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17 Long-Term Suppressive Therapy: Clinical Reality and Future Prospects Amy E. Hackmann and Robert W. Thompson Departments of Surgery (Section of Vascular Surgery), Radiology, and Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri, U.S.A. Scott A. LeMaire Division of Cardiothoracic Surgery, Michael E. DeBakey Department of Surgery, Baylor College of Medicine, and Cardiovascular Surgery Service, The Texas Heart Institute at St. Luke’s Episcopal Hospital, Houston, Texas, U.S.A. INTRODUCTION Progressive aortic dilatation and rupture are the inevitable consequences of untreated aortic aneurysms and dissections. The only treatments that effectively eliminate the risk of aortic rupture are surgical replacement of the diseased aortic segment with a graft and intraluminal exclusion of the segment with an endovascular stent graft. Because of the associated risks, aortic repair procedures are performed only in patients who are at significant risk of aortic rupture. The decision of when to repair an aneurysm is based primarily on the severity of aneurysmal disease—as indicated by symptoms, aortic diameter, and aortic expansion rate—in the context of other factors that increase the likelihood of rupture, such as connective tissue disorders or a family history of ruptured aneurysm. Patients who have not reached the clinical threshold for aortic repair receive nonoperative treatment and careful surveillance with imaging studies. Current nonoperative treatment is rather unsophisticated and comprises smoking cessation, avoidance of strenuous activity, and pharmacologic reduction of hemodynamic stress. Although this regimen successfully halts aortic expansion in some patients, aneurysms continue to enlarge and rupture in many patients, despite 309
310 Hackmann et al. treatment. New treatments are needed to stop aneurysm expansion and prevent rupture. Recent experimental work has focused on improving our understanding of the pathobiology of aortic aneurysms in hope of identifying new strategies for long-term suppressive therapy. PATHOBIOLOGY OF AORTIC ANEURYSMS Over the last two decades, research on the pathobiology of aortic aneurysms has greatly improved our understanding of the cellular and molecular mechanisms involved in progressive aortic dilatation. Most studies have focused on abdominal aortic aneurysm (AAA) formation. Until recently, most of the research regarding thoracic aortic aneurysms (TAAs) has concentrated on those related to connective tissue disorders, particularly Marfan syndrome (MFS). Relatively little is known about the pathobiology of TAAs related to chronic medial degeneration or dissection in patients without MFS. Studies in animals and human aortic tissue have shown that the development of aneurysms results from a cascade of interacting cellular and molecular processes, including matrix degeneration by elastin- and collagendegrading proteases, chronic inflammation, cytokine activity, and loss of smooth muscle cells (SMCs) (Fig. 1) (1). Together, these processes undermine the mechanical properties of the aortic wall, and lead to aneurysm expansion and rupture (2). Matrix Proteolysis The two proteins responsible for maintaining structural integrity of the aortic wall are elastin and collagen, which respectively confer elasticity and tensile strength. Figure 1 Diagram illustrating the overlapping cellular and molecular processes that contribute to aortic aneurysm formation.
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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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Acute Aortic Dissection 245 22. Bax
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Acute Aortic Dissection 247 62. Lin
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Acute Aortic Dissection 249 DISSCUS
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252 Elefteriades and Griepp ACUTE A
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254 Elefteriades and Griepp Figure
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256 Elefteriades and Griepp sometim
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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
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Page 307 and 308: 278 Brinster et al. registry arm (2
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Page 351 and 352: 322 Hackmann et al. ACKNOWLEDGMENTS
Page 353 and 354: 324 Hackmann et al. 34. Thompson RW
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Page 359 and 360: 330 Hackmann et al. DISCUSSION AND
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Page 371 and 372: 342 Elefteriades Figure 3 Computed
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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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