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Endovascular Thoracic Aortic Stent Grafting 293 use of neurophysiological monitoring in endovascular treatment of the thoracic aorta has been reported to also allow early detection and intervention to augment spinal cord perfusion pressure to decrease the risk (94). A proposed algorithm to manage the risk of spinal cord ischemia is demonstrated in Figure 12. The risk of stroke in endovascular repair is approximately 3% to 9%, which is similar to open repair (95). Therefore, stroke rates are 2–3 × higher than paraplegia rates for thoracic endografting. There are several possible reasons for this high stroke risk. Endovascular placement of thoracic aortic stent grafts requires multiple Figure 12 Proposed algorithm to manage the risk of spinal cord ischemia in patients undergoing endovascular stent repair of descending thoracic aortic aneurysms. Abbreviations: AAA, abdominal aortic aneurysm; CSF, cerebrospinal fluid; LE, lower extremity; MAP, mean arterial pressure; Rx, drug therapy; SEP, somatosensory evoked potential. Source: From Ref. 84.
294 Brinster et al. wire manipulations in the aortic arch. These manipulations may contribute to stoke risk by producing emboli. Other risk factors for stroke include history of previous stroke and grade V atheroma of the aortic arch (129). Stent Migration In most series, stent migration has been relatively rare (ranging from 1% to 3%). Early stent migration is usually a result of inadequate proximal or distal landing zone length. If the landing zone is inadequate, the stent can be displaced into the aneurismal sac, resulting in migration. Additionally, persistent type I endoleaks can cause aneurismal sac enlargement, which then may displace the stent from its apposition to the proximal or distal landing zone. Late stent migration is usually related to either continued tortuous lengthening of the native aorta, resulting in stent component separation, or continuous increases in native aortic landing zone diameter, which eventually results in a “free floating” stent within the enlarging aorta. FUTURE DIRECTIONS Early reports have suggested the possible beneficial use of TEVAR in a number of acute aortic syndromes involving the ascending aorta and arch. A very likely and appropriate application of ascending aortic TEVAR has been the treatment of isolated saccular aneurysms and pseudoaneurysms of the ascending aorta. These successful ascending aortic TEVAR applications have been characterized by limited coverage distances, normal aortic diameters proximal and distal to the psuedoaneurysm, and a corresponding high predicted mortality rate from standard redo open surgery. The present limitation of this therapy is the fact that thoracic endovascular devices have been designed for descending aortic diameters and lengths. Examples of treated catastrophic ascending aortic conditions have been cannulation site pseudoaneurysms and ascending aortic suture line disruptions. An acute proximal aortic presentation treated with adjunctive thoracic aortic stent grafting has been acute type A dissection. Most reports utilizing TEVAR in the setting of acute type A dissection revolve around the hybrid deployment of a descending stent anchored at the distal aortic arch after standard open type A dissection repair. The theoretical rationale for this TEVAR application is the knowledge that standard acute type A dissection repair is associated with an 80% to 100% rate of residual descending aorta dissection. Therefore, an adjunctive stent procedure on the distal arch and proximal descending aorta may allow improved “remodeling” of the residual dissected thoracoabdominal aorta compared to standard acute type A repair. Multiple investigators have reported on the adjunctive use of an aortic stent graft in the descending thoracic aorta during repair of acute type A dissection and its effect on aortic remodeling. Early reports by Fleck et al. (96) and Kato et al. (97) described preliminary results using home-grown stent grafts. The largest series, by Liu et al. (98), reported 36 consecutive patients with acute type A dissection treated with total arch repair with a simultaneous antegrade deployment of a “stented elephant trunk.” They demonstrated an obliteration rate of the false lumen in the
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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
Page 272 and 273: Acute Aortic Dissection 243 dissect
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Page 276 and 277: Acute Aortic Dissection 247 62. Lin
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Page 281 and 282: 252 Elefteriades and Griepp ACUTE A
Page 283 and 284: 254 Elefteriades and Griepp Figure
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Page 295 and 296: 266 Elefteriades and Griepp CONCLUS
Page 297 and 298: 268 Elefteriades and Griepp DISCUSS
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 317 and 318: 288 Brinster et al. conventional op
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Page 325 and 326: 296 Brinster et al. Thoracoabdomina
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Page 329 and 330: 300 Brinster et al. 60. Elefteriade
Page 331 and 332: 302 Brinster et al. 98. Liu ZG, Sun
Page 333 and 334: 304 Brinster et al. 131. Szeto WY,
Page 335 and 336: 306 Brinster et al. 100% 90% 80% 70
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Page 339 and 340: 310 Hackmann et al. treatment. New
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Page 343 and 344: 314 Hackmann et al. Table 1 Pharmac
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Page 347 and 348: 318 Hackmann et al. inhibits NF-κB
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Page 351 and 352: 322 Hackmann et al. ACKNOWLEDGMENTS
Page 353 and 354: 324 Hackmann et al. 34. Thompson RW
Page 355 and 356: 326 Hackmann et al. 70. LeMaire SA,
Page 357 and 358: 328 Hackmann et al. 105. Marra DE,
Page 359 and 360: 330 Hackmann et al. DISCUSSION AND
Page 361 and 362: 332 Elefteriades Diseases of the th
Page 363 and 364: 334 Elefteriades Table 1 Individual
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344 Elefteriades reviewed over the
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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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