A newly designed 0.018-in.-compatible inner dilator as a novel option for endovascular therapy with the crossover approach.

This study aimed to investigate the efficacy of guiding sheath delivery with the crossover approach using a newly customized inner dilator for a 0.018-in. guidewire of the Destination® guiding sheath (Terumo Corporation, Tokyo, Japan) (18-system), compared with that of the conventional-type 0.035-in. guidewires with inner dilators (35-system), and to predict failure of guiding sheath delivery. We conducted a prospective multicenter case series study of the contralateral crossover approach using Destination®, to determine whether the 18-system could be a rescue system in cases in which the conventional 35-system failed. To evaluate the efficacy of the 18-system, we created an in vitro aortoiliac bifurcation model by using a silicone vessel. We enrolled 172 cases consecutively. The initial crossover approach with the 35-system failed in 37 cases (21.5%), and a second attempt with the 18-system was successful in all failed cases. The bifurcation angles in the 35-system failure cases were significantly steeper than those in the 35-system success cases. A receiver operating characteristic curve analysis demonstrated that an aortoiliac bifurcation angle of 68° was the optimal cut-off value for predicting failure of the crossover procedure. Data from the analysis using the silicone vessel model suggested that the 18-system provided superior results, especially in aortoiliac bifurcation angles steeper than 60°, consistent with the in vivo findings. The results of the initial use of the 18-system with the crossover approach suggest that it may be superior to the conventional 35-system, especially in cases of steeper aortoiliac bifurcation angles.

Transcriptome Analysis of Yamame (Oncorhynchus masou) in Normal Conditions after Heat Stress.

Understanding the mechanism of high-temperature tolerance in cold-freshwater fish is crucial for predicting how certain species will cope with global warming. In this study, we investigated temperature tolerance in masu salmon (Oncorhynchus masou, known in Japan as 'yamame'), an important aquaculture species. By selective breeding, we developed a group of yamame (F2) with high-temperature tolerance. This group was subjected to a high-temperature tolerance test and divided into two groups: High-temperature tolerant (HT) and non-high-temperature tolerant (NT). RNA was extracted from the gill and adipose fin tissues of each group, and the mRNA expression profiles were analyzed using RNA sequencing. A total of 2893 differentially expressed genes (DEGs) from the gill and 836 from the adipose fin were identified by comparing the HT and NT groups. Functional analyses were then performed to identify associated gene ontology (GO) terms and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. The HT group showed a high expression of heat shock protein 70 (HSP70) gene and enriched gene expression in the extracellular matrix (ECM), cell junction, and adhesion pathways in gill tissues compared to the NT group. The HT group also exhibited highly expressed genes in glycolysis and showed lower expression of the genes in the p53 signaling pathway in adipose fin tissues. Taken together, the difference of expression of some genes in the normal condition may be responsible for the difference in heat tolerance between the HT and NT yamame in the heat stress condition.

Popliteal artery aneurysm treated with implantation of a covered stent graft (fluency(®)) reinforced with a nitinol stent (S.M.A.R.T. (®)).

A 60-year-old man was admitted for right knee pain provoked by an enlarging popliteal artery aneurysm (PAA) after endovascular therapy for thromboembolism in the right popliteal artery. The PAA was treated with implantation of a covered stent graft (Fluency(®)); however, acute thromboembolism occurred 6 months after the intervention. Therefore, we implanted a nitinol stent (S.M.A.R.T.(®)) in the proximal part of the covered stent where the major hinge point existed in addition to a stent fracture. No vascular event occurred during 4.5 years of follow-up.

A side-grooved guiding sheath as an effective treatment strategy for femoro-popliteal artery lesions.

During revascularization for chronic total occlusion (CTO) of the proximal superficial femoral artery (SFA), the guiding sheath may prolapse out of the common femoral artery (CFA) or may not be fully inserted during treatment. Therefore, we have developed a treatment strategy using a novel side-grooved guiding sheath, whereby a 5.0-Fr guiding sheath (45 cm long) with a 1.0 mm × 5.0 mm rectangular side-groove is inserted into the deep femoral artery, the side-groove is aligned with the bifurcation, and the SFA lesion treatment is performed via the side-groove. This technique provides good stability and maintains the wire's torque performance, while avoiding sheath prolapse from its position in the CFA. We have successfully treated seven cases of SFA-CTO with this guiding sheath, and did not observe any increase in complications, procedure time, or amount of contrast media (vs. the conventional procedure). Therefore, our side-grooved guiding sheath appears to be safe and effective for treating SFA-CTO, and we hope to perform additional development of this technique.

Stent dislodgement induced by a vasodilator used for severe coronary artery spasm caused by Kounis syndrome.

Coronary stent dislodgement is a rare but critical complication of percutaneous coronary intervention. It can potentially result in serious consequences, such as stent embolization and emergent coronary artery bypass graft surgery. Here, we describe the successful retrieval of an extracoronary dislodged stent, where dislodgement was induced by a vasodilator used for severe coronary artery spasm caused by Kounis syndrome.

Nifekalant and disopyramide in a patient with short QT syndrome: evaluation of pharmacological effects and electrophysiological properties.

We assessed several pharmacological effects on electrocardiogram parameters and effective refractory period (ERP) in a patient with a short QT syndrome (SQTS). Pharmacological challenge tests revealed that disopyramide and selective I(kr) blocker, nifekalant normalized QT interval, and ERP of the atrial and ventricular myocardium. This study suggested that disopyramide and nifekalant should be feasible for the drug treatment of the SQTS. Moreover, QT interval was paradoxically prolonged at higher heart rates induced with isoproterenol infusion or an exercise test, although the mechanism of this QT prolongation remains to be investigated.

Case report: Focal ablation for atrial fibrillation originating from the inferior vena cava and the posterior left atrium.

We identified a case of paroxysmal atrial fibrillation (AF) originating from inferior vena cava (IVC) and the low-posterior left atrium (LA). Both foci, the IVC and the low-posterior LA, simultaneously served not only as trigger but also as driver for maintenance of AF. During AF, the IVC and the low-posterior LA continuously demonstrated the rapid and fractionated potentials that exit into both atria with conduction block. Focal ablation for ectopic beats within the IVC and the low-posterior LA completely eliminated the storm of AF.

Echocardiographic diagnosis of pulmonary vein varix.

Pulmonary vein varix is a rare abnormality, often resembling a pulmonary or mediastinal mass on chest radiographs, and pulmonary angiography has been the mainstay of diagnosis. An unusual case of pulmonary vein varix was clearly defined by echocardiography performed in a 47-year-old woman with chest discomfort who had been found to have an abnormal structure behind the cardiac silhouette on a chest radiograph. The diagnosis of left lower pulmonary vein varix was noninvasively confirmed by transthoracic echocardiography and transesophageal echocardiography.

Effects of ACE inhibition on myocardial apoptosis in an ischemia-reperfusion rat heart model.

Myocardial ischemia-reperfusion injury involves necrosis and apoptosis. The inhibition of angiotensin-converting enzyme (ACE) has been reported to suppress infarct size. In this study, it was investigated whether an ACE inhibitor affected myocardial apoptosis and apoptosis-related proteins in rats with experimental myocardial infarction. Anesthetized Sprague-Dawley rats were divided into four groups. Group I underwent 30 minutes of left coronary artery occlusion followed by 24 hours of reperfusion (control group); Group II underwent oral administration of the ACE inhibitor quinapril (10 mg/kg/day) before coronary occlusion (quinapril group); Group III underwent administration of the bradykinin B(2)-receptor antagonist Hoe 140 (250 microg/kg/day, subcutaneously) with quinapril (quinapril + Hoe 140 group); and Group IV underwent administration of Hoe 140 alone (Hoe 140 group). After reperfusion, myocardial infarct size was determined by triphenyltetrazolium chloride staining. Myocardial apoptosis was detected immunohistologically using terminal deoxynucleotidyl transferase-mediated nick end labeling staining and DNA electrophoresis. Myocardial caspase-3 activation was analyzed by Western blot and the expressions of Bcl-xL and Bax proteins were detected immunohistochemically. Quinapril significantly reduced the ratio of myocardial infarct size in the ischemic area at risk. In addition, quinapril significantly suppressed the incidence of apoptotic myocytes around the necrotic region (from 18.9 +/- 0.8% to 8.6 +/- 1.0%; P < 0.0001), the intensity of DNA ladder formation, and the activation of caspase-3. Hoe 140 attenuated these protective effects of quinapril. In the immunohistochemical study, Bax and Bcl-xL were expressed in myocytes, and ischemia-reperfusion abolished both proteins in the center region of ischemia. The Bax staining was equally observed among all groups. However, Bcl-xL staining remained in the ischemic area widely after quinapril treatment. In addition, Hoe 140 also depleted this effect of quinapril. These results suggest that inhibition of ACE reduces myocardial infarction and apoptosis via the bradykinin B(2) receptor in part. The antiapoptotic effect of the ACE inhibitor is attributed to the changing expression of Bcl-xL.