Background: Spontaneous isolated dissection of abdominal visceral arteries without aortic dissection is rare and its pathology and prognosis are not yet clear; therefore, therapeutic strategies for this disease have not been established. The present multi-institution investigational study analyzed the clinical features of patients with spontaneous isolated dissection of abdominal visceral arteries. Methods: A total of 36 patients diagnosed as spontaneous isolated dissection of abdominal visceral arteries from January 2010 to October 2016 were enrolled. The medical data of the patients were retrospectively reviewed. Imaging characteristics were evaluated. Spontaneous isolated dissection of abdominal visceral arteries was detected on upper abdominal computed tomography examination in almost patients, and was detected on magnetic resonance imaging in one patient. Results: Of the 36 cases, 26 cases involved the superior mesenteric artery dissection, nine involved the celiac artery, two involved the splenic artery, one involved the common hepatic artery, one involved the gastroduodenal artery and one involved the left gastric artery. Among the 36 patients, 20 had hypertension and 14 were current smokers. Additionally, only one patient had diabetes and four patients had dyslipidemia. Moreover, 32 cases complained of pain including abdominal pain and back pain, one had cough and three had no symptoms. Of the 36 patients, 34 cases (94.4%) were treated conservatively, and two (5.6%) required intravascular treatment. All patients were discharged without complications. Conclusions: Our findings indicate that hypertension and smoking might be closely involved in the pathogenesis of spontaneous isolated dissection of abdominal visceral arteries, whereas dyslipidemia and diabetes might be less involved. Additionally, few asymptomatic patients were accidentally diagnosed, indicating that the absence of symptoms cannot be used to rule out the presence of this disease. Randomized clinical trials cannot be performed because a considerable number of cases are required. Therefore, detailed descriptions of clinical features, as provided in our report, are important.

ObjectiveLittle is known about the long-term effects of renin–angiotensin system inhibitors (RASI) on cardiovascular events in patients after acute myocardial infarction (AMI) with ischaemic mitral regurgitation (IMR). The purpose of this study was to investigate the association of RASI with the incidence of adverse cardiac events in patients with or without IMR after AMI.MethodsWe reviewed charts of 1208 consecutive patients admitted with AMI who underwent emergency coronary angiography between 2000 and 2012. After excluding patients who died within 30 days, 551 patients were diagnosed to have mild or greater MR by transthoracic echocardiography (patients with IMR); the remaining 505 patients had no or trivial MR (non-IMR patients).ResultsOf the study patients, 395 (72%) patients with IMR and 403 (80%) non-IMR patients received RASI. Survival analysis showed that freedom from cardiac death and the composite of cardiac death and heart failure (HF) was significantly higher in patients with IMR receiving RASI than in those not receiving RASI (P<0.001 and P<0.001, respectively). Moreover, adjusted survival analysis using the inverse probability treatment weighting method showed a significant association of RASI therapy with reduced cardiac death (P=0.010) and the composite of cardiac death and HF (P=0.044) in patients with IMR. However, in non-IMR patients, there were no significant associations between RASI therapy and the outcome measures.ConclusionsRASI therapy was associated with a lower incidence of adverse cardiac events in patients with IMR after AMI, but not in patients without IMR.

Rationale: The only treatment for drug-resistant heart failure is heart transplantation, however, it has problems such as donor shortages and rejection. Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-cardiomyocytes) are promising sources of regenerative medicine that can solve these problems. The engraftment potential of hiPSC-cardiomyocytes following the transplantation into the host heart should be improved to realize this therapy. Objective: We aim to discover a compound to enhance the engraftment of hiPSC-cardiomyocytes following the cell transplantation into the damaged heart. We also aim to realize a larger graft size and recover cardiac function. Methods and Results: We established an iPSC line constitutively expressing Fluorescent Ubiquitination-based Cell Cycle Indicator (FUCCI), which can show the cell cycle phase in real-time. We compared the engraftment capacity of hiPSC-cardiomyocytes in between the S/G2/M (activation) phase and G0/G1 (inactivation) phase for three months after transplantation, finding cell cycle activated hiPSC-cardiomyocytes showed significantly higher engraftment efficiency than those in inactivated. We, thus, conducted the screening to find cell-cycle activating compounds in the hiPSC-cardiomyocytes. The screening identified some candidates from more than 4000 compounds, and we focused on the most effective compound (CCA-1). An EdU assay and cell number count demonstrated the activation of proliferative capacity by CCA-1. Moreover, genetic analysis revealed a group of genes related to CCA-1-induced cell cycle activation. Finally, using in vivo bioluminescent imaging, we confirmed that CCA-1 treated hiPSC-cardiomyocytes showed enhanced graft size after transplantation into mice ischemic heart. Conclusions: This study highlights the effectiveness of the FUCCI system to analyze the cell cycle status in hiPSC-cardiomyocytes, and the cell cycle activation by CCA-1 is the efficient strategy to increase the graft size following the cell transplantation into the damaged heart.

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