Lower Atherosclerotic Burden in Familial Abdominal Aortic Aneurysm

OBJECTIVE: Despite the apparent familial tendency toward abdominal aortic aneurysm (AAA) formation, the genetic causes and underlying molecular mechanisms are still undefined. In this study, we investigated the association between familial AAA (fAAA) and atherosclerosis. METHODS: Data were collected from a prospective database including AAA patients between 2004 and 2012 in the Erasmus University Medical Center, Rotterdam, The Netherlands. Family history was obtained by written questionnaire (93.1% response rate). Patients were classified as fAAA when at least one affected first-degree relative with an aortic aneurysm was reported. Patients without an affected first-degree relative were classified as sporadic AAA (spAAA). A standardized ultrasound measurement of the common carotid intima-media thickness (CIMT), a marker for generalized atherosclerosis, was routinely performed and patients' clinical characteristics (demographics, aneurysm characteristics, cardiovascular comorbidities and risk factors, and medication use) were recorded. Multivariable linear regression analyses were used to assess the mean adjusted difference in CIMT and multivariable logistic regression analysis was used to calculate associations of increased CIMT and clinical characteristics between fAAA and spAAA. RESULTS: A total of 461 AAA patients (85% men, mean age, 70 years) were included in the study; 103 patients (22.3%) were classified as fAAA and 358 patients (77.7%) as spAAA. The mean (standard deviation) CIMT in patients with fAAA was 0.89 (0.24) mm and 1.00 (0.29) mm in patients with spAAA (P = .001). Adjustment for clinical characteristics showed a mean difference in CIMT of 0.09 mm (95% confidence interval, 0.02-0.15; P = .011) between both groups. Increased CIMT, smoking, hypertension, and diabetes mellitus were all less associated with fAAA compared with spAAA. CONCLUSIONS: The current study shows a lower atherosclerotic burden, as reflected by a lower CIMT, in patients with fAAA compared with patients with spAAA, independent of common atherosclerotic risk factors. These results support the hypothesis that although atherosclerosis is a common underlying feature in patients with aneurysms, atherosclerosis is not the primary driving factor in the development of fAAA.

Familial Abdominal Aortic Aneurysm Is Associated With More Complications After Endovascular Aneurysm Repair

OBJECTIVE: A familial predisposition to abdominal aortic aneurysms (AAAs) is present in approximately one-fifth of patients. Nevertheless, the clinical implications of a positive family history are not known. We investigated the risk of aneurysm-related complications after endovascular aneurysm repair (EVAR) for patients with and without a positive family history of AAA. METHODS: Patients treated with EVAR for intact AAAs in the Erasmus University Medical Center between 2000 and 2012 were included in the study. Family history was obtained by written questionnaire. Familial AAA (fAAA) was defined as patients having at least one first-degree relative affected with aortic aneurysm. The remaining patients were considered sporadic AAA. Cardiovascular risk factors, aneurysm morphology (aneurysm neck, aneurysm sac, and iliac measurements), and follow-up were obtained prospectively. The primary end point was complications after EVAR, a composite of endoleaks, need for secondary interventions, aneurysm sac growth, acute limb ischemia, and postimplantation rupture. Secondary end points were specific components of the primary end point (presence of endoleak, need for secondary intervention, and aneurysm sac growth), aneurysm neck growth, and overall survival. Kaplan-Meier estimates for the primary end point were calculated and compared using log-rank (Mantel-Cox) test of equality. A Cox-regression model was used to calculate the independent risk of complications associated with fAAA. RESULTS: A total of 255 patients were included in the study (88.6% men; age 72 ± 7 years, median follow-up 3.3 years; interquartile range, 2.2-6.1). A total of 51 patients (20.0%) were classified as fAAA. Patients with fAAA were younger (69 vs 72 years; P = .015) and were less likely to have ever smoked (58.8% vs 73.5%; P = .039). Preoperative aneurysm morphology was similar in both groups. Patients with fAAA had significantly more complications after EVAR (35.3% vs 19.1%; P = .013), with a twofold increased risk (adjusted hazard ratio, 2.1; 95% confidence interval, 1.2-3.7). Secondary interventions (39.2% vs 20.1%; P = .004) and aneurysm sac growth (20.8% vs 9.5%; P = .030) were the most important elements accounting for the difference. Furthermore, a trend toward more type I endoleaks during follow-up was observed (15.6% vs 7.4%; P = .063) and no difference in overall survival. CONCLUSIONS: The current study shows that patients with a familial form of AAA develop more aneurysm-related complications after EVAR, despite similar AAA morphology at baseline. These findings suggest that patients with fAAA form a specific subpopulation and create awareness for a possible increase in the risk of complications after EVAR.