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Matrix Metalloproteinases in Aortic Aneurysm 137 Hovespian et al. (47) were able to demonstrate concordance between circulating and tissue levels of MMPs in AAA disease. For human TAA, recent work at our center has demonstrated, for the first time, that there is a correlation between tissue levels of MMP-9 and circulating levels of this enzyme. This pilot study involved ten patients with thoracic aneurysms who underwent elective operative repair of ascending TAAs. We noted an extremely strong (R squared = .913) correlation between tissue and circulating MMP-9 levels (Fig. 4). We are currently continuing our work in this area, and if this correlation holds true, it could represent an advance in the way patients with early TAAs are monitored. MMPs as “biomarkers”? The fourth question is whether circulating MMPs are reflective of overall expansion and complication rates of TAAs. For AAAs, McMillan et al. demonstrated a relationship between circulating MMP 9 levels and abdominal aortic diameter (56). For TAAs, no published study to date has addressed this issue, but it is one on which work is progressing at our institution. Benefit from pharmacologic inhibition? The answer to the fifth question as to whether pharmacologic manipulation of MMPs can result in a beneficial change in aneurysm behavior is slowly beginning to become clear. The idea of medical therapy for TAAs is not new. For patients with early or inoperable TAAs, decreased growth rate with “anti-impulse therapy”—limiting the heart rate, blood pressure, and pressure up-slope in systole (Dp/Dt)—is a standard and well-accepted practice, both for AAAs and TAAs, which has met with varied success since its introduction in 1965 (62–64), mostly in limiting progression of aortic dissections. This therapy is based on the premise that if the forces on the aortic wall, most importantly the wall stress, can be limited, aortic expansion will also be ameliorated. The mainstay of anti-impulse therapy is currently beta-adrenergic receptor blockade. However, enthusiasm for aneurysm treatment with beta blockade should be tempered by the results of a randomized trial of propranolol for aneurysm Tissue MMP9 (pg/ml) 450000 400000 350000 300000 250000 200000 150000 100000 50000 0 0 200000 MMP Correlations with Plasma and Tissue y = 0.3536x + 21344 R 2 = 0.913 400000 600000 800000 1000000 1200000 Plasma MMP9 (pg/ml) Series1 Linear (Series1) Figure 4 Correlation between serum and tissue matrix metalloproteinase levels in thoracic aortic aneurysms. (Unpublished Yale data.)
138 Botta et al. management that was terminated early due to poor tolerability and increased mortality in the study group, although the aneurysm expansion rate was lessened (65). The beneficial effects of beta blockers on aneurysm expansion, however, may not be solely attributable to mechanical forces. Similar changes in heart rate, blood pressure, and Dp/Dt can be achieved with calcium channel blocking medications (66), but these medications have been shown to be independently associated with increased risk of AAA development, with an odds ratio of 2:6 over those who do not take this class of drugs (67). It is probably no coincidence that amlodipine, a calcium channel blocker, potentiates MMP activity and elastin degradation (68). It is also probably not coincidental that beta-adrenergic blockade is associated with decreased tumor necrosis factor alpha expression, which leads to decreased MMP production (69,70). Specific inhibition of MMPs may become the mainstay of pharmacologic therapy for TAAs. The literature is replete with reports of animal models demonstrating decreased formation or progression of aneurysms through either MMP inhibition or targeted MMP gene deletion. Mosorin et al. (71) published a randomized controlled trial, which demonstrated a decreased expansion rate in human AAAs after administration of doxycycline, an antibiotic with known MMP inhibitory properties. Further investigations of MMP inhibition using doxycycline and other MMP inhibitors in AAAs are ongoing. For TAAs in humans, this question has not been directly addressed, although reports of animal models of TAAs are yielding encouraging results. Recently, great interest has been focused on an article by Habashi et al. in which losartan, an angiotensin receptor type I (ATI) antagonist, was used in a murine model of Marfan’s syndrome to prevent aortic root aneurysms and pulmonary alveolar septation defects (72). Alhough the mechanism of beneficial effects of ATI blockade with losartan is not clearly elucidated, the authors postulated several possible explanations. These included decreased mechanical stress on the aorta, which the authors state is unlikely because the control group was treated with beta blockade to achieve similar blood pressure control to the study groups, direct inhibition of transforming growth factor beta (TGFB) expression, indirect inhibition of TGFB expression through inhibition of thrombospondin production, decreased proliferation of vascular smooth muscle cells (VSMCs) and subsequent vessel wall fibrosis, and decreased Smad-2 dependent signaling and fibrosis. If one carefully examines each of the postulated mechanisms, however, the downstream effect of each mechanism can lead to MMP inhibition. With regard to TGFB inhibition, TGFB has been shown to enhance MMP expression in sites of inflammation (73,74). VSMCs, whose proliferation is inhibited by losartan, are an abundant source of MMPs in TAAs (60). These findings, as well as preservation of VSMC density in early ascending thoracic aneurysms, were also demonstrated in our laboratory (75). Thrombospondin has also been shown to modulate MMP-2 activity in VSMCs (76). Concerning decreased Smad-2 dependent signaling, a study by Dixon et al. (77) demonstrated that chronic ATl receptor blockade abrogated this process, and led to decreased MMP1 and 2 production. When one carefully
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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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Page 117 and 118: 88 Raghupathy and Eagle is highly l
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Page 121 and 122: 92 Elefteriades and Rizzo Table 1 S
Page 123 and 124: 94 Elefteriades and Rizzo 70s, this
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
Page 141 and 142: 112 Milewicz et al. A genome wide s
Page 143 and 144: 114 Milewicz et al. Structural anal
Page 145 and 146: 116 Milewicz et al. assembly of a h
Page 147 and 148: 118 Milewicz et al. in the nuclei o
Page 149 and 150: 120 Milewicz et al. 22. Furlong J,
Page 151 and 152: 122 Milewicz et al. DISCUSSION AND
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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
Page 202 and 203: SECTION IV: TREATMENT OF ACUTE AORT
Page 204 and 205: Natural History of Thoracic Aortic
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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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