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

Background Although patients with abdominal aortic aneurysms (AAA) frequently have coexisting systemic atherosclerosis, the dilatative manifestation of AAA is the opposite of the occlusion characteristic of atherosclerotic disease. It has been suggested that this dilatative disease is caused by an alteration in connective tissue metabolism in systemic arterial wall. Such a condition might alter systemic arterial diameter and wall behavior. We investigated arterial characteristics in AAA patients, including morphologic changes and wall mechanics in the carotid artery. Methods and Results Atherosclerotic intimal changes such as intima-media thickness (IMT), plaque formation, diameter, and wall elasticity of the carotid artery were determined ultrasonographically in patients with AAA (n = 102) and compared with age-matched patients with the atherosclerotic diseases arteriosclerosis obliterans (ASO, N = 115) and coronary artery disease (CAD, N = 123) and with age-matched healthy control patients (CTL, N = 45). Intimal disease in AAA was significantly milder than in ASO, at the same level as CAD, and more severe than in CTL. Although end-diastolic luminal diameters (mm) in AAA (7.05 ± 1.08), ASO (6.74 ± 0.18), 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 (× 10–6 cm2 · dyne–1) in AAA (0.83 ± 0.48) was excessively decreased compared not only with CTL (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 blood pressure and luminal diameter. Intra–AAA group analysis showed that distensibility in ruptured cases (n = 14) was significantly lower than in nonruptured 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. (Am Heart J 2000;140:297-302.)