Methods

To assess the association of fasting serum lipids with AAA, we used subjects from the Health In Men Study. The Health In Men Study consisted of a cohort of men who originally participated in a trial of screening for AAA in 1996 to 1998. Each man completed a questionnaire assessing aspects of their history and lifestyle relevant to AAA. Diabetes and hypertension were defined by a history, or treatment, of diabetes or hypertension, respectively. Coronary heart disease was defined by a history of myocardial infarction, angina, or treatment of coronary artery disease (medication or endovascular or surgical methods). Smoking history was categorized as ever having smoked or a lifelong nonsmoker. Men were questioned about a history of high cholesterol or high triglycerides and asked whether they had been instructed to follow a diet or take medication to treat it. A history of dyslipidemia was recorded in men reporting a history of high cholesterol or high triglycerides. A history of treatment of dyslipidemia was noted in men reporting they had previously been given a diet or medication to treat fats. The height, weight, and circumference at the waist and hips were measured to calculate the body mass index and waist/hip ratio. From the initial sample of 12,203 community-dwelling men aged 65 to 83 years from Perth, Western Australia, 4,263 attended a follow-up visit from 2001 to 2004, at which time a fasting blood sample was obtained from 3,327 men (78%). At blood sampling, a drug history was obtained, allowing the identification of men receiving lipid-modifying medication, including statins, fibrates, and cholestryramine. The relevant committee granted ethics approval, and all men gave written informed consent for their involvement in the study.

The greatest diameter of the infrarenal aorta was measured at baseline (1996 to 1998) using a Toshiba Capasee ultrasound machine with a 3.75-MHz probe (Toshiba Australia, North Ryde, New South Wales, Australia). Ultrasound reproducibility was assessed during subject recruitment, and the 95% confidence intervals were <3 mm. AAA was defined as an infrarenal aortic diameter of ≥30 mm, as previously used in most studies.

Blood samples were collected after an overnight fast, and the serum was separated and analyzed for total cholesterol, triglycerides, LDL, and HDL using automated assays (Hitachi 917, Roche Diagnostics GmBH, Mannheim, Germany). The interassay coefficient of variation for these assays was 2.1% to 4.8%.

To assess the association of serum lipids with AAA, we initially divided patients into those receiving lipid-modifying medication and those who had not been prescribed this medication at blood sampling. We compared the serum lipids in patients with and without AAAs using the Mann-Whitney U test. We used multiple logistic regression analysis to assess the association of total cholesterol, triglycerides, LDL, and HDL with AAA, adjusting for other risk factors, including age, smoking, hypertension, diabetes, coronary heart disease, a history of dyslipidemia or past treatment (diet or medication) of dyslipidemia, and the waist/hip ratio, as previously described.

Results

Of the 3,327 men with fasting lipids measured, 245 (7.4%) had an AAA. At imaging, 1/3 (n = 1,102, 33%) had a history of dyslipidemia, and 700 gave a history of previous treatment (dietary modification or medication). A total of 237 men had previously been given a diet to treat dyslipidemia, and 621 had previously received medication for dyslipidemia (158 patients had previously received both a diet and medication for dyslipidemia). At the fasting lipid measurement, 1,043 (31%) of the 3,327 men were receiving lipid-modifying medication, including simvastatin (n = 475), atorvastatin (n = 287), pravastatin (n = 247), fluvastatin (n = 14), gemfibrozil (n = 23), and cholestryramine (n = 2). Of these 1,043 men, 1,019 were receiving a statin alone, 18 had been prescribed gemfibrozil alone, 1 was receiving cholestryramine alone, 4 were receiving a statin and gemfibrozil, and 1 was receiving cholestryramine and gemfibrozil. The risk factors and serum lipids of the men in relation to the concurrent use of lipid-modifying medication and AAA are listed in Table 1 .

The serum HDL concentrations were lower in the men with AAAs. The serum HDL level was independently and inversely associated with a reduced risk of having an AAA in men not receiving lipid-modifying medication, after adjusting for other risk factors (odds ratio 0.72, 95% confidence interval 0.56 to 0.93 per 0.4-mM increase; Table 2 ). A greater serum HDL level was also associated with a reduced risk of AAA in the total cohort of men in an analysis, which was adjusted for lipid-modifying medication and other risk factors (odds ratio 0.76, 95% confidence interval 0.63 to 0.91; Table 2 ). The serum triglyceride and LDL concentrations were not associated with the presence of an AAA. Lipid-modifying medication prescription was associated with the presence of an AAA ( Table 2 ).

Table 2

Independent correlates of abdominal aortic aneurysm (AAA) in men in relation to lipid-lowering prescription

Characteristic	Receiving Lipid-Lowering Therapy
	No (n = 2,284)			Yes (n = 1,043)			Combined (n = 3,327)
	OR	95% CI	p Value	OR	95% CI	p Value	OR	95% CI	p Value
Age per 4 years ⁎	1.38	1.16–1.65	<0.01	1.26	1.04–1.52	0.02	1.32	1.16–1.51	<0.01
Hypertension	1.32	0.88–1.97	0.18	1.14	0.77–1.69	0.69	1.28	0.97–1.70	0.09
Diabetes mellitus	1.07	0.54–2.15	0.84	0.87	0.45–1.70	0.87	0.99	0.61–1.59	0.96
Coronary heart disease	2.68	1.66–4.31	<0.01	1.46	0.96–2.21	0.08	1.86	1.35–2.57	<0.01
Current or past smoker	2.75	1.67–4.53	<0.01	3.51	2.08–5.92	<0.01	3.08	2.15–4.42	<0.01
History of dyslipidemia †	0.68	0.40–1.17	0.16	1.02	0.64–1.64	0.93	0.86	0.60–1.23	0.40
Previous treatment of dyslipidemia †	1.87	0.99–3.48	0.05	0.78	0.48–1.25	0.30	1.01	0.68–1.50	0.96
Waist/hip ratio per 0.05 ⁎	1.28	1.08–1.52	<0.01	1.11	0.94–1.32	0.20	1.19	1.06–1.34	<0.01
Triglycerides per 1 mM ⁎	0.93	0.69–1.25	0.62	0.98	0.73–1.31	0.87	0.94	0.76–1.16	0.55
Low-density lipoprotein per 1 mM ⁎	1.07	0.84–1.36	0.58	0.87	0.63–1.21	0.41	0.98	0.81–1.18	0.80
High-density lipoprotein per 0.4 mM ⁎	0.72	0.56–0.93	0.01	0.82	0.64–1.06	0.13	0.76	0.63–0.91	<0.01
Current lipid therapy							2.07	1.47–2.91	<0.01

For nominal variables, comparisons were to those without the risk factor.

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