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Elevated Lp(a) and Abdominal Aortic Aneurysm

Circulating biomarkers reflecting the development, progression, and rupture of abdominal aortic aneurysm (AAA) are needed. AAA is the most common arterial aneurysm and is characterized by a degradation of elastin fibers in the media and collagen fibers in the adventitia, leading to >50% expansion of the diameter of the aorta. The incidence of AAA is increasing with an aging population around the world. Evidence from epidemiologic and experimental investigations suggest that the pathogenesis of AAA is often related to atherosclerosis risk factors, particularly smoking, genetic influence, and the development of inflammatory atherosclerotic plaque formation, which results in degradation of the structural integrity of the aorta. Diagnostic methods, such as ultrasound screening, have been the key to the identification and management of AAA. Ultrasound screening of men older than 65 years have reduced deaths associated with AAA, and therefore, selective screening of men aged 65 years or older who have smoked at some stage of life was initiated in the United States. Surgical correction for AAAs >5.5 cm in diameter is currently advocated, but most identified AAAs are <5.5 cm. For example, in a screening study completed in Australia, of 12,203 men older than 65 years of age, 814 (6.7%) had an AAA 3.0 to 5.4 cm, whereas 61 (0.5%) patients had AAAs 5.5 cm. Unfortunately, surgical removal of <5.5 cm AAAs has not been shown to improve outcome. In the current era, endovascular repair is preferred when feasible, but it involves its own set of potential complications and should not be performed until a large AAAs has evolved. This increase in the detection of smaller AAAs highlights a number of opportunities for improving prevention, diagnosis, delaying progression, and managing this condition. Hence, additional biomarkers would aid in enhancing the accuracy of early diagnosis and appropriate tailored interventions that may delay the development of large AAAs which, in turn, would require intervention. Such an initiative may decrease morbidity and mortality. Lipoprotein(a) (Lp(a)) is a cholesterol and oxidized phospholipid rich particle that is composed of apolipoprotein B-100 covalently linked via a disulfide bond to apolipoprotein (a) (apo(a)). High plasma levels of Lp(a) are strongly associated with coronary artery disease, stroke, and peripheral artery disease. The LDL-like component of Lp(a) promotes atherosclerosis and the plasminogen-like apo(a) particle promotes both inflammation via its oxidized phospholipid content and potentially thrombosis by interfering with fibrinolysis. Lipoprotein(a) has a potent lysine-binding site that allows strong affinity for vessel wall fibrin and proteoglycans and is identified in high amounts in atherosclerotic plaques of the human aorta. In this issue of Angiology, Kotani et al conducted an updated meta-analysis of studies that evaluated Lp(a) levels and their association with AAA. The search identified 9 eligible studies (mainly case–control studies) published between 1988 and 2013 that included 1,564 patients with AAA. The authors appropriately did not add 2 studies of acute AAA rupture. Effect sizes were expressed as standardized mean difference (SMD) and 95% confidence interval (CI) due to different assays to determine Lp(a) levels, and therefore, an easily interpretable measure of clinical risk, such as an odds ratio, is not available. The analysis showed that patients with AAA had modest but significantly higher levels of Lp(a) compared to controls (SMD: 0.87, 95% CI: 0.41-1.33, P < .001), allowing the authors to conclude that circulating Lp(a) may be a useful biomarker in screening for the presence of AAA. This metaanalysis expands by 584 cases the results of a prior analysis that fundamentally shows similar results. This earlier study included 5 case–control studies with 982 cases with AAA and 1,296 controls, showing significantly higher Lp(a) levels in the