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Natural History of Thoracic Aortic Aneurysms 185 Arteriosclerosis Joyce et al. (51) in 1964 studied 107 patients who had nondissecting, nonsurgically treated TAAs. Approximately 73% were considered “arteriosclerotic” in origin, and the incidence of syphilitic aneurysms at that time had fallen to 20%. One of the reasons that the natural history of aortic aneurysms has been difficult to record is the fact that arteriosclerosis is so prevalent in this population. Joyce et al. (51) attributed the most deleterious effects on survival to the presence of associated coronary, cerebral, or other peripheral arterial occlusive or aneurysmal disease. In their study, approximately 50% of patients with aortic aneurysms were not alive at five years after diagnosis. Whether arteriosclerosis is a cause of aortic aneurysm formation, or simply a coexisting disease process, is still a matter of debate. EVIDENCE-BASED CLINICAL DECISION-MAKING FOR THORACIC AORTIC ANEURYSM TAAs are serious conditions that frequently require surgical intervention due to the threat of dissection or rupture. The natural history of aortic aneurysm is often related to the specific location and the primary cause of the disease. The decisionmaking process is further complicated by the greater risks of thoracic aortic replacement compared to abdominal aortic replacement. In developing management protocols for appropriate patient selection for surgery, it is essential to study risk factors that may influence the natural history of the disease. The specific objective is to select patients for whom the operative risks are justified. Our team at the Yale Center for Thoracic Aortic Disease has developed and maintained a robust clinical database to: 1. Further define the natural history of TAAs in terms of thoracic aortic growth, incidence of complications (dissection and rupture), and survival; 2. determine risk factors for thoracic aortic growth, dissection, and rupture; and 3. define scientific criteria for surgical intervention based on the natural history available from these patients. The Yale observations confirm that TAA is, over the long term, a lethal disease. Figure 7A illustrates that patients with TAA do, indeed, have a dramatically poorer natural outlook than an age and sex-matched general population. Figure 7B illustrates that patients with descending aneurysms do have a poorer outlook than those with ascending aneurysm. Figure 7C illustrates that patients with dissection fare more poorly than patients free of dissection. And, Figure 7D shows that prognosis depends on size of the aortic aneurysm: patients with larger aneurysms do more poorly. Careful scrutiny of Figure 7D reveals that that TAA is
186 Coady and Elefteriades Figure 7 Key natural history graphs from the Yale database. (A) Survival of patients with unrepaired thoracic aortic aneurysm compared to that of the age and sex-matched general population. (B) Poorer outlook of patients with descending compared to ascending thoracic aortic aneruysm. (C) Adverse impact of aortic dissection on outlook. (D) Larger aneurysms do more poorly in the long run. (E) Elective surgical therapy is very safe, and restores excellent long-term prognosis. Source: From Ref. 1. indeed a lethal disease, but that it takes years for this lethality to express itself. Please note that it is not until after three years of follow-up, even in the largest aneurysms, that the survival curve drops significantly. Figure 7E demonstrates the excellent survival after elective surgical therapy for TAA. Note that emergent surgical therapy leads to much poorer long-term survival. These graphs argue strongly for elective, prophylactic surgical extirpation of the aneurysmal thoracic aortic aorta, before rupture or dissection—which either result in death or require emergent surgery—have a chance to occur. Aortic Growth Our team has found that calculation of growth rate is more complicated than simply subtracting original size from current size and dividing by time. Rizzo (52), from the Yale School of Public Health, has developed exponential equations that permit rigorous calculation of growth rates for large populations of TAA patients. Growth rate estimates were obtained for our entire population and for subgroups with specific risk factors by means of a multivariable regression analysis in which aneurysm growth followed an exponential path. In particular, the natural logarithm of the difference between the last measured size and the first measured
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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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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
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Page 235 and 236: 206 Shahriari and Farkas properties
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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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