Enrico Cieri1, Paola De Rango2, Giacomo Isernia1, Gioele Simonte1, Andrea Ciucci1, Gianbattista Parlani1, Fabio Verzini1, Piergiorgio Cao3. 1. Unit of Vascular and Endovascular Surgery, Hospital S. Maria della Misericordia, University of Perugia, Perugia, Italy. 2. Unit of Vascular and Endovascular Surgery, Hospital S. Maria della Misericordia, University of Perugia, Perugia, Italy. Electronic address: plderango@gmail.com. 3. Unit of Vascular and Endovascular Surgery, Department of Cardiosciences, Hospital S. Camillo-Forlanini, Rome, Italy.
Abstract
BACKGROUND: This study analyzed predictors and the long-term consequence of type II endoleak in a large series of elective endovascular abdominal aneurysm repairs (EVARs). METHODS: Baseline characteristics and operative and follow-up data of consecutive patients undergoing EVAR were prospectively collected. Patients who developed type II endoleak according to computed tomography angiography and those without type II endoleak were compared for baseline characteristics, mortality, reintervention, conversion, and aneurysm growth after repair. RESULTS: In 1997-2011, 1412 consecutive patients (91.4% males; mean age, 72.9 years) underwent elective EVAR and were subsequently followed up for a median of 45 months (interquartile range, 21-79 months). Type II endoleak developed in 218. Adjusted analysis failed to identify significant independent predictors for type II endoleak with the exception of age (odds ratio, 1.03; 95% confidence interval, 1.01-1.05; P = .003) and intraluminal thrombus (odds ratio, 0.69; 95% confidence interval, 0.53-0.92; P = .010). Type II endoleak rates were comparable regardless of the device model. Late aneurysm-related survival was comparable (98.4% vs 99.5% at 60 months; P = .73) in patients with and without type II endoleak. However, at 60 months after EVAR, rates of aneurysm sac growth >5 mm (35.3% vs 3.3%; P < .0001) were higher in patients with type II endoleak. Cox regression identified type II endoleak as an independent predictor of aneurysm growth along with age and cardiac disease. The presence of type II endoleak led to reinterventions in 40% of patients and conversion to open surgery in 8%. However, assessment of these patients after reintervention showed similar 60-month freedom rates of persisting type II endoleak (present in more than two after computed tomography angiography scan studies) among those with and without reinterventions (49.8% vs 45.6%; P = .639). Aneurysm growth >5 mm persisted with comparable rates in type II endoleak patients after reintervention and in those who remained untreated (42.9% vs 57.4% at 60 months; P = .117). CONCLUSIONS: Reintervention for type II endoleak was common in our practice, yet such intervention did not reliably prevent the continued expansion of the abdominal aortic aneurysm. Our data indicate type II endoleak appears to be a marker of EVAR failure that is difficult to predict and treat effectively.
BACKGROUND: This study analyzed predictors and the long-term consequence of type II endoleak in a large series of elective endovascular abdominal aneurysm repairs (EVARs). METHODS: Baseline characteristics and operative and follow-up data of consecutive patients undergoing EVAR were prospectively collected. Patients who developed type II endoleak according to computed tomography angiography and those without type II endoleak were compared for baseline characteristics, mortality, reintervention, conversion, and aneurysm growth after repair. RESULTS: In 1997-2011, 1412 consecutive patients (91.4% males; mean age, 72.9 years) underwent elective EVAR and were subsequently followed up for a median of 45 months (interquartile range, 21-79 months). Type II endoleak developed in 218. Adjusted analysis failed to identify significant independent predictors for type II endoleak with the exception of age (odds ratio, 1.03; 95% confidence interval, 1.01-1.05; P = .003) and intraluminal thrombus (odds ratio, 0.69; 95% confidence interval, 0.53-0.92; P = .010). Type II endoleak rates were comparable regardless of the device model. Late aneurysm-related survival was comparable (98.4% vs 99.5% at 60 months; P = .73) in patients with and without type II endoleak. However, at 60 months after EVAR, rates of aneurysm sac growth >5 mm (35.3% vs 3.3%; P < .0001) were higher in patients with type II endoleak. Cox regression identified type II endoleak as an independent predictor of aneurysm growth along with age and cardiac disease. The presence of type II endoleak led to reinterventions in 40% of patients and conversion to open surgery in 8%. However, assessment of these patients after reintervention showed similar 60-month freedom rates of persisting type II endoleak (present in more than two after computed tomography angiography scan studies) among those with and without reinterventions (49.8% vs 45.6%; P = .639). Aneurysm growth >5 mm persisted with comparable rates in type II endoleak patients after reintervention and in those who remained untreated (42.9% vs 57.4% at 60 months; P = .117). CONCLUSIONS: Reintervention for type II endoleak was common in our practice, yet such intervention did not reliably prevent the continued expansion of the abdominal aortic aneurysm. Our data indicate type II endoleak appears to be a marker of EVAR failure that is difficult to predict and treat effectively.
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