Cost-effectiveness of endovascular versus open repair of acute complicated type B aortic dissections

ObjectiveThis study weighed the cost and benefit of thoracic endovascular aortic repair (TEVAR) vs open repair (OR) in the treatment of an acute complicated type B aortic dissection by (TBAD) estimating the cost-effectiveness to determine an optimal treatment strategy based on the best currently available evidence.MethodsA cost-utility analysis from the perspective of the health system payer was performed using a decision analytic model. Within this model, the 1-year survival, quality-adjusted life-years (QALYs), and costs for a hypothetical cohort of patients with an acute complicated TBAD managed with TEVAR or OR were evaluated. Clinical effectiveness data, cost data, and transitional probabilities of different health states were derived from previously published high-quality studies or meta-analyses. Probabilistic sensitivity analyses were performed on uncertain model parameters.ResultsThe base-case analysis showed, in terms of QALYs, that OR appeared to be more expensive (incremental cost of €17,252.60) and less effective (−0.19 QALYs) compared with TEVAR; hence, in terms of the incremental cost-effectiveness ratio, OR was dominated by TEVAR. As a result, the incremental cost-effectiveness ratio (ie, the cost per life-year saved) was not calculated. The average cost-effectiveness ratio of TEVAR and OR per QALY gained was €56,316.79 and €108,421.91, respectively. In probabilistic sensitivity analyses, TEVAR was economically dominant in 100% of cases. The probability that TEVAR was economically attractive at a willingness-to-pay threshold of €50,000/QALY gained was 100%.ConclusionsThe present results suggest that TEVAR yielded more QALYs and was associated with lower 1-year costs compared with OR in patients with an acute complicated TBAD. As a result, from the cost-effectiveness point of view, TEVAR is the dominant therapy over OR for this disease under the predefined conditions

Reduced pulsatile wall motion of abdominal aortic aneurysms after endovascular repair

AbstractPurpose: The reduced size of abdominal aortic aneurysms (AAAs) after endovascular repair suggests lowered intraaneurysmal pressure. In the presence of endoleaks, the size is not decreased. Although postoperative intraaneurysmal pressure is difficult to record, the pulsatile wall motion (PWM) of aneurysms can be measured noninvasively. The aim of this study was to assess the PWM of AAAs before and after endovascular repair and to relate the change in the PWM to aneurysmal size and presence of endoleaks. Methods: Forty-seven patients underwent endovascular repair of an AAA. The aneurysm diameter and PWM were measured with the use of ultrasonic echo-tracking scans preoperatively; at 1, 3, and 6 months; and thereafter biannually. Fifteen aneurysms developed endoleaks, whereas 32 were completely excluded. The leaks were characterized with the use of computed tomographic scanning and angiography. Median follow-up was 12 months (interquartile range, 5 to 24 months). Results: The preoperative PWM of the aneurysms was 1.0 mm (range, 0.8 to 1.3 mm). After complete endovascular exclusion, the PWM was 25% (range, 16% to 37%) of the preoperative value (p < 0.001), and aneurysm diameter decreased by 8 mm (range, 6 to 14 mm) (p < 0.001). After 18 months, no further diameter reduction occurred. In three patients without endoleaks but with enlarging aneurysms, the postoperative PWM showed less reduction (p < 0.05). Aneurysms with endoleaks showed no diameter decrease, and the postoperative PWM was 50% higher than that in the totally excluded cases (p < 0.01). In five patients with transient endoleaks, the PWM was reduced after leakage ceased (p < 0.05). Leaks of various sources displayed similar PWM. Conclusion: The size and PWM of aneurysms are reduced after endovascular repair. The diameter reduction may cease after 1.5 years. Endoleaks are associated with higher PWM than expected. Pressure may be transmitted without evidence of leaks. (J Vasc Surg 1998;27:624-31.

Endovascular repair of descending thoracic aortic aneurysms: an early experience with intermediate-term follow-up

AbstractPurpose: The purpose of this study was to report an initial experience with the endovascular repair of descending thoracic aortic aneurysm. Complications and intermediate-term morphologic changes were identified with the intent of altering patient selection and device design. Methods: Endografts were placed into 25 patients at high-risk for conventional surgical repair over a 3 ½–year period. Devices were customized on the basis of preoperative imaging information. Follow-up computed tomography scans were obtained at 1, 3, 6, and 12 months and yearly thereafter. Additional interventions occurred in the setting of endoleaks, migration, and aneurysm growth. Results: The overall 30-day mortality rate was 20% (12.5% for elective cases; 33% for emergent cases). There were 3 conversions to open repair. Neurologic deficits developed in 3 patients; 1 insult resulted in permanent paraplegia. Neurologic deficits were associated with longer endografts (P = .019). Three endoleaks required treatment, and 1 fatal rupture of the thoracic aneurysm treated occurred 6 months after the initial repair. Migrations were detected in 4 patients. The maximal aneurysm size decreased yearly by 9.15% (P = .01) or by 13.5% (P = .0005) if patients with endoleaks (n = 3 patients) were excluded. Both the proximal and distal neck dilated slightly over the course of follow-up (P = .019 and P = .001, respectively). The length of the proximal neck was a significant predictor of the risk for endoleakage (P = .02). Conclusion: The treatment of descending thoracic aortic aneurysms with an endovascular approach is feasible and may, in some patients, offer the best means of therapy. Early complications were primarily related to device design and patient selection. All aneurysms without endoleaks decreased in size after treatment. Late complications were associated with changing aneurysm morphologic features and device migration. The morphologic changes remain somewhat unpredictable; however, alterations in device design may result in improved fixation and more durable aneurysm exclusion. (J Vasc Surg 2000;31:147-56.

Persistent collateral perfusion of abdominal aortic aneurysm after endovascular repair does not lead to progressive change in aneurysm diameter

AbstractPurpose: To differentiate between the phenomenon of collateral perfusion from a side branch versus graft-related endoleaks after endovascular repair of abdominal aortic aneurysms (AAA), with respect to aneurysm size and prognosis. Methods: We successfully treated 64 AAA patients with endovascular grafting. We followed all the patients postoperatively with spiral computed tomography at one, three, six and 12 months, and biannually thereafter. We measured aneurysm diameters preoperatively and postoperatively. We calculated preoperatively the relation of maximum aortic diameter (D) to the thrombus-free lumen diameter (L) expressed as an L/D ratio. Median follow-up was 15 months. Results: Sixteen patients had collateral perfusion during follow-up. We successfully treated two patients with embolization. One patient showed resolution of collateral perfusion after we stopped warfarin treatment. Two patients died of unrelated causes during follow-up. One patient was converted to surgical treatment, and two patients showed spontaneous resolution of their collateral perfusion. The group of patients with perfusion showed no statistically significant change of their aortic diameter on follow-up. The group of patients without perfusion showed a median decrease in aortic diameter of 8mm (p < 0.0001) at 18 months postoperatively. The group of patients with perfusion had significantly less thrombus in their aneurysm sac preoperatively than the group without perfusion, as expressed by the L/D ratio (mean L/D 0,61 versus 0,78, respectively; p = 0.0021.) Conclusion: There was no significant increase in aortic diameter on an average 18 months postoperatively despite persistent collateral perfusion. This may indicate a halted disease progression in the short term. Embolization of collateral vessels is associated with risk of paraplegia. We recommend a conservative approach with close observation if aneurysm diameter is stable. (J Vasc Surg 1998;28:242-9.

Effect of preexcisional heparin anticoagulation on excised canine vein and artery prostanoid production

The effect of heparin, administered prior to vessel dissection and excision, on the luminal release of prostanoids from an excised vessel was assessed. Eight adult mongrel dogs underwent removal of the jugular vein and carotid artery on one side, followed by intravenous administration of heparin sodium (150 IU/kg) and subsequent removal of these same vessels from the contralateral neck. The excised vessels were perfused in an ex vivo system with Hanks' balanced salt solution for five consecutive 15-min periods. Prostacyclin release (measured as 6-keto-PGF1[alpha]) and thromboxane A2 (measured as thromboxane B2) release into the perfusate were quantitated by radioimmunoassay. Vessel segments were studied with and without first period thrombin stimulation (2 U/ml) and with arachidonic acid (4 [mu]g/ml) stimulation during the last perfusion period. Vein segments following heparin administration exhibited greater prostacyclin production than veins not exposed to heparin. This effect did not occur in arteries. Heparin did not influence thromboxane A2 release. Luminal endothelial cell coverage was not affected by the presence or absence of heparin. Thus heparin anticoagulation prior to dissection and excision of a vein, may enhance early preservation of its endothelial cell function as evident by increased luminal release of prostacyclin.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/27928/1/0000352.pd

Papaverine effects on PGI2 and TXA2 release from the canine vascular wall

Operative manipulation of blood vessels might lead to spasm, thereby destroying the endothelial cell function: the spasm can be prevented by the vasodilator papaverine. To study if this was mediated via the prostanoid pathway the following investigation was undertaken: canine jugular veins and carotid arteries were dissected with or without papaverine. Vessel segments were then perfused with Hank's balanced salt solution for five times 15 min. Prostacyclin was measured as the stable degradation product 6-keto-PGF1[alpha] and thromboxane as TXB2, by radioimmunoassay. Control arterial segments' 6-keto-PGF1[alpha] release was initially 129.5 + 20.1 pg/mm2/15 min, and 29.7 + 10.4 after 60 min (p2/15 min (p125I tracer. When using 3H tracer including absorption of free antigen to dextran coated charcoal, papaverine displaced the free tracer giving artificially low values. There was no effect of papaverine given intraoperatively on the TXB2 release, neither from arteries nor from veins. In another experiment the vessel wall tension was examined and the cyclooxygenase inhibitor diclofenac did not inhibit the vasodilating effect of papaverine. It is concluded that the vasodilating effect of papaverine is not mediated via prostacyclin release and that the vasodilating effect does not influence the prostacyclin release from arteries or veins. Finally, papaverine interacts with the 3H assay by displacing the antigen-antibody complex.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/29961/1/0000323.pd

Comparison of static incubation versus physiologic perfusion techniques for quantitation of luminal release of prostacyclin and thromboxane in canine arteries and veins

Intraluminal release of 6-keto-PGF1[alpha] and TxB2 in ex vivo canine arteries and veins was assessed during five consecutive 15-min periods using static incubation and physiologic perfusion techniques. Arterial segments were perfused with 90 ml/min pulsatile flow at 100 mm Hg and vein segments with 90 ml/min nonpulsatile flow at 7 mm Hg. During the final 15-min period vessels were stimulated with arachidonic acid (AAS). Perfusion of vein segments caused a higher release of 6-keto-PGF1[alpha] during the first 30 min (P P 1[alpha] for 45 min (P P 2 release was higher during the entire observation period in perfused arteries and veins compared to incubated vessels (P and 1[alpha] or TxB2 released when comparing values obtained by one technique to values obtained by the other (P&gt; 0.1). These data suggest that flow related shear stress alters vascular prostanoid production, and that such should be accounted for when interpreting results of studies on prostacyclin and thromboxane release from intact vessels.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/27222/1/0000226.pd

New insights regarding the incidence, presentation and treatment options of aorto-oesophageal fistulation after thoracic endovascular aortic repair: the European Registry of Endovascular Aortic Repair Complications

OBJECTIVES To review the incidence, clinical presentation, definite management and 1-year outcome in patients with aorto-oesophageal fistulation (AOF) following thoracic endovascular aortic repair (TEVAR). METHODS International multicentre registry (European Registry of Endovascular Aortic Repair Complications) between 2001 and 2011 with a total caseload of 2387 TEVAR procedures (17 centres). RESULTS Thirty-six patients with a median age of 69 years (IQR 56-75), 25% females and 9 patients (19%) following previous aortic surgery were identified. The incidence of AOF in the entire cohort after TEVAR in the study period was 1.5%. The primary underlying aortic pathology for TEVAR was atherosclerotic aneurysm formation in 53% of patients and the median time to development of AOF was 90 days (IQR 30-150). Leading clinical symptoms were fever of unknown origin in 29 (81%), haematemesis in 19 (53%) and shock in 8 (22%) patients. Diagnosis could be confirmed via computed tomography in 92% of the cases with the leading sign of a new mediastinal mass in 28 (78%) patients. A conservative approach resulted in a 100% 1-year mortality, and 1-year survival for an oesophageal stenting-only approach was 17%. Survival after isolated oesophagectomy was 43%. The highest 1-year survival rate (46%) could be achieved via an aggressive treatment including radical oesophagectomy and aortic replacement [relative risk increase 1.73 95% confidence interval (CI) 1.03-2.92]. The survival advantage of this aggressive treatment modality could be confirmed in bootstrap analysis (95% CI 1.11-3.33). CONCLUSIONS The development of AOF is a rare but lethal complication after TEVAR, being associated with the need for emergency TEVAR as well as mediastinal haematoma formation. The only durable and successful approach to cure the disease is radical oesophagectomy and extensive aortic reconstruction. These findings may serve as a decision-making tool for physicians treating these complex patient