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 IF1. Familial Abdominal Aortic Aneurysm Is Not Related to a Genetic Predisposition for Atherosclerosis

​Koen M. van de Luijtgaarden1, Frederico Bastos Goncalves1, Sanne E. Hoeks2, Danielle Majoor-Krakauer3, Robert J. Stolker2, Hence J. Verhagen1, Ellen V. Rouwet1
1Erasmus University Medical Center - Department of Vascular Surgery, Rotterdam, Netherlands; 2Erasmus University Medical Center - Department of Anesthesiology, Rotterdam, Netherlands; 3Erasmus University Medical Center - Department of Clinical Genetics, Rotterdam, Netherlands.

OBJECTIVES: Although genetic influences in abdominal aortic aneurysm (AAA) are clear, no major genetic cause has been identified so far. In this study, we investigated whether familial AAA (fAAA) is associated with a familial predisposition for atherosclerosis.

METHODS: Patients were derived from a prospective database, including AAA patients treated between 2004 -2012. Family history was obtained by written questionnaire (93% response rate). fAAA was defined as having at least one 1st-degree relative with an aortic aneurysm. A standardized ultrasound measurement of the common carotid intima-media thickness (CIMT), a marker for generalized atherosclerosis, was performed and clinical characteristics (demographics, cardiovascular risk factors, comorbidities and medication use) were recorded. Multivariable linear and logistic regression analyses were used to calculate the association of CIMT and fAAA versus sporadic AAA (spAAA).
 
RESULTS: A total of 461 AAA patients (85% men, age 70±8) were included in the study. One hundred three (22%) patients were classified as fAAA, and 358 patients as spAAA. The mean CIMT in patients with fAAA was 0.89±0.24mm vs. 1.00±0.29mm in patients with spAAA (p=0.001). Adjustment for the clinical characteristics showed a mean difference in CIMT of 0.09mm (95% CI, 0.03-0.16, p=0.007). Furthermore, a lower CIMT was independently associated with fAAA (Figure 1).
 
CONCLUSIONS: The CIMT was lower in patients with fAAA compared to patients with spAAA, suggesting that fAAA is not related to a genetic predisposition for atherosclerosis.
 
AUTHOR DISCLOSURES: F. Bastos Goncalves: Nothing to disclose; S. E. Hoeks: Nothing to disclose; D. Majoor-Krakauer: Nothing to disclose; E. V. Rouwet: Nothing to disclose; R. J. Stolker: Nothing to disclose; K. M. van de Luijtgaarden: Lijf & Leven foundation, Rotterdam, The Netherlands, Research grants; H. J. Verhagen: Cook Medical, Consulting fees or other remuneration (payment); Medtronic, Consulting fees or other remuneration (payment); Gore, Consulting fees or other remuneration (payment).
 
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Posted April 2013

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