Objective: Compression of the left common iliac vein (LCIV) by the right common iliac artery is an anatomic variant that may increase the risk for LCIV thrombosis. The incidence of LCIV compression in patients with abdominal aortic aneurysms (AAA) is unknown, however. The aim of this descriptive anatomic study was to determine (1) the incidence of LCIV compression in patients with and without AAA and (2) if endovascular AAA repair acutely alters the incidence of LCIV compression and, hence, the risk of LCIV thrombosis.
Method: A retrospective analysis of medical records and helical computed tomography (CT) scans was conducted in 100 AAA patients and 100 non-AAA patients (n = 200). Medical records were reviewed for symptoms and risk factors for deep vein thrombosis, and data were reported according to the Joint Society Reporting Standards for acute lower-extremity venous thrombosis. The minor diameters of the aorta, inferior vena cava, and common iliac arteries and veins were measured. For AAA patients, measurements were obtained from preoperative and 30-day postoperative CT scans.
Results: The mean age of the study cohort was 38 years (range, 17 to 85 years) for non-AAA subjects and 73 years (range, 51 to 89 years) for AAA subjects. The mean acute lower-extremity venous thrombosis risk factor score was low for both patient groups (non-AAA, 0.82 +/- 0.12; AAA, 2.63 +/- 0.14). Mean compression of the LCIV was 37.8% (range, 0% to 74.8%) for non-AAA patients but only 27.3% (range, 0% to 74.2%; P < .0006) for AAA patients. Of non-AAA patients with venous compression, the right common iliac artery was the compressing structure in 87% of cases. However, of AAA patients with venous compression, the left common iliac artery was the compressing structure in 76% of cases. There was no statistically significant change in the degree of compression of the LCIV before and after endovascular repair (27.3% vs 25.1%, respectively) nor was there a change in the structure that compressed the LCIV.
Conclusion: Patients with AAA were found to have more tortuous iliac arteries that led to less anatomic compression of the LCIV compared with nonaneurysmal patients. Furthermore, the left common iliac artery was found to compress the LCIV in most of the AAA patients, and the right iliac artery was found to compress the LCIV in most non-AAA patients. Endovascular AAA repair did not acutely alter these anatomic findings. Patients with AAA may therefore be at lower risk of developing LCIV thrombosis owing to the nature of their anatomy.