Preoperative relative abdominal aortic aneurysm thrombus burden predicts endoleak and sac enlargement after endovascular anerysm repair.

BACKGROUND: Endoleak and sac growth remain unpredictable occurrences after EVAR, necessitating regular surveillance imaging, including CT angiography. This study was designed to identify preoperative CT variables that predict AAA remodeling and sac behavior post-EVAR. METHODS: Pre- and postoperative CT scans from 136 abdominal aortic aneurysms treated with EVAR were analyzed using M2S (West Lebanon, NH) software for size measurements. Preoperative total sac volume and proportion of thrombus and calcium in the sac were assessed. Sac change was defined as a 3-mm difference in diameter and a 10-mm3 difference in volume when compared with preoperative measurements. Univariate analysis was performed for age, gender, AAA size, relative thrombus/calcium volume, device type, presence of endoleak, and the effects on sac size. RESULTS: Gender, device type, age, AAA size, and percent calcium were not predictive of sac change post-EVAR. Increased proportion of thrombus on pre-EVAR resulted in a greater likelihood of sac shrinkage (P=0.002). Patients with aneurysms that grew on postoperative CT scan had less sac thrombus on pre-EVAR (mean 27.5%) than patients without evidence of endoleak (mean 41.9%, P<0.0001). Only 2 of 30 patients with >50% pre-EVAR thrombus developed endoleak. A>50% thrombus burden resulted in endoleak in significantly fewer patients (6.7%) compared with those who had <50% thrombus (43.1%). CONCLUSIONS: The proportion of thrombus on preoperative CT may predict sac behavior after EVAR and development of an endoleak. Greater than 50% thrombus appears to predict absence of endoleak after EVAR. Aneurysms with large thrombus burden are less likely to grow and may require less vigilant postoperative surveillance than comparable AAA with relatively little thrombus.

Human endothelial progenitor cells from type II diabetics exhibit impaired proliferation, adhesion, and incorporation into vascular structures.

BACKGROUND: The recent discovery of circulating endothelial progenitor cells (EPCs) has altered our understanding of new blood vessel growth such as occurs during collateral formation. Because diabetic complications occur in conditions in which EPC contributions have been demonstrated, EPC dysfunction may be important in their pathophysiology. METHODS AND RESULTS: EPCs were isolated from human type II diabetics (n=20) and age-matched control subjects (n=20). Proliferation of diabetic EPCs relative to control subjects was decreased by 48% (P<0.01) and inversely correlated with patient levels of hemoglobin A1C (P<0.05). Diabetic EPCs had normal adhesion to fibronectin, collagen, and quiescent endothelial cells but a decreased adherence to human umbilical vein endothelial cells activated by tumor necrosis factor-alpha (TNF-alpha) (P<0.05). In a Matrigel assay, diabetic EPCs were 2.5 times less likely to participate in tubule formation compared with controls (P<0.05). CONCLUSIONS: These findings suggest that type II diabetes may alter EPC biology in processes critical for new blood vessel growth and may identify a population at high risk for morbidity and mortality after vascular occlusive events.