Rolf Alexander Jánosi1, Riccardo Gorla2, Konstantinos Tsagakis3, Philipp Kahlert2, Michael Horacek2, Florian Bruckschen2, Daniel-Sebastian Dohle3, Heinz Jakob3, Thomas Schlosser4, Holger Eggebrecht5, Eduardo Bossone6, Raimund Erbel7. 1. Department of Cardiology, West-German Heart and Vascular Center Essen and University Duisburg-Essen, Essen, Germany alexander.janosi@uk-essen.de. 2. Department of Cardiology, West-German Heart and Vascular Center Essen and University Duisburg-Essen, Essen, Germany. 3. Department of Thoracic and Cardiovascular Surgery, West-German Heart and Vascular Center Essen and University Duisburg-Essen, Essen, Germany. 4. Department of Diagnostic and Interventional Radiology and Neuroradiology, University Hospital Essen, University Duisburg-Essen, Essen, Germany. 5. Cardioangiological Center Bethanien (CCB), Frankfurt, Germany. 6. Heart Department, University Hospital, Salerno, Italy. 7. Institute of Medical Informatics, Biometry and Epidemiology (IMIBE), University Hospital Essen, University Duisburg-Essen, Essen, Germany.
Abstract
PURPOSE: To analyze an 11-year single-center experience of treating complicated penetrating aortic ulcer (PAU) using thoracic endovascular aortic repair (TEVAR). METHODS: This study included 63 consecutive patients (mean age 69.1±11.5 years; 40 men) with complicated PAU (42 symptomatic, 22 with rupture) who underwent TEVAR between 2002 and 2013. The PAUs were located in the aortic arch (n=11), the descending thoracic aorta (n=43), and the thoracoabdominal aorta (n=9). RESULTS: TEVAR was performed within 14 days of diagnosis in 33 (52.3%) cases (19 ruptures treated immediately); the other 30 (47.6%) patients had an average interval between diagnosis and intervention of 40±39 days. Technical success was 98.4% (62/63). One patient had a type I endoleak after stent-graft repair of a PAU in the aortic arch without great vessel transposition; another procedure was required for carotid-subclavian bypass and proximal stent-graft extension. No patient experienced spinal cord ischemia after TEVAR. Five (7.9%) patients died in-hospital; 3 had severe cardiac complications, 1 died from complications of aortic rupture, and the other succumbed to septic shock. Mean follow-up was 45.6±47.2 months, during which 12 (19.0%) patients needed a secondary intervention because of late endoleaks (n=4, 6.3%) or new complications due to disease progression. Multivariate analysis indicated that a PAU depth >15 mm was an independent predictor of mortality (hazard ratio 6.92, p=0.03). In the biomarker analysis, symptomatic patients had significantly higher D-dimer and troponin levels compared to asymptomatic patients [559.5±460.7 vs 283.2±85.2 µg/L (p=0.016) and 0.22±0.61 vs 0.02±0.03 ng/mL (p=0.04), respectively]. CONCLUSION: Patients with PAU suffer from underlying severe atherosclerotic disease and have a significant number of cardiovascular comorbidities that lead to relevant mortality and morbidity after TEVAR. As a PAU diameter >15 mm represented high risk for disease progression, these patients may be candidates for early intervention. D-dimer levels may help identify patients at risk and with progression of PAU.
PURPOSE: To analyze an 11-year single-center experience of treating complicated penetrating aortic ulcer (PAU) using thoracic endovascular aortic repair (TEVAR). METHODS: This study included 63 consecutive patients (mean age 69.1±11.5 years; 40 men) with complicated PAU (42 symptomatic, 22 with rupture) who underwent TEVAR between 2002 and 2013. The PAUs were located in the aortic arch (n=11), the descending thoracic aorta (n=43), and the thoracoabdominal aorta (n=9). RESULTS: TEVAR was performed within 14 days of diagnosis in 33 (52.3%) cases (19 ruptures treated immediately); the other 30 (47.6%) patients had an average interval between diagnosis and intervention of 40±39 days. Technical success was 98.4% (62/63). One patient had a type I endoleak after stent-graft repair of a PAU in the aortic arch without great vessel transposition; another procedure was required for carotid-subclavian bypass and proximal stent-graft extension. No patient experienced spinal cord ischemia after TEVAR. Five (7.9%) patients died in-hospital; 3 had severe cardiac complications, 1 died from complications of aortic rupture, and the other succumbed to septic shock. Mean follow-up was 45.6±47.2 months, during which 12 (19.0%) patients needed a secondary intervention because of late endoleaks (n=4, 6.3%) or new complications due to disease progression. Multivariate analysis indicated that a PAU depth >15 mm was an independent predictor of mortality (hazard ratio 6.92, p=0.03). In the biomarker analysis, symptomatic patients had significantly higher D-dimer and troponin levels compared to asymptomatic patients [559.5±460.7 vs 283.2±85.2 µg/L (p=0.016) and 0.22±0.61 vs 0.02±0.03 ng/mL (p=0.04), respectively]. CONCLUSION:Patients with PAU suffer from underlying severe atherosclerotic disease and have a significant number of cardiovascular comorbidities that lead to relevant mortality and morbidity after TEVAR. As a PAU diameter >15 mm represented high risk for disease progression, these patients may be candidates for early intervention. D-dimer levels may help identify patients at risk and with progression of PAU.
Authors: Gabriele Piffaretti; Federico Fontana; Marco Tadiello; Chiara Guttadauro; Filippo Piacentino; Ruth L Bush; Anna Maria Socrate; Matteo Tozzi Journal: Ann Cardiothorac Surg Date: 2019-07