Acute Aortic Disease.. - Index of

More documents

Recommendations

Info

Inflammation and Remodeling in the Thoracic Aorta 153 TAAs, protein production continues to occur, but this production becomes overwhelmed by protein destruction (36). The chief culprits in the breakdown of the matrix structure are the matrix metalloproteinases (MMPs). The MMPs are a group of zinc dependent enzymes whose role, in both physiologic and pathologic states, is to break down the extracellular matrix (37). Without the MMPs, normal growth and angiogenesis could not occur (38). These enzymes are active in a wide array of disease processes, from periodontal disease (39) to congestive heart failure (40–42). The activity of the MMPs is normally held in check by their natural inhibitors, known as the tissue inhibitors of metalloproteinases (TIMPs). When an imbalance between the MMPs and TIMPs exists, tissue destruction can ensue. In no disease process is the role of MMPs more clear than aneurysm disease, and thoracic aneurysms are no exception to this rule. A number of studies, including those in our laboratory, have noted increased expression of MMPs at the DNA, RNA, and protein level in TAAs. In particular, overexpression of MMP1, MMP2, MMP3, and MMP9 have been noted (43). In addition, we have noted an increase in the MMP to TIMP ratio in thoracic aneurysms, resulting in a condition that favors proteolysis (36). These enzymes serve to break down the building blocks of the thoracic aortic media, most importantly collagen and elastin. In animal models of TAA, inhibiting the production of these enzymes limits aneurysm formation and progression. Interplay Between Mechanical Forces and Remodeling Once the aneurysm process begins, its progress is usually assured. This is likely because the changes that occur in the thoracic aortic wall lead to increased wall stress, which leads to greater inflammation, which leads to further remodeling, perpetuating a vicious cycle. The components of wall stress include pressure, lumen diameter, and wall thickness. As the aneurismal aorta remodels, the lumen diameter increases, and the wall thins. Both of these conditions lead to increased wall stress. Increased wall stress leads to greater inflammatory and proteolytic activity within the aortic wall, and more outward remodeling. Once a critical diameter is reached, the aorta loses its elastic properties, and the energy transmitted during systole cannot be effectively absorbed. Once the tensile strength of the aorta is matched by the stress applied (usually at about six centimeters diameter at a pressure of 200 mmHg for the ascending aorta) aortic rupture or dissection ensues (44) (Fig. 5). WHAT IS MEASURABLE AND WHAT IS MODIFIABLE? A number of studies have recently been completed or are ongoing to answer these questions. Currently available imaging technology, coupled with a comprehensive database, has already allowed us to develop predictive models of thoracic aortic expansion and complications (45–50). While these models work well on a population based sample, further investigations are required to predict which patients with aneurysm require more urgent intervention. Targets of these investigations begin
154 Botta et al. Wall stress (kPa) 1000 800 600 400 200 0 Normals < 4cm 4.1-5cm 5.1-6cm > 6 cm aortic diameter(cm) Figure 5 From our mechanical studies on the aneurysmal ascending aorta. Note the exponential relationship between wall stress and aneurysm size in ascending aortic aneurysms. Dark bars represent blood pressure of 100 mmHg; light bars represent blood pressure of 200 mmHg. Lines at 800 to 1000 kPa represent range of maximum tensile strength of human aorta. It is no wonder that the aneurysmal aorta ruptures or dissects, especially under stress or exertion. at the DNA level in tissues, and proceed through the RNA and protein expression level (51–54). To assess risk without aortic tissue requirement, circulating biomarkers are beginning to be assessed. We have recently completed work that has identified a group of single nucleotide polymorphisms from peripheral blood samples that are reflective of aneurysm risk (55). Work is now underway to harness these data and develop a micro-array chip that would be broadly applicable as a predictive test for aneurysm propensity. We have also begun to investigate the correlation between tissue levels and circulating levels of MMP-9, which is responsible for the breakdown of elastin in TAAs. We have identified a correlation in MMP-9 levels between these two locations (blood and tissue) (56). Study is ongoing to determine if MMP-9, among other biomarkers is predictive of aneurysm expansion or complications. If so, measurement of serum MMP-9 levels would greatly enhance the decisionmaking process in those who are being evaluated for thoracic aneurysm disease. For aortic dissection, evaluation of circulating levels of d-dimers, which are products of cross-linked fibrin degradation, has emerged as an extremely sensitive tool for diagnosis (57,58). If the D-dimers are not elevated, an acute aortic dissection can almost certainly be excluded. Is it possible to prevent, arrest, or reverse the process of aortic remodeling? In animal models, the answer is affirmative (59–64), and limited data in humans seem to concur (65–68). A number of agents or modalities have been shown to
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
Page 31 and 32:
2 Nienaber and Ince Table 1 Risk Co
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
Page 39 and 40:
10 Nienaber and Ince Figure 4 Curve
Page 41 and 42:
12 Nienaber and Ince Figure 6 Evolu
Page 43 and 44:
14 Nienaber and Ince dissection, su
Page 45 and 46:
16 Nienaber and Ince (A) (B) Probab
Page 47 and 48:
18 Nienaber and Ince Table 5 Risk P
Page 49 and 50:
20 Nienaber and Ince of the predila
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
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 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
Page 99 and 100:
70 Raghupathy and Eagle Figure 1 Sp
Page 101 and 102:
72 Raghupathy and Eagle SIGNS A tho
Page 103 and 104:
74 Raghupathy and Eagle patients ma
Page 105 and 106:
76 Raghupathy and Eagle Table 5 Dia
Page 107 and 108:
78 Raghupathy and Eagle Table 6 A S
Page 109 and 110:
80 Raghupathy and Eagle Figure 6 (A
Page 111 and 112:
82 Raghupathy and Eagle Figure 9 (A
Page 113 and 114:
84 Raghupathy and Eagle EDITOR’S
Page 115 and 116:
86 Raghupathy and Eagle 30. Erbel R
Page 117 and 118:
88 Raghupathy and Eagle is highly l
Page 119 and 120:
90 Elefteriades and Rizzo required
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
Page 153 and 154: 124 Milewicz et al. Figure A Distri
Page 155 and 156: 126 Elefteriades and Koullias Figur
Page 157 and 158: 128 Elefteriades and Koullias prope
Page 160 and 161: 8 Matrix Metalloproteinases in Aort
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
Page 232:
Natural History of Thoracic Aortic
Page 235 and 236:
206 Shahriari and Farkas properties
Page 237 and 238:
208 Shahriari and Farkas Figure 2 E
Page 239 and 240:
210 Shahriari and Farkas Less than
Page 241 and 242:
212 Shahriari and Farkas helpful if
Page 243 and 244:
214 Shahriari and Farkas Figure 6 A
Page 245 and 246:
216 Shahriari and Farkas (68). Many
Page 247 and 248:
218 Shahriari and Farkas Figure 9 H
Page 249 and 250:
220 Shahriari and Farkas fistula is
Page 251 and 252:
222 Shahriari and Farkas MEGS is de
Page 253 and 254:
224 Shahriari and Farkas 26. Svenss
Page 255 and 256:
226 Shahriari and Farkas 63. Fehren
Page 258 and 259:
14 Acute Aortic Dissection: Anti-im
Page 260 and 261:
Acute Aortic Dissection 231 lamella
Page 262 and 263:
Acute Aortic Dissection 233 P t is
Page 264 and 265:
Acute Aortic Dissection 235 From th
Page 266 and 267:
Acute Aortic Dissection 237 Figure
Page 268 and 269:
Acute Aortic Dissection 239 concern
Page 270 and 271:
Acute Aortic Dissection 241 Table 2
Page 272 and 273:
Acute Aortic Dissection 243 dissect
Page 274 and 275:
Acute Aortic Dissection 245 22. Bax
Page 276 and 277:
Acute Aortic Dissection 247 62. Lin
Page 278:
Acute Aortic Dissection 249 DISSCUS
Page 281 and 282:
252 Elefteriades and Griepp ACUTE A
Page 283 and 284:
254 Elefteriades and Griepp Figure
Page 285 and 286:
256 Elefteriades and Griepp sometim
Page 287 and 288:
Page 289 and 290:
Page 291 and 292:
262 Elefteriades and Griepp to a se
Page 293 and 294:
264 Elefteriades and Griepp Natural
Page 295 and 296:
266 Elefteriades and Griepp CONCLUS
Page 297 and 298:
268 Elefteriades and Griepp DISCUSS
Page 299 and 300:
270 Brinster et al. thoracic aneury
Page 301 and 302:
272 Brinster et al. Figure 1 Retrop
Page 303 and 304:
274 Brinster et al. artery. Z3 land
Page 305 and 306:
276 Brinster et al. or ischemia of
Page 307 and 308:
278 Brinster et al. registry arm (2
Page 309 and 310:
280 Brinster et al. Table 3 Early P
Page 311 and 312:
282 Brinster et al. According to th
Page 313 and 314:
284 Brinster et al. ranged from 1 t
Page 315 and 316:
Table 4 Meta-Analysis of Tevar for
Page 317 and 318:
288 Brinster et al. conventional op
Page 319 and 320:
290 Brinster et al. using no (or lo
Page 321 and 322:
292 Brinster et al. Table 5 Risk Fa
Page 323 and 324:
294 Brinster et al. wire manipulati
Page 325 and 326:
296 Brinster et al. Thoracoabdomina
Page 327 and 328:
298 Brinster et al. 25. Hagan PG, N
Page 329 and 330:
300 Brinster et al. 60. Elefteriade
Page 331 and 332:
302 Brinster et al. 98. Liu ZG, Sun
Page 333 and 334:
304 Brinster et al. 131. Szeto WY,
Page 335 and 336:
306 Brinster et al. 100% 90% 80% 70
Page 337 and 338:
308 Brinster et al. ● “Long-ter
Page 339 and 340:
310 Hackmann et al. treatment. New
Page 341 and 342:
312 Hackmann et al. tissue than in
Page 343 and 344:
314 Hackmann et al. Table 1 Pharmac
Page 345 and 346:
316 Hackmann et al. Some anti-hyper
Page 347 and 348:
318 Hackmann et al. inhibits NF-κB
Page 349 and 350:
320 Hackmann et al. Patients with C
Page 351 and 352:
322 Hackmann et al. ACKNOWLEDGMENTS
Page 353 and 354:
324 Hackmann et al. 34. Thompson RW
Page 355 and 356:
326 Hackmann et al. 70. LeMaire SA,
Page 357 and 358:
328 Hackmann et al. 105. Marra DE,
Page 359 and 360:
330 Hackmann et al. DISCUSSION AND
Page 361 and 362:
332 Elefteriades Diseases of the th
Page 363 and 364:
334 Elefteriades Table 1 Individual
Page 365 and 366:
336 Elefteriades Table 1 Individual
Page 367 and 368:
338 Elefteriades Failure to Diagnos
Page 369 and 370:
340 Elefteriades of physicians on t
Page 371 and 372:
342 Elefteriades Figure 3 Computed
Page 373 and 374:
344 Elefteriades reviewed over the
Page 375 and 376:
346 Elefteriades DISCUSSION AND COM
Page 377 and 378:
348 Elefteriades Figure 1 (See colo
Page 379 and 380:
350 Elefteriades that are the subje
Page 382 and 383:
SECTION VII: SYNTHESIS 20 The Key L
Page 384 and 385:
The Key Lessons of This Book—In a
Page 386 and 387:
Page 388:
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
Page 397 and 398:
368 Index [Thoracic aortic aneurysm
Page 399 and 400:
Figure 1.C Note from schematic depi
Page 401 and 402:
Figure 8.1 Dramatic clinical exampl
Page 403 and 404:
Figure 11.2 Proposed schema for the
Page 405:
Figure 19.1 Future prospects in car
show all

Acute Aortic Disease.. - Index of

Create successful ePaper yourself

Delete template?

Save as template?