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Abdominal aortic aneurysm is a chronic degenerative disease that is usually silent until rupture occurs and this complication is still associated in contemporary era with a high rate of mortality. Screening programmes for abdominal aortic aneurysm have been shown to be effective in reducing global mortality in the screened population but these programmes are poorly implemented in the Western countries. As coronary artery disease and abdominal aorta aneurysmal disease share many risk factors, the cardiologist is centrally positioned in the screening strategy, not only to identify patients with higher risk of developing abdominal aortic aneurysm, but also to perform an opportunistic screening during echocardiography. This paper summarises evidence about the feasibility, indications, modalities, benefits and risks related to the opportunistic screening for abdominal aortic aneurysm during echocardiography with a particular emphasis on the population of patients with coronary artery disease.

Postischaemic reperfusion injury is often attributed to the generation of oxygenated free radicals which may subsequently promote lipid peroxidation in cell membranes. Electron paramagnetic resonance spectroscopy in association with the spin trap molecule α-phenyl- N-tert-butyl-nitrone allowed direct confirmation of lipid free radical production after renal ischaemia-reperfusion in an in vivo rabbit model. A 60-min period of ischaemia followed by reperfusion caused free radical production twofold greater than after 15min of ischaemia. Glutathione and a-tocopherol have been measured in renal tissue, as indirect markers of lipid peroxidation. After 15min of ischaemia followed by 10min of reperfusion, the mean(s.e.m.) glutathione content of the ischaemic kidney was slightly but significantly reduced by 11.9(2.5)% ( P < 0.003). The content of α-tocopherol was unchanged. However, 10min of reperfusion following 60 min of ischaemia led to significant decrease in mean(s.e.m.) content of both glutathione (30.4(3.7)%) (2.23(0.2) versus 3.14(0.18) μmol/g wet tissue, ( P < 0.001) and α-tocopherol (46.1(7.8)%) (0.57(0.10) versus 1.09(0.14) μg/g wet tissue. P < 0.001) when compared to the control kidney. Under these experimental conditions, desferrioxamine (15mg/kg administered intravenously before inducing ischaemia), a drug known to limit free radical production, significantly limited the decrease of α-tocopherol to 20.8(6.4)% (0.83(0.08) versus 1.05(0.04) μg/g wet tissue. P < 0.05), but did not prevent glutathione consumption in the reperfused kidney.