Martin Czerny1, Diana Reser2, Holger Eggebrecht3, Karin Janata4, Gottfried Sodeck4, Christian Etz5, Maximilian Luehr5, Fabio Verzini6, Diletta Loschi6, Roberto Chiesa7, Germano Melissano7, Andrea Kahlberg7, Philippe Amabile8, Wolfgang Harringer9, Rolf Alexander Janosi10, Raimund Erbel10, Jürg Schmidli11, Piergiorgio Tozzi12, Yutaka Okita13, Ludovic Canaud14, Ali Khoynezhad15, Gabriele Maritati16, Piergiorgio Cao17, Tilo Kölbel18, Santi Trimarchi19. 1. Department of Cardiovascular Surgery, University Hospital Zurich, Zurich, Switzerland martin.czerny@usz.ch. 2. Department of Cardiovascular Surgery, University Hospital Zurich, Zurich, Switzerland. 3. Cardioangiological Center Bethanien, Frankfurt, Germany. 4. Department of Emergency Medicine, Medical University of Vienna, Vienna, Austria. 5. Heart Center Leipzig, Leipzig, Germany. 6. Vascular and Endovascular Surgery Unit, Hospital S. Maria Misericordia, Perugia, Italy. 7. Department of Vascular Surgery, Scientific Institute H San Raffaele, Milan, Italy. 8. Department of Interventional Radiology, AP-HM-Hôpital Nord, Marseille, France. 9. Department of Cardiovascular and Thoracic Surgery, Braunschweig, Germany. 10. Department of Cardiology, West-German Heart Center Essen, Essen, Germany. 11. Department of Cardiovascular Surgery, Inselspital, University Hospital Berne, Berne, Switzerland. 12. Department of Cardiac Surgery, CHUV, Lausanne, Switzerland. 13. University, Division of Cardiovascular Surgery, Kobe University, Kobe, Japan. 14. Department of Vascular and Thoracic Surgery, Arnaud de Villeneuve Hospital, Montpellier, France. 15. Division of Cardiothoracic Surgery Cedars Sinai Medical Center, Los Angeles, CA, USA. 16. The Leeds Teaching Hospitals NHS Trust, Leeds, UK. 17. San Camillo Hospital, Rome, Italy. 18. Universitäres Herzzentrum Hamburg, Hamburg, Germany. 19. IRCCS Policlinico San Donato, Thoracic Aortic Research Center, Milan, Italy.
Abstract
OBJECTIVES: To learn upon incidence, underlying mechanisms and effectiveness of treatment strategies in patients with central airway and pulmonary parenchymal aorto-bronchial fistulation after thoracic endovascular aortic repair (TEVAR). METHODS: Analysis of an international multicentre registry (European Registry of Endovascular Aortic Repair Complications) between 2001 and 2012 with a total caseload of 4680 TEVAR procedures (14 centres). RESULTS: Twenty-six patients with a median age of 70 years (interquartile range: 60-77) (35% female) were identified. The incidence of either central airway (aorto-bronchial) or pulmonary parenchymal (aorto-pulmonary) fistulation (ABPF) in the entire cohort after TEVAR in the study period was 0.56% (central airway 58%, peripheral parenchymal 42%). Atherosclerotic aneurysm formation was the leading indication for TEVAR in 15 patients (58%). The incidence of primary endoleaks after initial TEVAR was n = 10 (38%), of these 80% were either type I or type III endoleaks. Fourteen patients (54%) developed central left bronchial tree lesions, 11 patients (42%) pulmonary parenchymal lesions and 1 patient (4%) developed a tracheal lesion. The recognized mechanism of ABPF was external compression of the bronchial tree in 13 patients (50%), the majority being due to endoleak formation, further ischaemia due to extensive coverage of bronchial feeding arteries in 3 patients (12%). Inflammation and graft erosion accounted for 4 patients (30%) each. Cumulative survival during the entire study period was 39%. Among deaths, 71% were attributed to ABPF. There was no difference in survival in patients having either central airway or pulmonary parenchymal ABPF (33 vs 45%, log-rank P = 0.55). Survival with a radical surgical approach was significantly better when compared with any other treatment strategy in terms of overall survival (63 vs 32% and 63 vs 21% at 1 and 2 years, respectively), as well as in terms of fistula-related survival (63 vs 43% and 63 vs 43% at 1 and 2 years, respectively). CONCLUSIONS: ABPF is a rare but highly lethal complication after TEVAR. The leading mechanism behind ABPF seems to be a continuing external compression of either the bronchial tree or left upper lobe parenchyma. In this setting, persisting or newly developing endoleak formation seems to play a crucial role. Prognosis does not differ in patients with central airway or pulmonary parenchymal fistulation. Radical bronchial or pulmonary parenchymal repair in combination with stent graft removal and aortic reconstruction seems to be the most durable treatment strategy.
OBJECTIVES: To learn upon incidence, underlying mechanisms and effectiveness of treatment strategies in patients with central airway and pulmonary parenchymal aorto-bronchial fistulation after thoracic endovascular aortic repair (TEVAR). METHODS: Analysis of an international multicentre registry (European Registry of Endovascular Aortic Repair Complications) between 2001 and 2012 with a total caseload of 4680 TEVAR procedures (14 centres). RESULTS: Twenty-six patients with a median age of 70 years (interquartile range: 60-77) (35% female) were identified. The incidence of either central airway (aorto-bronchial) or pulmonary parenchymal (aorto-pulmonary) fistulation (ABPF) in the entire cohort after TEVAR in the study period was 0.56% (central airway 58%, peripheral parenchymal 42%). Atherosclerotic aneurysm formation was the leading indication for TEVAR in 15 patients (58%). The incidence of primary endoleaks after initial TEVAR was n = 10 (38%), of these 80% were either type I or type III endoleaks. Fourteen patients (54%) developed central left bronchial tree lesions, 11 patients (42%) pulmonary parenchymal lesions and 1 patient (4%) developed a tracheal lesion. The recognized mechanism of ABPF was external compression of the bronchial tree in 13 patients (50%), the majority being due to endoleak formation, further ischaemia due to extensive coverage of bronchial feeding arteries in 3 patients (12%). Inflammation and graft erosion accounted for 4 patients (30%) each. Cumulative survival during the entire study period was 39%. Among deaths, 71% were attributed to ABPF. There was no difference in survival in patients having either central airway or pulmonary parenchymal ABPF (33 vs 45%, log-rank P = 0.55). Survival with a radical surgical approach was significantly better when compared with any other treatment strategy in terms of overall survival (63 vs 32% and 63 vs 21% at 1 and 2 years, respectively), as well as in terms of fistula-related survival (63 vs 43% and 63 vs 43% at 1 and 2 years, respectively). CONCLUSIONS: ABPF is a rare but highly lethal complication after TEVAR. The leading mechanism behind ABPF seems to be a continuing external compression of either the bronchial tree or left upper lobe parenchyma. In this setting, persisting or newly developing endoleak formation seems to play a crucial role. Prognosis does not differ in patients with central airway or pulmonary parenchymal fistulation. Radical bronchial or pulmonary parenchymal repair in combination with stent graft removal and aortic reconstruction seems to be the most durable treatment strategy.
Authors: Joseph S Coselli; Konstantinos Spiliotopoulos; Ourania Preventza; Kim I de la Cruz; Hiruni Amarasekara; Susan Y Green Journal: Gen Thorac Cardiovasc Surg Date: 2016-06-17