Pre-procedural prediction of termination of persistent atrial fibrillation by catheter ablation as an indicator of reverse remodeling of the left atrium. (1/11)

BACKGROUND: The pre-procedural prediction of atrial fibrillation (AF) termination by catheter ablation in patients with persistent AF has not been evaluated fully. The aim of this study was to evaluate the pre-procedural predictors of persistent AF termination by ablation associated with the possibility of reverse remodeling of the left atrium (LA). METHODS AND RESULTS: Seventy consecutive patients (mean age, 62+/-8 years) with persistent or long-standing persistent AF underwent ablation. They were divided into 2 groups: those with AF terminated by ablation (n=14; group 1) and those with AF terminated by cardioversion after ablation (n=56; group 2). The left atrial appendage (LAA) contraction velocity determined on transesophageal echocardiography was significantly decreased in group 2 as compared to group 1 (P<0.001). Kaplan-Meier analysis showed that the group 1 patients had a higher AF-free survival rate than those in group 2 during 12+/-4.1 months of follow-up (P=0.048). The LA reverse remodeling ratio, given as the volume difference between before and 3 months after ablation in group 1, was significantly greater after ablation than that in group 2 (25.8+/-13% vs. 15.0+/-15%, P=0.015). Multivariate logistic regression analysis indicated that the LAA contraction velocity was an independent predictor of persistent AF termination by ablation (P=0.018). CONCLUSIONS: The LAA contraction velocity was the only non-invasive pre-procedural predictor of persistent AF termination by ablation, indicating the possibility of reverse remodeling of the LA.  (+info)

Changes in microRNAs expression are involved in age-related atrial structural remodeling and atrial fibrillation. (2/11)

BACKGROUND: Small noncoding microRNAs regulate gene expression in cardiac development and disease and have been implicated in the aging process and in the regulation of extracellular matrix proteins. However, their role in age-related cardiac remodeling and atrial fibrillation (AF) was not well understood. The present study was designed to decipher molecular mechanisms underlying age-related atrial structural remodeling and AF. METHODS: Three groups of dogs were studied: adult and aged dogs in sinus rhythm and with persistent AF induced by rapid atrial pacing. The expressions of microRNAs were measured by quantitative real-time polymerase chain reaction. Pathohistological and ultrastructural changes were tested by light and electron microscopy. Apoptosis index of myocytes was detected by TUNEL. RESULTS: Samples of atrial tissue showed the abnormal pathohistological and ultrastructural changes, the accelerated fibrosis, and apoptosis with aging and/or in AF dogs. Compared to the adult group, the expressions of microRNAs-21 and -29 were significantly increased, whereas the expressions of microRNAs-1 and -133 showed obvious downregulation tendency in the aged group. Compared to the aged group, the expressions of microRNAs-1, -21, and -29 was significantly increased in the old group in AF; contrastingly, the expressions of microRNA-133 showed obvious downregulation tendency. CONCLUSION: These multiple aberrantly expressed microRNAs may be responsible for modulating the transition from adaptation to pathological atrial remodeling with aging and/or in AF.  (+info)

An Angiotensin receptor blocker prevents arrhythmogenic left atrial remodeling in a rat post myocardial infarction induced heart failure model. (3/11)

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Effect of renal sympathetic denervation on atrial substrate remodeling in ambulatory canines with prolonged atrial pacing. (4/11)

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MicroRNAs in pulmonary arterial remodeling. (5/11)

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Left atrial endocardial fibrosis and intra-atrial thrombosis - landmarks of left atrial remodeling in rats with spontaneous atrial tachyarrhythmias. (6/11)

INTRODUCTION: Histological abnormalities are common findings in the left atria (LA) of atrial fibrillation (AF) patients. We aimed to assess LA histological abnormalities in our model of spontaneous atrial tachyarrhythmias in rats. MATERIALS AND METHODS: LA sampling was performed in 12 spontaneously hypertensive rats (SHRs) and eight age-matched Wistar-Kyoto (WKY) rats. Tissue sections were stained with Masson's trichrome and Hematoxylin-Eosin-Safran and examined with a light microscope. A 0 to 3 scoring system was used to quantify the severity of LA structural abnormalities. LA von Willebrand factor (vWF) content was also assessed using immunohistochemical staining. RESULTS: In six of the eight SHRs, LA fibrosis, inflammatory infiltrates, and myocyte necrosis of varying grades of severity were observed. The most frequent feature was endocardial fibrosis, which was observed in six SHRs and in none of the WKY rats. Intra-atrial thrombosis was found in three SHRs and in none of the WKY rats. The intensity of vWF-related fluorescence was higher in the atrial endocardium of SHRs compared to age-matched WKY rats. CONCLUSIONS: Our findings reinforce the role of LA structural abnormalities in atrial arrhythmogenicity. However, two SHRs did not present LA histological abnormalities despite the presence of arrhythmias. This finding suggests that the LA remodeling-atrial tachyarrhythmia relationship could be highly nonlinear and that atrial fibrosis is more likely to be a facilitator of atrial arrhythmogenicity, rather than a prerequisite. We also provide evidence that intra-atrial thrombosis accompanies LA structural remodeling in arrhythmic rats. Increased endocardial platelet adhesion molecule vWF could contribute to this increased thrombogenicity.  (+info)

Mechanistic inquiry into the role of tissue remodeling in fibrotic lesions in human atrial fibrillation. (7/11)

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Atrial arrhythmia in ageing spontaneously hypertensive rats: unraveling the substrate in hypertension and ageing. (8/11)

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