Abdominal aortic grafting for spontaneous infrarenal abdominal aortic dissection.

This case report concerns a 62-year-old woman with spontaneous infrarenal abdominal aortic dissection, which developed into claudication and rest pain in the lower extremity. Multi-row detector computed tomography showed the entry site of the abdominal aortic dissection at the second lumbar artery, while the reentry site was found intraoperatively at the median sacral artery, indicating that the false lumen had progressed and compressed the true lumen. A direct approach involving grafting appears to be an effective procedure for resolving mesenteric and lower extremity hypoperfusion due to aortic dissection with a dilated false channel, even during the acute period.

Reoperation for a giant arch anastomotic pseudoaneurysm eleven years after total arch replacement with island reconstruction.

BACKGROUND: The long-term effects of some surgical treatment procedures of arch replacement for aortic dissection or aortic aneurysm are unknown. CASE PRESENTATION: The present study reports the case of a 68-year-old man admitted to our hospital for aortic arch anastomotic pseudoaneurysm with concomitant aortic root enlargement and coronary artery stenosis. Eleven years ago, at the age of 56 years, he underwent total arch replacement with island reconstruction for chronic aortic dissection. We performed a second total arch replacement, aortic root replacement, and coronary artery bypass, using a cardiopulmonary bypass with cannulation through the right subclavian artery, femoral artery, and femoral vein prior to re-sternotomy. We also used selective cerebral perfusion. Postoperatively, the patient temporarily required reintubation; however, he was discharged in good condition on the fiftieth postoperative day. CONCLUSIONS: This case suggests that island reconstruction has the potential to cause arch anastomotic pseudoaneurysms, particularly after a long postoperative period.

The Paracrine Effect of Skeletal Myoblasts Is Cardioprotective Against Oxidative Stress and Involves EGFR-ErbB4 Signaling, Cystathionase, and the Unfolded Protein Response.

Therapeutic effects of skeletal myoblast transplantation into the myocardium are mediated via paracrine factors. We investigated the ability of myoblast-derived soluble mediators to protect cardiomyocytes from oxidative stress. Fetal rat cardiac cells were treated with conditioned medium from cultures of myoblasts or cardiac fibroblasts, and oxidative stress was induced with H2O2. Myoblast-derived factors effectively prevented oxidative stress-induced cardiac cell death and loss of mitochondrial membrane potential. This protective effect was mediated via epidermal growth factor (EGF) receptor and c-Met signaling, and mimicked by neuregulin 1 but not EGF. Microarray analysis of cardiac cells treated with myoblast versus cardiac fibroblast-derived mediators revealed differential regulation of genes associated with antioxidative effects: cystathionine-γ-lyase (cst), xanthine oxidase, and thioredoxin-interacting protein as well as tribbles homolog 3 (trib3). Cardiac cell pretreatment with tunicamycin, an inducer of trib3, also protected them against H2O2-induced cell death. Epicardial transplantation of myoblast sheets in a rat model of acute myocardial infarction was used to evaluate the expression of CST and trib3 as markers of myoblasts' paracrine effect in vivo. Myoblast sheets induced expression of the CST as well as trib3 in infarcted myocardium. CST localized around blood vessels, suggesting smooth muscle cell localization. Our results provide a deeper molecular insight into the therapeutic mechanisms of myoblast-derived paracrine signaling in cardiac cells and suggest that myoblast transplantation therapy may prevent oxidative stress-induced cardiac deterioration and progression of heart failure.

Right ventricular thrombus in a patient with nephrotic syndrome.

We treated a 21-year-old man with right ventricular thrombus caused by nephrotic syndrome. The right ventricular thrombus was safely removed and his postoperative course was uneventful. Peri- and postoperative management after surgery for the worsened nephrotic syndrome was relatively unique and difficult, and critical care was essential for saving the patient's life and protecting renal function.

Bioengineered myocardium derived from induced pluripotent stem cells improves cardiac function and attenuates cardiac remodeling following chronic myocardial infarction in rats.

Cell-based therapies are promising strategies for myocardial repair following myocardial infarction. Induced pluripotent stem (iPS) cells have the potential to generate many cardiomyocytes, and they hold significant promise for the application of regenerative medicine to heart failure. Here, we developed cardiac tissue sheets, termed bioengineered myocardium (BM), from mouse iPS cells and measured cardiac performance following BM implantation in a rat chronic myocardial infarction model. Immunostaining analyses revealed that the α-actinin(+) cell population was isolated with more than 99% purity under specific culture conditions. To evaluate the contribution of BM to the improvements in cardiac performance, we induced myocardial infarction in 30 F344/NJcl-rnu/rnu rats by left anterior descending coronary ligation. The rats were randomly divided into two groups, 2 weeks after ligation: a BM implantation group (n = 15) and a sham group (n = 15). Echocardiography and catheter examination showed that the BM implantation significantly improved cardiac function and attenuated cardiac remodeling compared with the sham group. Histological analyses demonstrated that the implanted BM survived at the epicardial implantation site 4 weeks after implantation. The implanted BM survived and attenuated left ventricular remodeling in the rat chronic myocardial infarction model. Thus, BM derived from iPS cells might be a promising new treatment for heart failure.