Acute Aortic Disease.. - Index of

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Genetic Basis of Thoracic Aortic Aneurysms 105 Figure 2 (See color insert) Variable clinical presentation of individuals with transforming growth factor β receptor (TGFBR1 or TGFBR2) mutations. Individuals may present with hypertelorism and malar flattening (A); bifid uvula (B); marked hypertelorism with exotropia (C); premature fusion of the coronal suture of the skull (arrow, D); marked tortuosity of the aorta (arrow head ), aortic root and subclavian artery aneurysms (arrows) or tortuous abdominal aorta (arrow) (E,F,H); micrognathia, retrognathia, downslanting palpebral fissures, and skeletal features including pectus excavatum, scoliosis, and pes planus (G,I,J). Source: From Refs. 21, 51. Figure 3 Heterozygous germline transforming growth factor β receptor TGFBR1 and TGFBR2 mutations in syndromic and nonsyndromic aortic disease. Genomic and protein structure of the TGFBR1 and TGFBR2 genes showing known mutations previously identified in MFS, LDS, Furlong syndrome, and TAAD. Source: From Ref. 58.
106 Milewicz et al. Turner syndrome is a sex aneuploidy syndrome in which the most frequent chromosome constitution is 45, X (also written 45, XO to indicate the loss of one of the two X chromosomes). A significant number of patients with Turner syndrome have other karyotypes that involve mosaicism or abnormalities of the second X chromosome. The incidence of Turner syndrome is approximately 1 in 5000 live female births. The typical features of Turner syndrome include short stature, gonadal dysgenesis, unusual facial appearance, neck webbing, low posterior hairline, broad chest with widely spaced nipples, and an increased frequency of renal and cardiovascular abnormalities. The cardiovascular problems include bicuspid aortic valve (BAV), coarctation of the aorta, hypertension, and TAAD (29,30). Aortic root dilatation is present in approximately 40% of women with Turner syndrome. It has recently been suggested that the risk of aortic dissection in patients with Turner syndrome is increased with growth hormone treatment (31). Routine surveillance of the aortic root diameter is currently recommended for women with Turner syndrome. Noonan syndrome is an autosomal dominant condition that shares many phenotypic features with Turner syndrome. Congenital heart abnormalities, including pulmonary valve stenosis, hypertrophic cardiomyopathy, and other structural defects are present in 50% to 80% of patients. TAAD is a rare finding in patients with Noonan syndrome (32,33). Ehlers-Danlos syndrome Type IV “or the vascular form” is a disorder characterized by thin, translucent skin, spontaneous bowel rupture, and arterial fragility (34). The vascular fragility includes aneurysm with rupture and dissection. Although the aorta can be involved, it is typically the smaller arteries that rupture or dissect in this syndrome. This condition results from mutations in the COL3A1 gene, which encodes a polypeptide of Type III collagen. The vascular complications of this syndrome are difficulty to manage, leading to premature death at a median age of 48 years. A few other genetic conditions predispose individuals to TAAD. Polycystic kidney disease is an autosomal dominant, late onset disorder characterized by progressive cyst development and bilaterally enlarged polycystic kidneys. Although this disease is primarily associated with intracranial aneurysms, a rare patient will have TAAD (35). Ehlers-Danlos syndrome Type VI (kyphoscoliotic form) is characterized by kyphoscoliosis, joint laxity, and muscle hypotonia and is caused by deficient activity of the enzyme procollagen lysine hydroxylase (36). Vascular rupture is a life-threatening feature of this disorder, and both aortic dilatation/dissection and rupture of medium-sized arteries may occur. FAMILIAL THORACIC AORTIC ANEURYSMS AND DISSECTIONS The initial studies to determine if there was a genetic contribution to nonsyndromic TAAD were familial aggregation studies. Family histories were obtained on patients with ascending aortic aneurysms or dissections to determine if they had first-degree relatives with similar aortic disease. These studies have indicated that between 13% and 19% of individuals referred for repair of a TAAD have a
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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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Page 89 and 90: 60 Danias In conclusion, in the rig
Page 91 and 92: 62 Danias DISCUSSION AND COMMENTARY
Page 93 and 94: 64 Danias tomography, among others.
Page 95 and 96: 66 Danias cardiac silhouette. The a
Page 97 and 98: 68 Raghupathy and Eagle the inciden
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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
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Page 151 and 152: 122 Milewicz et al. DISCUSSION AND
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Page 176 and 177: 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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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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