Large Thoracic Aortic Aneurysm and Dissection with Rare Complication Nedaa Skeik,1 Aisha K. Ahmed,2 Clark W. Schumacher,3 Troy Decker,4 and Timothy M. Sullivan,4 Minneapolis, Minnesota
Thoracic aortic aneurysms can be found incidentally, however, patients can also present with acute dissection and or rupture that can be fatal. Symptoms that might indicate dissection include chest and back pain as well as lightheadedness. The diagnosis can be made with imaging studies such as computed tomography or magnetic resonance angiogram and sometimes transesophageal echocardiogram. Management is based on the aneurysmal size, location, extension, and the presence of complications. Although smaller localized and slow growing aneurysms can be monitored, larger and or complicated ones may warrant immediate repair. Lesscommon complications include compression over anatomic structures in the vicinity including vessels and the mediastinum. We report a unique case of a 71-year-old man who presented with a very large thoracic aortic aneurysm with dissection causing compression over the brachiocephalic veins and the mediastinum leading to facial and upper extremity swelling, dysphagia, and cough. This case represents a rare but significant complication of thoracic aortic aneurysm and emphasizes the challenges of its management.
CASE REPORT A 71-year-old man with history of repaired type A thoracic aortic dissection and large aneurysm who presented with a several week history of progressive bilateral upper extremity and facial swelling, intermittent dysphagia, and cough affecting his daily living activities. He had remote history of a 16-cm thoracic aortic aneurysm (TAA) with a Stanford type A dissection involving the aortic arch and the entire descending thoracic and abdominal aorta. This had been repaired 9 years earlier
1
Vascular Medicine, Minneapolis Heart Institute, Minneapolis, MN.
2
Minneapolis Heart Institute Research Foundation, Minneapolis,
MN. 3 Interventional Radiology, Abbott Northwestern Hospital, Minneapolis, MN. 4
Vascular Surgery, Minneapolis Heart Institute, Minneapolis, MN.
Correspondence to: Nedaa Skeik, MD, Vascular Medicine, Abbott Northwestern Hospital, Minneapolis Heart Institute, 800 East 28th Street, Suite H 2000, Minneapolis, MN 55407, USA; E-mail: nedaa. [email protected] Ann Vasc Surg 2014; 28: 1034.e9–1034.e12 http://dx.doi.org/10.1016/j.avsg.2013.12.020 Ó 2014 Elsevier Inc. All rights reserved. Manuscript received: September 4, 2013; manuscript accepted: December 5, 2013.
using a 28-mm straight Hemashield graft without the need for aortic valve replacement that was intact (Fig. 1A). Over 9 years, there was ongoing aneurysmal dilatation but the patient refused further intervention. Vital signs revealed a blood pressure of 140/70 mm Hg and a pulse of 62 beats/min. The physical examination revealed diffuse, hard, pitting edema with purple skin discoloration involving the face and the entire bilateral upper extremity. There was a harsh 3/6 late systolic murmur at the left sternal border. The remainder of the physical examination was unremarkable. An upright anteroposterior chest X-ray revealed nearcomplete opacification of the left hemithorax with rightward mediastinal shift secondary to mass effect from the large TAA (Fig. 1B). Coronal computed tomography angiogram (CTA) demonstrated the aneurysmal thoracic aortic dissection, which measured 16 cm at the aortic arch and 8.4 cm in the mid-descending thoracic aorta. This caused a rightward mediastinal shift (Fig. 1C). Dissection extending into the right internal carotid artery is not shown. To exclude other possible musculoskeletal or soft tissue causes for the patient’s symptoms, magnetic resonance (MR) studies were performed. MR arteriogram confirmed the large aortic aneurysm with the dissection flap extending into the right brachiocephalic and internal carotid arteries but not into the left common carotid or left subclavian artery (Fig. 1D). The MR venogram
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Annals of Vascular Surgery
Fig. 1. (A) Axial CTA illustrating Stanford type A dissection involving the aortic arch. (B) Chest x-ray (CXR) showing near-complete opacification of the left hemithorax. (C) Coronal CTA demonstrating rightward mediastinal shift caused by large thoracic aortic aneurysm with dissection. (D) Coronal MR arteriogram demonstrating right coronal carotid artery dissection that extends into the right internal carotid artery (arrow). Normal-appearing left coronal carotid artery is shown for comparison (star). (E) MR venogram depicting focal
stenosis at the right subclavian and brachiocephalic vein junction. (F) Left upper extremity venogram showing complete occlusion of the central left subclavian vein with extensive collateral flow. Collateral vessels cross midline and empty into the right innominate vein. (G) Catheter-based venogram showing distended right axillary, subclavian, and cephalic veins, because of compression on the right innominate vein by the aortic aneurysm.
demonstrated significant compression over the left brachiocephalic vein by the dilated aorta with a focal stenosis at the right subclavian and brachiocephalic vein junction (Fig. 1E). Both studies excluded other soft tissue pathology. Conventional venogram was performed for more detailed venous imaging and possible palliative intervention. It showed complete occlusion of the proximal left subclavian vein with extensive collateral flow emptying predominantly into the right innominate vein (Fig. 1F). On the right side, it showed distended right axillary, cephalic, and subclavian veins, because of compression over the right innominate vein by the aortic aneurysm. There was just a trickle of flow into the innominate vein and superior vena cava. Interestingly, there were very few collateral veins on the right side despite the venous compression (Fig. 1G). Unfortunately, vascular compression was severe and not amenable to straightforward palliative intervention. Furthermore, the patient refused further intervention. He was managed conservatively with bilateral arm compression and elevation and showed partial improvement. One month later, he returned to the emergency department with acute lightheadedness and severe
hypotension followed by cardiopulmonary arrest and death that was most likely secondary to the rupture of the aortic aneurysm.
DISCUSSION TAA is considered when there is 50% diameter increase compared with the normal segment.1 They are usually asymptomatic until they are large enough to compress the surrounding structures.2 As an aneurysm increases in size, patients may experience chest, abdominal, and/or upper back pain.3 Very large unrepaired aneurysms can lead to a variety of complications including compression of the surrounding structures, dissection, and rupture.3 Compression of nearby structures, such as vessels, soft tissue, left laryngeal and phrenic nerves, and mediastinal structures, rarely cause edema, hoarseness, dyspnea, cough, and dysphagia.4 Patients may present with heart failure because of aortic regurgitation caused by dilation of the valvular annulus. A thromboembolic event
Vol. 28, No. 4, May 2014
is another complication in aneurysms with mural thrombosis.5 Aneurysmal rupture is the most feared complication with mortality rate of 94%.6 Patients would present with severe tearing chest pain and hypotension.7 The initial anteroposterior (API) diameter and annual growth rate of the aneurysm are the most predictive factors for rupture risk.8 The optimal timing of repair is uncertain, particularly for smaller aneurysms, and most of the patients have concomitant cardiovascular disease that increases the risks for any planned surgery.7 Based on the current evidence and general consensus, aneurysmal repair is indicated in patients with an API diameter of 60 mm or an annual growth rate of 6 mm.8,9 Although open repair is still the gold standard, there are considerable surgical complications depending on the extent of repair required. Complications after the surgery include myocardial infarction, arrhythmia, stroke, paralysis, and kidney dysfunction.10 Thoracic endovascular aneurysm repair (TEVAR) is now considered a suitable alternative to open repair in many cases.11,12 Potential benefits of TEVAR include smaller incisions, elimination of aortic cross clamping, less blood loss, lower incidence of visceral, renal, and spinal cord ischemia, and quicker recovery.13 Aortic dissection is another life-threatening complication with very few noticeable signs and symptoms. The most evident distinction is a ripping sensation that causes the sudden onset of excruciating pain.14 Depending on where the dissection occurs, the pain will be localized in different areas of the body. If the dissection is type A, the pain is centered in the chest and spreads to the upper back. If the dissection is in the abdominal aorta, the pain will be centered in the lower back and spreads to the flanks.14 The presentations of aortic dissection can be very similar to the symptoms of other heart-related problems, such as myocardial infarction. These presentations are all variable, making the diagnosis challenging. The key symptom is the sudden onset of chest or back pain, which is a transient intrathoracic tearing sensation irradiating toward the lumbar region. Other concurrent symptoms may include syncope, shortness of breath, paraplegia, acute peripheral ischemia, and hemiplegia. Coma may also be a manifestation.15 The dissection location and affected branches would determine the end-organ ischemia, which can be in a form of stroke, limb ischemia, renal failure, or paraplegia.16 Death can also be caused by intrapericardial or intrapleural ruptures and acute aortic insufficiency leading to cardiac tamponade, hemothorax, and cardiogenic shock, respectively.17
Case reports 1034.e11
Although acute type A aortic dissection represents a surgical emergency requiring immediate repair, most uncomplicated type B dissections can be managed medically.18 In comparison to open repair, if feasible, endovascular repair is less invasive with faster recovery.12 Our patient presented with a large TAA along with extensive type A dissection that compressed the bilateral brachiocephalic veins resulting in severe bilateral upper extremity and facial edema. The aneurysm was large enough to cause right mediastinal shift resulting in intermittent dysphagia and cough. Large TAA is an unusual cause for upper extremity and facial edema and very rarely leads to dysphagia and cough.19 Management of such complication is not only very challenging but usually requires multidisciplinary approach that might include palliative intervention.20 Our patient refused treatment and unfortunately expired because of complications related to his enlarging TAA.
REFERENCES 1. Hiratzka LF, Bakris GL, Beckman JA, et al. 2010 ACCF/ AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with thoracic aortic disease: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine. Circulation 2010;121: e266. 2. Pressler V, McNamara JJ. Aneurysm of the thoracic aorta. Review of 260 cases. J Thorac Cardiovasc Surg 1985;89: 50e4. 3. Elefteriades JA. Thoracic aortic aneurysm: current approach to surgical timing. ACC Curr J Rev 2002;11:82e8. 4. Teixido MT, Leonetti JP. Recurrent laryngeal nerve paralysis associated with thoracic aortic aneurysm. Otolaryngol Head Neck Surg 1990;102:140e4. 5. Zhang Y. Encyclopedia of Global Health, Volume 1. Sage Publications, 2008. pp 137e8. 6. Johansson G, Markstrom U, Swedenborg J. Ruptured thoracic aortic aneurysms: a study of incidence and mortality rates. J Vasc Surg 1995;21:985e8. 7. Nuenninghoff DM, Hunder GG, Christianson TJ, et al. Incidence and predictors of large-artery complication (aortic aneurysm, aortic dissection, and/or large-artery stenosis) in patients with giant cell arteritis: a population-based study over 50 years. Arthritis Rheum 2003;48:3522. 8. Lobato AC, Puech-Le~ao P. Predictive factors for rupture of thoracoabdominal aortic aneurysm. J Vasc Surg 1998;27: 446e53. 9. Davies RR, Goldstein LJ, Coady MA, et al. Yearly rupture or dissection rates for thoracic aortic aneurysms: simple prediction based on size. Ann Thorac Surg 2002;73:17.
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10. Budillon AM, Nicolini F, Beghi C, et al. Surgical repair of thoracic aortic aneurysms: results and complications. Acta Biomed Ateneo Parmense 2001;72:33e43. 11. Matsumura JS, Cambria RP, Dake MD, et al. International controlled clinical trial of thoracic endovascular aneurysm repair with the Zenith TX2 endovascular graft: 1-year results. J Vasc Surg 2008;47:247. 12. Makaroun MS, Dillavou ED, Wheatley GH, et al. Five-year results of endovascular treatment with the Gore TAG device compared with open repair of thoracic aortic aneurysms. J Vasc Surg 2008;47:912. 13. Greenberg RK, Lu Q, Roselli EE, et al. Contemporary analysis of descending thoracic and thoracoabdominal aneurysm repair: a comparison of endovascular and open techniques. Circulation 2008;118:808. 14. Juang D, Braverman AC, Eagle K. Aortic dissection. Circulation 2008;118:e507e10.
Annals of Vascular Surgery
15. Rogers FB, Osler TM, Shackford SR. Aortic dissection after trauma: case report and review of the literature. J Trauma 1996;41:906e8. 16. Hebballi R, Swanevelder J. Diagnosis and management of aortic dissection. Contin Educ Anaesth Crit Care Pain 2009;9: 14e8. 17. Elefteriades JA. Thoracic aortic aneurysm: reading the enemy’s playbook. Curr Probl Cardiol 2008;33:203e77. 18. Suzuki T, Mehta RH, Ince H, et al. Clinical profiles and outcomes of acute type B aortic dissection in the current era: lessons from the International Registry of Aortic Dissection (IRAD). Circulation 2003;108(Suppl 1):II312. 19. Hiller HG, Lagattolla NRF. Thoracic aortic aneurysm presenting with dysphagia: a fatal delay in diagnosis. Thorac Surg Sci 2007;4. Doc01. 20. Tsai TT, Nienaber CA, Eagle KA. Acute aortic syndromes. Circulation 2005;112:3802.
Thoracic aortic aneurysms can be found incidentally, however, patients can also present with acute dissection and or rupture that can be fatal. Symptoms that might indicate dissection include chest and back pain as well as lightheadedness. The diagnosis can be made with imaging studies such as computed tomography or magnetic resonance angiogram and sometimes transesophageal echocardiogram. Management is based on the aneurysmal size, location, extension, and the presence of complications. Although smaller localized and slow growing aneurysms can be monitored, larger and or complicated ones may warrant immediate repair. Lesscommon complications include compression over anatomic structures in the vicinity including vessels and the mediastinum. We report a unique case of a 71-year-old man who presented with a very large thoracic aortic aneurysm with dissection causing compression over the brachiocephalic veins and the mediastinum leading to facial and upper extremity swelling, dysphagia, and cough. This case represents a rare but significant complication of thoracic aortic aneurysm and emphasizes the challenges of its management.
CASE REPORT A 71-year-old man with history of repaired type A thoracic aortic dissection and large aneurysm who presented with a several week history of progressive bilateral upper extremity and facial swelling, intermittent dysphagia, and cough affecting his daily living activities. He had remote history of a 16-cm thoracic aortic aneurysm (TAA) with a Stanford type A dissection involving the aortic arch and the entire descending thoracic and abdominal aorta. This had been repaired 9 years earlier
1
Vascular Medicine, Minneapolis Heart Institute, Minneapolis, MN.
2
Minneapolis Heart Institute Research Foundation, Minneapolis,
MN. 3 Interventional Radiology, Abbott Northwestern Hospital, Minneapolis, MN. 4
Vascular Surgery, Minneapolis Heart Institute, Minneapolis, MN.
Correspondence to: Nedaa Skeik, MD, Vascular Medicine, Abbott Northwestern Hospital, Minneapolis Heart Institute, 800 East 28th Street, Suite H 2000, Minneapolis, MN 55407, USA; E-mail: nedaa. [email protected] Ann Vasc Surg 2014; 28: 1034.e9–1034.e12 http://dx.doi.org/10.1016/j.avsg.2013.12.020 Ó 2014 Elsevier Inc. All rights reserved. Manuscript received: September 4, 2013; manuscript accepted: December 5, 2013.
using a 28-mm straight Hemashield graft without the need for aortic valve replacement that was intact (Fig. 1A). Over 9 years, there was ongoing aneurysmal dilatation but the patient refused further intervention. Vital signs revealed a blood pressure of 140/70 mm Hg and a pulse of 62 beats/min. The physical examination revealed diffuse, hard, pitting edema with purple skin discoloration involving the face and the entire bilateral upper extremity. There was a harsh 3/6 late systolic murmur at the left sternal border. The remainder of the physical examination was unremarkable. An upright anteroposterior chest X-ray revealed nearcomplete opacification of the left hemithorax with rightward mediastinal shift secondary to mass effect from the large TAA (Fig. 1B). Coronal computed tomography angiogram (CTA) demonstrated the aneurysmal thoracic aortic dissection, which measured 16 cm at the aortic arch and 8.4 cm in the mid-descending thoracic aorta. This caused a rightward mediastinal shift (Fig. 1C). Dissection extending into the right internal carotid artery is not shown. To exclude other possible musculoskeletal or soft tissue causes for the patient’s symptoms, magnetic resonance (MR) studies were performed. MR arteriogram confirmed the large aortic aneurysm with the dissection flap extending into the right brachiocephalic and internal carotid arteries but not into the left common carotid or left subclavian artery (Fig. 1D). The MR venogram
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Fig. 1. (A) Axial CTA illustrating Stanford type A dissection involving the aortic arch. (B) Chest x-ray (CXR) showing near-complete opacification of the left hemithorax. (C) Coronal CTA demonstrating rightward mediastinal shift caused by large thoracic aortic aneurysm with dissection. (D) Coronal MR arteriogram demonstrating right coronal carotid artery dissection that extends into the right internal carotid artery (arrow). Normal-appearing left coronal carotid artery is shown for comparison (star). (E) MR venogram depicting focal
stenosis at the right subclavian and brachiocephalic vein junction. (F) Left upper extremity venogram showing complete occlusion of the central left subclavian vein with extensive collateral flow. Collateral vessels cross midline and empty into the right innominate vein. (G) Catheter-based venogram showing distended right axillary, subclavian, and cephalic veins, because of compression on the right innominate vein by the aortic aneurysm.
demonstrated significant compression over the left brachiocephalic vein by the dilated aorta with a focal stenosis at the right subclavian and brachiocephalic vein junction (Fig. 1E). Both studies excluded other soft tissue pathology. Conventional venogram was performed for more detailed venous imaging and possible palliative intervention. It showed complete occlusion of the proximal left subclavian vein with extensive collateral flow emptying predominantly into the right innominate vein (Fig. 1F). On the right side, it showed distended right axillary, cephalic, and subclavian veins, because of compression over the right innominate vein by the aortic aneurysm. There was just a trickle of flow into the innominate vein and superior vena cava. Interestingly, there were very few collateral veins on the right side despite the venous compression (Fig. 1G). Unfortunately, vascular compression was severe and not amenable to straightforward palliative intervention. Furthermore, the patient refused further intervention. He was managed conservatively with bilateral arm compression and elevation and showed partial improvement. One month later, he returned to the emergency department with acute lightheadedness and severe
hypotension followed by cardiopulmonary arrest and death that was most likely secondary to the rupture of the aortic aneurysm.
DISCUSSION TAA is considered when there is 50% diameter increase compared with the normal segment.1 They are usually asymptomatic until they are large enough to compress the surrounding structures.2 As an aneurysm increases in size, patients may experience chest, abdominal, and/or upper back pain.3 Very large unrepaired aneurysms can lead to a variety of complications including compression of the surrounding structures, dissection, and rupture.3 Compression of nearby structures, such as vessels, soft tissue, left laryngeal and phrenic nerves, and mediastinal structures, rarely cause edema, hoarseness, dyspnea, cough, and dysphagia.4 Patients may present with heart failure because of aortic regurgitation caused by dilation of the valvular annulus. A thromboembolic event
Vol. 28, No. 4, May 2014
is another complication in aneurysms with mural thrombosis.5 Aneurysmal rupture is the most feared complication with mortality rate of 94%.6 Patients would present with severe tearing chest pain and hypotension.7 The initial anteroposterior (API) diameter and annual growth rate of the aneurysm are the most predictive factors for rupture risk.8 The optimal timing of repair is uncertain, particularly for smaller aneurysms, and most of the patients have concomitant cardiovascular disease that increases the risks for any planned surgery.7 Based on the current evidence and general consensus, aneurysmal repair is indicated in patients with an API diameter of 60 mm or an annual growth rate of 6 mm.8,9 Although open repair is still the gold standard, there are considerable surgical complications depending on the extent of repair required. Complications after the surgery include myocardial infarction, arrhythmia, stroke, paralysis, and kidney dysfunction.10 Thoracic endovascular aneurysm repair (TEVAR) is now considered a suitable alternative to open repair in many cases.11,12 Potential benefits of TEVAR include smaller incisions, elimination of aortic cross clamping, less blood loss, lower incidence of visceral, renal, and spinal cord ischemia, and quicker recovery.13 Aortic dissection is another life-threatening complication with very few noticeable signs and symptoms. The most evident distinction is a ripping sensation that causes the sudden onset of excruciating pain.14 Depending on where the dissection occurs, the pain will be localized in different areas of the body. If the dissection is type A, the pain is centered in the chest and spreads to the upper back. If the dissection is in the abdominal aorta, the pain will be centered in the lower back and spreads to the flanks.14 The presentations of aortic dissection can be very similar to the symptoms of other heart-related problems, such as myocardial infarction. These presentations are all variable, making the diagnosis challenging. The key symptom is the sudden onset of chest or back pain, which is a transient intrathoracic tearing sensation irradiating toward the lumbar region. Other concurrent symptoms may include syncope, shortness of breath, paraplegia, acute peripheral ischemia, and hemiplegia. Coma may also be a manifestation.15 The dissection location and affected branches would determine the end-organ ischemia, which can be in a form of stroke, limb ischemia, renal failure, or paraplegia.16 Death can also be caused by intrapericardial or intrapleural ruptures and acute aortic insufficiency leading to cardiac tamponade, hemothorax, and cardiogenic shock, respectively.17
Case reports 1034.e11
Although acute type A aortic dissection represents a surgical emergency requiring immediate repair, most uncomplicated type B dissections can be managed medically.18 In comparison to open repair, if feasible, endovascular repair is less invasive with faster recovery.12 Our patient presented with a large TAA along with extensive type A dissection that compressed the bilateral brachiocephalic veins resulting in severe bilateral upper extremity and facial edema. The aneurysm was large enough to cause right mediastinal shift resulting in intermittent dysphagia and cough. Large TAA is an unusual cause for upper extremity and facial edema and very rarely leads to dysphagia and cough.19 Management of such complication is not only very challenging but usually requires multidisciplinary approach that might include palliative intervention.20 Our patient refused treatment and unfortunately expired because of complications related to his enlarging TAA.
REFERENCES 1. Hiratzka LF, Bakris GL, Beckman JA, et al. 2010 ACCF/ AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with thoracic aortic disease: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine. Circulation 2010;121: e266. 2. Pressler V, McNamara JJ. Aneurysm of the thoracic aorta. Review of 260 cases. J Thorac Cardiovasc Surg 1985;89: 50e4. 3. Elefteriades JA. Thoracic aortic aneurysm: current approach to surgical timing. ACC Curr J Rev 2002;11:82e8. 4. Teixido MT, Leonetti JP. Recurrent laryngeal nerve paralysis associated with thoracic aortic aneurysm. Otolaryngol Head Neck Surg 1990;102:140e4. 5. Zhang Y. Encyclopedia of Global Health, Volume 1. Sage Publications, 2008. pp 137e8. 6. Johansson G, Markstrom U, Swedenborg J. Ruptured thoracic aortic aneurysms: a study of incidence and mortality rates. J Vasc Surg 1995;21:985e8. 7. Nuenninghoff DM, Hunder GG, Christianson TJ, et al. Incidence and predictors of large-artery complication (aortic aneurysm, aortic dissection, and/or large-artery stenosis) in patients with giant cell arteritis: a population-based study over 50 years. Arthritis Rheum 2003;48:3522. 8. Lobato AC, Puech-Le~ao P. Predictive factors for rupture of thoracoabdominal aortic aneurysm. J Vasc Surg 1998;27: 446e53. 9. Davies RR, Goldstein LJ, Coady MA, et al. Yearly rupture or dissection rates for thoracic aortic aneurysms: simple prediction based on size. Ann Thorac Surg 2002;73:17.
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10. Budillon AM, Nicolini F, Beghi C, et al. Surgical repair of thoracic aortic aneurysms: results and complications. Acta Biomed Ateneo Parmense 2001;72:33e43. 11. Matsumura JS, Cambria RP, Dake MD, et al. International controlled clinical trial of thoracic endovascular aneurysm repair with the Zenith TX2 endovascular graft: 1-year results. J Vasc Surg 2008;47:247. 12. Makaroun MS, Dillavou ED, Wheatley GH, et al. Five-year results of endovascular treatment with the Gore TAG device compared with open repair of thoracic aortic aneurysms. J Vasc Surg 2008;47:912. 13. Greenberg RK, Lu Q, Roselli EE, et al. Contemporary analysis of descending thoracic and thoracoabdominal aneurysm repair: a comparison of endovascular and open techniques. Circulation 2008;118:808. 14. Juang D, Braverman AC, Eagle K. Aortic dissection. Circulation 2008;118:e507e10.
Annals of Vascular Surgery
15. Rogers FB, Osler TM, Shackford SR. Aortic dissection after trauma: case report and review of the literature. J Trauma 1996;41:906e8. 16. Hebballi R, Swanevelder J. Diagnosis and management of aortic dissection. Contin Educ Anaesth Crit Care Pain 2009;9: 14e8. 17. Elefteriades JA. Thoracic aortic aneurysm: reading the enemy’s playbook. Curr Probl Cardiol 2008;33:203e77. 18. Suzuki T, Mehta RH, Ince H, et al. Clinical profiles and outcomes of acute type B aortic dissection in the current era: lessons from the International Registry of Aortic Dissection (IRAD). Circulation 2003;108(Suppl 1):II312. 19. Hiller HG, Lagattolla NRF. Thoracic aortic aneurysm presenting with dysphagia: a fatal delay in diagnosis. Thorac Surg Sci 2007;4. Doc01. 20. Tsai TT, Nienaber CA, Eagle KA. Acute aortic syndromes. Circulation 2005;112:3802.
