Giant hepatic hemangiomas, though often asymptomatic, may require intervention if rapid growth occurs. The imaging studies including the computed tomography, magnetic resonance imaging, and ultrasonography, and so on are effective for the diagnosis and the management of this tumor; however, due to its size and various patterns of these studies, we need to carefully consider the therapeutic methods. Compared to the cost needed for these modalities, recently developed and approved Perflubutane- (Sonazoid-) based contrast agent enhanced ultrasonography is reasonable and safe. The major advantage is the real-time observation of the vascular structure and function of the Kupffer cells. By this procedure, we can carefully follow the tumor growth or character change in a hemangioma and decide the timing of therapeutic intervention, since abdominal pain, abdominal mass, consumptive coagulopathy, and hemangioma growth are the signs for the therapeutic intervention. We reviewed recent reports about Sonazoid-based enhancement and also showed the representative images collected in our department. This is the first review showing the detailed findings of the giant hemangiomas using Perflubutane (Sonazoid). This review will help the physician in making the decision, and we hope that Sonazoid will gain widespread acceptance in the near future.

n important advancement in our understanding of atrial fibrillation (AF) during the past decade was the demonstration that rapid atrial excitation alters atrial electrophysiology to promote AF. [1][2][3][4] This process, termed "electrical remodeling", includes shortening and loss of rate-adaptation of the effective refractory period (ERP) as well as a reduction of conduction velocity. 1 With respect to the cellular mechanisms underlying such electrical remodeling, most previous studies have focused on the altered action potential (AP) configuration during the steady state, resulting from altered function and expression of sarcolemmal ion channels. For example, a shortening in ERP, which reflects a shortening of the AP duration (APD), has been attributed primarily to a reduction of the L-type Ca 2+ current (ICa,L) in association with a downregulation of pore-forming ICa,L -subunits. 2,3 In addition to changes in sarcolemmal ion channels, sustained rapid atrial excitation leads to profound changes in cellular Ca 2+ handling, 5 giving rise to significant contractile dysfunction. Such AF-related alterations in cellular Ca 2+ handling also could contribute to abnormal electrophysiologic properties of the atria. The information available on this issue is still limited. Hara et al reported that the dynamics of APD, in response to an abrupt change of stimulation cycle length (CL) in canine atria with AF, were different from normal atria. 4 They suggested an involvement of altered Ca 2+ handling, because the difference in APD dynamics was abolished by ryanodine. The present study was designed to obtain further insight into the role of Ca 2+ dynamics in modulating APD in atria subjected to chronic rapid atrial pacing.We hypothesized that alterations to the Ca 2+ handling in electrical remodeling could contribute to the abnormal APD dynamics favoring the initiation and perpetuation of fibrillation. Recent studies have shown that non-steady state AP characteristics have important implications for the development of arrhythmias. 6-10 Several studies have suggested that APD restitution kinetics are an important determinant of stability in several types of re-entrant circuits. 6-8 Burashnikov and Antzelevitch showed that late phase 3 triggered activity induced by early afterdepolarization (EAD) occurs after a long diastolic interval, causing immediate AF recurrence after AF termination in a cholinergically-mediated model of AF. 9 The purpose of this study was to test the following hypotheses: (1) that non-steady state APD dynamics, including APD restitution and APD transition after an abrupt change in CL, are related to intracellular Ca 2+ handling in canine atria; and that (2) APD dynamics are altered in association with altered Ca 2+ handling in the setting of electrical remodeling. Background Electrical instability following sustained rapid excitation has been attributed to altered ion channels. Alterations of Ca 2+ handling could also contribute to abnormal dynamics of action potential, favoring the initiation and perpetu...

AIMTo examine the effect of Helicobacter pylori (H. pylori) eradication therapy on the extra-gastrointestinal factors in elderly patients by a before-after observational study in community medicine.METHODSMedical records (1 May 2013-31 January 2014) of 130 patients who underwent H. pylori eradication therapy with 2-year after-eradication observation in our institute were reviewed. Data on sex; age; body weight; body mass index (BMI); mean corpuscular volume (MCV); total protein; low-density lipoprotein cholesterol, triglyceride, haemoglobin A1c and haemoglobin levels and gastric hyperplastic polyps (GHPs) at eradication was extracted. Two-year after-eradication change in data was analysed by paired-sample t-test; relationship between GHPs and subclinical iron deficiency anaemia (IDA) improvement was evaluated.RESULTSThe mean patient age (median, interquartile range) at eradication was 69.6 (71.5, 64-77) years. Paired-sample t-tests showed that body weight, BMI and MCV increased by 0.52 kg (P = 0.018), 0.25 kg/m2 (P = 0.006) and 0.83 fL (P < 0.001), respectively. The nonparametric Mann-Whitney test showed no significant difference in the change rate of MCV after eradication between the groups with and without GHPs (P = 0.892).CONCLUSIONH. pylori eradication therapy prevented weight loss and subclinical IDA in elderly individuals. GHPs were not associated with subclinical IDA.

Currently introduced retrograde approach may increase the success rate of percutaneous coronary interventions on chronic total occlusion (CTO) lesion. This article describes a case of CTO in the left circumflex artery (LCX), which did not allow the regular retrograde approach to deliver a guide wire. At first, a guide wire was attempted to advance from the apical collateral channel, which supplied the distal LCX. However, wiring was extremely difficult because the collateral channel was headed reversely against the direction that the wire was going. Different angle angiogram revealed the existence of another collateral artery, which supplied the distal RCA (posterior descending branch). A guide wire was successfully advanced from the distal RCA, through apical collateral channel, and reached the distal LCX. After the wire was retrieved from the guiding catheter engaged in the left main trunk, antegrade access for balloon and stent delivery was obtained. This method, a sort of "double retrograde" approach, would be worthy to consider when recanalization is failed by other approaches.