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  • Your support for the official journal of the Japan

    2019-05-05

    Your support for the , official journal of the Japan Heart Rhythm Society (JHRS) and the Asia Pacific Heart Rhythm Society (APHRS), is sincerely appreciated. We are pleased to announce that JOA has become an open access journal. Thus it is always available for readers online. All articles are accessible anytime at no charge to everyone using our journal home page and ScienceDirect .
    Introduction Delayed-enhancement magnetic resonance imaging (DE-MRI) is an established method for characterizing cardiac tissue in various disease processes [1]. Recently, DE-MRI has emerged as an effective method for noninvasively assessing and quantifying the extent of left atrium (LA) structural remodeling [2], which has been reported to be independent of the type of atrial fibrillation (AF) and associated comorbidities. Moreover, selecting appropriate treatment candidates based on the quality and quantity of atrial fibrosis detected using DE-MRI has shown to improve the procedural outcome and prevent unnecessary interventions [3]. Furthermore, a multicenter trial has also demonstrated that atrial fibrosis, as estimated by DE-MRI, is independently associated with the likelihood of recurrent arrhythmias [4]. We recognize the use and importance of DE-MRI for visualizing atrial fibrosis [3]. However, neither atrial fibrosis nor radiofrequency (RF) lesions can be visualized using DE-MRI in Japan, mainly due to the differences in diindolylmethane agents, volume-rendering tools and technical experience. Therefore, the objective of the current study was to visualize RF lesions and tissue fibrosis in the left atrium (LA) of Japanese patients who underwent AF ablation using commercially available tools for DE-MRI. In addition, we also investigated the clinical differences between the successful and unsuccessful MRI acquisitions groups.
    Material and methods
    Results
    Discussion
    Conclusion
    Conflict of interest
    Financial support
    Acknowledgments
    Introduction Activation of the renin–angiotensin–aldosterone system (RAAS) in the atrial tissue is a point of concern in patients with atrial fibrillation (AF), since increased generation of angiotensin II activates NADPH oxidase and enhances oxidative stress in vivo in these individuals [1,2]. Enhanced oxidative stress in turn activates matrix metalloproteinases (MMPs) [3], which are key enzymes in atrial remodeling [4,5]. The serum MMP-2 content was reported to be an independent predictor of post-ablation AF recurrence [6]. The oral direct renin inhibitor aliskiren is expected to block the RAAS completely when supplemented in treatment with conventional RAAS inhibitors, since addition of aliskiren was found to reduce in vivo oxidative stress and albuminuria in hypertensive diabetic patients with chronic kidney disease [7]. The aim of this study was to determine the effects of aliskiren on in vivo oxidative stress in AF patients.
    Materials and methods
    Discussion Aliskiren reduced in vivo oxidative stress and serum MMP-2 levels in patients with permanent AF, although it did not alter the symptoms of CHF or plasma BNP levels. Further, these biochemical markers seemed to have no association with echocardiographic parameters. One of the reasons for this lack of an association might be the irreversible atrial remodeling occurring in permanent AF.
    Conclusions Aliskiren reduced in vivo oxidative stress and serum MMP-2 levels in patients with permanent AF.
    Disclosure of conflict of interest
    Acknowledgments This work was supported by a research grant from Higashi-osaka City General Hospital to Dr. Yoshiyuki Kijima.
    Introduction Atrial fibrillation (AF), the most common type of sustained tachyarrhythmia, affecting approximately 0.9% of the population, is known to be associated with significant morbidity and mortality [1–4]. Recently, circumferential pulmonary vein isolation (CPVI) via catheter ablation has been established as a curative strategy for this type of arrhythmia, suggesting an important role of the thoracic veins in the mechanisms underlying AF. However, the success rate of CPVI ablation has been reported to decrease with increases in left atrial dimension (LAD) [5–7], similar to that of pharmacotherapy. This suggests potential pathological processes that invade the atrium from the pulmonary veins in a progressive manner in concert with the enlargement of the left atrium (LA).