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Importance Because of the similarity in clinical outcomes after elective open and endovascular repair of abdominal aortic aneurysm (AAA), cost may be an important factor in choosing a procedure. Objective To compare total and AAA-related use of health care services, costs, and cost-effectiveness between groups randomized to open or endovascular repair. Design, Setting, and Participants This unblinded randomized clinical trial enrolled 881 patients undergoing planned elective repair of AAA who were candidates for open and endovascular repair procedures. Patients were randomized from October 15, 2002, to April 15, 2008, at 42 Veterans Affairs medical centers. Follow-up was completed on October 15, 2011, and data were analyzed from April 15, 2013, to April 15, 2016, based on intention to treat. Main Outcomes and Measures Mean total and AAA-related health care cost per life-year and per quality-adjusted life-year (QALY). Results A total of 881 patients (876 men [99.4%]; 5 women [0.6%]; mean [SD] age, 70 [7.8] years) were included in the analysis. After a mean of 5.2 years of follow-up, mean life-years were 4.89 in the endovascular group and 4.84 in the open repair group ( P = .68), and mean QALYs were 3.72 in the endovascular group and 3.70 in the open repair group ( P = .82). Total mean health care costs did not differ significantly between the 2 groups (endovascular group, $142 745; open repair group, $153 533; difference, −$10 788; 95% CI, −$29 796 to $5825; P = .25). Costs related to AAA, including the initial repair, constituted nearly 40% of total costs and did not differ significantly between the 2 groups (endovascular group, $57 501; open repair group, $57 893; difference, −$393; 95% CI, −$12 071 to $7928; P = .94). Lower costs due to shorter hospitalization for initial endovascular repair were offset by increased costs from AAA-related secondary procedures and imaging studies. The probability of endovascular repair being less costly and more effective was 56.8% when effectiveness was measured in life-years and 55.4% when effectiveness was measured in QALYs for total costs and 31.3% and 34.3%, respectively, for AAA-related costs. Conclusions and Relevance In this multicenter randomized clinical trial with follow-up to 9 years, survival, quality of life, costs, and cost-effectiveness did not differ between elective open and endovascular repair of AAA. Trial Registration clinicaltrials.gov Identifier:NCT00094575

Background/Purpose: If the goal of partial liquid ventilation (PLV) with perfluorocarbons in the management of respiratory failure is to improve dynamic lung compliance (C dyn ) and pulmonary vascular resistance (PVR) while sustaing O 2 delivery, the optimal ventilatory management is unclear. The authors asked if volume-cycled or pressure-limited ventilation had different effects on PVR, cardiac index (CI), and C dyn in uninjured and injured neonatal piglet lungs. Methods: Anesthetized piglets (6 to 8 kg) were ventilated after tracheostomy. C dyn was measured by in-line Fleisch pneumotach/PC data acquisition terminal. Thermodilution instrumentation allowed determination of both Cl and PVR. Volume-control or pressure-limited ventilation was established in uninjured or injured (surfactant deficiency induced by saline lavage at 18 mL/kg) animals. After a stable 30-minute baseline, animals were assigned randomly to one of four groups: group I (n = 9), uninjured animals plus volume-cycled ventilation (intermittent mandatory ventilation [IMV], 10 bpm; tidal volume [TV], 15 mL/kg, positive end-expiratory pressure [PEEP], 5 cm H 2 O; Fio 2 , 1.0; and PLV for 150 minutes); group II (n = 9), uninjured animals plus pressure-limited ventilation (IMV, 10 bpm; peak inspiratory pressure (PIP), 25 cm H 2 O, PEEP, 5 cm H 2 O, Fio 2 , 1.0; and PLV for 150 minutes); group III (n = 7), injured animals plus volume-cycled ventilation (IMV, 10 bpm; TV, 15 mL/kg; PEEP, 5 cm H 2 O; Fio 2 , 1.0 for 30 minutes, followed by saline injury for 30 minutes, followed by PLV rescue for 120 minutes); group IV (n = 7), injured animals plus pressure-limited ventilation (IMV, 10 bpm; PIP, 25 cm H 2 O; PEEP, 5 cm H 2 O; Fio 2 , 1.0 for 30 minutes, followed by saline injury, and PLV rescue). Comparison within and between groups was accomplished by repeated measures analysis of variance (ANOVA) with Tukey correction. Results: There was no significant difference between volumecycled or pressure-limited ventilation in healthy lungs; however, in the setting of lung injury, dynamic compliance was 1.44 ± 0.15 after 180 minutes in the volume-cycled group and 0.91 ± 0.10 in the pressure-limited group after the same interval (mL/cm H 2 O · kg ± SEM). Similarly, PVR was 100 ± 6 in the volume-cycled group and 145 ± 12 in the pressurelimited group after 180 minutes of lung injury (mm Hg/L/kg · min ± SEM). Cardiac index declined significantly in all groups independent of ventilatory mode. Conclusions: These results suggest that in the setting of lung injury, C dyn and PVR improved significantly when volume-cycled, compared with pressure-limited ventilation was used. Although no difference existed between ventilatory modes in healthy lungs, pressure-limited ventilation, when combined with PLV in injured lungs, had adverse effects on lung compliance and pulmonary vascular resistance. Volume-cycled ventilation may optimize the ability of perfluorocarbon to recruit collapsed or atelectatic lung regions.

Objective Prior analysis in the Open vs Endovascular Repair Veterans Affairs (VA) Cooperative Study (CSP #498) demonstrated that survival, quality of life, and total health care costs are not significantly different between the open and endovascular methods of repair of abdominal aortic aneurysm. The device is a major cost of this method of repair, and the objective of this study was to evaluate the costs of the device, abdominal aortic aneurysm repair, and total health care costs when different endograft systems are selected for the endovascular repair (EVR). Within each selected system, EVR costs are compared with open repair costs. Methods The study randomized 881 patients to open (n = 437) or EVR (n = 444). Device selection was recorded before randomization; therefore, open repair controls were matched to each device cohort. Data were excluded for two low-volume devices, implanted in only 13 individuals, leaving 423 control and 431 endovascular patients: 166 Zenith (Cook Medical, Bloomington, Ind), 177 Excluder (W. L. Gore & Associates, Flagstaff, Ariz), and 88 AneuRx (Medtronic, Minneapolis, Minn). Mean device, hospitalization, and total health care costs from randomization to 2 years were compared. Health care utilization data were obtained from patients and national VA and Medicare data sources. VA costs were determined using methods previously developed by the VA Health Economics Resource Center. Non-VA costs were obtained from Medicare claims data and billing data from the patient's health care providers. Results Implant costs were 38% of initial hospitalization costs. Mean device (range, $13,600-$14,400), initial hospitalization (range, $34,800-$38,900), and total health care costs at 2 years in the endovascular (range, $72,400-$78,200) and open repair groups (range, $75,600-$82,100) were not significantly different among device systems. Differences between endovascular and corresponding open repair cohorts showed lower mean costs for EVR (range, $3200-$8300), but these were not statistically different. Conclusions The implant costs of endovascular aneurysm repair are substantial. When evaluating total health care system expenditures, there is large individual variability in costs, and there is no significant difference at 2 years among systems or when an individual system is compared with open repair.

Introduction : Partial liquid ventilation (PLV) with perfluorocarbons can be advantageous in treating lung injury. We studied this phenomenon in isolated piglet lungs devoid of systemic detractors by studying the changes in pulmonary vascular resistance (PVR) after lung injury with and without PLV. The following questions were asked. (1) Does PLV alone affect PVR in the uninjured lung? (2) Does PLV prevent the increase in PVR associated with oleic acid-induced lung injury? (3) Does PLV modify the increase in PVR associated with oleic acid lung injury? (4) Are the prophylactic and therapeutic effects of PLV on the increased PVR associated with oleic acid-induced lung injury different? Methods : Neonatal piglet (3 to 4 kg) lungs were prepared without pulmonary ischemia, hypoxia, or reperfusion injury for in situ study. Before pulmonary vascular isolation (eg, aortic and ductus arteriosus ligation) the pulmonary artery (PA) and left atrium (LA) were cannulated and attached to a blood-primed perfusion circuit (flow, 80 mL/kg/min). Pressure-limited volume-cycled ventilation (FIO 2 , 0.21; TV, 15 mL/kg; PIP, 25 cm H 2 O) was accomplished via occlusive tracheostomy. Blood gas parameters were monitored continuously and maintained within normal range (SpaO 2 , 75%; pH, 7.35 to 7.45; pCO 2 , 35 to 45 torr). Pulmonary artery pressure (P pa ), left atrial pressure (P ia ) and pulmonary blood flow (Q pa ) were recorded and PVR calculated (PVR = Ppa − PiaQpa). After achieving a stable baseline with gas ventilation only, the animal preparations were assigned to one of the following four groups. In group 1 (n = 7) PLV was given alone, using endotracheally administered perfluorodecalin (15 mL/kg). In group 2 (Prophylactic, n=7) PLV was given prophylactically 60 minutes before lung injury induced by injecting oleic acid (OA) at 0.08 mL/kg into the pulmonary artery. In group 3 (Therapeutic, n=8) PLV was given 60 minutes after OA-induced lung injury. P PA , P LA , and Q PA were measured and PVR was calculated. In group 4 (n = 7) OA was given alone. Significance of differences between groups was obtained by repeated measures analysis of variance (ANOVA). Results were expressed as mean ± SEM (mm Hg/L/Kg). Results : Group I showed baseline PVR of the normoxic gas ventilated animals was 127 ± 19 mm Hg/L/kg. PVR 180 minutes after PLV administration was 160 ± 15 mm Hg/L/kg ( P = ns v baseline). In group 2 after OA infusion, PVR increased from 109 ± 13 to 281 ± 26 mm Hg/L/kg ( P v baseline), and 60 minutes later, PVR decreased to 193 ± 22 mm Hg/L/kg ( P v OA). In group 3 PVR on gas ventilation, before lung injury, was 137 ± 28 mm Hg/L/kg. Sixty minutes after OA infusion, PVR increased to 314 ± 23 mm Hg/L/kg ( P v baseline). After 60 additional minutes of PLV, PVR decreased to 201 ± 31 mm Hg/L/kg, ( P v maximum). In group 4 baseline PVR was 96 ± 16 mm Hg/L/kg. After 120 minutes of OA injection, PVR increased to 414 ± 20 mm Hg/L/kg ( P v baseline). Endpoint analysis of PVR at the conclusion of the recording interval showed no difference between group 2 and group 3 (P = not significant [ns]). Conclusions : (1) PLV does not significantly alter PVR in the uninjured lung when given for 2 hours; (2) prophylactic administration of PLV prevents the sustained increase in PVR known to be induced by OA injury; (3) PLV abates OA-induced elevation in PVR when given therapeutically after injury; and (4) Prophylactic and therapeutic PLV have similar effects on PVR in the OA-injured lung.

PARTIAL LIQUID VENTILATION (PLV) AND LUNG INJURY: IS PLV ABLE TO MODIFY PULMONARY VASCULAR RESISTANCE (PVR)? † 1927