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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3734_Библиотеки_им_академика_М_И_Перельмана
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Management ofType B Aortic Dissection
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These medications also work to prevent reex tachycardia which can occur with
the use of vasodilator medications. In the event of contraindications to beta-blocker
usages such as asthma and heart failure, calcium channel blockers can be used as an
alternative. Heart rate should be kept below 60bpm with systolic blood pressure
below 120mmHg [2].
Hydralazine and sodium nitroprusside were used historically for the management of blood pressure, however, are closely associated with reex tachycardia and
increasing left ventricular contractile force (dP/dT), thus should be avoided in
patients with dissection. Nicardipine is a vasodilator of choice in patients with dissection. Patients often require multiple antihypertensive medications to achieve the
guideline recommendation of <120mmHg [35].
Pain control includes the use of morphine which also provides a reduction in
stress-induced hypertension due to its sedative properties. Poorly controlled pain can
lead to a hyperadrenergic state further potentiating the progression of dissection [36].
In the rare event of hypotension, it is crucial to conrm the absence of pseudohypotension as a result of measurement in an extremity with ow compromise. Blood
pressure should be measured in both arms and both legs to determine the highest
central blood pressure [2]. Fluid resuscitation should be performed with crystalloid,
PRBCs, or other colloid solutions.
During hospitalization for the uncomplicated type B dissection patient, continued blood pressure control should be maintained with the goal of SBP between
100–120 mmHg and heart rate <60 bpm [2]. This is most commonly initially
achieved through the use of parenteral medications, however during the hospital
stay, the patient should be transitioned to oral antihypertensives as a bridge to discharge and long-term blood pressure control. Continued telemetry monitoring and
arterial line monitoring are important measures during the patient’s stay in the
intensive care unit. As the patient stabilizes on oral medications, transfer to a telemetry unit, and subsequently to home is reasonable if there are no signs of end-organ
ischemia or malperfusion, blood pressure has been stabilized to goal with oral medications, and repeat imaging is without signicant progression of the disease.
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Endovascular Repair
Optimal medical therapy remains the standard of care for uncomplicated dissection,
however, this strategy fails to prevent long-term aortic-related morbidity and mortality. The paucity of supporting data has created controversy surrounding the optimal treatment strategy for acute type B dissection. Medical therapy has low early
mortality in centers experienced in the management of acute aortic syndrome, however, 30% of the patients will require an operation due to enlargement of the chronic
dissection within the rst ve years. Recent data and trends show a paradigm shift
favoring early TEVAR in acute type B dissection. TEVAR improves the chance of
reverse remodeling of the descending thoracic aorta and therefore reduced the rate
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of reoperations in the follow-up. TEVAR is a reasonable option for patients with
aortic disease, however, some concern remains regarding reintervention rates and
aneurysmal dilatation in the setting of dissection.
A meta-analysis was performed of 39 studies involving a total of 609 patients
who underwent stent-graft placement for a type B dissection [37]. Procedural success was reported in 98% of patients. Major complications were reported in 11%
with the most dreaded neurologic complications in 2.9% of patients. Periprocedural
stroke was encountered more frequently than paraplegia (1.9% versus 0.8%). The
major complication rate was signicantly higher for acute compared with chronic
dissection (21.7% versus 9.1%). Minor complications occurred in 2.5%. The rate of
complications compared favorably with previous reported surgical series. The inhospital mortality rate was 5.2%. Thirty-day mortality was 5.3% and was signicantly higher for acute compared with chronic dissection (9.8% versus 3.2%) [37].
Outcomes were much better in centers that had performed more than 20 endovascular procedures compared with fewer. This included signicantly lower rates of overall
complications (7.7 versus 20.9 percent), neurologic complications (1.0 versus 5.7 percent), and 30-day mortality (3.2 versus 8.5 percent). One report evaluated 19 patients
with an acute dissection (15 with type B) and an indication for surgery [37]. Complete
thrombosis of the false lumen was achieved in 79 percent, and revascularization with a
relief of ischemic symptoms occurred in 76 percent of obstructed aortic branch sites.
The 30-day mortality rate was 16 percent, and morbidity was 21 percent morbidities
included small bowel and renal infarction and lower extremity gangrene [37].
In an IRAD report of 384 type B dissections, 46 (12%) were managed with endovascular stent-grafting [38]. Stenting was only performed for patients who had at
least eight weeks of medical management. Inpatient mortality was only in three
patients (6.5%). Two-year follow up of 49 patients was performed for patients who
underwent stent-graft placement for treatment of acute or chronic type B dissection.
Serial computed tomography (CT) studies in the 32 patients with type B aortic dissection showed that, at two years, total occlusion of the false lumen was achieved
with acute dissection in 76 percent of patients [39].
ADSORB is a randomized trial that compared outcomes between patients with
acute uncomplicated TBAD who were treated with best medical therapy alone
(n=31) or medical treatment in addition to TEVAR (n=31) [40]. The 30-day mortality and neurological complication rates were 0% for both groups, but a signicantly higher rate of favorable remodeling (complete false lumen thrombosis) was
reported at 1year after stenting (57 vs. 3%, p<.001). The study was not powered
for mortality or late aortic intervention.
INSTEAD is the larger trial that prospectively randomized patients with uncomplicated chronic TBAD to continuing optimal medical therapy (n=68) or medical
therapy in addition to stent-graft placement (n=72) [41].
At 2years, despite a higher rate of favorable remodeling in the stented group,
all-cause and aorta-related mortality were similar between the two groups. There
was also no signicant difference in the rate of secondary interventions as crossovers to endovascular repair in the medical therapy group were balanced by stent
extensions and access-vessel repairs in the TEVAR group. Long-term analysis at
5years did, however, demonstrate a signicantly higher aorta-specic mortality in
Management ofType B Aortic Dissection
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389
medically managed patients than those who underwent elective stenting (19.3 vs.
6.9%, p=.045) [41].
INSTEAD, XL was a follow-up study of the subjects enrolled in the INSTEAD
trial and continued original analysis for 5years following the original procedure [42].
Analysis for subjects managed with optimal medical therapy (OMT) and TEVAR
(n=72) versus OMT alone (n=68) included all-cause mortality (0% versus 16.9%;
P=0.0003), aorta-specic mortality (0% versus 16.9%; P=0.0005), and progression
(4.1% versus 28.1%; P=0.004). Stent graft induced false lumen thrombosis at 5years
after TEVAR was associated with both improved survival and less progression of disease in 90.6% of subjects (P<0.0001) [42]. Despite this data, the treatment strategy for
acute type B dissection remains controversial. Early treatment has been suggested to
positively affect overall reverse aortic remodeling and visceral ow (Fig.1). High-risk
morphologic features including partial thrombosis in false lumen, total aortic diameter>4cm, false lumen diameter>2.2cm, and refractory pain should be considered
Pre 1yr
Fig. 1 Three year follow-up imaging on type B dissection following thoracic endovascular aortic
repair (TEVAR). Positive aortic remodeling demonstrated in post-TEVAR images with progressive
thrombosis of proximal false lumen over time
2 yrs
3 yrs
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when evaluating a patient for early TEVAR versus OMT alone. Additionally, given
that the benet associated with early TEVAR is not achieved until years following the
intervention as illustrated in the INSTEAD XL ndings, patient age and comorbidities
should be considered before deciding to proceed with TEVAR (Fig.2).
Complicated Acute Type B Dissection
Up to 50% of patients with uncomplicated type B dissection will experience
sequelae which can include further propagation of dissection either retrograde converting to a type A, or antegrade with risk for malperfusion syndromes. Additionally,
aneurysm degeneration and possible rupture can occur during the long-term follow
up of these patients [43]. Comorbidities that can be associated with the progression
of an uncomplicated dissection to a complicated state include a bicuspid aortic
valve, underlying connective tissue disorders (such as Marfan syndrome and Loeys
Dietz), aortic coarctation, poorly controlled hypertension, and cocaine abuse [44].
There is an unpredictable variability to blood ow patterns in the dissected aorta,
this can lead to spontaneous resolution of malperfusion syndromes in some cases.
Dynamic obstruction from the prolapse of intimal ap blocking ow into branch vessels can lead to intermittent signs and symptoms. In the event of a direct extension of
dissection into the branch vessel (static obstruction), a more sustained presentation
may occur [2]. Additional contributors to the development of malperfusion post-dissection include arterial thrombosis, embolization, compression of branch vessels from
false lumen expansion, rupture or leakage of the false lumen into surrounding structures, and distortion of the aortic valve leading to acute aortic valve insufciency [2].
Aortic Dissection Acuity
Uncomplicated
1. No rupture
2. No malperfusion
3. No high-risk features
High-Risk Features
1. Refractory pain
2. Refractory hypertension
3. Bloody pleural effusion
4. Aortic diameter>4cm
5. Radiographic only malperfusion
6. Readmission
7. Entry tear: lesser curve location
8. False lumen diameter>22mm
Complicated
1. Rupture
2. Malperfusion
From: Lombardi JV, Hughes GC, Appoo JJ, Bavaria JE, Beck AW, Cambria RP, Charlton-Ouw K,
Eslami MH, Kim KM, Leshnower BG, Maldonado T. Society for Vascular Surgery (SVS) and
Society of Thoracic Surgeons (STS) reporting standards for type B aortic dissections. The Annals
of Thoracic Surgery. 2020 Jan 27.
Management ofType B Aortic Dissection
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a1 a2
b1 b2
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c1 c2
Fig. 2 Pre and post-treatment IVUS images of perivisceral true lumen of uncomplicated TBD
dissection. True lumen in very small Celiac (a1) SMA (b1) and renal (c1) arteries, post-treatment
the true lumen has dramatically expanded after covering the entry tear with a stent graft (a2, b2, c2)
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The presence of malperfusion syndrome is a signicant contributor to mortality
in patients with type B aortic dissection. The most common cause of death in
patients with type B aortic dissection is mesenteric ischemia [2]. Fortunately, mesenteric ischemia is uncommon, presenting in only 3.7% of cases [45].
Endovascular stent grafting has been used as a less invasive alternative to open
surgery for the management of type B aortic dissection. The stent-graft is positioned
to cover the intimal ap to seal the entry site of the dissection, resulting in thrombosis of the false lumen [46]. With successful coverage of the intimal tear, perfusion is
restored in patients with dynamic aortic obstruction in approximately 95% of
patients.
Initial repair of the dissection often resolves peripheral ischemia; however additional distal stenting of the aorta or rarely fenestration of the intimal ap may be
required to achieve adequate perfusion in cases of persistent peripheral or visceral
ischemia.
Despite the favorable aortic remodeling reported after TEVAR in patients with
aortic dissection, a review of 1108 patients found that there is the continued growth
of the thoracic aorta in 6.6–84% of patients [47]. In a review of 397 patients with
TBAD, abdominal aorta growth was reported in 10–54% of cases [47].
Stabilization of the distal ap has been investigated using the PETTICOAT technique (provisional extension to induce complete attachment). In this approach, a
proximal endograft is placed in the true lumen, with a bare-metal stent extension
distally. With the deployment of the bare metal stent, the aim is to stabilize the distal
intimal ap and allow blood ow to the visceral vessels [48]. In one review which
investigated outcomes of acute (89 cases) and subacute (54) type B dissection, the
PETTICOAT procedure had an overall 30-day mortality rate of 4.9% and a clinical
success rate of 90.2% [49]. Early expansion of the true lumen of the thoracic and
abdominal aorta was observed; however there was no evidence of improved short
and mid-term survival when compared to standard stent-grafting [49].
The Study of Thoracic Aortic Type B Dissection Using Endoluminal Repair
(STABLE I) trial is a nonrandomized multicenter prospective study that was performed to evaluate the safety and performance of the Zenith Dissection endovascular stent system. This system is specically designed for the treatment of dissection
and is comprised of a proximal stent-graft with distal bare-metal stent based on the
PETTICOAT approach [50]. In this study, 86 patients were enrolled, inclusion criteria included acute phase and non-acute phase patients with TBAD presenting with
branch vessel obstruction or compromise, impending rupture, resistant hypertension, persistent pain or symptoms, or rapid aortic growth [50]. During this feasibility study, 30-day mortality was 5.5% for acute patients and 3.2% for nonacute [50].
Kaplan-Meier estimate of freedom from dissection-related mortality at 5years was
83.9% for acute patients and 90.1% for nonacute patients [50]. False lumen thrombosis was exhibited in 74.1% of acute patients and 58.8% of non-acute patients at
5years, and a majority of patients experienced stable or reduced thoracic aortic size
at 5years (acute, 65.5%; nonacute, 81.3%) [50].
The STABLE II study pivotal study was a follow up prospective, nonrandomized
multicenter study including 73 patients with acute type B aortic dissection again
Management ofType B Aortic Dissection
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evaluating the Zenith Dissection Endovascular System based on the PETTICOAT
procedure. Inclusion criteria were expanded in this trial to include rupture and malperfusion. The primary safety endpoint was freedom from adverse events at 30days
and the primary effectiveness endpoint was the rate of survival at 30days. The
Kaplan-Meier estimate of freedom from all-cause mortality was 80.3% (+/− 4.7%)
at one year. One year follow up identied complete or partial thrombosis in 100%
of patients at the stent site and 97.4% of the patient within the bare stent region.
Thoracic aortic growth >5mm after one year was observed in 14.9% of patients in
the area of the stent-graft, 38.5% of patients within the bare stent site.
In a comparative analysis performed by Sobocinski etal., TEVAR alone was
compared to the PETTICOAT technique for the treatment of acute complicated
TBAD by use of secondary analyses to compare cohorts from high-volume aortic
centers in Europe using TEVAR alone versus the STABLE cohorts [51].
Reintervention rates at one year were similar between the TEVAR and STABLE
cohorts (11.1% TEVAR, 12.8% STABLE). Both cohorts exhibited positive thoracic
aorta remodeling; however in the STABLE cohort, the investigators observed a statistically signicant increase in true lumen volume at the abdominal aorta while the
TEVAR group did not. Malperfusion related mortality was statistically lower in the
STABLE group versus TEVAR (2.3% vs. 12.2%) [51].
Building on the foundation of the PETTICOAT technique and STABLE I and
STABLE II, the concept of STABILISE was introduced. Stent assisted balloon
induced disruption and relamination in aortic dissection repair (STABILISE) was
rst described by Hofferberth etal. in 2014 [52]. In this approach, a stent-graft is
used to cover the proximal intimal tear with a bare-metal stent distally, with the
added step of serial balloon dilatation to the point of intimal ap disruption to return
the dissected intima to the aortic wall [52]. The 30-day mortality rate among the 41
patients treated was 2% with no aortic-related mortality at 12months. All patients
had complete aortic remodeling at the stent graft and bare stent level at follow up,
39% had complete aortic remodeling at the non-stented infrarenal aortoiliac level.
Of those who experienced persistent false-lumen ow at the bare-stent level, the
aortoiliac diameter remained stable in 92% at one year [53].
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Fenestration
Intimal ap fenestration can be performed to equalize pressure between the true and
false lumen as well as serving as an alternative to TEVAR in patients who are at high
risk for spinal cord ischemia or when the false lumen is perfusing a large number of
lumbar or intercostal branch vessels. Fenestration is rarely used in modern practice,
and typically reserved for patients with signicant peripheral or visceral malperfusion or cases where TEVAR may not be possible such as excessive aortic diameter
or intimal tear near crucial branch vessels. Fenestration can be useful for the management of dynamic obstruction; however if a static obstruction is also present,
stenting of the branch vessels should also be considered. It is technically
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demanding, time-consuming, and is associated with signicant patient morbidity.
The exact relationship of each major branch vessel to the intimal ap and false
lumen should be reviewed before the beginning of the procedure. In one study, a
17% early mortality rate was reported after endovascular fenestration with 7% of
these due to false lumen rupture and 10% to malperfusion complications [54]. Long
term outcomes showed freedom from aortic rupture or repair at 1, 5, and 8years of
80.2%, 67.7%, and 54.2% [54]. There are various techniques to achieve the fenestration of the dissection ap. Some authors report an approach by puncture through
the ap with a wire or needle with the subsequent deployment of an angioplasty
balloon to extend the fenestration. Other approaches described include a variety of
techniques centered around wire access in the false and true lumen with subsequent
downward traction to divide the ap longitudinally. These techniques are associated
with signicant potential risks, including intimal ap dehiscence as a result of “snag
and drag” instead of the desired longitudinal fenestration effect [54].
A. Khoynezhad et al.
Open Surgical Repair
Before the advent of TEVAR in the 1990s, open surgical repair provided the only
treatment option that offered any meaningful survival. Surgical repair, similar to
fenestration, is rarely used in modern practice. Since the advent of TEVAR, the
treatment of acute TBAD has shifted to endovascular therapy [55].
The University of Michigan reviewed their outcomes with open or endovascular
repair in patients with acute complicated TBAD.While there was statistically no
difference between the two cohort’s early and late survival, there was a higher rate
of mortality, higher ventilation time, use of blood product, and longer hospital stays
those patients treated with open repair. Also, the TEVAR were older with more
comorbidities [55].
In a retrospective review of the University of Pennsylvania experience from 2002
to 2010, Zeehan etal. reported 77 complicated TBAD treated acutely comparing
TEVAR to conventional treatment, including open surgical repair or optimal medical treatment [56]. 45 patients were treated with TEVAR (26 within 24h of presentation), and 32 patients were in the open surgical repair and optimal medical
treatment group. This group included 20 patients undergoing open surgery repair
(10 of those within 24h of presentation); the remainder were treated with medical
therapy. In hospital, mortality was 4% in the TEVAR group vs 40% in the group
treated with open and medical approaches [56]. Survival at 1, 3, and 5years for
those who underwent TEVAR versus those who underwent open surgical repair was
82%, 79%,79% versus 58%, 54%, 44% [56]. These ndings were confounded by
lumping open and medical treatment together.
In a series of complicated Type B dissections treated in the acute or subacute phase,
Wilkinson showed no signicant difference in hospital mortality, late mortality, or
freedom from re-intervention [55]. The long term follow-up of the patients treated in
the Zeehan series showed the best survival in those treated with TEVAR [56].
Management ofType B Aortic Dissection
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A combined retrospective and meta-analysis study showed no long-term survival
or reintervention benet to either open or endovascular repair of acute TBAD [57].
In the setting of chronic Type B dissections, van Bogerjen etal. showed no longterm survival benet, although the lower re-intervention rate in open compared to
endovascular repair [58]. They did note lower operative mortality in the chronic
setting as compared to that reported for open repairs in the acute phase [58]. Using
a slightly different treatment algorithm treating all complicated Type B with TEVAR
and uncomplicated with optimal medical therapy followed by open or endovascular
repair for OMT failures, Lou etal. found better long term survival in those patients
receiving open repair compared to TEVAR in the chronic phase. Those receiving
acute TEVAR fared better than those who underwent TEVAR for chronic dissection [59].
Despite the increased use of endovascular repair, there are still patients for whom
open repair may be indicated or required. Those beneting from open repair include
younger patients with connective tissue disorder or patients with anatomic constraints for TEVAR, and as a bail-out for complications of TEVAR in the setting of
acute TBAD.
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Outpatient Follow Up
Regardless of the treatment approach, more than 60% of those with aortic dissection
experience aneurysmal growth within 5years [60]. In the outpatient setting, continued close surveillance is vital as aortic remodeling continues. Guidelines recommend repeat imaging at 1, 3, 6, and 12 months following the index event, and
annually after that [2]. Those with stable ndings after 5years may be followed up
in longer intervals. Lifestyle recommendations for the dissection patient should
include the avoidance of strenuous lifting or other isometric exercises that increase
intrathoracic pressures [2]. Additionally, avoidance of activities that put the patient
at risk for sudden deceleration should be discussed. Blood pressure management is
an essential factor in the continued stabilization of aortic dissection, patients should
be counseled on the importance of following their prescribed regimen, as poorly
controlled hypertension can have a disastrous consequence to the dissected aorta.
Future Perspective
Given the suboptimal results of purely medical or surgical therapy in uncomplicated
type B AAD, there has been signicant interest in the use of TEVAR in this patient
cohort. The basis of endovascular therapy is the concept that obliteration and thrombosis of the false lumen may result in improved long-term outcomes and reduce the
need for future reoperation. Furthermore, the newer generation of stent-grafts,
including ones with a lower prole or with absorbable material are being evaluated.
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Once the reverse remodeling after acute TBAD has completed, the stent-graft may
become obsolete, and in these cases an absorb stent-graft would be very benecial
in reducing future complications including infection, migration, branch obstruction
or retrograde dissection.
References
1. Khoynezhad A, Walot I, Kruse MJ, Rapae T, Donayre CE, White RA.Distribution of intimo-
medial tears in patients with type B aortic dissection. J Vasc Surg. 2010 Sep 1;52(3):562–8.
2. Hiratzka LF, Bakris GL, Beckman JA, Bersin RM, Carr VF, Casey DE, Eagle KA, Hermann
LK, Isselbacher EM, Kazerooni EA, Kouchoukos NT. 2010 ACCF/AHA/AATS/ACR/ASA/
SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with thoracic aortic disease. J Am Coll Cardiol. 2010 Apr 6;55(14):e27–129.
3. Hagan PG, Nienaber CA, Isselbacher EM, Bruckman D, Karavite DJ, Russman PL, Evangelista
A, Fattori R, Suzuki T, Oh JK, Moore AG. The International Registry of Acute Aortic
Dissection (IRAD): new insights into an old disease. JAMA. 2000 Feb 16;283(7):897–903.
4. Januzzi JL, Isselbacher EM, Fattori R, Cooper JV, Smith DE, Fang J, Eagle KA, Mehta
RH, Nienaber CA, Pape LA.Characterizing the young patient with aortic dissection: results
from the International Registry of Aortic Dissection (IRAD). J Am Coll Cardiol. 2004 Feb
18;43(4):665–9.
5. Khoynezhad A, Rao R, Trento A, Gewertz B.Management of acute type B aortic dissections
and acute limb ischemia. J Cardiovasc Surg. 2011 Aug;52(4):507–17.
6. Klompas M. Does this patient have an acute thoracic aortic dissection? JAMA. 2002 May
1;287(17):2262–72.
7. Rosman HS, Patel S, Borzak S, Paone G, Retter K.Quality of history taking in patients with
aortic dissection. Chest. 1998 Sep 1;114(3):793–5.
8. Nienaber CA, Eagle KA.Aortic dissection: new frontiers in diagnosis and management: Part
I: from etiology to diagnostic strategies. Circulation. 2003 Aug 5;108(5):628–35.
9. Estrera AL, Miller CC, Goodrick J, Porat EE, Achouh PE, Dhareshwar J, Meada R, Azizzadeh
A, Sa HJ.Update on outcomes of acute type B aortic dissection. Ann Thorac Surg. 2007 Feb
1;83(2):S842–5.
10. Nienaber CA, Zannetti S, Barbieri B, Kische S, Schareck W, Rehders TC.INvestigation of
STEnt grafts in patients with type B Aortic Dissection: design of the INSTEAD trial—a prospective, multicenter, European randomized trial. Am Heart J. 2005 Apr 1;149(4):592–9.
11. Khoynezhad A, Donayre CE, Omari BO, Kopchok GE, Walot I, White RA.Midterm results
of endovascular treatment of complicated acute type B aortic dissection. J Thorac Cardiovasc
Surg. 2009 Sep 1;138(3):625–31.
12. Khoynezhad A, Donayre CE, White RA.Techniques and results of endovascular manage-
ment of acute complicated type B aortic dissection in North America. Rev Cardiovasc Med.
2012;13(4):e176–84.
13. Onitsuka S, Akashi H, Tayama K, Okazaki T, Ishihara K, Hiromatsu S, Aoyagi S.Long-term
outcome and prognostic predictors of medically treated acute type B aortic dissections. Ann
Thorac Surg. 2004 Oct 1;78(4):1268–73.
14. Tsai TT, Evangelista A, Nienaber CA, Trimarchi S, Sechtem U, Fattori R, Myrmel T, Pape
L, Cooper JV, Smith DE, Fang J.Long-term survival in patients presenting with type A acute
aortic dissection: insights from the International Registry of Acute Aortic Dissection (IRAD).
Circulation. 2006 Jul 4;114(1_supplement):I–350.
15. Tsai TT, Evangelista A, Nienaber CA, Myrmel T, Meinhardt G, Cooper JV, Smith DE, Suzuki
T, Fattori R, Llovet A, Froehlich J.Partial thrombosis of the false lumen in patients with acute
type B aortic dissection. N Engl J Med. 2007 Jul 26;357(4):349–59.
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