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Atherosclerosis continues to cause considerable morbidity and mortality, particularly in the western world. While risk factors have been clearly identified, their precise roles in early atherogenesis are complex. The early development of the plaque is dependent upon interactions between damaged endothelial cells, vessel wall smooth muscle cells and circulating inflammatory cells mediated by the release of cytokines, growth factors and cell adhesion molecules. Plaque formation may represent a cell-mediated immune phenomenon, with a variety of potential antigenic agents identified. Shear stress and flow considerations also play a part.
Atherosclerosis begins in childhood, but it takes decades for atherosclerosis to evolve into the mature plaques responsible for the onset of ischaemic symptoms. Whilst plaque growth due to smooth muscle cell proliferation, matrix synthesis and lipid accumulation may narrow the arterial lumen and ultimately limit blood flow, uncomplicated atherosclerosis is essentially a benign disease. The final clinical outcome depends on whether a plaque becomes unstable, leading to acute disruption of its surface and exposure of its thrombogenic core to the luminal blood flow. The concept of a ‘vulnerable plaque’ was initially described in 1990 and though this initially gained wide acceptance, many authors now favour the broader concept of a ‘vulnerable patient”, whereby certain systemic and haematological conditions (e.g. relative hypercaogulability) must also be met before plaque rupture will result in symptomatic thrombosis.
Mature atherosclerotic plaques are composed of a lipid core that is separated from the vessel lumen by a cap composed of fibrillar collagen.
Matt M. Thompson, Department of Vascular Surgery The St George's Vascular Institute St George's Hospital Blackshaw Road London SW17 0QT UK,
Ian Loftus, Department of Vascular Surgery The St George's Vascular Institute St George's Hospital Blackshaw Road London SW17 0QT UK
In the last five years, vascular surgery has undergone a considerable change in emphasis with respect to the breadth of conditions being treated and in the techniques used in therapy. The evidence base for vascular surgical intervention has broadened considerably, particularly in the fields of carotid intervention and the treatment of abdominal and thoracic aortic aneurysms. This newly gathered evidence base has been used to further define the indications for vascular reconstruction.
The emphasis on the development of new techniques for vascular intervention has continued, with the focus on minimally invasive and endovascular therapy. The application of endovascular therapy for the treatment of aortic and carotid disease is still largely confined to specialist centres but these techniques are likely to represent the future of vascular intervention. The change in direction of traditional vascular surgery has significant implications for anaesthetic practice as most of the newer vascular techniques are amenable to loco-regional anaesthesia. This chapter reviews the most recent advances in vascular practice for the treatment of aortic disease, carotid artery stenosis and varicose veins.
Advances in the treatment of abdominal aortic aneurysms
Aortic aneurysms are responsible for 13 000 deaths in the UK, with abdominal aneurysms causing 8000 of these. The principles that guide aneurysm treatment are to detect aneurysms prior to rupture, to electively repair these aneurysms with the lowest possible mortality and to treat the complications of aneurysmal disease (primarily rupture). Unfortunately, the majority of aneurysms are asymptomatic and many rupture before elective surgical repair can be contemplated.
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