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Genetic Basis of Thoracic Aortic Aneurysms 123 dissections have TGFBR1/2 mutational analysis to screen for mutations in these genes as a cause of disease because finding such a mutation has significant implications for the subsequent management of the patient and their family. We hope that in the future, more genes will be identified that can be screened for mutations in families with thoracic aortic aneurysms and dissections. Do you think that the ARB drugs will prove to be a panacea for aneurysm disease? Does this possibility seem almost too good to be true? It will be determined if the success of losartan in blocking the progressive aortic disease in a mouse model of MFS will also apply to humans with MFS, in a clinical trial comparing beta adrenergic blocking agents to losartan. The clinical trial, funded by NHLBI and using the Pediatric Heart Network, will recruit patients under the age of 26 years with MFS and randomize them to either drug. A similar trial of adults with MFS is in the planning stage. It is not certain if the success of losartan in the animal model of MFS will translate to humans with MFS. In addition, we do not know the role of TGF beta signaling in aortic disease in patients who do not have MFS. Further studies are needed to determine if ARB drugs will prove to be a panacea for aneurysm disease. References 1. Glesby MJ, Pyeritz RE. Association of mitral valve prolapse and systemic abnormalities of connective tissue. A phenotypic continuum. JAMA 1989; 262:523–528. 2. Dietz HC, McIntosh I, Sakai LY, et al. Four novel FBN1 mutations: significance for mutant transcript level and EGF-like domain calcium binding in the pathogenesis of Marfan syndrome. Genomics 1993; 17:468–475. Editor’s Comments Dr. Milewicz et al. have made extraordinary contributions to the fundamental genetic understanding of aortic diseases, which they enumerate clearly in this chapter. Their work reflects tremendous industry, acumen, and insight. The entire vascular community respects and is grateful for it. Our own team is working with molecular geneticists at Celera Diagnostics in California to explore the automated SNP avenue of investigation that Dr. Milewicz describes. Our preliminary findings have shown that (1) aneurysm disease has a unique “RNA signature” in the peripheral blood. (2) This signature, if confirmed in further investigations, promises to facilitate clinical diagnosis of aneurysm disease on a molecular genetic basis. Our separate investigations on 30,000 DNA SNPs is ongoing. We hope to identify specific alterations in the genome of aneurysm patients. The DNA studies look at the blueprint which programs the body is to be made. The RNA studies look at which proteins are actually upregulated or downregulated in terms of active manufacture at the time of sampling. In terms of clinical genetic patterns, our most recent examination of 520 family pedigrees of patients with thoracic aortic aneurysms indicates that there are distinct patterns of inheritance among family members. (3) Family members
124 Milewicz et al. Figure A Distribution of aneurysm sites among family of probands with thoracic aortic aneurysms. of patients with ascending aortic aneurysms are very likely to manifest their aneurysms in the ascending aorta as well. However, family members of patients with descending aortic aneurysms are more likely to manifest their aneurysms in the descending aorta (Fig. A). References 1. Elefteriades JA. Beating a sudden killer. Sci Am 2005; 293(2):64–71. 2. Elefteriades JA, Wang YY, et al. Gene Expression Profiling of Peripheral Blood for Diagnosis of Aortic Aneurysm. California: Cambridge Healthtech Institute’s Molecular Medicine Tri-Conference, San Francisco, February 22, 2006. 3. Albornoz G, Coady MA, Roberts M, et al. Familial thoracic aortic aneurysms and dissection: Incidence, modes of inheritance, and phenotypic patterns. Ann Thorac Surg (in press).
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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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Page 113 and 114: 84 Raghupathy and Eagle EDITOR’S
Page 115 and 116: 86 Raghupathy and Eagle 30. Erbel R
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Page 121 and 122: 92 Elefteriades and Rizzo Table 1 S
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Page 125 and 126: 96 Elefteriades and Rizzo Table 3 C
Page 127 and 128: 98 Elefteriades and Rizzo DISCUSSIO
Page 129 and 130: 100 Milewicz et al. KNOWN GENETIC S
Page 131 and 132: 102 Milewicz et al. Table 2 Quick G
Page 133 and 134: 104 Milewicz et al. ascending aorti
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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
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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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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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