 157 (28%) were ATP-induced (63 patients) and 397 (72%) were spontaneous. ATP-induced VTs were faster (cycle length 316 ± 62 ms vs 369 ± 83 ms; P < .001), less commonly inducible with invasive programmed stimulation (35% vs 52%; P < .001), and less commonly had identifiable target sites (21% vs 40%; P < .001) than were spontaneous VTs. During a median follow-up of 368 days [IQR: 68-1106] postablation, 71 VTs recurred (39 patients), none of which was a previously documented ATP-induced VT. A history of ATP-induced VT was associated with an increase in VT recurrence. CONCLUSION: ATP-induced VTs occur frequently in patients with prior myocardial infarction presenting for VT ablation procedures. The presence of ATP-induced VT is associated with a higher VT recurrence rate postablation. None of the ATP-induced VTs recorded before the ablation procedure recurred postablation, and therefore ATP-induced VTs represent a marker rather than the cause of VT recurrence.

Thromboembolic prophylaxis protocol with warfarin after radiofrequency catheter ablation of infarct-related ventricular tachycardia.

INTRODUCTION: Ablation in the left ventricle (LV) is associated with a risk of thromboembolism. There are limited data on the use of specific thromboembolic prophylaxis strategies postablation. We aimed to evaluate a thromboembolic prophylaxis protocol after ventricular tachycardia (VT) ablation. METHODS AND RESULTS: The index procedures of 217 patients undergoing ablation for infarct-related VT with open irrigated-tip catheters were included. Patients with large LV endocardial ablation area (>3 cm between ablation lesions) were started on low-dose, slowly escalating unfractionated heparin (UFH) infusion 8 hours after access hemostasis, followed by 3 months of anticoagulation. Patients with less extensive ablation were treated only with antiplatelet agents postablation. Postablation bridging anticoagulation was used in 181 (83%) patients. Of them, 11 (6%) patients experienced bleeding events (1 required endovascular intervention) and 1 (0.6%) experienced lower extremity arterial embolism requiring vascular surgery. Systemic anticoagulation was prescribed in 190 (89%) of 214 patients discharged from the hospital (warfarin in 98%), while the rest received single- or dual-antiplatelet therapy alone. Patients treated with an anticoagulant had significantly longer radiofrequency time compared to patients treated with antiplatelet agents only. One (0.5%) of the patients treated with oral anticoagulation experienced major bleeding 2 weeks postablation. No thromboembolic events were documented in either the anticoagulation or the "antiplatelet only" group postdischarge. CONCLUSION: A slowly escalating bridging regimen of UFH, followed by 3 months of oral anticoagulation, is associated with low thromboembolic and bleeding risks after infarct-related VT ablation. In the absence of extensive ablation, antiplatelet therapy alone is reasonable.

Association of preprocedural cardiac magnetic resonance imaging with outcomes of ventricular tachycardia ablation in patients with idiopathic dilated cardiomyopathy.

BACKGROUND: Knowledge of complex arrhythmogenic substrates can help plan ventricular tachycardia (VT) ablation in patients with idiopathic dilated cardiomyopathy (DCM). OBJECTIVE: The purpose of this study was to assess whether preprocedural late gadolinium enhancement magnetic resonance imaging (LGE-MRI) can improve ablation outcomes in DCM. METHODS: Consecutive patients (N = 96) with idiopathic DCM underwent VT ablation with open-irrigated catheters (2006-2016). Before 2012, LGE-MRI was not performed at our institution in patients with implanted devices, but it has been performed routinely in all patients after implementation of a new MRI protocol in 2012. We retrospectively compared acute and long-term outcomes of initial VT ablation procedures in patients with (n = 41) and those without (n = 55) preprocedural LGE-MRI. Procedural outcome was classified as successful if VT was not inducible postablation. RESULTS: The 2 groups had a similar mean age and ejection fraction, comorbidities, and frequency of epicardial ablation. Preablation LGE-MRI was independently associated with improved procedural success (63% vs 24%) by logistic regression analysis (adjusted odds ratio [OR] 7.86, P <.001). This result was consistent even when patients with nondiagnostic MRIs due to artifact were included in the imaging group (OR 4.87, P = .005). Preablation imaging was also associated with improved survival free of the composite endpoint of VT recurrence, heart transplantation, or death, which was met by 11 (27%) and 33 (60%) patients in the imaging and no imaging groups, respectively, after median 7.6 months of follow-up (unadjusted log-rank P = .02). However, there was no association with long-term outcomes after adjustment for other covariates. CONCLUSION: Preprocedural imaging with LGE-MRI may be associated with improved outcomes of VT ablation in DCM.

Contemporary measures to reduce the risk of embolic events in patients with atrial fibrillation.

Atrial fibrillation is a common arrhythmia with significant risk of embolic events. Patients with atrial fibrillation should undergo a careful assessment using validated risk score calculators to estimate the risk of embolic events and the risk of bleeding. Patients deemed to be at a high risk for arterial thromboembolism should be advised to take an oral anticoagulant with a vitamin K antagonist or a target-specific oral anticoagulant unless contraindicated. These agents significantly reduce the risk of embolic events, but at the expense of a higher risk of bleeding. Antiplatelet agents do not confer the same degree of protection and their use should limited. When antithrombotic treatment is contraindicated, novel approaches such as left atrial appendage occlusion should be considered.