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Introduction: 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. Methods: PubMed was searched from inception to October 2020 following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses statement protocol. Results: 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, p < 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%, p < 0.001). Conservative or stent intervention was an independent risk factor for mortality. Age (adjusted odds ratio, 1.063, p = 0.004), presentation with neurological symptoms (adjusted odds ratio, 5.706, p = 0.017), and presentation with gastrointestinal bleeds (adjusted odds ratio, 3.009, p = 0.045) were also predictors of mortality. Conclusions: 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. [ABSTRACT FROM AUTHOR]

Abstract: 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. [ABSTRACT FROM AUTHOR]

Objectives: To investigate the association between serum uric acid and mortality in a Chinese population of hypertensive patients. Methods and results: A total of 2757 Chinese hypertensive patients from department of cardiology of several hospitals in Shanghai in China were followed up for about six years in this prospective study. Mortality was recorded and related factors were evaluated. Hyperuricemia was diagnosed by serum uric acid levels of >420 µmol/L in males or >357 µmol/L in females. A total of 2585 hypertensive patients with complete data were included in the final statistical analysis. Totally 709 deaths (27.4%) occurred during the six-year follow-up, of which 475 deaths were attributable to cardiovascular disease (CVD). All-cause and CVD mortality of hypertensive patients with hyperuricemia was significantly higher than that of patients without hyperuricemia. The Cox regression analysis indicated that hazards ratios (HRs) of hyperuricemia for all-cause and CVD mortality were 1.206 (95% CI: 1.002-1.453) and 1.085 (95% CI: 1.002-1.271) respectively. All-cause and CVD mortality of hypertensive patients was significantly increased (both p < 0.05) when uric acid levels increased. HRs of uric acid levels >536 µmol/L to all-cause and CVD mortality of hypertensive patients were 2.115 (95% CI: 1.596-2.801) and 1.861 (95% CI: 1.296-2.673), respectively, compared with those of uric acid levels ≤357 µmol/L. Conclusions: The data from this cohort study indicate that hyperuricemia can predict increased all-cause and CVD mortality in hypertensive patients. [ABSTRACT FROM AUTHOR]

Mol Med Rep 12: [Related article:] 5746–5752, 2015; DOI: 10.3892/mmr.2015.4193 Following the publication of this article on-line ahead of print, an interested reader drew to our attention some anomalies associated with the presentation of Fig. 1. In the lower panel, the fourth image from the left resembled a mirror image representation of the image in the first panel; the fifth image from the left bore a marked resemblance to a section of the third image, albeit displaced at an angle and with a different magnification; and an internal office investigation drew our attention to the fact that the sixth image in the upper panel resembled a section of the image in the third panel, although rotated through 180°.

An immerging role of TNF-α in collagen synthesis and cardiac fibrosis implies the significance of TNF-α production in the development of myocardial remodeling. Our previous study showed a reduction of TNF-α and attenuated cardiac remodeling in CXCR6 knockout (KO) mice after ischemia/reperfusion injury. However, the potential mechanism of TNF-α-mediated cardiac fibrosis with pressure overload has not been well elucidated. In the present study, we aim to investigate the role of CXCR6 in TNF-α release and myocardial remodeling in response to pressure overload. Pressure overload was performed by constriction of transverse aorta (TAC) surgery on CXCR6 KO mice and C57 wild-type (WT) counterparts. At 6 weeks after TAC, cardiac remodeling was assessed by echocardiography, cardiac TNF-α release and its type I receptor (TNFRI), were detected by ELISA and western blot, collagen genes Col1a1 (type I) and Col3a1 (type III) were examined by real-time PCR. Compared with CXCR6 WT mice, CXCR6 KO mice exhibited less cardiac dysfunction, reduced expression of TNFRI, Col1a1 and Col3a. In vitro, we confirmed that CXCR6 deficiency led to reduced homing and infiltration of CD11b(+) monocytes, which contributed to attenuated TNF-α release in myocardium. Furthermore, TNFRI antagonist pretreatment blocked AT1 receptor signaling and NOX4 expression, reduced collagen synthesis, and blunted the activity of MMP9 in CXCR6 WT mice after TAC, but these were not observed in CXCR6 KO mice. In the present work, we propose a mechanism that CXCR6 is essential for pressure overload-mediated myocardial recruitment of monocytes, which contributes to cardiac fibrosis through TNF-α-dependent MMP9 activation and collagen synthesis.

Objective: To observe changes in connexin 43 (Cx43) after ventricular fibrillation (VF) and the effects of rotigaptide (ZP123) on Cx43., Methods: Thirty domestic pigs were randomly assigned to three groups (10 in each group): sham group, model group and ZP123 group. VF was induced by an 80 V AC transthoracic shock for 5 seconds with the use of subcutaneous needles. Before the induction of VF, animals in ZP123 group were administered with ZP123 (1 μg/kg bolus+10 μg×kg(-1)×h(-1) dissolved in 50 ml normal saline and pumped for 15 minutes ). Those in model group received 50 ml normal saline pumped for 15 minutes. For pigs in sham group VF was not induced and no fluid was given. After 8 minutes of VF, animals were euthanized and myocardial tissues were harvested along the long axis of each left ventricular free wall. Immunofluorescence combined with laser scanning confocal microscope was used to detect the distribution of Cx43. Western blotting was used for quantitative determination of Cx43 protein expression., Results: Immunofluorescence signals for Cx43 in sham group were strong and regularly distributed. In model group, Cx43 signals were weak and distributed in heterogeneity, while in ZP123 group, Cx43 signals were enhanced and their distribution were much more orderly. Compared with sham group, the percentage area and the optical densities (A value) of Cx43 fluorescence signals and Cx43 protein expression were significantly decreased in model group [the percentage area: (0.64±0.36)% vs.(1.27±0.19)%, A value: 15 201± 2 613 vs. 30 634±4 975, Cx43 protein expression: 0.72±0.08 vs. 0.97±0.07, all P<0.05]. The level of Cx43 expression in ZP 123 group [the percentage area (0.96±0.16)%, A value 22 100±4 404, Cx43 protein expression 0.82±0.04] was much higher than model group (all P<0.05)., Conclusion: During VF, down-regulation of myocardial Cx43 expression occurred, which could be attenuated by administration of ZP123.