Survival after Acute Type B Aortic Dissection: A Single-Center Experience

Survival after Acute Type B Aortic Dissection: A Single-Center Experience

S184 J Am Coll Surg Scientific Forum Abstracts INTRODUCTION: Tunneled dialysis-catheter (TDC) infections remain a leading cause of morbidity and mo...

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S184

J Am Coll Surg

Scientific Forum Abstracts

INTRODUCTION: Tunneled dialysis-catheter (TDC) infections remain a leading cause of morbidity and mortality in end-stage renal disease (ESRD) patients. Arteriovenous fistulas (AVF) and grafts (AVG) require concurrent TDC while maturing. Early cannulation AVGs (ECAVG) permit immediate hemodialysis (HD) and avoid the use of TDCs. The purpose of this study was to evaluate short-term outcomes after dialysis access. METHODS: Patients with ESRD on HD who underwent placement of a TDC, AVF, AVG (4 to 7 tapered PTFE), or ECAVG (ACUSEAL, WL Gore & Associates, Inc.) were followed over 6 months. Infection, reintervention, and comparison with national cohorts were determined using the 2012 National and State Inpatient Samples with readmission identifiers. Actual costs were projected to 1 year using a propensity score-matched cohort. RESULTS: The rate of sepsis requiring hospitalization per 1,000 dialysis days was 1.4 for TDC, 0.3 for AVF, and 0.5 for AVG/ ECAVG (p<0.001). The initial cost of care was $1,800 for TDC, $1,497 for AVF, $2,200 for AVG, and $2,473 for ECAVG (p<0.05). The total cost of care at 1 year using national and state data project costs at $10,056 for TDC, $6,442 for AVF, $8,325 for AVG, and $5,422 for ECAVG (p<0.05; Table). Primary-assisted patency was 100% for all dialysis access at 6 months with no deaths. Month

TDC, $

AVF, $

AVG, $

ECAVG, $

0 1 3 6 9 12

1,800 2,488 3,176 5,928 7,992 10,056

1,497 4,132 4,968 5,558 6,000 6,442

2,200 4,934 5,867 6,850 7,587 8,325

2,473 2,719 2,964 3,947 4,684 5,422

CONCLUSIONS: Early cannulation AVG has the lowest cost of care after 3 months, a significantly lower rate of infection compared with TDC, and 100% primary patency at 6 months. A more comprehensive financial analysis including other complications of dialysis access and long-term results is needed. Stimulation of EphB4 Alters Arteriovenous Fistula Maturation Trenton Foster, MD, Takuya Hashimoto, MD, PhD, Hualong Bai, MD, Go Kuwahara, MD, Mo Wang, MD, Kirstyn Brownson, MD, Kota Yamamoto, MD, PhD, Alan Dardik, MD, PhD, FACS Yale University School of Medicine, New Haven, CT INTRODUCTION: Although the arteriovenous fistula (AVF) is the gold standard for dialysis access, low rates of fistula maturation prevent optimal fistula use. We have previously shown that stimulation of Eph-B4 in vein grafts alters venous remodeling and that Eph-B4 is present in the remodeling AVF. We

hypothesized that stimulation of Eph-B4 would improve fistula maturation. METHODS: The infrarenal aorto-caval AVF model was created in wild-type C57BL/6 mice, as has been previously described. Mice were treated with 20 mg intraperitoneal injections of either EphrinB2/Fc or a control vehicle at 48-hour intervals over a 21-day study period. Fistula maturation was monitored with weekly ultrasound measurements of inferior vena cava (IVC) diameter. At 21 days, infrarenal IVC wall thickness was measured using computerized morphometry. Cellular proliferation was analyzed using immunohistochemistry. RESULTS: Stimulation of Eph-B4 was associated with reduced fistula diameter at days 14 and 21 compared with that in control mice (45% vs 98.6%, p<0.05 ANOVA). Eph-B4 stimulation also reduced fistula wall thickness (8.9mm vs 20.0mm, p¼0.0261, ttest). Immunohistochemistry results found a reduced rate of cellular proliferation (24.7% vs 16.6%, p¼0.0245, t-test) but showed no difference in the rate of apoptosis. CONCLUSIONS: These results show that Eph-B4 signaling controls venous remodeling to the arterial environment. Stimulation of Eph-B4 during AVF maturation leads to less venous dilation, reduced venous wall thickness, and a reduction in cellular proliferation. These findings suggest strategies to inhibit Eph-B4 signaling may result in improved fistula maturation. Survival after Acute Type B Aortic Dissection: A SingleCenter Experience Farah HA Mohammad, MB, BS, Loay Kabbani, MD, Efstathios Karamanos, MD, Alexander D Shepard, MD, FACS Henry Ford Hospital, Detroit, MI INTRODUCTION: We aimed to review our 10-year experience with acute type B aortic dissections (TBAD) with a specific focus on associated renal dysfunction, and early and long-term survival. METHODS: All patients presenting with a confirmed TBAD to our referral center were reviewed. Demographics, treatment, complications, hospital mortality, and survival were analyzed. The occurrence of acute kidney injury (AKI) was analyzed using the RIFLE (risk, injury failure, loss, end-stage renal disease)/ Acute Kidney Injury Network criteria. Long-term survival was assessed using the Michigan Social Security Death Index. RESULTS: Between January 2003 and October 2012, 116 patients (75 men) were treated for TBAD. Mean age was 61 years (range 20-94). A history of hypertension was found in 89% of patients and illicit drug use in 17%. Early surgical intervention was required in 20 patients (18%). Acute kidney injury occurred in 65 patients (61%). Predictors of AKI development were male sex (p ¼0.022; odds ratio [OR] 3.05, 95% CI, 1.17-7.30) and abdominal or lower back pain on presentation (p¼0.037; OR 2.13, 95% CI, 1.23-6.54). Thirty-day mortality was 12.5%-35% when operative intervention was required and 7% when medical management was maintained. Thirty-day mortality was associated with surgery

Vol. 221, No. 4S1, October 2015

(p¼0.001), AKI (p¼0.054), systolic blood pressure at presentation to the emergency room (p¼0.02; adjusted OR 1.03, 95% CI, 1.011.06) and persistent/uncontrolled hypertension when the patient reached the ICU (p¼0.039; OR 1.08, 95% CI, 1.04-1.09). Median follow-up was 7.6 years. Kaplan-Meier 5- and 10-year survival estimates for TBAD were 67% and 36% respectively. CONCLUSIONS: Type B aortic dissection has significant morbidity and mortality; AKI is common and usually mild. Early mortality is associated with the need for emergent surgery, AKI, systolic blood pressure on presentation, and uncontrolled hypertension at the time of admission to the ICU. Synthetically Engineered Targeted Gold Nanoparticles for the Prevention of Restenosis after Vascular Interventions Molly A Wasserman, MD, Qun Jiang, MD, Jonathan Rink, PhD, Melina R Kibbe, MD, FACS, FAHA, Colby S Thaxton, MD, PhD Northwestern University, Chicago, IL, Simpson Querrey Institute for BioNanotechnology in Medicine, Chicago, IL INTRODUCTION: Surgical therapies for severe atherosclerotic disease often fail due to the development of neointimal hyperplasia with resultant arterial restenosis. The objective of this study was to evaluate the biocompatibility and targeting specificity of a novel therapeutic delivery vehicle to prevent restenosis. METHODS: A 5-nm gold-nanoparticle (AuNP) functionalized with a collagen-binding peptide and fluorophore was exposed to rat aortic endothelial cells, vascular smooth muscle cells (VSMC), and adventitial fibroblasts (0-100nM). In vitro assessment of cell viability and proliferation was performed at 24 hours. In vivo assessment of targeting specificity was accomplished using the rat carotid artery balloon injury model in male Sprague-Dawley rats. After angioplasty, the targeted AuNP (4.9-15.6nM) was instilled into the left carotid artery for 5 minutes and either harvested immediately (n¼6) or harvested after restoration of circulation for 20 minutes (n¼9). Fluorescence was assessed using in-vivo imaging systems (IVIS). RESULTS: There was no significant effect of the targeted AuNP on cell proliferation, viability, or death (p¼NS) in endothelial cells, VSMC, and adventitial fibroblasts at any concentration in vitro. Mean cell viabilities were: endothelial cells 98%-99%, VSMC 94%-97%, and adventitial fibroblasts 91%-95%. In vivo, the collagen-targeted AuNP bound only to the site of arterial injury. Binding was maintained after restoration of blood flow for 20 minutes. CONCLUSIONS: Our targeted AuNP delivery vehicle is biocompatible with vascular cells and binds with specificity to vascular injury. Ultimately, our goal is to systemically administer a therapeutic agent in a targeted manner to prevent neointimal hyperplasia and arterial restenosis.

Scientific Forum Abstracts

S185

The Role of Model of End-Stage Liver Disease Score in Predicting Outcomes of Carotid Endarterectomy in Patients with Liver Disease Brianna M Krafcik, Denis Rybin, Gheorghe Doros, PhD, Mohammed H Eslami, MD, FACS, Alik Farber, MD, FACS, Jeffrey A Kalish, MD, FACS, Elizabeth G King, MD, Jeffrey Siracuse, MD Boston University School of Medicine, Boston, MA INTRODUCTION: The Model of End-Stage Liver Disease (MELD) score is often used to characterize and prioritize liver transplantation; however, it has recently been shown to have value in predicting outcomes for patients with a wide variety of conditions with hepatic and renal dysfunction. Our objective was to use MELD score to predict outcomes in asymptomatic patients undergoing carotid endarterectomy (CEA). METHODS: Patients undergoing CEA were identified in the NSQIP data set (2005 to 2012). The MELD score was calculated using serum bilirubin, creatinine, and the international normalized ratio (INR). Patients were grouped into low (<9), moderate (9-14), and high (15+) MELD classifications. Multivariable logistic and gamma regressions, propensity matching, and propensity weighting were used to analyze results. The primary outcome was major adverse cardiovascular events (MACE: composite stroke, cardiac arrest, myocardial infarction, and death). RESULTS: There were 8,826 CEAs performed in asymptomatic patients. Low (<9), moderate (9-14), and high (>15) MELD scores were noted in 6,366 (72%), 2,126 (24%), and 334 (4%) patients, respectively. Moderate and high MELD

Table. Predictors of Complications Based on Model for End-stage Liver Disease Score

Perioperative complication

Moderate MELD p (9-14) Value

High MELD (>15)

p Value

0.22 0.41 Odds OR 1.45, ratio (OR) Death/myocardial 95% CI, infarction/stroke 1.14, 95% CI, 0.80-2.64 0.83- 1.57 (MACE) Bleeding OR 1.87, 0.004 OR 1.28, 0.6 1 95% CI, 95% CI, 1.22-2.88 0.50-3.30 Return to OR 1.17, 0.17 OR 0.99, 0.96 operating 95% CI, 95% CI, room 0.94-1.45 0.62-1.58 0.03 0.28 OR 1.05, Operative time OR 1.01, 95% CI, 95% CI, l.00-1.10 0.99-1.03 <0.001 OR 1.25, <0.001 Length of stay OR 1.15, 95% CI, 95% CI, 1.15-1.35 1.11-1.20