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A Hanging Mass in the Ascending Aorta Diagnosed by Transthoracic Echocardiography in a Totally Asymptomatic Subject
A Hanging Mass in the Ascending Aorta Diagnosed by Transthoracic Echocardiography in a Totally Asymptomatic Subject Umberto Baldini, MD, Francesca Chiaramonti, MD, Gaetano Minzioni, MD, and Michele Galli, MD, Livorno and Pisa, Italy
Aortic mural thrombosis is generally associated with several diseases, including coagulopathies, aortic dissection or trauma, tumors, and complicated atherosclerotic plaques. The development of a friable mobile thrombus, especially in the ascending aorta or proximal aortic arch, is a rare event with potentially ominous consequences because of a life-threatening risk of stroke and peripheral embolization. The treatment of choice of this condition is still controversial. We report a case of an absolutely asymptomatic 57-year-old patient with a mobile, pedunculated mass attached to the posterior wall of an otherwise normal ascending aorta. The aortic mass, identified by transthoracic echocardiography, was surgically removed and demonstrated to be a thrombus, and the aortic wall specimen was microscopically normal. (J Am Soc Echocardiogr 2009;22:1197.e5-1197.e7.) Keywords: Ascending aorta, Echocardiography, Surgery, Thrombosis
Sessile masses in the ascending aorta are infrequent, and most of the cases are found at autopsy. Aortic tumors involving the intima and growing into the vessel lumen are unusual.1-4 Rare also is the occurrence of a mobile aortic thrombi in the ascending aorta or the arch,5-12,17 generally originated from complicated atherosclerotic plaques. The development of a friable mobile thrombus, especially in the ascending aorta or the proximal aortic arch, may cause ominous consequences, and once the diagnosis is established, treatment is mandatory. We report a case of a mobile aortic mass found in an otherwise asymptomatic subject undergoing transthoracic echocardiography for screening evaluation; the mass, surgically removed, proved to be a mobile thrombus attached to an nonaneurysmal ascending aorta, in the absence of significant atherosclerotic disease. CASE REPORT In September 2007, a 57-year-old man underwent transthoracic echocardiography in the laboratory of Livorno Hospital Cardiology Division. Three years earlier, the patient had received the diagnosis of non-Hodgkin’s lymphoma, with a complete remission after induction and consolidation chemotherapy with the cyclophosphamide, doxorubicin (Adriamycin, Bedford Laboratories, Bedford, OH), vincristine, prednisone, and rituxan regimen; in addition, he had received recombinant human granulocyte colony-stimulating factor (rhG-CSF) and thoracic radiation. Any cancer treatment was discontinued in August 2005. He had no history of opportunistic infections, and his medFrom the Cardiology Division, Spedali Riuniti, Livorno, Italy (U.B., M.G.); and Heart Surgery Department, Cisanello Hospital and University of Pisa, Pisa, Italy (F.C., G.M.). Reprint requests: Umberto Baldini, MD, Cardiology Division, Spedali Riuniti, Viale Vittorio Alfieri, 36, 57124 Livorno, Italy (E-mail: [email protected]). 0894-7317/$36.00 Copyright 2009 by the American Society of Echocardiography. doi:10.1016/j.echo.2009.04.017
ical history was otherwise not significant, in the absence of cardiovascular risk factors. The patient’s blood pressure was 135/70 mm Hg and pulse rate was 90 beats/min. The echocardiographic examination was performed using a Philips iE33 (Philips Medical Systems, Bothell, WA) echocardiography system equipped with a 3.5-MHz transducer. The heart was imaged using the standard views, and the aortic arch was visualized from the suprasternal view. The echocardiographic examination of the aortic arch documented a mobile mass moving into and out of the image plane at the level of the proximal aortic arch (Video 1). Modified suprasternal and right supraclavear approaches clearly showed a large pedunculated and mobile mass attached to the posterior wall of the ascending aorta, approximately 6 cm above a normal aortic valve and extending into the proximal portion of the aortic arch (Video 2). At the time of the examination, the patient was asymptomatic, without neurologic deficit or signs of peripheral embolization. Routine laboratory results were normal, and a complete coagulation profile was normal. Echocardiographic findings were confirmed by angio-TC scan (Figure 1). Soon after the diagnosis of a mobile mass into the ascending aorta, the patient was referred to the nearest heart surgery department for mass excision and histologic examination. Anticoagulants or thrombolytic agents were avoided because of possible untoward drugs effects or embolization of fragments. At surgery, the aorta was approached via a median sternotomy and the ascending aorta was incised longitudinally. With cardiotomy suckers in place, a large 4.5 1.5 cm pedunculated mass was removed from the posterior aortic wall (Figure 2); at visual inspection the aortic wall appeared normal. The mass was removed, as well as a small button of the aortic wall surrounding the mass pedicle (Figure 3). Histologic examination of the mass revealed a fresh thrombus composed of a fibrinous material and platelets. Histologic examination of the aortic specimen confirmed the absence of significant atherosclerotic disease. The hospital course was uneventful, and the patient was discharged after 7 days of warfarin therapy. At echocardiographic 1197.e5
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Journal of the American Society of Echocardiography October 2009
Figure 3 The excised thrombotic mass with a small button of the aortic wall surrounding its pedicle. Figure 1 CT angiography. The floating mass located in the ascending aorta.
Figure 2 Operative view of the pedunculated thrombus attached to the posterior wall of ascending aorta.
reevaluation 1 year later, the ascending aorta and the aortic arch were normal, and the vessel lumen was free of thrombus.
DISCUSSION Aortic mural thrombosis is generally associated with several diseases, including coagulopathies, aortic dissection or trauma, tumors, and complicated atherosclerotic plaques.5,6,7,10 Few cases of mobile thrombi of the ascending aorta in the absence of concomitant aortic disease have been reported.9-11 In this case, ultrasound imaging by transthoracic echocardiography allowed the identification of a large, pedunculated mass attached to the posterior wall of an otherwise normal ascending aortic tract, without macroscopic and histologic evidence of significant atherosclerotic disease. Histologic examination confirmed the thrombotic nature of the mass. In the absence of a coagulopathy, aortic wall degeneration, or atherosclerotic disease, mechanisms leading to the thrombus formation in the proximal aortic tract remain obscure in our patient.13-17
The patient received therapeutic irradiation for non-Hodgkin’s disease. The inadvertent inclusion of the heart within the irradiation field may cause, over the next 10 to 20 years, pathologic changes of all the structures in the heart, including the heart valves, pericardium, myocardium, and conduction system. Standard therapeutic doses of radiation can cause endothelial proliferation, fibroblast proliferation, collagen deposition, and fibrosis within the large branches of the coronary arteries: These changes can lead to an accelerated form of atherosclerosis and an increased risk of experiencing nonfatal and fatal myocardial infarctions. Atherosclerotic disease progression is also enhanced by chest or neck radiation therapy.18-21 Among the various cardiac sequelae of mediastinal irradiation, scant data are available regarding the radiotherapy-induced supra-aortic trunk sequelae.22 A focal radiation-induced endothelial damage could have predisposed the aortic wall to thrombus development. In addition, our patient received rhG-CSF hematopoietic support to reduce the toxic effects of chemotherapy. Several in vitro studies showed that administration of G-CSF may induce activation of both coagulation and endothelial cells.23-25 Shimoda et al.26 report that low doses of rhG-CSF may induce platelet activation (G-CSF receptors are expressed on platelets surface) with a greater risk of thromboembolic events. Neurologic symptoms or signs of peripheral embolism are the most common early manifestations of proximal aortic thrombosis.5-10,12,13 Appropriateness of echocardiographic screening in an otherwise asymptomatic subject who received chest or neck radiation is questionable. On the contrary, basal and serial echocardiographic re-evaluation in patients who underwent therapy with cardiotoxic agents is appropriate.27 In our totally asymptomatic subject, a comprehensive transthoracic echocardiographic examination, including a suprasternal approach, proved to be extremely useful to detect a mobile thrombus of the ascending aorta, which could have ultimately caused ominous complications. Transesophageal echocardiography was not performed because of the clear definition of the mass at transthoracic echocardiography and its location at the level of the distal ascending aorta, frequently a ‘‘blind spot’’ during transesophageal echocardiography. The presence of the mobile mass in the ascending aorta was confirmed by computed tomography angiography. Magnetic resonance could be useful for better noninvasive imaging of the mass to differentiate clots from other solid tumors; however, access to this diagnostic modality is limited in many parts of the world. The best treatment of mobile aortic thrombi without evidence of aortic atherosclerotic disease is still controversial. Aggressive intravenous anticoagulation (thrombolysis or heparin followed by oral anticoagulants) has been proposed.15-17 However, the complete resolution
Journal of the American Society of Echocardiography Volume 22 Number 10
of a mobile, friable thrombus in this location with long-term anticoagulation carries a high risk of partial lysis and embolization, with potential catastrophic consequences. An immediate surgical approach has also been suggested; 8,12,14,28 despite surgical thrombus removal from the aorta, recurrent aortic thrombosis and subsequent embolization may still occur.11,14
CONCLUSIONS In this case, surgical resection allowed a definite diagnosis of isolated thrombus. The absence of recurrence at the 1-year follow-up confirmed the appropriateness of our therapeutic decision. REFERENCES 1. Schipper J, van Oostayen JA, den Hollander JC, van Seyen AJ. Aortic tumours: report of a case and review of the literature. Br J Radiol 1989; 62:35-40. 2. Davierwala PM, David TE, Butany J. A large lipoma of the ascending aorta. Ann Thorac Surg 2004;77:1079-80. 3. Glock Y, Laghzaoui A, Wang J, Delisle MB, Bachaud JM, Massabuau P, et al. Leiomyosarcoma fissure´ del’aorte thoracique descendante. A propos d’un cas, revue de la litte´rature (in French). Arch Mal Coeur Vaiss 1997; 90:1317-20. 4. Iorgulescu DG, White AL. Leiomyosarcoma of the thoracic aorta. Aust N Z J Surg 1999;67:537-40. 5. Bruno P, Massetti M, Babatasi G, Khayat A. Catastrophic consequences of a free floating thrombus in ascending aorta. Eur J Cardiothorac Surg 2001; 19:99-101. 6. Laperche T, Laurian C, Roudaut R, Steg PG. Mobile thromboses of the aortic arch without aortic debris: a transesophageal echocardiographic finding associated with unexplained arterial embolism. Circulation 1997;96:288-94. 7. Choi JB, Choi SH, Kim NH, Jeong JW. Floating thrombus in proximal aortic arch. Tex Heart Inst J 2004;31:432-4. 8. Kolvekar SK, Chaubey S, Firmin R. Floating thrombus in the aorta. Ann Thorac Surg 2001;72:925-7. 9. Kalangos A, Baldovinos A, Vuille C, Montessuit M, Faidutti B. Floating thrombus in the ascending aorta: a rare cause of peripheral emboli. J Vasc Surg 1997;26:150-4. 10. Farah MG, Hawawini H. Thrombus of the ascending aorta as a source of cerebral embolism. Chest 1993;104:1604-5. 11. Soyer H, Laudinat JM, Lemaitre C, Pommier JL, Delepine G, Poncet A, et al. Recurrent mobile thrombus of the ascending aorta diagnosed by transesophageal echocardiography. Arch Mal Coeur Vaiss 1993;86: 1769-71. 12. Mandegar MH, Roshanali F, Kocharian A. Complicate course consequences of a floating thrombus in ascending aorta. Eur J Echocardiogr 2008;9:846-8.
Baldini et al 1197.e7
13. Reber PU, Patel AG, Stauffer E, Muller MF, Do DD, Kniemeyer HW. Mural aortic thrombi: an important cause of peripheral embolization. J Vasc Surg 1999;30:1084-9. 14. Lozano P, Gomez FT, Julia J, M-Rimbau E, Garcia F. Recurrent embolism caused by floating thrombus in the thoracic aorta. Ann Vasc Surg 1998;12: 609-11. 15. Lau LS, Blanchard DG, Hye RG. Diagnosis and management of patients with peripheral macroemboli from thoracic aortic pathology. Ann Vasc Surg 1997;11:348-53. 16. Blackshear JL, Jahangir A, Oldenburg WA, Safford RE. Digital embolization from plaque related thrombus in the thoracic aorta. Identification with transesophageal echocardiography and resolution with warfarin therapy. Mayo Clin Proc 1993;68:268-72. 17. Hausman D, Gulba D, Borgheer K, Niedermeyer J, Comess KA, Daniel WG. Successful thrombolysis of an arch thrombus in a patient after mesenteric embolism (letter). N Engl J Med 1992;327:500-1. 18. Hannock SL, Tucker M, Hoppe RT. Factors affecting late mortality from heart disease after treatment of Hodgkin’s disease. Jama 1993;270: 1949-55. 19. Stewart JR, Fajardo LF, Gillette SM, Constine LS. Radiation injury to heart. Int J Radiat Oncol Biol Phys 1995;31:1205-11. 20. Basavaraju SR, Easterly CE. Pathophysiological effects of radiation on atherosclerosis development and progression, and incidence of cardiovascular complications. Med Phys 2002;29:2391-403. 21. Dorresteijn LD, Kappelle AC, Scholz NM, Munneke M, Scholma JT, Balm AJ, et al. Increased carotid wall thickening after radiotherapy on the neck. Eur J Cancer 2005;41:1026-30. 22. Hassen-Khodja R, Kieffer E. Radiotherapy-induced supra-aortic trunk disease: early and long-term results of surgical and endovascular reconstruction. J Vasc Surg 2004;40:254-61. 23. Barbui T, Finazzi G, Grassi A, Marchioli R. Thrombosis in cancer patients treated with hematopoietic growth factors—a meta-analysis. Thromb Hemostas 1996;75:368-71. 24. Kawachi Y, Watanabe A, Uchida T, Toshizawa K, Kurooka N, Setsu K. Acute arterial thrombosis due to platelet aggregation in a patient receiving granulocyte colony-stimulating factor. Br J Haematol 1996;94:413-6. 25. Kaptan K, Ifran A, Beyan C, Sertkaya D. Recombinant human granulocyte colony-stimulating factor (rhG-CSF) promotes in vitro platelet aggregation. Hematology 2007;12:441-4. 26. Shimoda K, Okamura S, Harada N, Kondo S, Okamura T, Niho Y. Identification of a functional receptor for granulocyte colony stimulating factor on platelets. J Clin Invest 1993;91:1310-3. 27. Douglas PS, Khandheria B, Stainback RF, Weissman NJ. ACCF/ASE/ ACEP/ASNC/SCAI/ SCCT/SCMR 2007 appropriateness criteria for transthoracic and transesophageal echocardiography. J Am Coll Cardiol 2007;50:187-204. 28. Kalangos A, Vala D, Bednarkiewicz M, Faidutti B. Technical implications regarding surgical removal of a floating thrombus located in the ascending aorta or aortic arch. Ann Vasc Surg 1999;13:115-20.
Aortic mural thrombosis is generally associated with several diseases, including coagulopathies, aortic dissection or trauma, tumors, and complicated atherosclerotic plaques. The development of a friable mobile thrombus, especially in the ascending aorta or proximal aortic arch, is a rare event with potentially ominous consequences because of a life-threatening risk of stroke and peripheral embolization. The treatment of choice of this condition is still controversial. We report a case of an absolutely asymptomatic 57-year-old patient with a mobile, pedunculated mass attached to the posterior wall of an otherwise normal ascending aorta. The aortic mass, identified by transthoracic echocardiography, was surgically removed and demonstrated to be a thrombus, and the aortic wall specimen was microscopically normal. (J Am Soc Echocardiogr 2009;22:1197.e5-1197.e7.) Keywords: Ascending aorta, Echocardiography, Surgery, Thrombosis
Sessile masses in the ascending aorta are infrequent, and most of the cases are found at autopsy. Aortic tumors involving the intima and growing into the vessel lumen are unusual.1-4 Rare also is the occurrence of a mobile aortic thrombi in the ascending aorta or the arch,5-12,17 generally originated from complicated atherosclerotic plaques. The development of a friable mobile thrombus, especially in the ascending aorta or the proximal aortic arch, may cause ominous consequences, and once the diagnosis is established, treatment is mandatory. We report a case of a mobile aortic mass found in an otherwise asymptomatic subject undergoing transthoracic echocardiography for screening evaluation; the mass, surgically removed, proved to be a mobile thrombus attached to an nonaneurysmal ascending aorta, in the absence of significant atherosclerotic disease. CASE REPORT In September 2007, a 57-year-old man underwent transthoracic echocardiography in the laboratory of Livorno Hospital Cardiology Division. Three years earlier, the patient had received the diagnosis of non-Hodgkin’s lymphoma, with a complete remission after induction and consolidation chemotherapy with the cyclophosphamide, doxorubicin (Adriamycin, Bedford Laboratories, Bedford, OH), vincristine, prednisone, and rituxan regimen; in addition, he had received recombinant human granulocyte colony-stimulating factor (rhG-CSF) and thoracic radiation. Any cancer treatment was discontinued in August 2005. He had no history of opportunistic infections, and his medFrom the Cardiology Division, Spedali Riuniti, Livorno, Italy (U.B., M.G.); and Heart Surgery Department, Cisanello Hospital and University of Pisa, Pisa, Italy (F.C., G.M.). Reprint requests: Umberto Baldini, MD, Cardiology Division, Spedali Riuniti, Viale Vittorio Alfieri, 36, 57124 Livorno, Italy (E-mail: [email protected]). 0894-7317/$36.00 Copyright 2009 by the American Society of Echocardiography. doi:10.1016/j.echo.2009.04.017
ical history was otherwise not significant, in the absence of cardiovascular risk factors. The patient’s blood pressure was 135/70 mm Hg and pulse rate was 90 beats/min. The echocardiographic examination was performed using a Philips iE33 (Philips Medical Systems, Bothell, WA) echocardiography system equipped with a 3.5-MHz transducer. The heart was imaged using the standard views, and the aortic arch was visualized from the suprasternal view. The echocardiographic examination of the aortic arch documented a mobile mass moving into and out of the image plane at the level of the proximal aortic arch (Video 1). Modified suprasternal and right supraclavear approaches clearly showed a large pedunculated and mobile mass attached to the posterior wall of the ascending aorta, approximately 6 cm above a normal aortic valve and extending into the proximal portion of the aortic arch (Video 2). At the time of the examination, the patient was asymptomatic, without neurologic deficit or signs of peripheral embolization. Routine laboratory results were normal, and a complete coagulation profile was normal. Echocardiographic findings were confirmed by angio-TC scan (Figure 1). Soon after the diagnosis of a mobile mass into the ascending aorta, the patient was referred to the nearest heart surgery department for mass excision and histologic examination. Anticoagulants or thrombolytic agents were avoided because of possible untoward drugs effects or embolization of fragments. At surgery, the aorta was approached via a median sternotomy and the ascending aorta was incised longitudinally. With cardiotomy suckers in place, a large 4.5 1.5 cm pedunculated mass was removed from the posterior aortic wall (Figure 2); at visual inspection the aortic wall appeared normal. The mass was removed, as well as a small button of the aortic wall surrounding the mass pedicle (Figure 3). Histologic examination of the mass revealed a fresh thrombus composed of a fibrinous material and platelets. Histologic examination of the aortic specimen confirmed the absence of significant atherosclerotic disease. The hospital course was uneventful, and the patient was discharged after 7 days of warfarin therapy. At echocardiographic 1197.e5
1197.e6 Baldini et al
Journal of the American Society of Echocardiography October 2009
Figure 3 The excised thrombotic mass with a small button of the aortic wall surrounding its pedicle. Figure 1 CT angiography. The floating mass located in the ascending aorta.
Figure 2 Operative view of the pedunculated thrombus attached to the posterior wall of ascending aorta.
reevaluation 1 year later, the ascending aorta and the aortic arch were normal, and the vessel lumen was free of thrombus.
DISCUSSION Aortic mural thrombosis is generally associated with several diseases, including coagulopathies, aortic dissection or trauma, tumors, and complicated atherosclerotic plaques.5,6,7,10 Few cases of mobile thrombi of the ascending aorta in the absence of concomitant aortic disease have been reported.9-11 In this case, ultrasound imaging by transthoracic echocardiography allowed the identification of a large, pedunculated mass attached to the posterior wall of an otherwise normal ascending aortic tract, without macroscopic and histologic evidence of significant atherosclerotic disease. Histologic examination confirmed the thrombotic nature of the mass. In the absence of a coagulopathy, aortic wall degeneration, or atherosclerotic disease, mechanisms leading to the thrombus formation in the proximal aortic tract remain obscure in our patient.13-17
The patient received therapeutic irradiation for non-Hodgkin’s disease. The inadvertent inclusion of the heart within the irradiation field may cause, over the next 10 to 20 years, pathologic changes of all the structures in the heart, including the heart valves, pericardium, myocardium, and conduction system. Standard therapeutic doses of radiation can cause endothelial proliferation, fibroblast proliferation, collagen deposition, and fibrosis within the large branches of the coronary arteries: These changes can lead to an accelerated form of atherosclerosis and an increased risk of experiencing nonfatal and fatal myocardial infarctions. Atherosclerotic disease progression is also enhanced by chest or neck radiation therapy.18-21 Among the various cardiac sequelae of mediastinal irradiation, scant data are available regarding the radiotherapy-induced supra-aortic trunk sequelae.22 A focal radiation-induced endothelial damage could have predisposed the aortic wall to thrombus development. In addition, our patient received rhG-CSF hematopoietic support to reduce the toxic effects of chemotherapy. Several in vitro studies showed that administration of G-CSF may induce activation of both coagulation and endothelial cells.23-25 Shimoda et al.26 report that low doses of rhG-CSF may induce platelet activation (G-CSF receptors are expressed on platelets surface) with a greater risk of thromboembolic events. Neurologic symptoms or signs of peripheral embolism are the most common early manifestations of proximal aortic thrombosis.5-10,12,13 Appropriateness of echocardiographic screening in an otherwise asymptomatic subject who received chest or neck radiation is questionable. On the contrary, basal and serial echocardiographic re-evaluation in patients who underwent therapy with cardiotoxic agents is appropriate.27 In our totally asymptomatic subject, a comprehensive transthoracic echocardiographic examination, including a suprasternal approach, proved to be extremely useful to detect a mobile thrombus of the ascending aorta, which could have ultimately caused ominous complications. Transesophageal echocardiography was not performed because of the clear definition of the mass at transthoracic echocardiography and its location at the level of the distal ascending aorta, frequently a ‘‘blind spot’’ during transesophageal echocardiography. The presence of the mobile mass in the ascending aorta was confirmed by computed tomography angiography. Magnetic resonance could be useful for better noninvasive imaging of the mass to differentiate clots from other solid tumors; however, access to this diagnostic modality is limited in many parts of the world. The best treatment of mobile aortic thrombi without evidence of aortic atherosclerotic disease is still controversial. Aggressive intravenous anticoagulation (thrombolysis or heparin followed by oral anticoagulants) has been proposed.15-17 However, the complete resolution
Journal of the American Society of Echocardiography Volume 22 Number 10
of a mobile, friable thrombus in this location with long-term anticoagulation carries a high risk of partial lysis and embolization, with potential catastrophic consequences. An immediate surgical approach has also been suggested; 8,12,14,28 despite surgical thrombus removal from the aorta, recurrent aortic thrombosis and subsequent embolization may still occur.11,14
CONCLUSIONS In this case, surgical resection allowed a definite diagnosis of isolated thrombus. The absence of recurrence at the 1-year follow-up confirmed the appropriateness of our therapeutic decision. REFERENCES 1. Schipper J, van Oostayen JA, den Hollander JC, van Seyen AJ. Aortic tumours: report of a case and review of the literature. Br J Radiol 1989; 62:35-40. 2. Davierwala PM, David TE, Butany J. A large lipoma of the ascending aorta. Ann Thorac Surg 2004;77:1079-80. 3. Glock Y, Laghzaoui A, Wang J, Delisle MB, Bachaud JM, Massabuau P, et al. Leiomyosarcoma fissure´ del’aorte thoracique descendante. A propos d’un cas, revue de la litte´rature (in French). Arch Mal Coeur Vaiss 1997; 90:1317-20. 4. Iorgulescu DG, White AL. Leiomyosarcoma of the thoracic aorta. Aust N Z J Surg 1999;67:537-40. 5. Bruno P, Massetti M, Babatasi G, Khayat A. Catastrophic consequences of a free floating thrombus in ascending aorta. Eur J Cardiothorac Surg 2001; 19:99-101. 6. Laperche T, Laurian C, Roudaut R, Steg PG. Mobile thromboses of the aortic arch without aortic debris: a transesophageal echocardiographic finding associated with unexplained arterial embolism. Circulation 1997;96:288-94. 7. Choi JB, Choi SH, Kim NH, Jeong JW. Floating thrombus in proximal aortic arch. Tex Heart Inst J 2004;31:432-4. 8. Kolvekar SK, Chaubey S, Firmin R. Floating thrombus in the aorta. Ann Thorac Surg 2001;72:925-7. 9. Kalangos A, Baldovinos A, Vuille C, Montessuit M, Faidutti B. Floating thrombus in the ascending aorta: a rare cause of peripheral emboli. J Vasc Surg 1997;26:150-4. 10. Farah MG, Hawawini H. Thrombus of the ascending aorta as a source of cerebral embolism. Chest 1993;104:1604-5. 11. Soyer H, Laudinat JM, Lemaitre C, Pommier JL, Delepine G, Poncet A, et al. Recurrent mobile thrombus of the ascending aorta diagnosed by transesophageal echocardiography. Arch Mal Coeur Vaiss 1993;86: 1769-71. 12. Mandegar MH, Roshanali F, Kocharian A. Complicate course consequences of a floating thrombus in ascending aorta. Eur J Echocardiogr 2008;9:846-8.
Baldini et al 1197.e7
13. Reber PU, Patel AG, Stauffer E, Muller MF, Do DD, Kniemeyer HW. Mural aortic thrombi: an important cause of peripheral embolization. J Vasc Surg 1999;30:1084-9. 14. Lozano P, Gomez FT, Julia J, M-Rimbau E, Garcia F. Recurrent embolism caused by floating thrombus in the thoracic aorta. Ann Vasc Surg 1998;12: 609-11. 15. Lau LS, Blanchard DG, Hye RG. Diagnosis and management of patients with peripheral macroemboli from thoracic aortic pathology. Ann Vasc Surg 1997;11:348-53. 16. Blackshear JL, Jahangir A, Oldenburg WA, Safford RE. Digital embolization from plaque related thrombus in the thoracic aorta. Identification with transesophageal echocardiography and resolution with warfarin therapy. Mayo Clin Proc 1993;68:268-72. 17. Hausman D, Gulba D, Borgheer K, Niedermeyer J, Comess KA, Daniel WG. Successful thrombolysis of an arch thrombus in a patient after mesenteric embolism (letter). N Engl J Med 1992;327:500-1. 18. Hannock SL, Tucker M, Hoppe RT. Factors affecting late mortality from heart disease after treatment of Hodgkin’s disease. Jama 1993;270: 1949-55. 19. Stewart JR, Fajardo LF, Gillette SM, Constine LS. Radiation injury to heart. Int J Radiat Oncol Biol Phys 1995;31:1205-11. 20. Basavaraju SR, Easterly CE. Pathophysiological effects of radiation on atherosclerosis development and progression, and incidence of cardiovascular complications. Med Phys 2002;29:2391-403. 21. Dorresteijn LD, Kappelle AC, Scholz NM, Munneke M, Scholma JT, Balm AJ, et al. Increased carotid wall thickening after radiotherapy on the neck. Eur J Cancer 2005;41:1026-30. 22. Hassen-Khodja R, Kieffer E. Radiotherapy-induced supra-aortic trunk disease: early and long-term results of surgical and endovascular reconstruction. J Vasc Surg 2004;40:254-61. 23. Barbui T, Finazzi G, Grassi A, Marchioli R. Thrombosis in cancer patients treated with hematopoietic growth factors—a meta-analysis. Thromb Hemostas 1996;75:368-71. 24. Kawachi Y, Watanabe A, Uchida T, Toshizawa K, Kurooka N, Setsu K. Acute arterial thrombosis due to platelet aggregation in a patient receiving granulocyte colony-stimulating factor. Br J Haematol 1996;94:413-6. 25. Kaptan K, Ifran A, Beyan C, Sertkaya D. Recombinant human granulocyte colony-stimulating factor (rhG-CSF) promotes in vitro platelet aggregation. Hematology 2007;12:441-4. 26. Shimoda K, Okamura S, Harada N, Kondo S, Okamura T, Niho Y. Identification of a functional receptor for granulocyte colony stimulating factor on platelets. J Clin Invest 1993;91:1310-3. 27. Douglas PS, Khandheria B, Stainback RF, Weissman NJ. ACCF/ASE/ ACEP/ASNC/SCAI/ SCCT/SCMR 2007 appropriateness criteria for transthoracic and transesophageal echocardiography. J Am Coll Cardiol 2007;50:187-204. 28. Kalangos A, Vala D, Bednarkiewicz M, Faidutti B. Technical implications regarding surgical removal of a floating thrombus located in the ascending aorta or aortic arch. Ann Vasc Surg 1999;13:115-20.