Dilation and reduced distensibility of carotid artery in patients with abdominal aortic aneurysms

Background Although patients with abdominal aortic aneurysms (AAA) frequent ly have coexisting systemic atherosclerosis, the dilatative manifestation o f AAA is the opposite of the occlusion characteristic of atherosclerotic di sease. It has been suggested that this dilatative disease is caused by an a lteration in connective tissue metabolism in systemic arterial wall. Such a condition might alter systemic arterial diameter and wall behavior. We inv estigated arterial characteristics in AAA patients, including morphologic c hanges and wall mechanics in the carotid artery. Methods and Results Atherosclerotic intimal changes such as intima-media th ickness (IMT), plaque Formation, diameter, and wall elasticity of the carot id artery were determined ultrasonographically in patients with AAA (n = 10 2) and compared with age-matched patients with the atherosclerotic diseases arteriosclerosis obliterans (ASO, n = 115) and coronary artery disease (CA D, n = 123) and with age-matched healthy control patients (CTL, n = 45). In timal disease in AAA was significantly milder than in ASO, at the same leve l as CAD, and more severe than in CTL. Although end-diastolic luminal diame ters (mm) in AAA (7.05 +/- 1.08), ASO (6.74 +/- 0.1.8), and CAD (6.66 +/- 0 .83) were significantly higher than in CTL (5.97 +/- 0.93), they were also excessively increased compared with the equivalent diameters seen in ASO (P <.01) and CAD (P <.01). Luminal distensibility (x 10(-6) cm(2) . dyne(-1)) in AAA (0.83 +/- 0.48) was excessively decreased compared not only with CT L (1.70 +/- 1.11, P <.01) but also with ASO (1.12 +/- 0.47, P <.01) and CAD [1.18 +/- 0.59, P <.01). These relations remained true when adjusted for b lood pressure and luminal diameter. Intra-AAA group analysis showed that di stensibility in ruptured cases (n = 14) was significantly lower than in non ruptured cases (n = 88) (0.58 +/- 0.24 vs 0.88 +/- 0.50, P <.05). Conclusions Excessive arterial dilation and reduced distensibility without severe intimal disease were found in the carotid arteries of patients with AAA. This suggests that these patients may be subject to systemic arterial alterations, including structural and functional abnormalities.