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Aims: Among patients with structural heart disease with ventricular tachycardia (VT) refractory to medical therapy and catheter ablation, cardiac stereotactic body radiotherapy (SBRT) is a paradigm-changing treatment option. This study aims to assess the efficacy of cardiac SBRT in refractory VT by comparing the rates of VT episodes, anti-tachycardia pacing (ATP) therapies, and implantable cardioverter-defibrillator (ICD) shocks post-SBRT with pre-SBRT.

Methods and results: We performed a comprehensive literature search and included all clinical studies reporting outcomes on cardiac SBRT for VT. Treatment efficacy was evaluated as random-effects pooled rate-ratios of VT episodes, ATP therapies and ICD shocks post-SBRT (after 6-week blanking) and pre-SBRT, with patients serving as their own controls. Post-SBRT overall survival was assessed using Kaplan-Meier method. We included 23 studies published 2017-24 reporting on 225 patients who received cardiac SBRT, with median follow-up 5.8-28 months. There was significant heterogeneity among the studies for all three efficacy endpoints (P < 0.00001). The random-effects pooled rate-ratios of VT episodes, ATP therapies and ICD shocks post- vs. pre-SBRT were 0.10 (95% CI 0.06, 0.16), 0.09 (0.05, 0.15), and 0.09 (0.05, 0.17), respectively (all P < 0.00001). The most common reported complications included pericardial (8.0%, including 0.9% late oesophagogastro-pericardial fistula) and pulmonary (5.8%). There was no change in left ventricular ejection fraction post-SBRT (P = 0.3) but some studies reported an increase in mitral regurgitation. The combined 3-, 12-, and 24-month overall patient survival was 0.86 (0.80, 0.90), 0.72 (0.65, 0.78), and 0.57 (0.47, 0.67), respectively.

Conclusion: Among patients with refractory VT in context of structural heart disease, VT burden and ICD shocks are dramatically reduced following cardiac SBRT. The overall mortality in this population with heart failure and refractory VT receiving palliative cardiac SBRT remains high.

It was widely accepted that malignant ventricular arrhythmias (VA) are the main direct initial cause for cardiac arrest and sudden cardiac death (SCD), but diverging data tended to demonstrate that asystole or pulseless activity were becoming the most prevalent cardiac rhythms at the time of cardiac arrest. We challenge here these conceptions and reinforce the persisting prominent role of VA in SCD.

Aims: Ventricular arrhythmias (VAs), which can lead to sudden cardiac death, are the primary cause of mortality in patients with heart failure (HF). However, the precise mechanisms underlying these arrhythmias are not well understood. Recent studies have implicated tumour necrosis factor alpha-induced protein 3-interacting protein 3 (TNIP3) in pathological cardiac hypertrophy. Nevertheless, its role in isoproterenol (ISO)-associated VAs remains elusive.

Methods and results: We overexpressed TNIP3 in the myocardium using an adeno-associated virus 9 system, administered via tail vein injection. C57BL/6 mice received daily subcutaneous injections of ISO for two consecutive weeks to establish an HF model. We performed histopathology and electrophysiological studies to assess ventricular structural remodelling, electrical remodelling, and susceptibility to VAs. Additionally, RNA sequencing (RNA-Seq) and western blot analysis were conducted to elucidate the underlying mechanisms. The expression of TNIP3 was up-regulated following ISO treatment. TNIP3 overexpression significantly reversed ISO-induced cardiac dysfunction, fibrosis, electrical remodelling, and VAs susceptibility. Accordingly, RNA-Seq identifies that the inflammatory response takes an important role in ISO-induced Vas, and TNIP3 overexpression could alleviate ISO-induced cardiac proinflammatory response by promoting M1 to M2 macrophage polarization. Mechanistically, PI3K/Akt/NF-κB signalling is responsible for the protective effect of TNIP3 overexpression on ISO-induced HF. And PI3K/Akt signalling activation offset the protective effect of TNIP3 overexpression on ISO-induced cardiac inflammation and VAs.

Conclusion: The findings of this study highlight the critical role of TNIP3 in ISO-associated cardiac remodelling and VAs, which are induced by the inhibited activation of the PI3K/Akt/NF-κB signalling pathway.

Aims: Utilization of transvenous lead extraction/removal (TLE) for the management of cardiac implantable electronic device (CIED)-associated infective endocarditis (IE) remains low. The aim of this study was to examine the impact of hospital TLE procedural volume on TLE utilization and outcomes for patients with CIED-associated IE.

Methods and results: Using the Nationwide Readmissions Database, we evaluated 21 545 admissions for patients (mean age 70 years, 39% female) with CIEDs hospitalized with IE at TLE centres. Hospitals were categorized based on annual volume tertiles: (i) low-volume (1-17 TLEs/year), (ii) medium-volume (18-45 TLEs/year), and (iii) high-volume centres (>45 TLEs/year). Between 2016 and 2019, 57% of admissions in the study were to low-volume TLE centres. Transvenous lead extraction/removal was performed during 6.9, 19.3, and 26% of admissions for CIED-associated IE at low-, medium-, and high-volume TLE centres, respectively (P < 0.001). After adjustment for age and comorbidities, hospitalization for IE at high-volume centres was independently associated with TLE when compared with low-volume centres (adjusted odds ratio 4.26; 95% confidence interval 3.53-5.15). Transvenous lead extraction/removal-associated complication rates were similar at 2.5, 2.3, and 3.4% at low-, medium-, and high-volume centres, respectively (P = 0.493). Overall inpatient mortality during admissions to low-, medium-, and high-volume centres was also similar.

Conclusion: Admissions to high-volume TLE centres were associated with higher utilization of TLE for management of CIED-associated IE. Transvenous lead extraction/removal-associated complications and mortality among patients hospitalized with CIED-associated IE were similar when stratified by hospital TLE volume, but this needs to be considered in context of significant differences in patient comorbidity burden between centres.