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Natural History of Thoracic Aortic Aneurysms 177 P042 P145 P188 P286 P470 P518 P557 P571 P007 P518 P167 P271 P330 P511 P546 P563 P572 P027 P588 P141 P184 P284 P422 P547 P565 P580 Figure 3 Thoracic aortic aneurysm (TAA) family pedigrees selected from over 500 family pedigrees. Squares represent men and circles, women. An arrow indicates the proband with a TAA. Blackened circles or squares represent affected patients with aortic aneurysms. new elastin is limited. In the aortic wall, collagen is responsible for the tensile strength of the vessel, whereas elastin is responsible for its recoil capacity. Fibrillin is another structural protein that contributes to the microfibrillar organization of the extracellular matrix. The microfibrillar construction functions as scaffolding for the deposition of elastin during elastogenesis. A mutation in fibrillin has been demonstrated in patients with Marfan’s syndrome. The aorta is categorized as an elastic artery with three defined layers—the intima, media, and adventitia. The intima consists of single layer of endothelial cells that rest on a basal lamina. The intimal cells rest on a subendothelial tissue comprised of collagen and elastin fibers, fibroblasts, and a mucoid ground substance.
178 Coady and Elefteriades The internal elastic lamina separates the intimal layer from the media. The internal elastic lamina, composed primarily of elastin, has fenestrae that allow substances from the lumen to diffuse to nourish cells within the aortic wall. The media is composed of smooth muscle cells within a matrix of elastin, collagen, and ground substance. The elastic fibers in the aortic wall are arranged in the media as circumferential lamellae. The thoracic aorta consists of 45 to 56 lamellar units (concentric elastic lamellae with smooth muscle cells, collagen, and ground substance); the abdominal aorta contains only 28 units (18). The number of lamallar units is preserved throughout the mammalian species, with the exception of the human abdominal aorta, which consists of fewer units than expected given the load it bears. This may be a contributing factor in the prevalence of abdominal aorta aneurysm (AAA) compared to aneurysms in the thoracic aorta. The lamallar units provide a structural framework for the media. These elastic lamellae serve to maintain the forward flow of blood during diastole: during systole, the diameter of these lamellae increases; the elastic fibers recoil during diastole (19). Smooth muscle cells within the medial layer maintain vascular resistance, serve a macrophage-like function, and are capable of collagen synthesis when stimulated (20). Humans lose the ability to produce elastic fibers in early life, and little elastin synthesis can be detected within the aortic wall beyond infancy (21). In most patients with aortic aneurysm, histology examination reveals loss of elastic fibers—so called “medial degenerative disease.” The mechanisms for this degeneration are not known, but fragmentation and retrogression of elastic fibers within the aortic media are clearly evident. More advanced medial degeneration (as in Marfan patients) leads to loss of smooth muscle cells. Histologic examination reveals significant reduction in the number of smooth muscle cells within the tunica media, and multiple interspersed lakes of mucopolysaccharide (“cystic medial necrosis”). White et al. (22) however, emphasize that loss of smooth muscle cells of the media should not directly affect the maximal outer diameter of the aorta. They and other others believe that loss of smooth muscle cells may play an important role in the formation of aortic aneurysm and growth through their degradative and synthetic functions but not through loss of contractile function (23). Loss of structural integrity of the adventitia, not the media, is required for aneurysm formation (24). The biomechanical function of the adventitia is the maintenance of the maximal aortic outer diameter (23). Destruction of elastin within the aortic wall results in pathologic dilation of the vessel, whereas destruction of the collagen within the vessel has been shown to cause rupture (23). Therefore, at least in AAA, it is presently believed that maintenance of adventitial elastin is critical for sustaining the integrity of the aortic wall. Since it is well recognized clinically that it is unusual for aneurysm formation to occur after an endarterectomy if the adventitia remains intact, White et al. (24) believe that aneurysmal disease must be a disorder of the adventitia. The integrity of this layer is critical for maintenance of aortic wall integrity under wall stress
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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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Page 160 and 161: 8 Matrix Metalloproteinases in Aort
Page 162 and 163: Matrix Metalloproteinases in Aortic
Page 176 and 177: INTRODUCTION 9 Inflammation and Rem
Page 178 and 179: Inflammation and Remodeling in the
Page 190 and 191: 10 Weight Lifting and Aortic Dissec
Page 192 and 193: Weight Lifting and Aortic Dissectio
Page 198 and 199: 11 Timing of Acute Aortic Events: H
Page 200 and 201: Timing of Acute Aortic Events 171 F
Page 202 and 203: SECTION IV: TREATMENT OF ACUTE AORT
Page 204 and 205: Natural History of Thoracic Aortic
Page 232: Natural History of Thoracic Aortic
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Page 245 and 246: 216 Shahriari and Farkas (68). Many
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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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262 Elefteriades and Griepp to a se
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264 Elefteriades and Griepp Natural
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266 Elefteriades and Griepp CONCLUS
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268 Elefteriades and Griepp DISCUSS
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270 Brinster et al. thoracic aneury
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272 Brinster et al. Figure 1 Retrop
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274 Brinster et al. artery. Z3 land
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276 Brinster et al. or ischemia of
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278 Brinster et al. registry arm (2
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280 Brinster et al. Table 3 Early P
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282 Brinster et al. According to th
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284 Brinster et al. ranged from 1 t
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Table 4 Meta-Analysis of Tevar for
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288 Brinster et al. conventional op
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290 Brinster et al. using no (or lo
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292 Brinster et al. Table 5 Risk Fa
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294 Brinster et al. wire manipulati
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296 Brinster et al. Thoracoabdomina
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298 Brinster et al. 25. Hagan PG, N
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300 Brinster et al. 60. Elefteriade
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302 Brinster et al. 98. Liu ZG, Sun
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304 Brinster et al. 131. Szeto WY,
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306 Brinster et al. 100% 90% 80% 70
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308 Brinster et al. ● “Long-ter
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310 Hackmann et al. treatment. New
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312 Hackmann et al. tissue than in
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314 Hackmann et al. Table 1 Pharmac
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316 Hackmann et al. Some anti-hyper
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318 Hackmann et al. inhibits NF-κB
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320 Hackmann et al. Patients with C
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322 Hackmann et al. ACKNOWLEDGMENTS
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324 Hackmann et al. 34. Thompson RW
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326 Hackmann et al. 70. LeMaire SA,
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328 Hackmann et al. 105. Marra DE,
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330 Hackmann et al. DISCUSSION AND
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332 Elefteriades Diseases of the th
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334 Elefteriades Table 1 Individual
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336 Elefteriades Table 1 Individual
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338 Elefteriades Failure to Diagnos
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340 Elefteriades of physicians on t
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342 Elefteriades Figure 3 Computed
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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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