[Rhythm management in patients with heart failure].

INTRODUCTION: Arrhythmias manifest frequently in individuals with heart failure, posing a notable threat of mortality and morbidity. While the prevention of sudden cardiac death through ICD therapy remains pivotal, accurate risk stratification remains a challenging task even in 2024. Recent data underscore the early consideration of catheter ablation for ventricular tachycardias. Although antiarrhythmic drug therapy serves as an ancillary measure for symptomatic patients, it does not confer prognostic advantages. The holistic management of arrhythmias in heart failure necessitates a systematic, multidimensional approach that initiates with evidence-based medical therapy for heart failure and integrates device-based and interventional therapies. Noteworthy clinical studies have illustrated the positive prognostic impact of early rhythm control strategies, particularly catheter ablation, in individuals managing heart failure and atrial fibrillation.

Performance and safety of temperature- and flow-controlled radiofrequency ablation for ventricular arrhythmia.

AIMS: High-power ablation is effective for ventricular arrhythmia ablation; however, it increases the risk of steam pops. The aim of this study was to define the safety and efficacy of QMODE ablation in the ventricle and the risk of steam pop. METHODS AND RESULTS: Consecutive patients undergoing ventricular ablation using QDOT were included in a prospective single-centre registry. Procedural data, complications, and follow-up were systematically analysed and compared with a historical ventricular tachycardia (VT) and premature ventricular complexes (PVC) cohort ablated using STSF. QMODE (≤50 W) ablation was performed in 107 patients [age 62 ± 13 years; 76% male; VT (n = 41); PVC (n = 66)]. A total of 2456 applications were analysed [power: 45.9 ± 5.0 W with minimal power titration (90% > 95% max power); duration 26 ± 8 s; impedance drop 9.4 ± 4.7 Ω; ablation index: 569 ± 163; mean-max temperature 44.3 ± 2.6°C]. Ventricular tachycardia ablation was associated with shorter radiofrequency (RF) time and a trend towards shorter procedure times using QDOT (QDOT vs. STSF: 20.1 ± 14.7 vs. 31 ± 17 min; P = 0.002, 151 ± 59 vs. 172 ± 48 min; P = 0.06). Complications, VT recurrence, and mortality rates were comparable (QDOT vs. STSF: 2% vs. 2%; P = 0.9, 24% vs. 27%; P = 0.82, and 2% vs. 4%; P = 0.67). Five audible steam pops (0.02%) occurred. Premature ventricular complex ablation was associated with comparable RF and procedure times (QDOT vs. STSF: 4.8 ± 4.6 vs. 3.9 ± 3.1 min; P = 0.25 and 96.1 ± 31.9 vs. 94.6 ± 24.7 min; P = 0.75). Complication and PVC recurrence were also comparable (QDOT vs. STSF: 0% vs. 3%; P = 0.17 and 19% vs. 22%; P = 0.71). CONCLUSION: Ventricular ablation using QMODE ≤ 50 W is safe and effective for both VT and PVC ablation and is associated with a low risk for steam pop.

Prevalence and outcomes of heart failure phenotypes in patients with atrial fibrillation.

BACKGROUND: Atrial fibrillation (AF) is common in patients with heart failure (HF). Real-world data about long-term outcomes and rhythm control interventions use in AF patients with and without HF remain scarce. METHODS: AF patients from two prospective, multicentre studies were classified based on the HF status at baseline into: HF with preserved ejection fraction (HFpEF), HF with reduced or mildly reduced ejection fraction (HFrEF/HFmrEF), and no HF. The prespecified primary outcome was risk of HF hospitalisation. Other outcomes of interest included mortality, cardiovascular events, AF progression, and quality of life. RESULTS: A total of 1265 patients with AF were analysed (mean age 69.6 years, women 27.4%) with a median follow-up of 5.98 years. Patients with HFpEF (n = 126) had a 2.69-fold and patients with HFrEF/HFmrEF (n = 308) had a 2.12-fold increased risk of HF hospitalisation compared to patients without HF (n = 831, p < 0.001). Similar results applied for all-cause and cardiovascular mortality. The risk for AF progression was higher for patients with HFpEF and HFrEF/HFmrEF (6.30 and 6.79 per 100 patient-years, respectively) compared to patients without HF (4.20). The use of rhythm control strategies during follow-up was least in the HFpEF population (4.56 per 100 patient-years) compared to 7.74 in HFrEF/HFmrEF and 8.03 in patients with no HF. With regards to quality of life over time, this was worst among HFpEF patients. CONCLUSIONS: The presence of HFpEF among patients with AF carried a high risk of HF hospitalisations and AF progression, and worse quality of life. Rhythm control interventions were rarely offered to HFpEF patients. These results uncover an unmet need for enhanced therapeutic interventions in patients with AF and HFpEF.

Sex-specific association of cardiovascular drug doses with adverse outcomes in atrial fibrillation.

OBJECTIVES: Sex differences occur in atrial fibrillation (AF), including age at first manifestation, pathophysiology, treatment allocation, complication rates and quality of life. However, optimal doses of cardiovascular pharmacotherapy used in women with AF with or without heart failure (HF) are unclear. We investigated sex-specific associations of beta-blocker and renin-angiotensin system (RAS) inhibitor doses with cardiovascular outcomes in patients with AF or AF with concomitant HF. METHODS: We used data from the prospective Basel Atrial Fibrillation and Swiss Atrial Fibrillation cohorts on patients with AF. The outcome was major adverse cardiovascular events (MACEs), including death, myocardial infarction, stroke, systemic embolisation and HF-related hospitalisation. Predictors of interest were spline (primary analysis) or quartiles (secondary analysis) of beta-blocker or RAS inhibitor dose in per cent of the maximum dose (reference), in interaction with sex. Cox models were adjusted for demographics, comorbidities and comedication. RESULTS: Among 3961 patients (28% women), MACEs occurred in 1113 (28%) patients over a 5-year median follow-up. Distributions of RAS inhibitor and beta-blocker doses were similar in women and men. Cox models revealed no association between beta-blocker dose or RAS inhibitor dose and MACE. In a subgroup of patients with AF and HF, the lowest hazard of MACE was observed in women prescribed 100% of the RAS inhibitor dose. However, there was no association between RAS dose quartiles and MACE. CONCLUSIONS: In this study of patients with AF, doses of beta-blockers and RAS inhibitors did not differ by sex and were not associated with MACE overall.

Antithrombotic properties of Tafamidis: An additional protective effect for transthyretin amyloid cardiomyopathy patients.

INTRODUCTION: Tafamidis is a molecular chaperone that stabilizes the transthyretin (TTR) homo-tetramer, preventing its dissociation and consequent deposition as amyloid fibrils in organ tissues. Tafamidis reduces mortality and the incidence of hospitalization for cardiovascular causes in patients with TTR amyloid (ATTR) cardiomyopathy. As ATTR cardiomyopathy is associated with a high risk of thromboembolic complications, we hypothesized that tafamidis may have a direct ancillary anti-thrombotic effect. METHODS: Primary human aortic endothelial cells (HAECs) were treated with tafamidis at clinically relevant concentrations and with plasma of patients, before and after the initiation of treatment with tafamidis. The expression of TF was induced by incubation with Tumor Necrosis Factor α (TNFα). Intracellular expression of tissue factor (TF) was measured by western blot. TF activity was measured by a colorimetric assay. Gene expressions of TF were measured by quantitative polymerase chain reaction. RESULTS: Treatment with tafamidis dose-dependently reduced the expression and activity of TNFα-induced TF. This effect was confirmed in cells treated with patients' plasma. Signal Transducer and Activator of Transcription 3 (STAT3) phosphorylation was significantly inhibited by tafamidis. Incubation of HAECs with tafamidis and the STAT3 activator colivelin partially rescued the expression of TF. CONCLUSIONS: Treatment with tafamidis lowers the thrombotic potential in human primary endothelial cells by reducing TF expression and activity. This previously unknown off-target effect may provide a novel mechanistic explanation for the lower number of thromboembolic complications in ATTR cardiomyopathy patients treated with tafamidis.