A 77-year-old woman underwent an upper gastrointestinal (UGI) endoscopy screening examination, and a 10-mm reddish, submucosal tumor-like lesion was found on the posterior wall of the fornix. Biopsy was performed, but there was no evidence of malignancy, so annual follow-up by UGI endoscopy was decided upon. After 12 years, examination of another biopsy specimen revealed an adenocarcinoma of the fundic gland type. There had been no significant change in the size or shape of the lesion over the long follow-up period. Endoscopic submucosal dissection (ESD) was performed, and en bloc resection was achieved. Histopathologically, the tumor appeared as a flat elevated lesion measuring 11 × 10 mm. It was composed of irregularly shaped glands and invaded the submucosa up to 300 µm. Immunohistochemical examination involving specific antibodies to pepsinogen I, MIST-1, MUC6, and H+/K+-ATPase confirmed the fundic gland differentiation of the irregularly shaped glands together with a very low Ki-67 labeling index. Thus, gastric adenocarcinoma of the fundic gland type (GAFG) was diagnosed. Four years have passed since the ESD, and there has been no recurrence. To the best of our knowledge, this is the first report of the long-term natural history of GAFG. Over the 12 years, no morphologic changes were observed; the tumor remained within the submucosal layer. Our observations in this case strengthen the notion that GAFG is a specific type of gastric adenocarcinoma of low-grade malignancy.

Background: An adaptive cardiac resynchronization therapy (aCRT) algorithm has been described for synchronized left ventricular (LV) pacing and continuous optimization of cardiac resynchronization therapy (CRT). However, there are few algorithmic data on the effect of changes during exercise. Methods and Results: We enrolled 27 patients with availability of the aCRT algorithm. Eligible patients were manually programmed to optimal atrioventricular (AV) and interventricular (VV) delays by using echocardiograms at rest or during 2 stages of supine bicycle exercise. We compared the maximum cardiac output between manual echo-optimization and aCRT-on during each phase. After initiating exercise, the optimal AV delay progressively shortened (P<0.05) with incremental exercise levels. The manual-optimized settings and aCRT resulted in similar cardiac performance, as demonstrated by a high concordance correlation coefficient between the LV outflow tract velocity time integral (LVOT-VTI) during each exercise stage (Ex.1: r=0.94 P<0.0008, Ex.2: r=0.88 P<0.001, respectively). Synchronized LV-only pacing in patients with normal AV conduction could provide a higher LVOT-VTI as compared with manual-optimized conventional biventricular pacing at peak exercise (P<0.05). Conclusions: The aCRT algorithm was physiologically sound during exercise by patients.

Introduction: High shock impedance is associated with conversion failure among patients with subcutaneous implantable cardioverter defibrillators (S-ICD). Currently, there is no preoperative assessment method for predicting high shock impedance. This study aimed to examine the efficacy of chest computed tomography (CT) as a preoperative evaluation tool to assess the shock impedance of S-ICDs. Methods and Results: The amount of adipose tissue adjacent to the device and the anteroposterior diameter at the basal heart region were measured preoperatively using a chest CT. We examined the correlation between these measurements and shock impedance at the conversion test. We enrolled 43 patients with S-ICDs (age: 54±15 years, body mass index: 23±4 kg/m , PRAETORIAN score: 30–270 points, amount of adipose tissue 1250±716 cc), who underwent intraoperative conversion tests by inducing ventricular fibrillation, which was terminated with a 65 J shock. A strong concordance correlation coefficient was observed between the shock impedance and the amount of adipose tissue (r=0.616, p < 0.01) and anteroposterior diameter (r=0.645, p < 0.01). Moreover, these were identified as independent predictive factors of shock impedance (amount of adipose tissue: β=0.439, p = 0.009; anteroposterior diameter: β=0.344, p = 0.038) in the stepwise multiple regression analysis. Conclusions: Preoperative CT-measured amount of adipose tissue and basal heart anteroposterior diameter are independent predictors of shock impedance. These may provide better accuracy in identifying high shock impedance in patients with S-ICDs.

Introduction: Atrial arrhythmia (AA) and left ventricular systolic dysfunction (LVSD) frequently co-exist, which loom as burgeoning public health problems. It is difficult to determine whether a tachycardia is the indicator or consequence of LVSD in patients with tachycardia and LVSD. Tachycardia mediated cardiomyopathy (TCM) raises a “chicken or egg” question. Regardless of the etiology, the patients with severe LVSD are considered as the candidate for the implantation of cardioverter defibrillator as primary prevention. It is well known that the LVSD improves after the successful treatment of AA in TCM population. However, enlarged left ventricular end-diastolic dimension (LVDd) is considered as a parameter of irreversible LVSD. Hypothesis: Enlarged LVDd could not be a predictor for irreversible LVSD in patients with AA. Methods: We assessed patients with persistent AA and heart failure (Ejection Fraction (EF) <45%) who were received aggressive rhythm control therapy and maintained sinus rhythm with catheter ablation, electrical cardioversion and anti arhythmic drugs. Echocardiographic parameters and brain natriuretic peptide (BNP) were evaluated before and after the treatment. Results: Twenty-five patients with persistent AA and LVSD (23 men; mean age 63.8±9.3 years) were enrolled in this study. After restored and maintained SR, EF and left ventricular end-systolic volume (ESV) and BNP were improved in all patients respectively (EF 30.7±10.7 to 54.0±7.3%, ESV; 82.1±32.4 to 50.6±24.1ml, BNP; 379.2±237.9 to 48.0±29.7pg/ml P<0.001). In the other hand, there were no significant improvement of LVDd and left ventricular end-diastolic volume (EDV) (LVDd; 54.7±7.6 to 54.3±5.5mm P=0.68, EDV; 120.1±37.9 to 108.2±38.0ml P=0.16). Enlarged LVDd >60mm were observed in 5 patients (25%) before the treatment. EF was normalized in patients with severe LVSD (EF<35%, n=13; 52%). Conclusions: The unnecessary device implantation could be avoided in patients with AA and severe LVSD with aggressive rhythm control therapy. Even in the patients with severe LVSD and enlarged LVDd, LVSD is reversible when AA exists.

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