Atherosclerosis in Abdominal Aortic Aneurysms: A Causal Event or a Process Running in Parallel? The Tromsø Study

Abstract

The pathogenesis of abdominal aortic aneurysm (AAA) formation is poorly understood. We investigated the relationship between carotid, femoral, and coronary atherosclerosis and abdominal aortic diameter, and whether atherosclerosis was a risk marker for AAA. Ultrasound of the right carotid artery, the common femoral artery, and the abdominal aorta was performed in 6446 men and women from a general population. The burden of atherosclerosis was assessed as carotid total plaque area, common femoral lumen diameter, and self-reported coronary heart disease. An AAA was defined as maximal infrarenal aortic diameter > or =30 mm. No dose-response relationship was found between carotid atherosclerosis and abdominal aortic diameter <27 mm. However, significantly more atherosclerosis and coronary heart disease was found in aortic diameter > or =27 mm and in AAAs. The age- and sex-adjusted odds ratio (OR) (95% CI) for AAA in the top total plaque area quintile was 2.3 (1.5 to 3.4), as compared with subjects without plaques. The adjusted OR (95% CI) was 1.7 (1.1 to 2.6). No independent association was found between femoral lumen diameter and AAA. The lack of a consistent dose-response relationship between atherosclerosis and abdominal aortic diameter suggests that atherosclerosis may not be a causal event in AAA but develops in parallel with or secondary to aneurismal dilatation.