Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3925_Библиотеки_им_академика_М_И_Перельмана
.pdf
https://t.me/med1917
353
20
The Key Lessons of This
Book—In a Nutshell
John A. Elefteriades
Section of Cardiothoracic Surgery, Yale University,
New Haven, Connecticut, U.S.A.
The various chapters of this textbook have provided up-to-the minute information
from authorities in a wide variety of disciplines impacting on acute aortic
diseases—from genetics to pathophysiology to imaging to clinical presentation
and diagnosis to surgical treatment and future prospects. It is hoped that this infor-
mation will benefit a multidisciplinary group of medical professionals interested
in and involved with these disorders and, ultimately, contribute to the clinical care
of affected patients.
Every chapter likely includes some information not previously familiar to
each of us, even those of as intimately involved in the scientific investigation
and/or clinical care of acute aortic diseases.
For purposes of review and ease of assimilation, the key points from each
chapter are summarized in Table 1.
Osler said a hundred years ago that “there is no disease more conducive to
clinical humility than aneurysm of the aorta.” Although this is still true, through
our combined efforts in many related disciplines, we are definitely gaining ground
against this disease—in favor of our patients.
SECTION VII: SYNTHESIS
https://t.me/med1917
354 Elefteriades
Table 1 A Summary of the Key Points of Each Chapter
Chapters Title Author names Key points
1 Terminology and
Classification
Nienaber Dr. Nienaber classifies aortic dissections based on:
Etiology
Anatomy
Acuity
Clinical predictive patterns.
The Stanford classification (Type A = ascending, Type B = descending) has been
most widely adopted.
Alternate classifications (e.g., Lansman’s) are more detailed anatomically
and accommodate more of the precise information now available from
three-dimensional imaging.
2 Symptoms and Signs Isselbacher Aortic dissection is “the great masquerader,” with protean potential manifestations.
Abrupt onset of pain distinguishes dissection from myocardial infarction.
“One cannot make a diagnosis that one does not consider.”
3 Imaging Danias CT, MRI, and TEE are all acceptable imaging modalities for the diagnosis of
aneurysm and dissection.
In ambiguous cases, dual modalities should be employed.
4 Putting It All Together Eagle The most reliable presenting symptom characteristic of aortic dissection is sudden
onset of severe pain in the anterior chest or back.
Anterior chest pain suggests ascending dissection.
Interscapular back pain suggests descending dissection.
Painless aortic dissection can occur (6% of cases), especially in the elderly and in
diabetics.
Hypotension on presentation with aortic dissection portends poor prognosis
(mortality >50%).
Differentiation from MI is essential, as anticoagulation may have disastrous
consequences in case of aortic dissection.
Diagnosis of aortic dissection requires a flap: “No flap, no dissection.” IMH and
PU are nonflap variants of dissection-type disease.
https://t.me/med1917
The Key Lessons of This Book—In a Nutshell 355
5 Epidemiology: Incidence,
Prevalence, and
Trends
Elefteriades/Rizzo Aneurysm causes more deaths in the U.S. than HIV disease
Aneurysm and dissection are truly increasing in frequency (not just being
diagnosed more effectively).
Ruptured AAA affects about 10/100,000 patients per year.
Ruptured AAA or AAD affect about 7/100,000 patients per year.
If a screening abdominal ultrasound exam is negative at 65 years of age, that
patient will never die of ruptured AAA.
6 Genetics of Aortic
Aneurysm and
Dissection
Milewicz Marfan’s disease is autosomal dominant.
Three-fourth of Marfan’s cases are transmitted from parents, but one-fourth
represent new mutations.
Over 600 specific mutations have been registered, producing the Marfan’s
abnormality in fibrillin-1.
A second Marfan’s locus has recently been identified.
Loeys–Dietz is a newly described genetic syndrome associated with aneurysm disease.
Familial thoracic aneurysm disease occurs frequently, in the absence of named
genetic syndromes like Marfan’s disease.
Dr. Milewicz’s ground-breaking work has identified the following loci for familial
aortic aneurysm:
TAAD1 (20–30% of cases)
FAA1
TGFBR2 (5% of cases)
MYH11.
Much attention is currently being focused on the TGF-β pathway and its potential
blocking by Losartan.
7 Mechanical Properties Elefteriades/Koullias Biomechanical properties of the aorta can be calculated from echocardiographic
measurements.
Distensibility becomes seriously impaired and wall stress increases dangerously
at an aortic diameter of 6 cm.
Monitoring of mechanical properties of the aorta may become feasible in the near
future.
(Continued )
https://t.me/med1917
356 Elefteriades
Table 1 A Summary of the Key Points of Each Chapter (Continued )
Chapters Title Author names Key points
8 MMPs in Aortic Disease Botta/Elefteriades MMPs are definitely involved in the pathogenesis of aortic aneurysm and dissection.
MMP levels are elevated in abdominal and thoracic aneurysms.
Blood levels mirror tissue levels of MMPs.
Inhibition of MMPs makes physiologic sense for impeding aneurysm growth.
The ARBs (Losartan) have shown promise in very preliminary studies
9 Molecular Biology of
Aortic Destruction
Botta/Tang/Tellides/
Elefteriades
The aorta “plays a game of catch” with the stroke volume, absorbing some of the
force in systole and transmitting this stored energy back in diastole. Thus, the
aorta is “much more than a tube.”
VSMCs serve both a motile and a secretory function.
The balance between production and destruction of matrix proteins is largely
orchestrated by the VSMCs.
MMPs are excessively active in aneurysm disease, leading to excess proteolsis in
the aortic wall.
Aneurysm formation proceeds through a combination of inflammation,
inflammation-induced proteolysis, and mechanical forces.
Once the aneurysm process begins, its progress is assured.
10 Weight Lifting and
Aortic Dissection
Elefteriades Evidence is mounting that weight lifting brings on acute dissection via extreme
elevation of BP during the effort cycle.
Aneurysm patients should be cautioned against heavy lifting or straining.
Individuals embarking on strenuous exercise programs should be screened for
occult aortic dilation.
11 Timing of Acute Aortic
Events
Elefteriades Extreme emotion or exertion bring on dissection in an aorta susceptible by virtue
of pre-existing enlargement.
12 Natural History of
Aortic Aneurysm
Coady/Elefteriades Aortic aneurysm is lethal, but indolent, growing at about 0.1 cm/yr for the
ascending aorta.
Acute aortic events (rupture and dissection) begin to occur with frequency at
5.5–6 cm diameter of the ascending aorta.
Pre-emptive surgical intervention before those sizes are reached is prudent.
https://t.me/med1917
The Key Lessons of This Book—In a Nutshell 357
13 Ruptured Aneurysm:
Abdominal and
Thoracic
Ashirari/Farkas/
Elefteriades
For ruptured AAA, caution in fluid resuscitation is warranted, even at the expense
of moderate hypotension, so as to prevent free rupture prior to clamp
application.
For AAA, initial supraceliac clamping is often essential.
For AAA, catheter-based therapy for rupture is growing in popularity.
For TAA, the “clamp and sew” technique (without perfusion adjuncts) is appropriate
when free rupture has occurred.
Surgical techniques are depicted in chapter figures.
14 Acute Aortic Dissection:
Anti-Impulse Therapy
Fuster Death rate is 1–2%/hr early after acute aortic dissection.
Elastin (distensible) absorbs the force of cardiac contraction, but collagen
(inelastic) supplies the tensile strength of the aorta.
The adventitia is the “strength” layer of the aorta.
By Laplace’s law, thickness of the arterial wall decreases wall stress.
The maximal rate of pressure rise (dp/dt
max
) appears to be the most important
determinant of aortic rupture and the progression of dissection.
IV esmolol is a nearly ideal agent for initial lowering of dp/dt for acute aortic
dissection, because of its:
Rapid onset of action
Short half-life of distribution
Rapid elimination
Suitability in renal/hepatic disease (hydrolyzed by erythrocytes).
When β-blockers are contraindicated, calcium channel blockers are the next line
agents, although conclusive evidence of a beneficial action on dp/dt is lacking.
Nitroprusside should not be used without β-blockade, as alone it can increase
dp/dt.
Pericardiocentesis appears to be contraindicated for tamponade from acute Type A
aortic dissection, even as an interim measure before the OR.
(Continued )
https://t.me/med1917
358 Elefteriades
Table 1 A Summary of the Key Points of Each Chapter (Continued )
Chapters Title Author names Key points
15 Surgical Therapy: A
Primer
Elefteriades/Griepp First job is to achieve patient survival:
Discretion should be used in replacing the aortic arch.
Discretion should be used in replacing the aortic root.
An open distal anastomosis, under DHCA, is preferable.
Descending dissections can achieve a survival of 80–90% with “anti-impulse”
therapy alone.
Operation for descending dissection is required in case of rupture, uncontrolled
symptoms or rapid enlargement, or organ ischemia.
Surgical techniques are depicted in chapter figures.
16 Stent Therapy Bavaria Complications of stent therapy arise most commonly from accessing the central
aorta from the femoral or iliac arteries.
Stent therapy appears to have a role in treatment of:
Aortic transection
Certain descending dissections
IMH and PAU
Ruptured descending aneurysms.
Stent therapy has no current role in ascending dissections.
Longer term f/u is required to determine the durability and appropriate role of
stent therapy.
Paraplegia, stroke, and renal failure still occur, even with stent therapy.
17 Long-Term Suppressive
Therapy
LeMaire/Thompson Aneurysm formation involves:
Extracellular matrix proteolysis
Chronic inflammation
Cytokine activity
SMC loss.
https://t.me/med1917
The Key Lessons of This Book—In a Nutshell 359
The benefit of β-blockers for long-term prevention of aneurysm expansion and
rupture is far from proven.
Potential future treatment options include:
Statin medications
Anti-inflammatory agents (COX-2 inhibitors)
Immunosuppressants (rapamycin)
Antibiotics (doxycycline)
ARBs (Losartan).
Suppressive therapy may have a role in treatment of patients with predisposing
conditions, patients with small aneurysms, patients who are poor surgical
candidates, patients with chronic aortic dissection, patients who have already
undergone open or endovascular repair (to protect the remaining aorta), and
patients with aneurysms undergoing nonaortic operations (to prevent aneurysm
“activation” and early rupture).
18 Litigation Elefteriades Consider aortic dissection.
Check D-dimer (100% sensitive).
Image liberally.
Consider the “Triple Rule-Out CT scan” (PE, CAD, dissection).
19 Future Prospects Elefteriades DNA diagnosis of aneurysm diathesis.
RNA diagnosis of acute dissection.
Biomarkers for clinical followup.
Genetic-guided conventional drug development.
Control of physical and emotional stress.
20 Key Lessons Elefteriades See this Table.
Abbreviatons: AAA, abdominal aortic aneurysm; ARBs, angiotensin receptor blockers; BP, blood pressure; CAD, coronary artery disease; CT, computed tomography;
DHCA, deep hypothermic circulatory arrest; IMH, intramural hematoma (of aorta); IV, intravenous; MI, myocardial infarction; MMPs, matrix metalloproteinases;
MRI, magnetic resonance imaging; OR, operating room; PE, pulmonary embolism; PAU, penetrating ulcer (of aorta); SMC, smooth muscle cells; TAA, thoracic
aortic aneurysm; TEE, transesophageal echocardiography; VSMC, vascular smooth muscle cells.
https://t.me/med1917
https://t.me/med1917
361
Index
AAA. See Abdominal aortic aneurysm
Abdominal aortic aneurysm (AAA), 133
endovascular repair, 217–221
epidemiology of, 207–308
open repair, 217–219
Abdominal pain, 32–33
Abnormal blood pressure, 34–35
Acuity classification, 13–15
acute phase, 13–14
subacute phase, 14
Acute aortic diseases, legal
considerations, 329–342
delay in surgical therapy, 340
failure to diagnose, 335–339
failure to prevent paraplegia, 341
family patterns, 341
review of cases, 331–334
Acute aortic dissection, 227–241
anti-impulse therapy, 233–234
aortic wall
disruption, 229–234
structure, 228–229
blood pressure control, 233–234
clinical diagnosis of, 29–37
dyspnea, 34
pain, 30–33
signs, 34–36
syncope, 33–34
medical treatment of, 234–241
general considerations, 234–237
pharmacological therapy, 237–241
[Acute aortic dissection
pharmacological therapy]
beta blockers, 237, 240
calcium channel blockers, 240
intravenous agents, 238–239
trimethaphan camsylate, 240–241
vasodilators, 241
symptoms, 30
Acute aortic syndrome
thoracic aortic endovascular repair
and, 278–289
rupture, 288–289
type A dissection, 278
type B dissection, 279–286
traumatic transection, 286–288
type B dissection, meta-analysis,
283–284
Acute ascending aortic dissection
chronic arch dissection, 260
operation type, 254–259
aortic valve management, 256
closed distal anatomosis, 256
dissected aortic tissue handling, 257
formal aortic arch replacement,
257–259
open distal anatomosis, 256
proximal resection extent, 255–256
resected aortic arch, 256–257
retrograde extension, 250–251
surgical procedures and, 250
Acute descending aortic dissection, 260–263
https://t.me/med1917
Соседние файлы в папке Библиотека им академика М.И. Перельмана