Publications

BACKGROUND: The decision to continue or discontinue oral anticoagulation (OAC) after catheter ablation for atrial fibrillation (AF) requires balancing thromboembolic and bleeding risks, and the need for long-term OAC after a successful procedure remains unclear. Thus, we aim to evaluate the safety of discontinuing OAC compared with continuation after apparently successful AF ablation.

METHODS: PubMed, Embase, Cochrane Central, and Web of Science were searched for randomized controlled trial and cohort studies comparing OAC discontinuation with continuation. Eligible studies required no evidence of AF recurrence before group allocation. A random-effects model with Hartung-Knapp-Sidik-Jonkman adjustment was used to estimate pooled risk ratios (RR) and hazard ratios (HR) with 95% confidence intervals (CI).

RESULTS: Thirteen studies encompassing 249,452 patients were included. No difference was observed between groups for thromboembolic events (RR 0.932; 95% CI 0.624 to 1.393; GRADE: very low quality of evidence), nor when stratifying for patients with CHA2DS2-VASc ≥ 2 (RR 1.289; 95% CI 0.673 to 2.469) or < 2 (RR 0.786; 95% CI 0.353 to 1.751). For major bleeding, discontinuing OAC was associated with a significant reduction in events (RR 0.332; 95% CI 0.167 to 0.659; GRADE: low quality of evidence). Finally, for all-cause mortality, no difference between groups was observed (HR 0.977; 95% CI 0.889 to 1.073; GRADE: very low quality of evidence).

CONCLUSION: Discontinuing OAC after successful AF ablation may reduce the risk of major bleeding while not increasing the risk of thromboembolism. However, further studies with proper designs are needed to confirm these associations.

BACKGROUND AND OBJECTIVE: Ventricular arrhythmias (VAs) remain a pervasive and deadly arrhythmia in patients with left ventricular assist devices (LVADs). Catheter ablation has emerged as a treatment option for refractory VAs, yet evidence in the era of the HeartMate 3 (HM3) remains limited. This review aims to synthesize contemporary evidence for VA ablation in LVAD recipients.

METHODS: A systematic review was performed across major electronic databases. The primary efficacy outcome was the recurrence of ventricular tachycardia (VT), and the primary safety outcome was the rate of procedural complications. The secondary outcomes were inability to induce any VT, all-cause mortality at 12 months, orthotropic heart transplantation (OHT). Sub-analyses were performed for patients with HM3 LVADs.

RESULTS: Twenty-seven studies encompassing 300 LVAD recipients undergoing 325 VT ablations, after a mean follow-up of 327 ± 175 days post VT ablation, VT recurred in 38% (95% CI, 28% to 49%) of cases and the complication rate was 8% (95% CI, 1.6% to 15.7%). VT was non-inducible in 61% of cases. One-year all-cause mortality was 26%, and 16% had OHT. Among HM3 recipients, electromagnetic interference (EMI) occurred in 51%, and no cases of device thrombosis were reported; one stroke was observed.

CONCLUSIONS: Catheter ablation is a safe and feasible treatment for refractory VAs in LVAD patients as evidenced by low complication rates and reasonable acute success. Yet, the persistence of considerable VT recurrence and all-cause mortality reflects the clinical complexity of this population. Procedural challenges include mapping limitations caused by EMI, particularly in the HM3 era.

AIMS: Catheter ablation is the standard treatment for symptomatic atrial fibrillation (AF) and can be performed under general anaesthesia (GA) or varying levels of sedation to optimize patient comfort and lesion formation. However, the effect of different anaesthesia strategies on AF recurrence rates remains uncertain.

METHODS AND RESULTS: We systematically searched PubMed, Embase, Cochrane, and ClinicalTrials.gov for randomized controlled trials (RCTs) and observational studies comparing outcomes of catheter ablation under GA vs. sedation (including deep, moderate, and conscious sedation). We pooled risk ratios (RR) with 95% confidence intervals (CI) with a random effects model. R version 4.4.1 was used for statistical analyses. Our systematic review and meta-analysis included 6 RCTs and 17 observational studies, corresponding to 12 302 patients assigned to either sedation (n = 8952) or GA (n = 3350). There was no difference in recurrence of atrial tachyarrhythmias (ATAs) between groups (RR 1.15; 95% CI 0.97-1.36; P = 0.10; 95% prediction interval 0.66-2.01). There was no significant subgroup interaction in the recurrence of AF according to sedation type (conscious vs. mild vs. moderate sedation vs. deep sedation) (P = 0.20) or AF type (persistent AF vs. non-persistent) (P = 0.20).

CONCLUSION: In patients undergoing catheter ablation for AF, there was no significant difference in recurrence of ATA between GA and sedation.

BACKGROUND: Implantable cardioverter-defibrillator (ICD) intervention is an established prophylactic measure. Identifying high-benefit patients poses challenges.

PURPOSE: To assess the prognostic value of cardiac magnetic resonance imaging (MRI) parameters including myocardial deformation for risk stratification of ICD intervention in non-ischemic cardiomyopathy (NICM) while accounting for competing mortality risk.

STUDY TYPE: Retrospective and prospective.

POPULATION: One hundred and fifty-nine NICM patients eligible for primary ICD (117 male, 54 ± 13 years) and 49 control subjects (38 male, 53 ± 5 years).

FIELD STRENGTH/SEQUENCE: Balanced steady state free precession (bSSFP) and three-dimensional phase-sensitive inversion-recovery late gadolinium enhancement (LGE) sequences at 1.5 T or 3 T.

ASSESSMENT: Patients underwent MRI before ICD implantation and were followed up. Functional parameters, left ventricular global radial, circumferential and longitudinal strain, right ventricular free wall longitudinal strain (RV FWLS) and left atrial strain were measured (Circle, cvi42). LGE presence was assessed visually. The primary endpoint was appropriate ICD intervention. Models were developed to determine outcome, with and without accounting for competing risk (non-sudden cardiac death), and compared to a baseline model including LGE and clinical features.

STATISTICAL TESTS: Wilcoxon non-parametric test, Cox's proportional hazards regression, Fine-Gray competing risk model, and cumulative incidence functions. Harrell's c statistic was used for model selection. A P value <0.05 was considered statistically significant.

RESULTS: Follow-up duration was 1176 ± 960 days (median: 896). Twenty-six patients (16%) met the primary endpoint. RV FWLS demonstrated a significant difference between patients with and without events (-12.5% ± 5 vs. -16.4% ± 5.5). Univariable analyses showed LGE and RV FWLS were significantly associated with outcome (LGE: hazard ratio [HR] = 3.69, 95% CI = 1.28-10.62; RV FWLS: HR = 2.04, 95% CI = 1.30-3.22). RV FWLS significantly improved the prognostic value of baseline model and remained significant in multivariable analysis, accounting for competing risk (HR = 1.73, 95% CI = 1.12-2.66).

DATA CONCLUSIONS: In NICM, RV FWLS may provide additional predictive value for predicting appropriate ICD intervention.

LEVEL OF EVIDENCE: 2 TECHNICAL EFFICACY: Stage 5.

BACKGROUND: Myocardial electrical heterogeneity is critical for normal cardiac electromechanical function, but abnormal or excessive electrical heterogeneity is proarrhythmic. The spatial ventricular gradient (SVG), a vectorcardiographic measure of electrical heterogeneity, has been associated with arrhythmic events during long-term follow-up, but its relationship with short-term inducibility of ventricular arrhythmias (VAs) is unclear.

OBJECTIVE: This study was designed to determine associations between SVG and inducible VAs during electrophysiology study.

METHODS: A retrospective study was conducted of adults without prior sustained VA, cardiac arrest, or implantable cardioverter-defibrillator who underwent ventricular stimulation for evaluation of syncope and nonsustained ventricular tachycardia or for risk stratification before primary prevention implantable cardioverter-defibrillator implantation. The 12-lead electrocardiograms were converted into vectorcardiograms, and SVG magnitude (SVGmag) and direction (azimuth and elevation) were calculated. Odds of inducible VA were regressed by logistic models.

RESULTS: Of 143 patients (median age, 69 years; 80% male; median left ventricular ejection fraction [LVEF], 47%; 52% myocardial infarction), 34 (23.8%) had inducible VAs. Inducible patients had lower median LVEF (38% vs 50%; P < .0001), smaller SVGmag (29.5 vs 39.4 mV·ms; P = .0099), and smaller cosine SVG azimuth (cosSVGaz; 0.64 vs 0.89; P = .0007). When LVEF, SVGmag, and cosSVGaz were dichotomized at their medians, there was a 39-fold increase in adjusted odds (P = .002) between patients with all low LVEF, SVGmag, and cosSVGaz (65% inducible) compared with patients with all high LVEF, SVGmag, and cosSVGaz (4% [n = 1] inducible). After multivariable adjustment, SVGmag, cosSVGaz, and sex but not LVEF or other characteristics remained associated with inducible VAs.

CONCLUSION: Assessment of electrical heterogeneity by SVG, which reflects abnormal electrophysiologic substrate, adds to LVEF and identifies patients at high and low risk of inducible VA at electrophysiology study.

Chagas cardiomyopathy caused by infection with the intracellular parasite Trypanosoma cruzi is the most common and severe expression of human Chagas disease. Heart failure, systemic and pulmonary thromboembolism, arrhythmia, and sudden cardiac death are the principal clinical manifestations of Chagas cardiomyopathy. Ventricular arrhythmias contribute significantly to morbidity and mortality and are the major cause of sudden cardiac death. Significant gaps still exist in the understanding of the pathogenesis mechanisms underlying the arrhythmogenic manifestations of Chagas cardiomyopathy. This article will review the data from experimental studies and translate those findings to draw hypotheses about clinical observations. Human- and animal-based studies at molecular, cellular, tissue, and organ levels suggest 5 main pillars of remodeling caused by the interaction of host and parasite: immunologic, electrical, autonomic, microvascular, and contractile. Integrating these 5 remodeling processes will bring insights into the current knowledge in the field, highlighting some key features for future management of this arrhythmogenic disease.