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Objectives Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) has been used clinically to limit torso bleeding and restore central perfusion. The objective of this study was to determine the sequelae of prolonged REBOA in a nonhuman primate animal model. Summary background data Prolonged duration of REBOA is associated with adverse clinical outcomes. Threshold occlusion values tied to relative risk have yet to be determined. Methods Juvenile baboons were subjected to 40% to 55% total blood volume hemorrhage to achieve profound hypotension and shock. Zone I REBOA was performed for 60 minutes to assess acute injury and survival at 4 hours (group 1; n = 7). Post-REBOA 10-day survival and complications were then compared between 60 minutes (group 2; n = 8) and 30 minutes (group 3; n = 6) REBOA animals. Results Overall survival was 20/21 (95%). IL-6 and IL-8 were elevated at 1 and 4 hours in group 1 (P = 0.005; P = 0.001). Comparing 60-minute REBOA with 30-minute REBOA, there was (1) hypertension compared with normotension (P = 0.005), (2) increased base deficit (P = 0.003), (3) elevated Troponin I (P = 0.04), and histological evidence of kidney injury (P = 0.004). In addition, group 2 demonstrated paralysis with histopathologic changes of spinal cord ischemia (SCI) in 4/8 (50%), with no SCI in group 3 (P = 0.033). Conclusions REBOA limits mortality in the primate model of severe hemorrhagic shock. However, unopposed balloon inflation in the distal thoracic aorta for 60 minutes results in high rates of spinal cord ischemia, an effect mitigated by limiting balloon inflation to 30 minutes.

Acute lower extremity ischemia is a common vascular disease and is a cause of considerable morbidity and mortality. In 2000, abdominal aortic and lower extremity arterial embolism and thrombosis affected 213,000 patients in the United States.1 Hospitalization costs of treating the individual patient range from $6000 to $45,000.2-4 In an evolving era of less invasive therapies, several randomized controlled clinical trials have suggested that catheter-directed thrombolysis is as effective as surgical revascularization in preventing limb-loss and mortality in these patients.4-8 Unfortunately, most such trials included patients with ischemic insults ranging from 7 to 14 days in duration. These patients may have subacute, not critical, limb ischemia, having a longer window for re-establishing blood flow and a lesser reperfusion injury. In addition, many patients in these trials had a history of chronic occlusive disease and some had prior arterial bypasses as the target for thrombolytic therapy. A distinction between subacute (SVS Class I) and true limb-threatening ischemia (SVS classes IIa, Iib, and III) becomes relevant regarding the urgency of care and risk of limb loss.9 Endovascular catheter-directed thrombolysis may be appropriate for limb-threatening ischemia, but it usually takes longer to return blood flow to the limb, is associated with increased risk of major hemorrhage, and increases costs due to repeated arteriography and longer ICU care compared with surgical therapy. The latter shortcomings must be balanced against open thrombectomy’s greater physiological stress on an already ill patient and the possibility that an urgent bypass may be needed.10-11 Obvious factors related to improved outcomes are: (1) precise patient categorization of the degree of ischemia; (2) etiology as judged by history and physical examination; and (3) an appropriate therapeutic intervention. The current study was undertaken using a database representing the United States population to define the contemporary national impact of acute lower extremity ischemia, coupled with a retrospective review of data from a single institution that carefully restricted the categorization of ischemia and identified those factors that reduce the rates of amputation and death.

BACKGROUND Endovascular approaches (thoracic endovascular aortic repair) have revolutionized treatment of thoracic aortic disease. OBJECTIVE We report our 20-year experience with this therapy. METHODS Four hundred twenty patients (mean age = 69.0 years; 54% male) underwent thoracic endovascular aortic repair (1993-2013), predominantly for fusiform aneurysm (n = 144), saccular aneurysm (n = 94), acute (n = 64) or chronic (n = 36) dissection, or traumatic injury (n = 39). Rupture was present in 80 patients (19.1%). Most patients (78.3%) were at high risk for open repair. Mean aortic diameter was 5.5 cm. Extent of repair included arch in 218 patients, total descending aorta in 193 patients, and thoracoabdominal aorta in 35 patients. RESULTS Thirty-day mortality occurred in 20 patients (4.8%). Neurologic events included stroke (5.0%) and spinal cord ischemia (permanent 1.7%, temporary 7.9%). Although dialysis was only required in 1.4% of the patients, 19% had renal failure by RIFLE (Risk, Injury, Failure) criteria. Endoleak occurred in 32.9% of the patients. Ten-year freedom from dissection, rupture, or need for reintervention in treated or adjacent aortic segments (ie, treatment failure) was 63.2%. Independent predictors included presentation with rupture, preexisting renal failure, or intervention on the arch aorta (all Ps < 0.03). Aortic pathology also independently predicted treatment failure (P = 0.026). The 15-year survival rate was 32.3%. Advancing age, presence of coronary artery disease, rupture, or postoperative renal failure (all Ps < 0.05), but not treatment failure (P = 0.926), independently predicted late mortality. CONCLUSIONS Thoracic endovascular aortic repair can be performed with acceptable results in a high-risk population. The risk of treatment failure persists, underscoring the importance of continued long-term endograft surveillance, but this does not seem to impact late mortality.

To determine whether F-fluorodeoxyglucose (F-FDG) micro-positron emission tomography (micro-PET) can predict abdominal aortic aneurysm (AAA) rupture.An infrarenal AAA model is needed to study inflammatory mechanisms that drive rupture. F-FDG PET can detect vascular inflammation in animal models and patients.After exposing Sprague-Dawley rats to intra-aortic porcine pancreatic elastase (PPE) (12 U/mL), AAA rupture was induced by daily, subcutaneous, β-aminopropionitrile (BAPN, 300 mg/kg, N = 24) administration. Negative control AAA animals (N = 15) underwent daily saline subcutaneous injection after PPE exposure. BAPN-exposed animals that did not rupture served as positive controls [nonruptured AAA (NRAAA) 14d, N = 9]. Rupture was witnessed using radiotelemetry. Maximum standard uptakes for F-FDG micro-PET studies were determined. Aortic wall PAI-1, uPA, and tPA concentrations were determined by western blot analyses. Interleukin (IL)-1β, IL-6, IL-10, and MIP-2 were determined by Bio-Plex bead array. Neutrophil and macrophage populations per high-power field were quantified. Matrix metalloproteinase (MMP) activities were determined by zymography.When comparing ruptured AAA (RAAA) to NRAAA 14d animals, increased focal F-FDG uptakes were detected at subsequent sites of rupture (P = 0.03). PAI-1 expression was significantly less in RAAA tissue (P = 0.01), with comparable uPA and decreased tPA levels (P = 0.02). IL-1β (P = 0.04), IL-6 (P = 0.001), IL-10 (P = 0.04), and MIP-2 (P = 0.02) expression, neutrophil (P = 0.02) and macrophage presence (P = 0.002), and MMP9 (P0.0001) activity were increased in RAAA tissue.With this AAA rupture model, increased prerupture F-FDG uptake on micro-PET imaging was associated with increased inflammation in the ruptured AAA wall. F-FDG PET imaging may be used to monitor inflammatory changes before AAA rupture.