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Background Tissue engineering techniques have been employed successfully in the management of wounds, burns and cartilage repair. Current prosthetic alternatives to autologous vascular bypass grafts remain poor in terms of patency and infection risk. Growing biological blood vessels has been proposed as an alternative. Methods This review is based on a literature search using Medline, PubMed, ISIS and CAS of original articles and reviews, and unpublished material and abstracts. Results and conclusions Complete incorporation into host tissues and the maintenance of a viable and self-renewing endothelial layer are the fundamental goals to be achieved when developing a tissue-engineered blood vessel. Sourcing of cells and modulating their interaction with extracellular matrix and supporting scaffold have been the focus of intense research. Although the use of tissue-engineered blood vessels in humans is so far limited, advances in our knowledge of stem cell precursors and the development of new biomaterials should enable this technology to reach routine clinical practice within a decade.

Myocardial infarction accounts for over 50 per cent of mortality following elective abdominal aortic surgery. Previous history of ischaemic heart disease and abnormal ECGs, common in vascular patients, are unreliable parameters for predicting myocardial response to stress. Exercise ECGs are often valueless, as claudication may mask myocardial insufficiency. Myocardial performance was studied preoperatively in 29 consecutive patients undergoing elective aortic bifurcation grafting, using a Swann-Ganz catheter to measure the rise in pulmonary artery wedge pressure (PAWP) produced by rapid intravenous infusion of plasma (200–400 ml). A Frank-Starling Curve was obtained by plotting LVSWI against PAWP. Two important values were obtained: (a) ‘Upslope’ or gradient of the ascending portion of the curve. Low values identify patients most at risk from cardiac complications. Six patients who suffered from postoperative cardiac complications had a mean ‘upslope’ value of 1·568 ± 0·681 (1 s.e.m.), whereas the 23 who did not, had a mean value of 7·094 ± 0·745 (1 s.e.m.), a significant difference (P < 0·001); (b) ‘PAWPmax’, the ventricular filling pressure above which work output dropped. Infusion beyond this may precipitate pulmonary oedema. PAWP was observed at levels greater than PAWPmax in all 6 patients who developed either pulmonary oedema or myocardial infarction. The myocardial performance curve can reliably identify high risk patients and permit control of intravenous therapy within individual safety limits, thereby preventing pulmonary oedema.