Acquired Post-Traumatic Aortic Coarctation Presenting as New-Onset Congestive Heart Failure: Treatment with Endovascular Repair Norris B. Thompson,1 Alireza Hamidian Jahromi,2 David H. Ballard,1 Vyas R. Rao,2 and Navdeep S. Samra,2 Shreveport, Louisiana
Acquired coarctation of the thoracic aorta is a rare phenomenon in adults. The etiology is often idiopathic, but severe stenosis can develop from prior surgery, blunt thoracic aortic injuries, or severe atherosclerotic/atheroembolic disease. Common symptomatic presentations include refractory upper extremity hypertension and new-onset congestive heart failure. We present the case of a 52-year-old man who developed acquired thoracic aortic coarctation 30 years after a blunt trauma and deceleration injuries to the aorta requiring open surgical aortic repair. He presented with poorly controlled hypertension and new-onset heart failure and was treated surgically with endovascular repair.
Thoracic coarctation (narrowing) of the aorta (TCA) is typically a congenital anomaly presenting during infancy or childhood; however, it occasionally goes undiagnosed and presents during adulthood. Acquired aortic coarctation, aortic coarctation secondary to traumatic etiologies, aortic surgeries, and severe atherosclerotic/atheroembolic disease is much more uncommon but has been reported after blunt or penetrating thoracic injuries.1 Nonetheless, the clinical presentation remains unchanged regardless of the etiology and includes refractory upper extremity hypertension, congestive heart failure, delayed femoral pulses, significant systolic and diastolic pressure gradient between the
Disclosures: All authors claim no conflicts of interest or disclosures. 1 School of Medicine, Louisiana State University Health-Shreveport, Shreveport, LA. 2 Department of Surgery, Louisiana State University HealthShreveport, Shreveport, LA. Correspondence to: Navdeep S. Samra, MD, Division of Trauma and Critical Care Surgery, Department of Surgery, Louisiana State University Health Shreveport, 1501 Kings Highway, Shreveport, LA 71130, USA; E-mail: [email protected] Ann Vasc Surg 2015; 29: 838.e11e838.e15 http://dx.doi.org/10.1016/j.avsg.2014.11.016 Ó 2015 Elsevier Inc. All rights reserved. Manuscript received: September 17, 2014; manuscript accepted: November 7, 2014; published online: February 12, 2015.
upper and lower extremities, and premature and/or sudden death. With a mean life expectancy of 35 years and 90% of cases resulting in death by age 50 years, the life expectancy of patients with TCA is greatly reduced compared with the normal population.2 Surgery, successfully used since 1945, is accepted as the gold standard for long-term management of aortic coarctation.3,4 Enduring and progressive improvements in symptom recognition, patient selection, postoperative complications, and surgical techniques have maintained a linear trajectory.4 The first notable surgical coarctation correction technique was reported by Crafoord and Nylin in 1945, when they successfully performed resection with end-to-end anastomosis of the coarctation segment of the aorta in 2 cases with TCA.5 Later advances introduced the subclavian flap aortoplasty, percutaneous balloon angioplasty in 1982, and the vastly used expandable endovascular stents.6
CASE REPORT A 52-year-old white man presented to the emergency department with a 3-day history of progressive newonset shortness of breath. His medical and surgical history was remarkable for poorly controlled hypertension despite maximal doses of 3 different antihypertensives, and 30 years earlier, a deceleration polytrauma from a 838.e11
838.e12 Case reports
Annals of Vascular Surgery
Fig. 1. (A) Axial computed tomography showing concentric stenosis of the thoracic aorta (arrow). (B) Three-dimensional reconstruction showing a significant
defect/area of stenosis in the descending thoracic aorta. Arrowheads show proximal and distal borders of the stenosed area.
motor vehicle collision. This deceleration polytrauma resulted in a thoracic aortic injury and ischemic bowel, which required an urgent open aortic surgical repair (details of the previous operation were unknown to us) and a partial colectomy with end colostomy. The patient underwent a colostomy take down and reanastomosis of the bowel at a later date. Physical examination revealed the right and left brachial blood pressures of 198/90 mm Hg and 198/ 88 mm Hg, and the lower limb blood pressures were 70/40 mm Hg (right) and 70/30 mm Hg (left), respectively. Other notable findings included a holosystolic murmur best heard in the fifth left intercostal space at the midclavicular line that radiated to the back, bibasilar crackles, strong radial pulses, and very weak dorsalis pedis pulses. An electrocardiogram demonstrated normal sinus rhythm with nonspecific T-wave abnormalities. Hematologic profile was normal, and on serial examinations, troponin and cardiac enzymes were not raised. The brain natriuretic peptide was markedly elevated at 1394 pg/mL (normal range, 0.5e30 pg/mL), and on metabolic panel evaluation, patient was found to have a prerenal azotemia (blood urea nitrogen of 95 mg/dL [normal 7e 18 mg/dL] and creatinine of 1.3 mg/dL [normal 0.6e 1.2 mg/dL]). A chest X-ray was unremarkable, but computed tomography (CT) and CT angiography scans revealed calcifications in the proximal descending thoracic aorta causing significant concentric stenosis (Fig. 1). The distal aorta, iliofemoral arteries, and their distal arterial branches were all patent. Transesophageal echocardiogram revealed concentric left ventricular hypertrophy with diastolic dysfunction, minimal mitral and tricuspid valve regurgitation, and moderate aortic root dilatation (4.1 cm). There was no aortic regurgitation and the ejection fraction was estimated to be 55e60%.
Surgical Intervention The patient was taken to the operating room with the presumptive diagnosis of a TCA with the aim of performing an endovascular repair of the stenosed segment of the descending aorta (patient did not want an open surgery and was only agreeable to that in case the endovascular repair will fail). The right femoral artery, which appeared much smaller than expected considering the patient size, had no palpable pulse and was cannulated using ultrasound guidance. Although the femoral artery pressure was only 70/50 mm Hg at the time of the procedure, the radial blood pressure was 150/70 mm Hg. Under fluoroscopic guidance, a guidewire was advanced through the femoral artery to the midthoracic aorta. Subsequently, a 9-Fr sheath was advanced over the guidewire. Resistance was encountered at the stenosed region of the midthoracic aorta. A glide catheter was placed over the guidewire and successfully navigated past this stenosed area. A Lunderquist wire (Cook Medical, Bloomington, IN) was inserted, and its tip was advanced to the proximal ascending aortal. At this time, the left femoral artery was cannulated and a glide wire was introduced through the left femoral artery and through the sheath into the aorta to maneuver it through the proximal thoracic aorta. In this stage, an intravascular ultrasound device (Volcano Co., San Diego, CA) was introduced into the left femoral artery and advanced to the thoracic aorta. The proximal aorta’s diameter was measured at 28 mm and the distal at 22 mm. The length of the stenotic area was approximately 10 mm. A Valiant 28 10 mm2 thoracic aortic graft (Medtronic Vascular, Santa Rosa, CA) was prepared and mounted on its delivery system. After removal of the intravascular ultrasound, the graft was introduced and advanced beyond the area of stenosis. It was positioned so that the graft’s edge was inferior to the subclavian
Vol. 29, No. 4, May 2015
artery, and its body was extended beyond the borders of the stenosis. After achieving the optimal position, the device was unfurrowed. The graft opened without incident, but the center of the graft appeared to be narrowed relative to the proximal and distal portions (due to the external pressure of the stenotic segment). For this reason, the decision was made to balloon dilate the graft. A Reliant balloon (Medtronic Vascular, Santa Rosa, CA) was passed over the stiff wire and placed into position. Before dilatation, the pressure in the radial artery was 150/70 mm Hg and the pressure in the femoral artery was 70/50 mm Hg. We then dilated the Reliant balloon at the proximal end of the Valiant thoracic aortic graft, the midportion, and finally, the distal aspect. At this time, the pressure in the radial artery dropped to 119/ 60 mm Hg; however, the pressure in the femoral artery remained approximately 70/50 mm Hg. With a pressure gradient still present, it was decided to remove the Reliant balloon and use a noncompliant balloon. A #16 size Siemen balloon (Siemens, Munich, Bavaria) was initially passed into the thoracic aortic graft through the right femoral artery on top of the Lunderquist wire. After dilatation, the gradient reduced to approximately 30 mm Hg with the proximal radial systolic pressure at 110 mm Hg and the femoral artery systolic pressure at approximately 80 mm Hg. The balloon was gradually upsized up to a 20 size, which resulted in a gradient reduction of 12 mm Hg; the radial artery demonstrated a systolic pressure of approximately 106 mm Hg and the femoral artery was 89e94 systolic with a mean gradient difference of approximately 8 mm Hg. The narrowing of the midportion of the graft appeared minimal, and the balloon was removed to perform an angiogram. A pigtail catheter was passed over the stiff wire, and the wire was subsequently removed to inject the dye through the pigtail at the aortic arch. The angiogram demonstrated a smooth curve in the midthoracic aorta and the narrowing, which had opened to approximately 80e90% of the expected diameter of the lumen (Fig. 2). As the graft was nicely positioned and already deployed, the midportion narrowing was minimal with an acceptable pressure gradient, we opted not to exchange the graft and/or use a large balloon-expandable stent. Good flow was appreciated from the proximal to distal aorta with almost complete reduction in proximal hypertension. After a riskebenefit analysis of further intervention, it was concluded that more intervention would risk tearing of the artery, and this 80e90% resolution of the stenosis was accepted. After removing the catheter, good femoral artery pulsation was appreciated distal to the insertion site. After the procedure, the patient had an unremarkable recovery. The patient was doing well at 1, 3, and 6 month clinical follow-up with resolution of both congestive heart failure symptoms and refractory hypertension. A 1-month follow-up, CT scan showed the narrowest portion of the graft at 1.51 cm (Fig. 3); a 6-month CT showed similar findings with the same graft diameter.
Case reports 838.e13
Fig. 2. Intraoperative aortogram after balloon dilatation of the stenosed midportion of the graft (arrows).
DISCUSSION Blunt thoracic aortic injuries (BTAIs) from motor vehicle collision or fall from a height (deceleration injuries) are among the most common causes of death in the United States. Up to 90% of those with blunt aortic trauma die at the scene and nearly half of those who survive the initial injury live through the initial hospital admission.7 The current treatment of BTAI is immediate endovascular repair. The most well-documented long-term complication after endovascular repair of a BTAI is aortic dilatation. This known complication can be followed with serial CT scans.8 Our patient had open surgical repair of BTAI, and 30 years later, developed symptomatic acquired aortic coarctation. Adult-onset aortic coarctation is rare, often idiopathic, and often amendable to endovascular stenting.9 We are currently lacking long-term data on durability of endovascular repair for adult-onset aortic coarctation from large studies. Acquired aortic coarctation after aortic surgeries has been reported.10 Rangasetty et al.11 reported a similar case in which a patient who had a motor vehicle collision 30 years before presented with a new-onset congestive heart failure. The imaging and clinical findings were consistent with pseudoaneurysm and acquired coarctation of the thoracic aorta at the aortic isthmus. The authors elected to bypass the stenosed segment, which were successful.11 Surgery is considered the treatment of choice for coarctation, but it is not curative.4 Therefore, regular screening for coarctation recurrence manifested
838.e14 Case reports
Annals of Vascular Surgery
Fig. 3. (A) Postoperative axial computed tomography showing the narrowest portion of the graft (arrow); the endoluminal diameter measured 1.51 cm. (B) Three-
dimensional reconstruction showing the proximal and distal extents of the graft (arrowheads).
by a systolic blood pressure gradient is essential. It is recommended that pressure gradients between the upper and lower extremities be measured and documented during each visit via a large cuff and auscultation of the brachial and popliteal arteries. If a systolic gradient greater than 20 mm Hg is discovered, reinvestigation for a possible recoarctation should begin. A multiple detector CT scan with contrast and or an magnetic resonance imaging strengthened with velocity vector mapping has been proposed for the radiologic evaluation of these cases.12e14 In a large retrospective study, Brown et al. reviewed the patients undergoing surgical repair of the aortic coarctation and suggested that preoperative hypertension had no association with late hypertension. Furthermore, the presence and degree of the native hypertension had no bearing on postoperative prognosis.12 However, some authors have linked the postoperative hypertension, especially high systolic pressures, directly to the risk of death in the patients.15 Although blood pressure monitoring may have surveillance values in the patients, it is considered as a preventive measure for recoarctation and the risk of death as well. It is paramount that patients, who use tobacco, be strongly encouraged to undergo a cessation plan and all patients adopt behaviors that reduce their risk of vascular disease. In conclusion, acquired coarctation of the thoracic aorta is rare in adults, but it can develop after prior aortic surgeries, BTAIs, or severe atherosclerotic/atheroembolic disease. In patients who are at risk for developing acquired coarctation of the thoracic aorta and present with
refractory upper extremity hypertension and or new-onset congestive heart failure radiologic, evaluation for possible acquired coarctation of the thoracic aorta is essential and diagnosis requires a high index of suspicion. Our case demonstrates that acquired post-traumatic coarctation of the thoracic aorta can be safely managed using endovascular repair.
The authors would like to thank Mr. John Cyrus who provided us editorial assistance.
REFERENCES 1. Kinley CE, Chandler BM. Traumatic aneurysm of thoracic aorta: a case presenting as a coarctation. Can Med Assoc J 1967;96:279e81. 2. Brown JW, Ruzmetov M, Hoyer MH, et al. Recurrent coarctation: is surgical repair of recurrent coarctation of the aorta safe and effective? Ann Thorac Surg 2009;88:1923e31. 3. Corno AF, Botta U, Hurni M, et al. Surgery for aortic coarctation: a 30 years experience. Eur J Cardiothorac Surg 2001;20:1202e6. 4. Simon AB, Zloto AE. Coarctation of the aorta. Longitudinal assessment of operated patients. Circulation 1974;50: 456e64. 5. Crafoord C, Nylin G. Congenital coarctation of the aorta and its surgical treatment. J Thorac Surg 1945;14:347e61. 6. Jenkins NP, Ward C. Coarctation of the aorta: natural history and outcome after surgical treatment. QJM 1999;92: 365e71. 7. Schulman CI, Carvajal D, Lopez PP, et al. Incidence and crash mechanisms of aortic injury during the past decade. J Trauma 2007;62:664e7. 8. Forbes TL, Harris JR, Lawlor DK, et al. Aortic dilatation after endovascular repair of blunt traumatic thoracic aortic injuries. J Vasc Surg 2010;52:45e8.
Vol. 29, No. 4, May 2015
9. Malebranche AD, McPherson T. Aortic coarctation in a 49year-old female. BCMJ 2014;56:278e81. 10. Starc TJ, Abramson SJ, Bierman FZ, et al. Acquired coarctation of the aorta. Pediatr Cardiol 1992;13:33e6. 11. Rangasetty UC, Raza S, Lick S, et al. Chronic pseudoaneurysm and coarctation of the aorta: a rare delayed complication of trauma. Tex Heart Inst J 2006;33:368e70. 12. Brown ML, Burkhart HM, Connolly HM, et al. Coarctation of the aorta: lifelong surveillance is mandatory following surgical repair. J Am Coll Cardiol 2013;62:1020e5.
Case reports 838.e15
13. Freeman LA, Young PM, Foley TA, et al. CT and MRI assessment of the aortic root and ascending aorta. AJR Am J Roentgenol 2013;200:W581e92. 14. Bogren HG, Mohiaddin RH, Yang GZ, et al. Magnetic resonance velocity vector mapping of blood flow in thoracic aortic aneurysms and grafts. J Thorac Cardiovasc Surg 1995;110:704e14. 15. Cohen M, Fuster V, Steele PM, et al. Coarctation of the aorta. Long-term follow-up and prediction of outcome after surgical correction. Circulation 1989;80:840e5.
Acquired coarctation of the thoracic aorta is a rare phenomenon in adults. The etiology is often idiopathic, but severe stenosis can develop from prior surgery, blunt thoracic aortic injuries, or severe atherosclerotic/atheroembolic disease. Common symptomatic presentations include refractory upper extremity hypertension and new-onset congestive heart failure. We present the case of a 52-year-old man who developed acquired thoracic aortic coarctation 30 years after a blunt trauma and deceleration injuries to the aorta requiring open surgical aortic repair. He presented with poorly controlled hypertension and new-onset heart failure and was treated surgically with endovascular repair.
Thoracic coarctation (narrowing) of the aorta (TCA) is typically a congenital anomaly presenting during infancy or childhood; however, it occasionally goes undiagnosed and presents during adulthood. Acquired aortic coarctation, aortic coarctation secondary to traumatic etiologies, aortic surgeries, and severe atherosclerotic/atheroembolic disease is much more uncommon but has been reported after blunt or penetrating thoracic injuries.1 Nonetheless, the clinical presentation remains unchanged regardless of the etiology and includes refractory upper extremity hypertension, congestive heart failure, delayed femoral pulses, significant systolic and diastolic pressure gradient between the
Disclosures: All authors claim no conflicts of interest or disclosures. 1 School of Medicine, Louisiana State University Health-Shreveport, Shreveport, LA. 2 Department of Surgery, Louisiana State University HealthShreveport, Shreveport, LA. Correspondence to: Navdeep S. Samra, MD, Division of Trauma and Critical Care Surgery, Department of Surgery, Louisiana State University Health Shreveport, 1501 Kings Highway, Shreveport, LA 71130, USA; E-mail: [email protected] Ann Vasc Surg 2015; 29: 838.e11e838.e15 http://dx.doi.org/10.1016/j.avsg.2014.11.016 Ó 2015 Elsevier Inc. All rights reserved. Manuscript received: September 17, 2014; manuscript accepted: November 7, 2014; published online: February 12, 2015.
upper and lower extremities, and premature and/or sudden death. With a mean life expectancy of 35 years and 90% of cases resulting in death by age 50 years, the life expectancy of patients with TCA is greatly reduced compared with the normal population.2 Surgery, successfully used since 1945, is accepted as the gold standard for long-term management of aortic coarctation.3,4 Enduring and progressive improvements in symptom recognition, patient selection, postoperative complications, and surgical techniques have maintained a linear trajectory.4 The first notable surgical coarctation correction technique was reported by Crafoord and Nylin in 1945, when they successfully performed resection with end-to-end anastomosis of the coarctation segment of the aorta in 2 cases with TCA.5 Later advances introduced the subclavian flap aortoplasty, percutaneous balloon angioplasty in 1982, and the vastly used expandable endovascular stents.6
CASE REPORT A 52-year-old white man presented to the emergency department with a 3-day history of progressive newonset shortness of breath. His medical and surgical history was remarkable for poorly controlled hypertension despite maximal doses of 3 different antihypertensives, and 30 years earlier, a deceleration polytrauma from a 838.e11
838.e12 Case reports
Annals of Vascular Surgery
Fig. 1. (A) Axial computed tomography showing concentric stenosis of the thoracic aorta (arrow). (B) Three-dimensional reconstruction showing a significant
defect/area of stenosis in the descending thoracic aorta. Arrowheads show proximal and distal borders of the stenosed area.
motor vehicle collision. This deceleration polytrauma resulted in a thoracic aortic injury and ischemic bowel, which required an urgent open aortic surgical repair (details of the previous operation were unknown to us) and a partial colectomy with end colostomy. The patient underwent a colostomy take down and reanastomosis of the bowel at a later date. Physical examination revealed the right and left brachial blood pressures of 198/90 mm Hg and 198/ 88 mm Hg, and the lower limb blood pressures were 70/40 mm Hg (right) and 70/30 mm Hg (left), respectively. Other notable findings included a holosystolic murmur best heard in the fifth left intercostal space at the midclavicular line that radiated to the back, bibasilar crackles, strong radial pulses, and very weak dorsalis pedis pulses. An electrocardiogram demonstrated normal sinus rhythm with nonspecific T-wave abnormalities. Hematologic profile was normal, and on serial examinations, troponin and cardiac enzymes were not raised. The brain natriuretic peptide was markedly elevated at 1394 pg/mL (normal range, 0.5e30 pg/mL), and on metabolic panel evaluation, patient was found to have a prerenal azotemia (blood urea nitrogen of 95 mg/dL [normal 7e 18 mg/dL] and creatinine of 1.3 mg/dL [normal 0.6e 1.2 mg/dL]). A chest X-ray was unremarkable, but computed tomography (CT) and CT angiography scans revealed calcifications in the proximal descending thoracic aorta causing significant concentric stenosis (Fig. 1). The distal aorta, iliofemoral arteries, and their distal arterial branches were all patent. Transesophageal echocardiogram revealed concentric left ventricular hypertrophy with diastolic dysfunction, minimal mitral and tricuspid valve regurgitation, and moderate aortic root dilatation (4.1 cm). There was no aortic regurgitation and the ejection fraction was estimated to be 55e60%.
Surgical Intervention The patient was taken to the operating room with the presumptive diagnosis of a TCA with the aim of performing an endovascular repair of the stenosed segment of the descending aorta (patient did not want an open surgery and was only agreeable to that in case the endovascular repair will fail). The right femoral artery, which appeared much smaller than expected considering the patient size, had no palpable pulse and was cannulated using ultrasound guidance. Although the femoral artery pressure was only 70/50 mm Hg at the time of the procedure, the radial blood pressure was 150/70 mm Hg. Under fluoroscopic guidance, a guidewire was advanced through the femoral artery to the midthoracic aorta. Subsequently, a 9-Fr sheath was advanced over the guidewire. Resistance was encountered at the stenosed region of the midthoracic aorta. A glide catheter was placed over the guidewire and successfully navigated past this stenosed area. A Lunderquist wire (Cook Medical, Bloomington, IN) was inserted, and its tip was advanced to the proximal ascending aortal. At this time, the left femoral artery was cannulated and a glide wire was introduced through the left femoral artery and through the sheath into the aorta to maneuver it through the proximal thoracic aorta. In this stage, an intravascular ultrasound device (Volcano Co., San Diego, CA) was introduced into the left femoral artery and advanced to the thoracic aorta. The proximal aorta’s diameter was measured at 28 mm and the distal at 22 mm. The length of the stenotic area was approximately 10 mm. A Valiant 28 10 mm2 thoracic aortic graft (Medtronic Vascular, Santa Rosa, CA) was prepared and mounted on its delivery system. After removal of the intravascular ultrasound, the graft was introduced and advanced beyond the area of stenosis. It was positioned so that the graft’s edge was inferior to the subclavian
Vol. 29, No. 4, May 2015
artery, and its body was extended beyond the borders of the stenosis. After achieving the optimal position, the device was unfurrowed. The graft opened without incident, but the center of the graft appeared to be narrowed relative to the proximal and distal portions (due to the external pressure of the stenotic segment). For this reason, the decision was made to balloon dilate the graft. A Reliant balloon (Medtronic Vascular, Santa Rosa, CA) was passed over the stiff wire and placed into position. Before dilatation, the pressure in the radial artery was 150/70 mm Hg and the pressure in the femoral artery was 70/50 mm Hg. We then dilated the Reliant balloon at the proximal end of the Valiant thoracic aortic graft, the midportion, and finally, the distal aspect. At this time, the pressure in the radial artery dropped to 119/ 60 mm Hg; however, the pressure in the femoral artery remained approximately 70/50 mm Hg. With a pressure gradient still present, it was decided to remove the Reliant balloon and use a noncompliant balloon. A #16 size Siemen balloon (Siemens, Munich, Bavaria) was initially passed into the thoracic aortic graft through the right femoral artery on top of the Lunderquist wire. After dilatation, the gradient reduced to approximately 30 mm Hg with the proximal radial systolic pressure at 110 mm Hg and the femoral artery systolic pressure at approximately 80 mm Hg. The balloon was gradually upsized up to a 20 size, which resulted in a gradient reduction of 12 mm Hg; the radial artery demonstrated a systolic pressure of approximately 106 mm Hg and the femoral artery was 89e94 systolic with a mean gradient difference of approximately 8 mm Hg. The narrowing of the midportion of the graft appeared minimal, and the balloon was removed to perform an angiogram. A pigtail catheter was passed over the stiff wire, and the wire was subsequently removed to inject the dye through the pigtail at the aortic arch. The angiogram demonstrated a smooth curve in the midthoracic aorta and the narrowing, which had opened to approximately 80e90% of the expected diameter of the lumen (Fig. 2). As the graft was nicely positioned and already deployed, the midportion narrowing was minimal with an acceptable pressure gradient, we opted not to exchange the graft and/or use a large balloon-expandable stent. Good flow was appreciated from the proximal to distal aorta with almost complete reduction in proximal hypertension. After a riskebenefit analysis of further intervention, it was concluded that more intervention would risk tearing of the artery, and this 80e90% resolution of the stenosis was accepted. After removing the catheter, good femoral artery pulsation was appreciated distal to the insertion site. After the procedure, the patient had an unremarkable recovery. The patient was doing well at 1, 3, and 6 month clinical follow-up with resolution of both congestive heart failure symptoms and refractory hypertension. A 1-month follow-up, CT scan showed the narrowest portion of the graft at 1.51 cm (Fig. 3); a 6-month CT showed similar findings with the same graft diameter.
Case reports 838.e13
Fig. 2. Intraoperative aortogram after balloon dilatation of the stenosed midportion of the graft (arrows).
DISCUSSION Blunt thoracic aortic injuries (BTAIs) from motor vehicle collision or fall from a height (deceleration injuries) are among the most common causes of death in the United States. Up to 90% of those with blunt aortic trauma die at the scene and nearly half of those who survive the initial injury live through the initial hospital admission.7 The current treatment of BTAI is immediate endovascular repair. The most well-documented long-term complication after endovascular repair of a BTAI is aortic dilatation. This known complication can be followed with serial CT scans.8 Our patient had open surgical repair of BTAI, and 30 years later, developed symptomatic acquired aortic coarctation. Adult-onset aortic coarctation is rare, often idiopathic, and often amendable to endovascular stenting.9 We are currently lacking long-term data on durability of endovascular repair for adult-onset aortic coarctation from large studies. Acquired aortic coarctation after aortic surgeries has been reported.10 Rangasetty et al.11 reported a similar case in which a patient who had a motor vehicle collision 30 years before presented with a new-onset congestive heart failure. The imaging and clinical findings were consistent with pseudoaneurysm and acquired coarctation of the thoracic aorta at the aortic isthmus. The authors elected to bypass the stenosed segment, which were successful.11 Surgery is considered the treatment of choice for coarctation, but it is not curative.4 Therefore, regular screening for coarctation recurrence manifested
838.e14 Case reports
Annals of Vascular Surgery
Fig. 3. (A) Postoperative axial computed tomography showing the narrowest portion of the graft (arrow); the endoluminal diameter measured 1.51 cm. (B) Three-
dimensional reconstruction showing the proximal and distal extents of the graft (arrowheads).
by a systolic blood pressure gradient is essential. It is recommended that pressure gradients between the upper and lower extremities be measured and documented during each visit via a large cuff and auscultation of the brachial and popliteal arteries. If a systolic gradient greater than 20 mm Hg is discovered, reinvestigation for a possible recoarctation should begin. A multiple detector CT scan with contrast and or an magnetic resonance imaging strengthened with velocity vector mapping has been proposed for the radiologic evaluation of these cases.12e14 In a large retrospective study, Brown et al. reviewed the patients undergoing surgical repair of the aortic coarctation and suggested that preoperative hypertension had no association with late hypertension. Furthermore, the presence and degree of the native hypertension had no bearing on postoperative prognosis.12 However, some authors have linked the postoperative hypertension, especially high systolic pressures, directly to the risk of death in the patients.15 Although blood pressure monitoring may have surveillance values in the patients, it is considered as a preventive measure for recoarctation and the risk of death as well. It is paramount that patients, who use tobacco, be strongly encouraged to undergo a cessation plan and all patients adopt behaviors that reduce their risk of vascular disease. In conclusion, acquired coarctation of the thoracic aorta is rare in adults, but it can develop after prior aortic surgeries, BTAIs, or severe atherosclerotic/atheroembolic disease. In patients who are at risk for developing acquired coarctation of the thoracic aorta and present with
refractory upper extremity hypertension and or new-onset congestive heart failure radiologic, evaluation for possible acquired coarctation of the thoracic aorta is essential and diagnosis requires a high index of suspicion. Our case demonstrates that acquired post-traumatic coarctation of the thoracic aorta can be safely managed using endovascular repair.
The authors would like to thank Mr. John Cyrus who provided us editorial assistance.
REFERENCES 1. Kinley CE, Chandler BM. Traumatic aneurysm of thoracic aorta: a case presenting as a coarctation. Can Med Assoc J 1967;96:279e81. 2. Brown JW, Ruzmetov M, Hoyer MH, et al. Recurrent coarctation: is surgical repair of recurrent coarctation of the aorta safe and effective? Ann Thorac Surg 2009;88:1923e31. 3. Corno AF, Botta U, Hurni M, et al. Surgery for aortic coarctation: a 30 years experience. Eur J Cardiothorac Surg 2001;20:1202e6. 4. Simon AB, Zloto AE. Coarctation of the aorta. Longitudinal assessment of operated patients. Circulation 1974;50: 456e64. 5. Crafoord C, Nylin G. Congenital coarctation of the aorta and its surgical treatment. J Thorac Surg 1945;14:347e61. 6. Jenkins NP, Ward C. Coarctation of the aorta: natural history and outcome after surgical treatment. QJM 1999;92: 365e71. 7. Schulman CI, Carvajal D, Lopez PP, et al. Incidence and crash mechanisms of aortic injury during the past decade. J Trauma 2007;62:664e7. 8. Forbes TL, Harris JR, Lawlor DK, et al. Aortic dilatation after endovascular repair of blunt traumatic thoracic aortic injuries. J Vasc Surg 2010;52:45e8.
Vol. 29, No. 4, May 2015
9. Malebranche AD, McPherson T. Aortic coarctation in a 49year-old female. BCMJ 2014;56:278e81. 10. Starc TJ, Abramson SJ, Bierman FZ, et al. Acquired coarctation of the aorta. Pediatr Cardiol 1992;13:33e6. 11. Rangasetty UC, Raza S, Lick S, et al. Chronic pseudoaneurysm and coarctation of the aorta: a rare delayed complication of trauma. Tex Heart Inst J 2006;33:368e70. 12. Brown ML, Burkhart HM, Connolly HM, et al. Coarctation of the aorta: lifelong surveillance is mandatory following surgical repair. J Am Coll Cardiol 2013;62:1020e5.
Case reports 838.e15
13. Freeman LA, Young PM, Foley TA, et al. CT and MRI assessment of the aortic root and ascending aorta. AJR Am J Roentgenol 2013;200:W581e92. 14. Bogren HG, Mohiaddin RH, Yang GZ, et al. Magnetic resonance velocity vector mapping of blood flow in thoracic aortic aneurysms and grafts. J Thorac Cardiovasc Surg 1995;110:704e14. 15. Cohen M, Fuster V, Steele PM, et al. Coarctation of the aorta. Long-term follow-up and prediction of outcome after surgical correction. Circulation 1989;80:840e5.
