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Abdominal aortic aneurysms (AAA) have a prevalence between 1.3-8.9% in men and 1.0-2.2% in women aged above 55 years. Furthermore, AAA cause 1-3% of all deaths among men aged 65-85 years in developed countries. As the disorder is invariably associated with severe atherosclerotic damage of the arterial wall, it has traditionally been regarded as a direct consequence of generalized atherosclerotic disease. In patients with occlusive aortic disease, dyslipidemia is a well established risk factor. However, in patients with aneursymatic aortic disease, the association between dyslipidemia and the development of AAA is less clear. Large clinical trials in patients with cardiac and peripheral arterial disease have shown the strong relation between dyslipidemia, statin therapy and the risk of cardiovascular disease. Importantly, the effects of statin therapy were still present irrespective of the decrease in serum cholesterol levels. These findings resulted in the discussion of potential non-lipid lowering effects of statin therapy. These ''pleiotropic effects'' compose a diversity of cellular events which have an effect on several components of the arterial wall, including: 1) endothelial cells; 2) smooth muscle cells; 3) platelets; 4) monocytes/macrophages; and 5) the process of inflammation. In the general population the role of dyslipidemia as an independent risk factor for AAA is debated. However, as patients with AAA frequently have concomitant arterial disease, statin therapy is often recommended. As a result, the non-lipid lowering effects of statins on aneurysm expansion rate are hardly studied, and most evidence comes from experimental and animal studies. In the current review article we provide an overview of all available literature on the effects of dyslipidemia, statin therapy and the risk of AAA expansion and rupture. In the first part we summarize all population-based studies that investigated the relation between hypercholesterolemia and the development of AAA. In the second part, the available literature regarding the effects of statins on aneurysm growth, expansion rate and the risk of rupture is summarized, including in vitro, animal and clinical human studies.

Abdominal aortic aneurysms (AAA) and coronary artery disease (CAD) have traditionally been regarded as two separate vessel disorders with a common background. Atherosclerosis has always been considered as the basic pathophysiologic process. However, during the last decade, evidence has emerged with differences between AAA and CAD. Firstly, data regarding the prevalence of AAA and CAD are different. Secondly, the risk profiles between AAA and CAD differ, mainly regarding gender, age and diabetes mellitus. Thirdly, despite the intensive treatment of CAD and improved outcome, the prevalence of AAA has not changed during the last decade. In this review we will discuss the characteristics of CAD in patients with AAA. In the first part we focus on epidemiological data of CAD in AAA patients. The pathophysiology of both AAA and CAD will be described in the second part. There is a common pathway between pathophysiology and risk profiles that is discussed in the third chapter. Based on the presence of risk factors and their influence on cardiovascular events, the preoperative work-up and testing for CAD in AAA has gained an important role. The role of (non)-invasive testing will be described in the fourth chapter. The treatment of AAA traditionally consisted solely of surgery. However, due to the influence of CAD on adverse outcomes, medical intervention is potentially useful. Surgical approaches for the treatment of both AAA and CAD, and most importantly, their influence on long-term outcome will be discussed in the fifth chapter.