Eiichiro Hatta

Thoracic Endovascular Aortic Repair for Challenging Aortic Arch Diseases Using Fenestrated Stent Grafts From Zone 0

BACKGROUND Although previous reports have described the repair of distal aortic arch aneurysms through debranching and chimney techniques, these methods invariably involve surgical management of the carotid artery. We report clinical results of thoracic endovascular aortic repair (TEVAR) using fenestrated stent grafts in the treatment of aortic arch aneurysms located less than 15 mm from the left common carotid artery. METHODS A semi-custom-made fenestrated stent graft designed to fit aortic arch tortuosity and preserve blood flow at least into the brachiocephalic and left common carotid arteries was placed from zone 0. RESULTS From 2007 through 2013, TEVAR from zone 0 was performed on 37 high-risk patients for open surgery (mean age 78.2 years). The mean length between the left common carotid artery and aortic aneurysm was 11.1 mm (range, 5 to 15 mm). The left subclavian artery was preserved for 26 patients (70.3%) through surgical reconstruction (n = 19) and graft fenestration (n = 7). The early mortality rate was 0%. Postoperative strokes and spinal cord ischemia occurred in 2 (5.4%) and 3 (8.1%) patients, respectively. Although type I endoleaks at discharge were noted in 12 (32.4%) patients, aneurysm enlargement was noted during follow-up in 6 (16.2%). Four patients (10.8%) underwent secondary interventions consisting of 3 coil embolization procedures; 2 re-TEVARs and 1 open conversion. There were no aorta-related late deaths. Survival and aorta-related event-free rates at 2 years were 86.3% and 88.8%, respectively. CONCLUSIONS Thoracic endovascular aortic repair using fenestrated stent graft from zone 0 can be considered as one of therapeutic options for high-risk patients with aortic arch diseases.

Norepinephrine release and ventricular fibrillation in myocardial ischemia/reperfusion : Roles of angiotensin and bradykinin

Exogenous bradykinin (BK), acting at B2-receptors, enhances norepinephrine (NE) release and exacerbates arrhythmias (VF) in myocardial ischemia/reperfusion. Inhibition of BK formation (with serine proteinase inhibitors) alleviates NE release and VF, whereas prevention of BK degradation (with kininase inhibitors) potentiates them. Yet serine proteinase and kininase inhibitors also prevent the formation of angiotensin (AII), a potent NE-release enhancer. Thus we assessed the respective contribution of AII and BK to NE release and VF by using selective B2- and AT1-receptor antagonists. Isolated guinea pig hearts were subjected to 10- and 20-min global ischemia and 45-min reperfusion. NE overflow (pmol/g) was approximately 8 (exocytotic) and approximately 750 (carrier mediated). VF, associated with carrier-mediated NE release, lasted approximately 2 min. The B2-receptor antagonist Hoe 140 (30 nM) affected neither NE overflow nor VF. In contrast, the AT1-receptor antagonist EXP3174 (100 nM) markedly reduced exocytotic and carrier-mediated NE release and shortened VF. When EXP3174 was combined with Hoe 140, NE overflow and VF were decreased even further. Thus in myocardial ischemia, local AII production contributes to NE release and VF via AT1-receptors. Although BK production increases in myocardial ischemia, the effects of BK on adrenergic nerve terminals are uncovered only when BK half-life is prolonged and/or when AII effects are suppressed.