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Acute Aortic Dissection 241 Table 2 Advantages and Disadvantages of Intravenous Agents for the Management of Acute Aortic Dissection Drug Anti-impulse agents Advantages Disadvantages Beta blockers Decrease dp/dtmax Contraindicated in bradycardia, and blood pressure bronchospasm Esmolol Rapid onset, short duration High fluid volume, drug levels increased by morphine Metoprolol Inexpensive, widely available Longer duration of action Labetalol Alpha and beta blockade, maintains cardiac output Longer duration of action Propranolol Inexpensive, widely available Longer duration of action Calcium Decrease blood pressure and Contraindicated in bradycardia blockers maybe dp/dtmax Verapamil Ganglionic blocker Can be used in setting of bronchospasm Constipation, limited evidence Trimethaphan Can be used when beta Unpredictable hemodynamics, blockers contraindicated anticholinergic, tachyphylaxis Vasodilator Decrease blood pressure Increase force of left ventricular agents ejection, reflex tachycardia Nitroprusside Most rapid onset and shortest duration Thiocyanate toxicity Enalaprilat Useful in high renin states Very long duration of action Fenoldopam Intermediate onset and Tachyphylaxis, contraindicated duration in glaucoma Calcium blockers Nicardipine Can be used in the setting Long elimination half life; of bronchospasm interaction with anesthetic agents Diltiazem Can use in bronchospasm, Peripheral edema, gastrointestinal some negative inotropic effect side effects, limited evidence Source: From Refs. 37, 73, 81, and 94. or high-grade heart block, and should be used with caution if there is a history of congestive heart failure or bronchospasm. Esmolol hydrochloride has the advantages of rapid onset on action, short half-life of distribution (two minutes) and elimination (nine minutes), and brief duration of action. Serum drug levels are undetectable 20 to 30 minutes after cessation of infusion. Esmolol is hydrolyzed by erythrocyte cytosol esterases into methanol and an acid metabolite with a low affinity for beta receptors. Therefore, its pharmacokinetic properties are not significantly altered in the setting of renal insufficiency or liver disease (76). Esmolol interacts with several commonly used drugs, including those that play a role in the medical and surgical management of patients with aortic
242 Sanz et al. dissection, although these interactions are of minimal clinical significance. Administered concurrently with morphine, serum esmolol levels were found in an open-label study to be 46% higher than in esmolol infusion alone; morphine levels were unchanged (77). This effect can be compensated for simply by prudent dose titration. In another study, esmolol was found to delay recovery from succinylcholine-induced neuromuscular blockade by less than three minutes (78). Similarly, in rabbits, esmolol decreased the neuromuscular blocking potency of mivacurium and prolonged its effect by 30% (79). Side effects from esmolol are typical of those for beta blockers, although, due to its short duration of action, this drug is the best choice in its class for a trial in patients for whom there is concern about bronchospasm. Caution should be used in patients with a history of congestive heart failure, as esmolol may be responsible for a large fluid load with the current 10 mg/mL formulation, especially at high doses. A double-strength, 20 mg/mL preparation is available. In sum, esmolol has been called an “ideal” beta blocker for critically ill patients due to its favorable pharmacokinetic, hemodynamic, and metabolic properties (80). Alternative beta-blocking agents include metoprolol tartrate, which is inexpensive and widely available, as well as propranolol and labetalol. The latter is both an alpha and nonspecific beta blocker, with an alpha to beta-blocking ratio of 1:7. It has been shown to be safe and effective in the management of hypertensive emergencies, and it maintains cardiac output (81). Calcium Channel Blockers For patients for whom beta blockade is contraindicated or not tolerated, calcium channel blockers are commonly used for the management of acute aortic dissection. The use of calcium channel blockers in this setting is based on an understanding of their pharmacology, but no data exists supporting this practice (37). Verapamil, in particular, has been shown to decrease contractility and dp/dtmax in some studies (82,83), although not all (84,85). Impulse appears to be unchanged by diltiazem, whereas dp/dtmax was increased by nifedipine in a canine model (86). Thus, for patients not receiving beta blockers, verapamil might be a reasonable alternative, although conclusive evidence for its use is lacking. For patients already receiving intravenous beta-blocker therapy, calcium channel blockers are not typically used. Infact, concomitant use of intravenous beta blockers and calcium channel antagonists is generally considered contraindicated, due to potential for severe toxicity (brady cardia and hypotension). Nicardipine is a 1,4-dihydropyridine with potent vasodilatory and blood pressure lowering effects. It may cause reflex sympathetic activity, and thus patients receiving this drug should be monitored closely (87). It also potentiates neuromuscular blockade from vecuronium (88), and its effects are modified by flurane inhalational anesthetics (89). Trimethaphan Camsylate Trimethaphan is an older, uncommonly used agent with a significant side effect profile, but one that may be particularly effective for patients with acute aortic
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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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Page 220 and 221: Natural History of Thoracic Aortic
Page 232: Natural History of Thoracic Aortic
Page 235 and 236: 206 Shahriari and Farkas properties
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Page 239 and 240: 210 Shahriari and Farkas Less than
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Page 245 and 246: 216 Shahriari and Farkas (68). Many
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Page 262 and 263: Acute Aortic Dissection 233 P t is
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Page 266 and 267: Acute Aortic Dissection 237 Figure
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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
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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
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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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