Acute Aortic Disease.. - Index of

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Imaging of Aneurysms and Dissections 63 Imaging technology advances at a rapid pace. Over the last few years, CT technology has evolved from single slice to spiral to multislice technology, and the number of detectors in multislice scanners has increased from 4 to 16 to 64. One hundred and eight- and 256-slice scanners are in development and likely to be in clinical practice soon. With the increasing number of detectors, one issue of concern is that radiation exposure increases proportionately. With the 64 detectors, the absorbed radiation dose for a cardiac study is ∼11 mSv, almost double that of a 16-slice scanner (Reference 18, above). This may in fact become a limiting factor in the widespread applicability of scanners with higher number of radiation detectors. A different approach to conventional CT imaging is represented in the so-called flat-panel technology. This approach does not use rotating detectors but rather a flat detecting surface that allows for volumetric high-resolution imaging. Preliminary application of this technology has been reported for imaging of the coronary arteries in an excised swine heart (1). At the present time, the computing power needed for in vivo cardiovascular imaging is not practical, although in the future computer technology may surpass this frontier. Do you anticipate that in the future interventional vascular procedures can be performed under “CT fluoro,” obviating the need for angiographic control of these procedures? Currently, interventional vascular procedures are performed under fluoroscopy. One drawback of this approach is the considerable radiation exposure. CT fluoroscopy, at least with current technology, could potentially facilitate the three-dimensional appreciation of the inter-relationships of the anatomic structures visualized during interventional procedures. CT guidance, however, would not eliminate the radiation exposure, and in fact the radiation dose would likely be higher than the current projection angiographic approach. On the other hand, real-time MR guidance would be a significant advance, as this would eliminate ionizing radiation exposure. Catheters equipped with receiver coils at tip have been developed and shown to be adequately imaged at a rate of a few frames per second. MR advancement of catheters in the aorta of experimental animals has been shown to be possible (2), and even feasibility data in peripheral arterial interventions in humans have been described (3). Because of the minimal biologic cost that this approach offers, it is likely that this technology will become a clinical tool in the not too distant future. Are there any totally new imaging modalities on the horizon, different from CT or MR? Technology advances at a rapid pace. Over the last decade we have witnessed a shift from macro-anatomical imaging to micro-molecular and cellular imaging. Developments have focused more on coronary atherosclerosis, as this is the major cause of morbidity and mortality in humans. These developments, however, can be applied to the entire vascular tree, where atherosclerosis can develop. Newer technologies that attempt to assess the atherosclerotic plaque include thermography, angioscopy, spectroscopy, elastography, and optical coherence
64 Danias tomography, among others. Excellent reviews of these new technologies have recently been published (4,5). Positron-emission-tomography (PET) has also been reported to visualize atherosclerotic plaque by way of selective FDG uptake at the vessel wall. This may be an indicator of increased metabolic activity at the plaque, and may carry additional prognostic information (6,7). Finally combination technologies are now being developed, whereby anatomic information is merged to functional-metabolic data. The most commonly used such technology is PET-CT, although PET-MRI, ultrasound-MRI and X-ray-MRI systems have been or are being developed. It is certain not only that the technological developments in the years to come will allow us to accurately evaluate the anatomic macroscopic appearance of the cardiovascular system, but also to get insights into the pathophysiologic mechanisms of cardiovascular disease that can lead to more targeted therapeutic approaches. References 1. Knollmann F, Pfoh A. Image in cardiovascular medicine. Coronary artery imaging with flat-panel computed tomography. Circulation 2003; 107(8):1209. 2. Bock M, Volz S, Zuhlsdorff S, et al. MR-guided intravascular procedures: real-time parameter control and automated slice positioning with active tracking coils. J Magn Reson Imaging 2004; 19(5):580–589. 3. Dick AJ, Raman VK, Raval AN, et al. Invasive human magnetic resonance imaging: feasibility during revascularization in a combined XMR suite. Catheter Cardiovasc Interv 2005; 64(3):265–274. 4. Pasterkamp G, Falk E, Woutman H, Borst C. Techniques characterizing the coronary atherosclerotic plaque: influence on clinical decision making? J Am Coll Cardiol 2000; 36(1):13–21. 5. Davies JR, Rudd JH, Weissberg PL. Molecular and metabolic imaging of atherosclerosis. J Nucl Med 2004; 45(11):1898–1907. 6. Tatsumi M, Cohade C, Nakamoto Y, Wahl RL. Fluorodeoxyglucose uptake in the aortic wall at PET/CT: possible finding for active atherosclerosis. Radiology 2003; 229(3):831–837. 7. Okane K, Ibartaki M, Toyoshima H, et al. 18F-FDG accumulation in atherosclerosis: use of CT and MR co-registration of thoracic and carotid arteries. Eur J Nucl Med Mol Imaging 2006; 33(5):589–594. Editor’s Counterpoint Dr. Danias, in his superlative review of diagnostic imaging in aortic diseases, gently impugns the utility of the plain chest x-ray in thoracic aortic aneurysm and dissection. The Editor respectfully takes issue with this, believing that the plain film contributes immensely to the early diagnosis of aneurysm and dissection. The plain chest x-ray shows the contours of the thoracic aorta quite well, given the contrast between the air-filled lungs and the fluid-filled aorta. The normal contours of the aorta are quite familiar and generally very well seen (Figs. A and B). The ascending aorta, if substantially enlarged, will appear outside the upper right
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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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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
Page 67 and 68: 38 Isselbacher 3. Nallamothu BK, Me
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
Page 77 and 78: 48 Danias faster, with higher resol
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: 62 Danias DISCUSSION AND COMMENTARY
Page 95 and 96: 66 Danias cardiac silhouette. The a
Page 97 and 98: 68 Raghupathy and Eagle the inciden
Page 99 and 100: 70 Raghupathy and Eagle Figure 1 Sp
Page 101 and 102: 72 Raghupathy and Eagle SIGNS A tho
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Page 107 and 108: 78 Raghupathy and Eagle Table 6 A S
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Page 113 and 114: 84 Raghupathy and Eagle EDITOR’S
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Page 117 and 118: 88 Raghupathy and Eagle is highly l
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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
Page 135 and 136: 106 Milewicz et al. Turner syndrome
Page 137 and 138: 108 Milewicz et al. dissection in t
Page 139 and 140: 110 Milewicz et al. Figure 5 Haplot
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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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