Acute Aortic Disease.. - Index of

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Future Prospects 349 1 0 1 Y: [PCA component 20(8.324% variance)] Z: [PCA component 3 (5.972% variance)] 0 1 Case Control X: [PCA component 1 (62.27% variance)] Figure 2 (See color insert) RNA “Signature” analysis allows effective discrimination (in three- dimensional space) of aneurysm patients (“cases”) from controls, on the basis of examination of peripheral blood alone. evidence suggest, this is only the beginning (4,5). Predictions are that CT scanners will become so compact that they will be carried by paramedics in the field and on ambulances, relaying images to the emergency department from the moment of arrival on the scene. Diagnosis will be expedited dramatically. Catheters may be replaced by “remote-controlled electronic devices that … like microscopic missiles, travel through vessels to reach organs or tissues”(4). These devices are powered by the energy of an MRI field. Tissue imaging and molecular imaging are on the horizon. Improved imaging has been the cornerstone of advancement in the diagnosis and treatment of aneurysms and dissections. More of the same appears to be in store. BIOMARKERS FOR CLINICAL FOLLOWUP, EVENT PREDICTION, AND SURGICAL DECISION MAKING As we have seen in Chapter 12, on the natural history of thoracic aortic aneurysms, the diameter of the aorta is key in determining the patient’s future and in our making the decision for pre-emptive surgical extirpation of the aneurysmal aorta. However, dimensional criteria, while very helpful, are far from ideal. The potential to use biomarkers to study the progression of aortic disease is very real. It is now becoming clear that serum levels of matrix metalloproteinases (MMPs) are quite reflective of tissue levels for both abdominal and thoracic aortic aneurysms (see Chapters 8 and 17). This raises the potential to follow the aneurysm state by serial assessment of serum MMPs. One study (6) already shows that MMP serum levels rise as aneurysms increase in size. Another (7) suggests that MMP rise may precede or accompany acute aortic dissection. Our “RNA Signature” profile may also change over time. It may be that a “blip” in one or more of these potential biomarkers may herald the onset of the acute aortic events
350 Elefteriades that are the subject of this textbook. Such a “blip” may alert us that pre-emptive surgery should be carried out. MECHANICAL PROPERTIES AS MONITORS AND PREDICTORS As explained in Chapter 7, on mechanical properties of the aorta, we have accumulated evidence that aortic distensibility and wall stress can be measured by epiaortic echocardiography. If we can make similar measurements by TEE, then this can become a clinical tool. We may, in the future, monitor not only size on a yearly basis, but also aortic distensibility and aortic wall stress. We may be able to develop criterion levels of these biomechanical parameters that signal looming adverse events and mandate surgical intervention. CONTROL OF ENVIRONMENTAL FACTORS As detailed in Chapters 10 and 11, it is becoming clear that physical exertion and extreme emotion are often the triggers that cause aortic dissection in an individual who is susceptible on the basis of genetic predisposition and underlying aortic enlargement. We are already beginning to limit physical activity in patients with known aortic enlargement. Although we cannot live our lives without stress, it is possible that altering a patient’s life milieu (e.g., job change) may decrease episodes of stress. Also, medications may be applied to limit emotional stress in extremely vulnerable individuals. We have also recommended widespread screening of individuals engaging in extreme physical training, to uncover occult aortic enlargement and prevent tragic deaths. We hope that this recommendation will see application, despite societal and economic restraints. MATRIX METALLOPROTEINASE ANTAGONISTS TO PREVENT ANEURYSM GROWTH We are on the cusp of effective treatment for aneurysm disease. The role of beta blockers, which have emerged as standard of care therapy despite a paucity of evidence, has been controversial for decades. New evidence, presented in Chapters 8 and 17, suggests that direct MMP inhibitors may slow the process of aneurysmal degeneration. Although the antibiotic doxycycline has been used most widely, in the pioneering efforts of Dr. Thompson, many specific MMP inhibitors are under development and hold great promise for the future. Medical science has been excited by the work of Dietz et al., with the angiotensin receptor blocker Losartan in preventing aneurysm growth in an animal model of Marfan’s disease. As Dr. Botta explains in Chapter 7, this drug as well may work through a final MMP-related pathway. The future is bright for drug therapy based on breakthroughs in understanding the molecular pathophysiology of aneurysm disease.
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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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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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Page 391 and 392: 362 Index Aging, aortic aneurysms a
Page 393 and 394: 364 Index Cytokines, aortic aneurys
Page 395 and 396: 366 Index Pathoanatomy classificati
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Page 399 and 400: Figure 1.C Note from schematic depi
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Page 403 and 404: Figure 11.2 Proposed schema for the
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