PMAT-LOMs following PVI or valve surgery accounted for up to 11% of PMATs. The bidirectional block of either MB-LA or CS-MB connections is required to eliminate PMAT-LOMs.

AimsRemodelling of the extracellular matrix (ECM) plays an important role in the production of arrhythmogenic substrate for atrial fibrillation (AF), and is considered to be promoted by the connective tissue growth factor (CTGF). Our objective was to assess the relationship between CTGF and ECM synthesis, and the effect of olmesartan on these processes.Methods and resultsFifteen canine AF models were produced by rapid atrial stimulation. They were divided into three groups: pacing control (n = 5): 6-week pacing, pacing + olmesartan (n = 5): pacing with olmesartan (2 mg/kg/day), and non-pacing group (n = 5). In the pacing control group, messenger ribonucleic acid expressions of CTGF and collagen types 1 and 3 were up-regulated in comparison with the non-pacing group (P < 0.05) while transforming growth factor-β (TGF-β) did not exhibit a significant difference. In the pacing + olmesartan group, these up-regulations were suppressed (P < 0.05). In fluorescent immunostaining, the expression of CTGF was localized in the cytoplasm. The protein level of collagen type 3 was increased in the pacing control and it was suppressed in the pacing + olmesartan group.ConclusionsCTGF and associated genes were up-regulated in the atria with the appearance of fibrosis. Because this up-regulation was independent of TGF-β and suppressed by olmesartan, CTGF up-regulation was considered to be mediated by angiotensin II.

The presence of ER, especially with day-to-day variation, can help predict VF recurrence in VSA patients. Implantable cardioverter defibrillator implantation is a reasonable approach for the secondary prevention of VF in high-risk VSA patients.

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Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jp lthough it has been suggested that oxidative stress plays a causative role in arteriosclerosis, 1,2 aging, 3 heart failure, 4,5 and reperfusion injury during ischemia, 6 the primary role of oxidative stress in the development of each of these pathological situations is unclear. We have documented that N-acetylcysteine, a precursor of glutathione, suppressed ventricular remodeling and arrhythmia in experimental autoimmune myocarditis of rats. 7 Therefore, oxidative stress played a key role in promoting electrical and structural remodeling in a model of myocarditis. Similarly, several reports have demonstrated electrophysiological changes that might be caused by oxidative stress in disease-model animals. 7-11 However, oxidative stress appears with the progression of pathological conditions (eg, inflammation, ischemia, hypertrophy etc), so it is technically difficult to evaluate the effect of hyperoxidative stress separately from other pathological factors in such disease models. As a result, the precise mechanism of the remodeling caused by primary oxidative stress is unclear in these models.In the present study, we designed a rat model of primary hyperoxidative stress without any other structural abnormalities in order to evaluate the role of primary oxidative stress in the promotion of myocardial electrical and structural remodeling. MethodsGlutathione-Depleted Hyperoxidative Rat Model 8-week-old Sprague-Dawley rats (CLEA Japan, Inc, Tokyo, Japan) were treated with L-buthionine-sulfoximine (BSO) (0 or 30 mmol · L -1 · day -1 , control group n=21, BSO group n=18) in drinking water for 14 days. On day 7 and/or 14, the Received October 26, 2010; revised manuscript received January 11, 2011; accepted January 28, 2011; released online April 16, 2011 Time for primary review: 28 days Department of Cardio-Angiology, Kitasato University School of Medicine, Sagamihara, Japan Name of grant: no grant. Mailing address: Sayaka Kurokawa, MD, Department of Cardio-Angiology, Kitasato University School of Medicine, 1-15-1 Kitasato, Minami-ku, Sagamihara 252-0374, Japan. E-mail: ksayaka@med. Background: Although oxidative stress is considered to promote arrhythmogenic substrates in diseased model animals, it is difficult to evaluate its primary role. In this study, we evaluated the promotion of arrhythmogenic substrates in the primary hyperoxidative state.

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Background. Clinical characteristics and prognosis of patients with a solitary Peutz-Jeghers polyp (PJP) have not been fully investigated. Methods. Solitary PJP was diagnosed when a single hamartomatous lesion was identified in the gastrointestinal tract of patients without mucocutaneous pigmentation or a family history of Peutz-Jeghers syndrome. We retrospectively reviewed 51 patients (32 men and 19 women) with a solitary PJP and analyzed the sex, age at diagnosis, endoscopic features, and outcomes in this patient group. The STK11/LKB1 germline mutation was not investigated in any of the patients. Results. The mean age of the 51 patients was 66.1 years. The polyp was found in the duodenum (N=10), jejunum (N=2), cecum (N=2), transverse colon (N=5), sigmoid colon (N=21), or rectum (N=11). Most of the polyps presented as a pedunculated lesion (N=40), followed by semipedunculated (N=9) and sessile (N=2) morphologies. The mean size of a solitary PJP was 15.6 mm (range: 5 to 33 mm). During a mean endoscopic follow-up period of 4.5 years (range: 0.1 to 16.1 years), no recurrence was identified. Eighteen of the enrolled patients had a history of cancer or concomitant cancer. Five patients died due to non-gastrointestinal-related causes. No additional cancer or death directly related to solitary PJP was observed. Conclusions. Solitary PJPs did not recur in this study. Although examination of the entire gastrointestinal tract using esophagogastroduodenoscopy, enteroscopy, and colonoscopy is desirable to exclude Peutz-Jeghers syndrome, follow-up endoscopy after endoscopic polyp resection may be unnecessary, once the diagnosis of a solitary PJP is made.

Background and study aims  Salvage therapy for esophageal cancer following chemo-radiation therapy (CRT) has not been established. We aimed to evaluate endoscopic submucosal dissection (ESD) as a salvage therapy based on histopathological features of lesions. Patients and methods  We compared 10 lesions in eight patients with local residual, recurrent, or metachronous esophageal squamous cell carcinoma treated by ESD after CRT (CRT group) and 59 lesions treated by ESD without CRT (non-CRT group) during the same period. Results  The en bloc resection rate was 100 % while the complete resection rate was 80.0 % in the lesions after CRT, indicating no difference between the CRT and non-CRT groups. Pathological examination showed that fibrosis was more intense in the lamina propria mucosa, muscularis mucosa, and submucosa. The muscularis mucosa was thicker in both non-tumor and tumor sites in the CRT group compared to the non-CRT group. However, severe submucosal fibrosis was observed only in one lesion in the CRT group. The maximum diameter of the submucosal artery was significantly larger in the CRT group ( P  < 0.001). Conclusions  Compared to the non-CRT group, the lesions in the CRT group were accompanied by fibrosis while the muscularis mucosa were thicker; however, severe fibrosis of the submucosa was rare. It is important to dissect the muscularis mucosa appropriately during ESD, which makes successful dissection of the submucosa possible. Attention should be paid to bleeding from large arteries.