Aortic dissection is a life-threatening condition caused by a tear in the intimal layer of the aorta or bleeding within the aortic wall, resulting in the separation (dissection) of the layers of the aortic wall. Aortic dissection is most common in those 65-75 years of age, with an incidence of 35 cases per 100,000 people per year in this population. Other risk factors include hypertension, dyslipidaemia and genetic disorders that involve the connective tissue, such as Marfan syndrome. Swift diagnostic confirmation and adequate treatment are crucial in managing affected patients. Contemporary management is multidisciplinary and includes serial non-invasive imaging, biomarker testing and genetic risk profiling for aortopathy. The choice of approach for repairing or replacing the damaged region of the aorta depends on the severity and the location of the dissection and the risks of complication from surgery. Open surgical repair is most commonly used for dissections involving the ascending aorta and the aortic arch, whereas minimally invasive endovascular intervention is appropriate for descending aorta dissections that are complicated by rupture, malperfusion, ongoing pain, hypotension or imaging features of high risk. Recent advances in the understanding of the underlying pathophysiology of aortic dissection have led to more patients being considered at substantial risk of complications and, therefore, in need of endovascular intervention rather than only medical or surgical intervention.

Nuclear factor B (NF-B) activation has been observed in human atherosclerotic plaques and is enhanced in unstable coronary plaques, but whether such activation has a protective or pathophysiological role remains to be determined. We addressed this question by developing a short-term culture system of cells isolated from human atherosclerotic tissue, allowing efficient gene transfer to directly investigate signaling pathways in human atherosclerosis. We found that NF-B is activated in these cells and that this activity involves p65, p50, and c-Rel but not p52 or RelB. This NF-B activation can be blocked by overexpression of IB␣ or dominant-negative IB kinase (IKK)-2 but not dominant-negative IKK-1 or NF-B-inducing kinase, resulting in selective inhibition of inflammatory cytokines (tumor necrosis factor ␣, IL-6, and IL-8), tissue factor, and matrix metalloproteinases without affecting the antiinflammatory cytokine IL-10 or tissue inhibitor of matrix metalloproteinases. Our results demonstrate that the canonical pathway of NF-B activation that involves p65, p50, c-Rel, and IKK-2 is activated in human atherosclerosis and results in selective upregulation of major proinflammatory and prothrombotic mediators of the disease.

Early results of visceral hybrid stent-grafts for types I, II, and III thoracoabdominal aneurysms are encouraging, with no paraplegia in this particularly high-risk group of patients. These results have encouraged us to perform the new procedure, in preference to open surgery, in Crawford type I, II, and III thoracoabdominal aortic aneurysms.