Effect of ethnicity and insurance type on the outcome of open thoracic aortic aneurysm repair.

OBJECTIVES: Mortality and complication rates for open thoracic aortic aneurysm repair have declined but remain high. The purpose of this study is to determine the influence of ethnicity and insurance type on procedure selection and outcome after open thoracic aneurysm repair. METHODS: Using the Nationwide Inpatient Sample database, ethnicity and insurance type were evaluated against the outcome variables of mortality and major complications associated with open thoracic aneurysm repair. The potential cofounders of age, gender, urgency of operation, and Deyo index of comorbidities were controlled. RESULTS: Between 2001 and 2005, a total of 10,557 patients were identified who underwent elective open thoracic aneurysm repair, with a significantly greater proportion of white patients (n = 8524) compared with black patients (n = 819), Hispanic patients (n = 556), and patients categorized as other (n = 658). Most patients (67%) were male. Almost half (45%) of the procedures were performed for urgent/emergent indications. Overall mortality was 10.7% (n = 1126) and the rate of spinal cord ischemia was 0.4% (n = 43). Univariate analysis revealed significant differences among race with regard to surgery type, income, hospital region, hospital bed size, and insurance type (P < 0.0001). Differences between insurance coverage were significant for gender, surgery type, income, hospital region, and race (P < 0.0001). Bivariate analysis by race revealed differences for death (P < 0.0001), pneumonia (P < 0.0001), renal complications (P = 0.011), implant complications (P < 0.0001), temporary tracheostomy (P = 0.004), transfusion (P < 0.0001), and intubation (P < 0.0001). In terms of payer status, bivariate analysis by insurance coverage revealed differences in death (P < 0.0001), central nervous system complications (P = 0.008), pneumonia (P < 0.0001), myocardial infarction (P = 0.001), infection (P < 0.0001), renal complications (P < 0.0001), malnutrition (P < 0.0001), temporary tracheostomy (P < 0.0001), spinal cord ischemia (P = 0.001), transfusion (P < 0.0001), and intubation (P < 0.0001). CONCLUSIONS: A high percentage of open thoracic procedures (45%) are performed urgently or emergently in the United States, which is associated with increased morbidity and mortality. Both ethnicity and payer status were associated with significant differences in surgical outcomes, including mortality and frequency of complications after open thoracic aortic aneurysm repair.

In vitro analysis of type II endoleaks and aneurysm sac pressurization on longitudinal stent-graft displacement.

PURPOSE: To evaluate the effects of type II endoleaks and sac pressurization on stent-graft displacement following endovascular aneurysm repair (EVAR). METHODS: Experimental silicone infrarenal aneurysm (6-cm) models were "treated" with a Talent stent-graft deployed with 20-mm proximal and distal landing zones. Inflow and outflow vessels were created as part of the silicone model to control flow into the aneurysm sac. All aneurysm models were uniform, with a diameter neck of 31 mm, a neck length of 20 mm, and iliac artery diameters of 16 mm. The aortic model was secured in a water bath to a pulsatile pump under physiological conditions; the output phase ratio (%systole/%diastole) was set at 65/35 with a pump rate of 80 beats per minute. Commercially available bifurcated stent-grafts were then displaced in vitro utilizing a linear motion apparatus attached to a force gauge. The mean arterial pressure (MAP) and pulse pressure (PP) at the aortic inflow were 60.1 ± 3.1 and 38.3 ± 7.8 mmHg, respectively. Peak force to cause initial stent-graft migration with and without a type II endoleak was recorded and compared. RESULTS: In aneurysm sacs with no endoleak, the MAP and sac PP were 32 ± 6.4 and 6 ± 1.3 mmHg, respectively (p<0.01). In aneurysm sacs with a type II endoleak, the MAP and sac PP were 54.1 ± 9.7 and 16.1 ± 4.1 mmHg, respectively (p<0.02). Peak force to initiate migration was 16.0 ± 1.41 N (range 15-18) with no endoleak vs. 23.2 ± 2.2 N (range 20-25) in those with a type IIa endoleak and 23.5 ± 2.5 N (range 20-26) in those with a type IIb endoleak (p<0.001). CONCLUSION: Type II endoleaks are associated with a significantly increased sac pressure. Increased sac pressurization from type II endoleaks results in a significantly greater force to displace a stent-graft longitudinally. Type II endoleaks may therefore inhibit migration and offer a benefit following EVAR; however, clinical correlation of these results is required.