[Traction-assisted Negative Pressure Wound Therapy for Pediatric Poststernotomy Mediastinitis:Report of Two Cases].

We herein report two cases of pediatric poststernotomy mediastinitis treated by traction-assisted negative pressure wound therapy (NPWT) with Zip Surgical Skin Closure (Zip), which is a non-invasive skin closure device. We used this device with NPWT in cases of pediatric poststernotomy mediastinitis to stabilize the sternum and reduce the natural retractive forces of the skin. The patients were two boys (two and three months old), with an onset of infection at 13 and eight postoperative days, respectively. The culture examination detected methicillin-susceptible Staphylococcus aureus in both cases. Traction-assisted NPWT with Zip was performed at-75 mmHg for 16 and 33 days, and the wounds healed completely. In conclusion, this modification was successfully applied to treat pediatric poststernotomy mediastinitis and may help reduce the duration of treatment.

[In situ Replacement with Bovine Pericardial Roll Graft for Infected Aneurysm of the Thoracoabdominal Aorta].

A 63-year-old man presented to a nearby doctor with fever and lumbago. Enhanced computed tomography showed a thoracoabdominal aortic aneurysm and enhancement of soft tissue around the aneurysm. He was diagnosed with an infected thoracoabdominal aortic aneurysm and given antibiotics. After 2 weeks, the infection was controlled and he underwent in situ replacement with a bovine pericardial roll graft. A week after the operation, the inflammatory reaction was increased, but the bovine pericardial roll graft was not infected. This suggests that a bovine pericardial roll graft is a suitable material for use in patients with bacterial infections.

A free-floating left atrial thrombus develops intermittent entrapment in the mid-ventricle during diastole.

Free-floating left atrial thrombi are rare. Here we report a case of a 75-year-old woman with atrial fibrillation who was admitted for treatment of acute myocardial infarction. A free-floating left atrial thrombus was found incidentally on echocardiography. Ten days after percutaneous coronary intervention, the patient had mild faintness with transient hypotension, and it was found that the left atrial thrombus had developed intermittent entrapment in the mid-ventricle during diastole, with abrupt rebound back to the left atrial cavity during systole. Urgent removal of the thrombus was performed successfully. Although the free-floating thrombus had appeared to be spherical, like a ball thrombus, on echocardiography, the excised thrombus was pedunculated. A cut section revealed a laminated thrombus with an onion-skin-like appearance.

STAT signaling in ischemic heart: a role of STAT5A in ischemic preconditioning.

We recently demonstrated that ischemic preconditioning (PC) induced by cyclic episodes of short duration of ischemia and reperfusion potentiates a signal transduction cascade involving Janus kinase (JAK) 2 and signal transducer and activator of transcription 3 (STAT3). A rapid activation of JAK and several STATs, including STAT3, STAT5A, and STAT6 also occurred during myocardial ischemia and reperfusion. This study sought to examine whether STAT5A and STAT6 were also involved in PC. Two different animal models were used: isolated perfused working rat hearts and STAT5A and STAT6 knockout mouse hearts. The results of our study indicated phosphorylation of STAT 5A and STAT6 in the preconditioned myocardium. Tyrphostin AG490, a JAK2 inhibitor, or 4-amino-5-(4-methylphenyl)-7-(t-butyl)-pyrazolo-3,4-d-pyrimidine (PPI), a Src kinase blocker, blocked STAT5A phosphorylation, whereas STAT6 phosphorylation was blocked only with tyrphostin. As expected, significant cardioprotection was achieved in the preconditioned heart as evidenced by reduced myocardial infarct size and decreased number of apoptotic cardiomyocytes. PC-mediated cardioprotection was partially abolished when hearts were pretreated with tyrphostin, PPI, or LY-294002, a phosphatidylinositol (PI)-3 kinase inhibitor. Studies with STAT5A and STAT6 knockout mouse hearts revealed that STAT6 knockout mouse hearts, and not STAT5A knockout mouse hearts, were resistant to myocardial ischemia-reperfusion injury. The hearts from STAT5A knockout mice could not be preconditioned, whereas those from STAT6 knockout mice were easily preconditioned. The results of the present study demonstrate that STAT5A, and not STAT6, plays a role in ischemic PC. For the first time, the results also indicated a role of Src kinase pathway in STAT5A PC and PI-3 kinase-Akt pathways appear to be the downstream regulator for STAT5A-STAT6 signaling pathway.

Real-time cerebral monitoring using multichannel near-infrared spectroscopy in total arch replacement.

Multichannel near-infrared spectroscopy (NIRS) could detect change in the regional cerebral oxygenation by following animated pictures of oxy-hemoglobin (OxyHb), deoxy-hemoglobin (DeoxyHb) and total hemoglobin in operations for three surgical cases of thoracic aortic aneurysm with selective cerebral perfusion (SCP). Simultaneously measured jugular venous oxygen saturation (SjO2) showed no change in parallel to OxyHb or DeoxyHb of NIRS. It was concluded that SjO2 represented the entire rather than the local findings of the cerebral oxidative metabolism. Assessment of the intra cranial oxidative metabolism using a multichannel NIRS provided real-time information about the efficacy of SCP, while SjO2 had a comprehensive limited value. The animation enabled the detection of regional hypoperfusion visually and instantly during SCP. This multichannel NIRS was a new real-time monitoring method and was useful to prevent cerebral neurological complication due to hypoperfusion during SCP.

Hypoxic preconditioning triggers myocardial angiogenesis: a novel approach to enhance contractile functional reserve in rat with myocardial infarction.

A modern experimental strategy for treating myocardial ischemia is to induce neovascularization of the heart by the use of "angiogens", mediators that induce the formation of blood vessels, or angiogenesis. Studies demonstrated that coronary collateral vessels protect ischemic myocardium after coronary obstruction; therefore we sought to examine a novel method of stimulating myocardial angiogenesis through hypoxic preconditioning at both capillary (using anti-CD31) and arteriolar (using anti- alpha smooth muscle actin) levels and also investigate whether such treatments could preserve left ventricular contractile functional reserve and regional blood flow by increasing vascular endothelial growth factor (VEGF). Male Sprague-Dawley rats were randomly divided into four groups: normoxia+sham surgery (CS), normoxia+permanent left anterior descending coronary artery (LAD) occlusion (CMI), hypoxic preconditioning+sham surgery (HS) and hypoxic preconditioning+permanent LAD occlusion (HMI). Rats in the preconditioned groups were subjected to systemic hypoxemic hypoxic exposure (10+/-0.4% O(2)) for 4 h followed by a 24 h period of normoxic reoxygenation prior to undergoing LAD occlusion. Rats in the normoxia group were time matched with the preconditioned group and maintained under normoxic conditions for a 28 h period prior to LAD occlusion. Western blot analysis was performed to measure VEGF expression and TUNEL staining with endothelial cell-specific antibody, anti-VWF, was used to examine endothelial apoptosis. One, two and three weeks after the LAD occlusion, baseline left ventricular pressures were monitored and recorded. Pharmacological stress tests with dobutamine infusion in progressively increasing doses revealed significantly elevated contractile reserve at each dose point in the HMI group compared to the CMI group. The HMI group displayed statistically significant increases in capillary as well as arteriolar density after 1, 2 and 3 weeks post-operation. Blood flow was also significantly elevated in the HMI groups when compared to the CMI group. The extent of endothelial cell apoptosis was found to be inversely proportional to VEGF expression. It was concluded that hypoxic preconditioning stimulates myocardial angiogenesis to an extent sufficient to exert significant cardioprotection in a rat model of myocardial infarction progressing to heart failure as evidenced by increased capillary/arteriolar density and enhanced ventricular contractile functional reserve.