<b><i>Introduction:</i></b> Atrial-esophageal fistula (AEF) is a rare but life-threatening complication of catheter ablation. The clinical presentation and mortality risk factors of AEF have not been fully elucidated. The aim of this study was to systematically review the clinical characteristics and prognosis of AEF. <b><i>Methods:</i></b> PubMed was searched from inception to October 2020 following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses statement protocol. <b><i>Results:</i></b> A total of 190 AEF patients were included. The mean age was 59.29 ± 11.67 years, 74.21% occurred in males, and 81.58% underwent radiofrequency ablation. AEF occurred within 30 days after ablation in 80.82% of patients and occurred later in patients presenting with neurological symptoms compared with other symptoms (median of onset time: 27.5 days vs. 16 days, <i>p</i> < 0.001). Clinical presentation included fever (81.58%) and neurological symptoms (80.53%). Chest computed tomography (abnormal rate of 91.24%) was the preferred diagnostic test, followed by magnetic resonance imaging of the brain (abnormal rate of 90.91%). Repeated testing improved diagnostic evaluation sensitivity. Distinctive imaging results included free air in the mediastinum (incidence rate of 81.73%) and air embolism of the brain (incidence rate of 57.53%). The overall mortality was 63.16%, with worse nonsurgical treatment outcomes compared with outcomes of surgical treatment (94.19% vs. 33.71%, <i>p</i> < 0.001). Conservative or stent intervention was an independent risk factor for mortality. Age (adjusted odds ratio, 1.063, <i>p</i> = 0.004), presentation with neurological symptoms (adjusted odds ratio, 5.706, <i>p</i> = 0.017), and presentation with gastrointestinal bleeds (adjusted odds ratio, 3.009, <i>p</i> = 0.045) were also predictors of mortality. <b><i>Conclusions:</i></b> AEF is a fatal ablation complication. AEF can be diagnosed using a combination of a clinical history of ablation, infection, or neurological symptoms and an abnormal chest CT. Our analysis supports that surgical treatment reduces the mortality rate.
Background
Left atrial appendage occlusion (LAAO) is usually performed via the guidance of procedural transesophageal echocardiography (TEE) companied by general anesthesia (GA).
Objective
To investigate the feasibility and safety of LAAO guided by procedural fluoroscopy only.
Methods
The patients eligible for LAAO were enrolled into the current study and received implantation of either Watchman device or LAmbre device. The procedure was carried out with procedural fluoroscopy only and no companied GA; the position, shape, and leakage of the device were assessed by contrast angiography. TEE was performed after 3‐month follow‐up to evaluate the thrombosis, and leakage of device.
Results
Ninety‐seven patients with atrial fibrillation (AF) with either Watchman device (n = 49) or LAmbre device (n = 48) were consecutively enrolled. Watchman device group was of lower CHA2DS2‐VASc and HAS‐BLED scores compared with LAmbre device groups (p < .05); the two groups had similar distributions of other baseline characteristics (p > .05), including procedural success rate (98.0% vs. 97.9%), mean procedure time, mean fluoroscopy time, total radiation dose, contrast medium dose, percentage of peri‐device leakage. Pericardial effusions requiring intervention occurred in two of the Watchman group. TEE follow‐up found no patient with residual leakage ≥5 mm at 3 months and no device related thrombosis (DRT). During the 22.0 ± 11.1 months follow‐up, two patients experienced ischemic stroke.
Conclusions
LAAO with the procedural imaging of fluoroscopy only exhibited the promising results of efficacy and safety. A prospective randomized multicenter study would be required to verify the observations in this study.
Atrial myocyte hypertrophy is one of the most important substrates in the development of atrial fibrillation (AF). The TWEAK/Fn14 axis is a positive regulator of cardiac hypertrophy in cardiomyopathy. This study therefore investigated the effects of Fn14 on atrial hypertrophy and underlying cellular mechanisms using HL‐1 atrial myocytes. In patients with AF, Fn14 protein levels were higher in atrial myocytes from atrial appendages, and expression of TWEAK was increased in peripheral blood mononuclear cells, while TWEAK serum levels were decreased. In vitro, Fn14 expression was up‐regulated in response to TWEAK treatment in HL‐1 atrial myocytes. TWEAK increased the expression of ANP and Troponin T, and Fn14 knockdown counteracted the effect. Inhibition of JAK2, STAT3 by specific siRNA attenuated TWEAK‐induced HL‐1 atrial myocytes hypertrophy. In conclusion, TWEAK/Fn14 axis mediates HL‐1 atrial myocytes hypertrophy partly through activation of the JAK2/STAT3 pathway.
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