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Endovascular Thoracic Aortic Stent Grafting 295 distal thoracoabdominal aorta approaching 92%. Panos and coworkers (99) reported on five patients undergoing similar surgical strategy using the Endofit endoluminal stent graft (Endomed Inc., Phoenix, Arizona, U.S.A.) with complete obliteration in two patients and partial obliteration in three patients. At the University of Pennsylvania, we have attempted to alter the prognosis and natural history of the residual type B dissection following acute type A dissection repair by stenting the distal aortic arch and descending thoracic aorta. We have presented a method for simultaneous open repair of the aortic dissection and antegrade “stented elephant trunk” stabilization of the descending aorta using thoracic aortic stent grafts (Fig. 4) (101). To date, nine patients have been treated with this technique, with five patients (56%) demonstrating complete thrombosis and stabilization of the false lumen in the entire aorta (Fig. 5). Two patients (22%) had stabilization of the descending thoracic aorta with persistence of the false lumen in the aorta beginning at the level of the celiac axis. Two patients (22%) had persistent false lumen in the descending thoracic aorta. Paraplegia did not develop in any of the nine patients. Other reports of similar combined open and aortic stent graft repair of acute type A dissection demonstrated comparable results of false lumen obliteration and prevention of distal aortic aneursymal remodeling (96–99). Arch Hybrids Conventional repair of atherosclerotic aortic arch aneurysm is technically demanding, requiring CPB and deep hypothermic circulatory arrest. Despite recent improvements in surgical technique, total arch repairs of large atherosclerotic arch aneurysms still have significant morbidity and mortality (102–105). In contrast to nonatherosclerotic aortic arches, large atherosclerotic saccular aneurysms of the arch are extremely high risk for perioperative stroke, as this disease is a grave marker of extensive arch and brachiocephalic atheromatous disease. In this subset of high risk patients, even the most recent series indicate in-hospital mortality rates ranging from 6.3% to 20%, with stroke rates up to 12% (43,106–111). Beginning with descending thoracic aortic aneurysms, endovascular stent graft technology has evolved as a safe and effective treatment for various thoracic aortic diseases (20,46,50,112–115). Because of the anatomical features of the aortic arch, endovascular therapy of arch aneurysms remains a technical challenge (130,131). Maintaining cerebral perfusion and eliminating embolic events during deployment are crucial for optimal neurologic outcome. Limited to Europe and Japan due to the availability of stent graft devices, small series of combined extraanatomical bypass of the great vessels with endovascular deployment of a stent graft in the arch have been reported with promising results (102,116–121). With FDA approval in 2005, the Gore TAG (W.L. Gore, Flagstaff, Arizona, U.S.A.) thoracic endoprosthesis became available commercially in the United States. Previously, these patients have been considered prohibitively high risk for conventional open arch repair due to their comorbidities, including the atherosclerotic burden in the arch and the associated high stroke risk.
296 Brinster et al. Thoracoabdominal Aneurysms Thoracic aortic stent grafting has now been utilized in the treatment of elective thoracoabdominal aneurysms (122,123). Although this advance has not been applicable in acute catastrophic presentations such as rupture or secondary dissection, thoracoabdominal aortic applications will undoubtedly be utilized in the future. These are complex procedures requiring branch artery revascularization. Postoperative Pseudoaneurysms Psueodaneurysms of the thoracic aorta are an excellent indication for TEVAR. Most general series report a small subset of patients treated with TEVAR for pseudoaneurysms of previous thoracic aortic suture lines. Technically, this urgent aortic condition is eminently suitable for stent grafting, as either the proximal or distal landing zone is usually within a previously placed Dacron graft, which is ideal for stent deployment (132). Mycotic Aneurysms TEVAR has been applied to a broad range of thoracic aortic diseases with mycotic or septic characteristics. These have included isolated mycotic aneurysms, broncho-aortic fistulas, aorto-esophageal communications, and infected grafts and stent grafts (124–126). In general, the effectiveness of TEVAR for “mycotic” type indications has been poor in the long-term. However, there maybe a role for thoracic aortic stent grafting in the setting of mycotic or infected thoracic aortic diseases as a “bridge,” to “defuse” the potentially catastrophic situation, while allowing the patient to recover sufficiently for a definitive procedure. CONCLUSION In summary, it is precisely in acute aortic events that application of TEVAR may be most beneficial. Since traditional open surgical procedures for acute aortic conditions have historically had a high morbidity and mortality, the application of TEVAR to these pathologies may offer significant survival benefits. As device technology improves and clinical experience expands, TEVAR applications are also likely to expand. REFERENCES 1. Rehders TCNC. Complications of Thoracic Aortic Stent Grafts. Vol. 1. New york: Editions Futura Publishing, 2001. 2. Krohg-Sorensen K, Hafsahl G, Fosse E, Geiran OR. Acceptable short-term results after endovascular repair of diseases of the thoracic aorta in high risk patients. Eur J Cardiothorac Surg 2003; 24(3):379–387. 3. Grabenwoger M, Fleck T, Czerny M, et al. Endovascular stent graft placement in patients with acute thoracic aortic syndromes. Eur J Cardiothorac Surg 2003; 23(5):788–793.
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Acute Aortic Disease
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15. Heart Failure: Basic Science an
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52. Clinical, Interventional, and I
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Informa Healthcare USA, Inc. 270 Ma
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Introduction Informa Healthcare has
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Foreword There is no disease more c
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Preface Over 100 years ago, the gre
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Preface xi Some distinguishing feat
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xiv Acknowledgments Above all, than
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xvi Contents 6. Genetic Basis of Th
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Contributors Nili Avidan Division o
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Contributors xxi Arun Raghupathy Di
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2 Nienaber and Ince Table 1 Risk Co
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4 Nienaber and Ince In addition to
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6 Nienaber and Ince CLASSIFICATION
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8 Nienaber and Ince Lansman’s Cla
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10 Nienaber and Ince Figure 4 Curve
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12 Nienaber and Ince Figure 6 Evolu
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14 Nienaber and Ince dissection, su
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16 Nienaber and Ince (A) (B) Probab
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18 Nienaber and Ince Table 5 Risk P
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20 Nienaber and Ince of the predila
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22 Nienaber and Ince 34. Pieters FA
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24 Nienaber and Ince 75. Mehta RH,
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26 Nienaber and Ince hematoma (IMH)
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28 Nienaber and Ince One good featu
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30 Isselbacher SYMPTOMS Pain Experi
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32 Isselbacher and wane in severity
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34 Isselbacher The mechanisms are u
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36 Isselbacher deficits are most co
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38 Isselbacher 3. Nallamothu BK, Me
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40 Danias spinal arteries) and the
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42 Danias Figure 2 Anteroposterior
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44 Danias However, due to the dista
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46 Danias TEE is highly sensitive f
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48 Danias faster, with higher resol
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50 Danias Figure 6 Transverse slice
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52 Danias hematoma, CT was reported
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54 Danias Figure 9 Transverse black
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56 Danias Figure 12 Single phase-co
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58 Danias restricted to the absolut
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60 Danias In conclusion, in the rig
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62 Danias DISCUSSION AND COMMENTARY
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64 Danias tomography, among others.
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66 Danias cardiac silhouette. The a
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68 Raghupathy and Eagle the inciden
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70 Raghupathy and Eagle Figure 1 Sp
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72 Raghupathy and Eagle SIGNS A tho
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74 Raghupathy and Eagle patients ma
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76 Raghupathy and Eagle Table 5 Dia
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78 Raghupathy and Eagle Table 6 A S
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80 Raghupathy and Eagle Figure 6 (A
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82 Raghupathy and Eagle Figure 9 (A
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84 Raghupathy and Eagle EDITOR’S
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86 Raghupathy and Eagle 30. Erbel R
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88 Raghupathy and Eagle is highly l
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90 Elefteriades and Rizzo required
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92 Elefteriades and Rizzo Table 1 S
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94 Elefteriades and Rizzo 70s, this
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96 Elefteriades and Rizzo Table 3 C
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98 Elefteriades and Rizzo DISCUSSIO
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100 Milewicz et al. KNOWN GENETIC S
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102 Milewicz et al. Table 2 Quick G
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104 Milewicz et al. ascending aorti
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106 Milewicz et al. Turner syndrome
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108 Milewicz et al. dissection in t
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110 Milewicz et al. Figure 5 Haplot
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112 Milewicz et al. A genome wide s
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114 Milewicz et al. Structural anal
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116 Milewicz et al. assembly of a h
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118 Milewicz et al. in the nuclei o
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120 Milewicz et al. 22. Furlong J,
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122 Milewicz et al. DISCUSSION AND
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124 Milewicz et al. Figure A Distri
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126 Elefteriades and Koullias Figur
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128 Elefteriades and Koullias prope
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8 Matrix Metalloproteinases in Aort
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Matrix Metalloproteinases in Aortic
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INTRODUCTION 9 Inflammation and Rem
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Inflammation and Remodeling in the
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10 Weight Lifting and Aortic Dissec
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Weight Lifting and Aortic Dissectio
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11 Timing of Acute Aortic Events: H
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Timing of Acute Aortic Events 171 F
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SECTION IV: TREATMENT OF ACUTE AORT
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Natural History of Thoracic Aortic
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206 Shahriari and Farkas properties
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208 Shahriari and Farkas Figure 2 E
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210 Shahriari and Farkas Less than
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212 Shahriari and Farkas helpful if
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214 Shahriari and Farkas Figure 6 A
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216 Shahriari and Farkas (68). Many
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218 Shahriari and Farkas Figure 9 H
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220 Shahriari and Farkas fistula is
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222 Shahriari and Farkas MEGS is de
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224 Shahriari and Farkas 26. Svenss
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226 Shahriari and Farkas 63. Fehren
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14 Acute Aortic Dissection: Anti-im
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Acute Aortic Dissection 231 lamella
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Acute Aortic Dissection 233 P t is
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Acute Aortic Dissection 235 From th
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Acute Aortic Dissection 237 Figure
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Acute Aortic Dissection 239 concern
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Acute Aortic Dissection 241 Table 2
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Acute Aortic Dissection 243 dissect
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Page 295 and 296: 266 Elefteriades and Griepp CONCLUS
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Page 299 and 300: 270 Brinster et al. thoracic aneury
Page 301 and 302: 272 Brinster et al. Figure 1 Retrop
Page 303 and 304: 274 Brinster et al. artery. Z3 land
Page 305 and 306: 276 Brinster et al. or ischemia of
Page 307 and 308: 278 Brinster et al. registry arm (2
Page 309 and 310: 280 Brinster et al. Table 3 Early P
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Page 335 and 336: 306 Brinster et al. 100% 90% 80% 70
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Page 351 and 352: 322 Hackmann et al. ACKNOWLEDGMENTS
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Page 359 and 360: 330 Hackmann et al. DISCUSSION AND
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346 Elefteriades DISCUSSION AND COM
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348 Elefteriades Figure 1 (See colo
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350 Elefteriades that are the subje
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SECTION VII: SYNTHESIS 20 The Key L
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The Key Lessons of This Book—In a
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362 Index Aging, aortic aneurysms a
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364 Index Cytokines, aortic aneurys
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366 Index Pathoanatomy classificati
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368 Index [Thoracic aortic aneurysm
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Figure 1.C Note from schematic depi
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Figure 8.1 Dramatic clinical exampl
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Figure 11.2 Proposed schema for the
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Figure 19.1 Future prospects in car
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