Acute Aortic Disease.. - Index of

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Classification of Aortic Dissection 19 Figure 11 Graphical display of International Registry of Acute Aortic Dissection-code of entry site locations in relation to 30-day-mortality. The more proximal the entry site location the higher the in-hospital mortality in percent. imaging technology, differentiates type A dissections, based on location of the most proximal entry site, into subgroups with distinct prognoses. Moreover, by defining dissection according to proximity to the aortic valve, we found a declining death rate with increasing distance between entry site and aortic valve. Not surprisingly, IRAD had previously identified shock and tamponade as significant predictors of death (40,74,75,78,79), supporting the concept of a correlation of entry site and prognosis (Fig. 11). Through incorporation of diagnostic imaging information from modern technology, the IRAD classification system ideally connects anatomic detail with prognostic information. The knowledge of entry location, thus, may help to estimate the individual risk in proximal dissection better than either the Stanford or DeBakey classification. Prognosis in proximal dissection is diverse considering differences of 30-day-mortality related to entry location. Patients may be classified according to the IRAD-code as A1, A2, and A3. Type B dissection is prognostically the same, regardless of entry site, and the IRAD subclassification, B1 to B3, is useful only from a descriptive perspective. Various mechanisms may explain the inverse relationship between the anatomic proximity of the entry site and the outcome in patients with acute dissection. First, the more proximal the origin of the dissected aortic layer, the more likely is a mechanical obstruction of coronary ostia, rupture within the pericardial sac (79), and/or new aortic regurgitation. Second, loss of elasticity in proximal aortic segments may predispose to aortic wall disintegrity preferentially adjacent to the sinuses of valsalva (80). Third, cyclic changes of aortic radius and distensibility (pressure strain elastic modulus) are most compromised at the level
20 Nienaber and Ince of the predilated sinus junction, according to the law of Laplace (81). In addition, the proximal segment of the aortic wall is known to lose distensibility with hypertension or increasing age. In this context, aortic regurgitation and the fluid dynamics of a bicuspid aortic valve may relate to these pathophysiologic mechanisms. CONCLUSION With the historic evolution of different classifications of aortic dissection, various prognostic mechanisms and management strategies have eventually emerged. The medical community faces the responsibility to integrate the clinical complexity of the disorder, improving classification algorithms and eventually understanding aortic dissection better via improved classification. REFERENCES 1. Fuster V, Halperin JL. Aortic dissection: a medical perspective. J Card Surg 1994; 9:713–728. 2. DeSanctis RW, Doroghazi RM, Austen WG, et al. Aortic dissection. N Engl J Med 1987; 317:1060–1067. 3. Kodolitsch Y, Schwartz AG, Nienaber CA. Clinical prediction of acute aortic dissection. Arch Intern Med 2000; 160:2977–2982. 4. Cigarroa JE, Isselbacher FM, DeSanetis RW, et al. Diagnostic imaging in the evaluation of suspected aortic dissection: old standards and new directions. N Engl J Med 1993; 238:38–43. 5. De Paepe A, Devereux R, Dietz H, et al. Revised diagnostic criteria for the Marfan syndrome. Am J Med Genet 1996; 62:417–426. 6. Sakai L, Keene D, Engvall E. Fibrillin. A new 350 kD glycoprotein is a compound of extracellular microfibrills. J Cell Biol 1986; 103:2499–2509. 7. Collod G, Babron MC, Jondeau G, et al. A second locus for Marfan syndrome maps to chromosome 3p24.2–p25. Nat Genet 1994; 8:264–268. 8. Milewicz DM, Pyeritz RE, Crawford ES, et al. Marfan syndrome: defective synthesis, secretion and extracellular matrix formation of fibrillin by cultured dermal fibroblasts. J Clin Invest 1992; 89:79–86. 9. Ramirez F. Fibrillin mutations in Marfan syndrome and related phenotypes. Curr Opin Genet Dev 1996; 6:309–315. 10. Aoyama T, Francke U, Dietz H, et al. Quantitative differences in biosynthesis and extracellular deposition of fibrillin in cultured fibroblasts distinguish five groups of Marfan syndrome patients and suggest distinct pathogenetic mechanisms. J Clin Invest 1994; 94:130–137. 11. Boileau D, Jondeau G, Babron MC, et al. Autosomal dominant Marfan-like connectivetissue disorder with aortic dilatation and skeletal anomalies not linked to the fibrillin genes. Am J Hum Genet 1993; 53:46–54. 12. Lesauskaite V, Tanganelli P, Sassi C, et al. Smooth muscle cells of the media in the dilatative pathology of ascending thoracic aorta: morphology, immunoreactivity for osteopontin, matrix metalloproteinases, and their inhibitors. Hum Pathol 2001; 32:1003–1011.
Page 2 and 3: Acute Aortic Disease
Page 4 and 5: 15. Heart Failure: Basic Science an
Page 6: 52. Clinical, Interventional, and I
Page 9 and 10: Informa Healthcare USA, Inc. 270 Ma
Page 12 and 13: Introduction Informa Healthcare has
Page 14 and 15: Foreword There is no disease more c
Page 16 and 17: Preface Over 100 years ago, the gre
Page 18: Preface xi Some distinguishing feat
Page 21 and 22: xiv Acknowledgments Above all, than
Page 23 and 24: xvi Contents 6. Genetic Basis of Th
Page 26 and 27: Contributors Nili Avidan Division o
Page 28: Contributors xxi Arun Raghupathy Di
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Page 33 and 34: 4 Nienaber and Ince In addition to
Page 35 and 36: 6 Nienaber and Ince CLASSIFICATION
Page 37 and 38: 8 Nienaber and Ince Lansman’s Cla
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Page 51 and 52: 22 Nienaber and Ince 34. Pieters FA
Page 53 and 54: 24 Nienaber and Ince 75. Mehta RH,
Page 55 and 56: 26 Nienaber and Ince hematoma (IMH)
Page 57 and 58: 28 Nienaber and Ince One good featu
Page 59 and 60: 30 Isselbacher SYMPTOMS Pain Experi
Page 61 and 62: 32 Isselbacher and wane in severity
Page 63 and 64: 34 Isselbacher The mechanisms are u
Page 65 and 66: 36 Isselbacher deficits are most co
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Page 69 and 70: 40 Danias spinal arteries) and the
Page 71 and 72: 42 Danias Figure 2 Anteroposterior
Page 73 and 74: 44 Danias However, due to the dista
Page 75 and 76: 46 Danias TEE is highly sensitive f
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Page 79 and 80: 50 Danias Figure 6 Transverse slice
Page 81 and 82: 52 Danias hematoma, CT was reported
Page 83 and 84: 54 Danias Figure 9 Transverse black
Page 85 and 86: 56 Danias Figure 12 Single phase-co
Page 87 and 88: 58 Danias restricted to the absolut
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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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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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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