Eiki Woo

Minimizing Cerebral Embolism in Resection of Distal Aortic Arch Aneurysm Through a Left Thoracotomy

BACKGROUND In order to reduce the risk of cerebral embolism during aortic replacement through a left thoracotomy, we performed ascending or arch aortic cannulation (AAC) as well as early extracorporeal perfusion (EEP) under deep hypothermic circulatory arrest (DHCA). In this study we examined the effectiveness of these modifications in preventing cerebral embolism after distal arch replacement. METHODS Between January 2006 and March 2010, 40 patients underwent distal arch replacement through a left thoracotomy, using 2 pieces of an artificial graft. In all patients, AAC, EEP, and the open technique for aortic anastomosis were performed under DHCA. The AAC resulted in the proximal aortic perfusion from the proximal site of the diseased aorta. The EEP was induced by aortic distal perfusion from the side branch of a distal graft. After completion of the proximal anastomosis under EEP and DHCA, anastomosis between the proximal and distal grafts was made during rewarming. Neurologic deficit in the brain and spinal cord, as well as early surgical results, were clinically evaluated. RESULTS There was no permanent neurologic deficit after the surgery in the operative survivors. No patient had a stroke (0%). Temporary paraplegia and paraparesis occurred in 1 and 2 patients, respectively (7.7%); all 3 patients were able to walk prior to their discharge from hospital. Mortality in this series was 5.0% (2 of 40 patients); the cause of death was rupture of an esophageal ulcer and cardiogenic shock possibly due to myocardial infarction. CONCLUSIONS The AAC and EEP, in addition to deep hypothermia and DHCA, minimized the risk of cerebral embolism after distal arch aortic replacement by the left lateral approach.

Capillary Degeneration and Right Ventricular Remodeling Due to Hypoxic Stress with Sugen5416

BACKGROUND Sugen5416 (semaxinib) is an inhibitor of the vascular endothelial growth factor (VEGF) receptor. A rat model of Pulmonary Arterial Hypertension (PAH), created with Sugen5416 and chronic hypoxia, is known to have similar histological findings to those of PAH patients. OBJECTIVE To evaluate the pathophysiological mechanisms of cardiac remodeling due to hypoxic stress with Sugen5416 in vivo. METHODS Male Sprague-Dawley rats were exposed to hypoxia (10 ± 1% O2) for 2 weeks after a single injection of Sugen5416 (SU-hypoxia group) or the vehicle (V-hypoxia group). RESULTS Hypoxia elevated right ventricular (RV) systolic pressure and caused RV remodeling on Day 14. By electron microscopy, metamorphosis of capillaries with endothelial cell occlusive degeneration was observed in the RV myocardium of the SU-hypoxia group from Day 3. After reoxygenation, progressive RV remodeling with extensive degeneration of cardiomyocytes was observed in the SUhypoxia group, associated with a significant increase of oxidative stress and TUNEL-positive cells in both RV and left ventricular myocardium on Day 84. The expression of VEGF mRNA in the RV myocardium was significantly suppressed in the SU-hypoxia group on Day 3, whereas delayed activation of VEGF/extracellular signal-regulated kinase (ERK) signaling pathway on Day 14 were observed. CONCLUSION Capillary degeneration and activation of VEGF/ERK signaling pathway might be crucial to accelerate the cardiac remodeling due to hypoxic stress with Sugen5416.