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FIGURE 39.4 Plan view of streamwise velocity contours for bileaflet mechanical heart valve and trileaflet mechanical heart valve with valve implanted
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at 0 degrees. Cross-sectional positions Z = 1D, 2D and 4D downstream along the center line were shown with different geometric models.
FIGURE 39.5 Velocity plots at cross-sectional view of Z = 1D, 2D and 4D for both (A) bileaflet mechanical heart valve and (B) trileaflet mechanical
heart valve during mid-acceleration t = 0.07 s, peak systole t = 0.115 s and mid-deceleration t = 0.22 s as viewed from the outlet.
Risk of Thrombosis in Downstream Flow of Mechanical Aortic Valves: A Computational Approach Chapter | 39 437
Velocity (m/s)
Radial Distance from centerline (m)
3
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(t = 0.22 s), triple-jet structure of the flow in the BMHV model has decreased in strength while central orifice jet flow was
higher in the TMHV at position Z = 1D. The velocity plots showed higher vorticity forming along the curvature of the sinus
in the BMHV compared to TMHV. This feature appeared strongly in all three time-points in BMHV, whereas in the BMHV,
the vorticity was less visible at mid-acceleration and peak systole. At position Z = 2D, the higher velocity flow was observed
nearer to the inner arch at mid-acceleration for both BMHV and TMHV, although higher velocity plots were found in
the BMHV model. At peak systole, the velocity plots and profiles in the BMHV and TMHV were completely different.
There were several regions of high velocity gradients in the BMHV, with the majority of the high velocity flow around the
wall of the aorta nearer to the inner arch. Meanwhile, the central orifice flow was more evenly distributed in the TMHV.
The vortices at the BMHV were located nearer to the center-line away toward the outer arch, whereas the vortices in the
TMHV were located near the wall toward the inner arch. At mid-deceleration, two vortices in the BMHV were still visible
in the same region. Meanwhile, the vorticity in the TMHV was no longer visible with a more evenly distributed velocity
plot along the centerline. At position Z = 4D, the velocity plots and profiles during mid-acceleration were similar for both
BMHV and TMHV. During peak systole, the vortices in the BMHV were still visible at this position. At mid-deceleration,
the two vortices in the BMHV combined into one with a more complex flow profile compared to the TMHV.
Fig. 39.6 shows the velocity profiles at each cross-sectional plane at the three locations Z = 1D, 2D, and 4D for both the
BMHV and TMHV at peak systole t = 0.115 s. At this point, the peak velocity of BMHV was 2.5 m/s while the peak velocity
for TMHV was 2.75 m/s. Two regions of recirculation in the BMHV were observed with velocity of about 0.87 m/s. On the
other hand, the TMHV displayed minimal recirculation flows with lower velocity values recorded at 0.36 m/s. This was quite
different compared to the mid-acceleration phase and could be attributed to the majority of the flow through the central orifice
for the TMHV compared to BMHV. At position Z = 2D, the triple-jet structure and lateral jets of the BMHV shifted toward the
inner arch. For the TMHV, the central orifice jet was still prominent at this location. The hexagonal shape disappeared at this
stage. The difference between the BMHV and TMHV was obvious with three different peaks observed in the BMHV, whereas
only one peak was observed in the TMHV. The peak velocity values were 2.42 and 2.65 m/s in the BMHV and TMHV, respectively. At position Z = 4D, the flow velocity was reduced to a magnitude of 1.73 m/s. The velocity shape and profile observed
2.5
2
1.5
1
0.5
0
0 degree BMHV
0 degree TMHV
Position Z = 4D
2.5
2
1.5
1
Velocity (m/s)
0.5
0
–0.5
–0.02–0.015 –0.01–0.005 0.0050.010.015 0.020
Position Z = 2D
Radial Distance from centerline (m)
0 degree BMHV
0 degree TMHV
Position Z = 1D
3
2
1
0
–1
–0.02–0.025 –0.015 –0.01–0.005 0.0050.010.015 0.020
Radial Distance from centerline (m)
Velocity (m/s)
0 degree BMHV
0 degree TMHV
FIGURE 39.6 Comparison of velocity profiles between bileaflet mechanical heart valve and trileaflet mechanical heart valve at positions Z = 1D, 2D
and 4D at peak systole t = 0.115 s.
–0.5
–0.02
–0.015 –0.01–0.005 0.0050.010.015 0.020
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(i)
Bileaflet mechanical heart valve
(ii)
Trileaflet mechanical heart valve
all Shear Stress /kPa
ll Shear Stress /kPa
(A)
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for the two models were generally similar except the region from the centerline toward the inner arch. At this position, both the
BMHV and TMHV displayed a central orifice jet that shifted more toward the outer wall of the arch’s curvature, with regions
of low velocity and recirculation at the inner wall. The centrifugal force was prevailing due to the curvature of the aortic arch.
regions of high wall shear stress in the BMHV were mainly on the leading and trailing hinges at 0.255 kPa. On the other
hand, the concentration of high wall shear stress for the TMHV was within 10% of the BMHV at 0.27 kPa. The distribution
of the wall shear stress regions was mainly on the leading hinges nearer to the inlet and appeared to be in a bigger region
compared to BMHV. The TMHV also has an evenly distributed wall shear stress on the peripheral gap between the leaflets
and the valve holder. Fig. 39.7B shows the wall shear stress distribution at the sinus region and the downstream aorta wall.
The sinus region in the BMHV has a higher wall shear stress compared to the TMHV. Meanwhile, the wall shear stress also
appeared to be distributed more evenly in the TMHV compared to BMHV, although the area seemed to have higher wall
Fig. 39.7A shows the wall shear stress at the hinge region of the BMHV and TMHV at peak systole t = 0.115 s. The
W
0.25
0.2
0.1
0
(B)
(C)
Inlet view
Flow direction
(i)
Bileaflet mechanical heart valve
Flow
direction
Bileaflet mechanical
(i)
heart valve
Side view
(ii)
Trileaflet mechanical heart valve
Trileaflet mechanical
(ii)
heart valve
Flow direction
Flow
direction
Wa
Wall Shear Stress /kPa
0.50
0.40
0.30
0.20
0.10
0
0.25
0.2
0.1
0
FIGURE 39.7 Wall shear stress at the (A) hinge region, (B) aorta wall and sinus region, and (C) valve leaflets of the bileaflet mechanical heart valve and
trileaflet mechanical heart valve at peak systole t = 0.115 s.
Risk of Thrombosis in Downstream Flow of Mechanical Aortic Valves: A Computational Approach Chapter | 39 439
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shear stress. The wall shear stress of the valve leaflets is shown in Fig. 39.7C. The side profile showed the wall shear stress
distributed across the external surface of the BMHV. For the TMHV, the wall shear stress was observed at the region where
leaflets were contained within the valve holder. From the inlet view, it was shown that the higher wall shear stress distributions were observed at the inner edge of the leaflets. High wall shear stress also occurred at the hinge of the leaflets for both
BMHV and TMHV, although it was observed that the stress concentration on the hinges was lesser in the TMHV model.
For the BMHV, nonuniform distributions of high wall shear stress regions were observed at the hinge regions. The difference in the wall shear stress distribution was largely due to the design of the two valves. When the TMHV was fully open,
there were gaps between the leaflets and the valve holder. The flow through the gap caused a slightly elevated wall shear
stress compared to the BMHV. The regions of high wall shear stress were found at the frontal side of the leaflets.
It was observed that the wall shear stress was the highest at the inner edge of the valve leaflet. At fully open position, the
BMHV leaflets were at 85 degrees from the transverse plane tilting toward lateral side, whereas the TMHV leaflets were
at 90 degrees from the transverse plane. Therefore, the leaflet surface at the lateral side would be exposed more to the fluid
flow, which caused elevated wall shear stress at the lateral surface.
The associated increase in wall shear stress often correlates to higher risk of hemolysis and platelet activation. One of
the common congenital conditions of the aortic valve is the bicuspid aortic valve, where the aortic valvular leaflets are fused
during the development. As a result, instead of a normal tricuspid configuration, a bicuspid valve appears. Bicuspid aortic
valve often leads to nonphysiological flow hemodynamics as well as the tendency to develop ascending aortic aneurysm
due to the higher wall shear stress along the surface of aorta arch. Similarly, it was observed that, due to higher wall shear
stress, the sinus regions of the BMHV are susceptible to increased risk of aortic aneurysm compared to TMHV. The lysis
of red blood cell occurs at approximately 400 Pa, below which a sublethal region of zero hemolysis has been observed [13].
Meanwhile, irreversible platelet aggregation can occur at shear stresses as low as 10 Pa [14–16].
The blood elements experienced higher rate of collision with the valve wall due to the vorticity formed near the wall
as a result of turbulent flow. The platelet activation by high wall shear stresses may lead to thromboembolic complications
[17,18]. These regions were often associated with high wall shear stress and may lead to hemolysis and platelet activation.
The high wall shear stress at the hinge regions for both BMHV and TMHV showed that the hinge joints are critical to
the design of an artificial heart valve. The concentrated area of wall shear stress in this study was consistent with earlier
findings [6,19,20]. The design of the hinge in mechanical heart valve is important to minimize any undesirable flow features
and wall shear stress during the cardiac cycle. It can also be used as an important tool to characterize potential thromboembolic complications in regions that cannot be measured experimentally due to the design and opacity of the hinge.
Generally, the major drawback associated with the implantation of mechanical heart valves is the need for chronic daily
anticoagulation therapy to reduce the risk of thrombosis and thromboembolic complications. Patients with such therapies are
exposed to an increased risk of bleeding, infection, and/or autoimmune response [21]. The present numerical study has shown
that the TMHV provided a flow condition that is more similar to the natural valve due to its large central free region compared
to the triple jet structures of BMHV. The central orifice flow in TMHV presented a configuration with smaller resistance for
blood flow. The velocity gradient in any radial direction in the TMHV is also smaller compared to the BMHV. Clinically, this
will reduce the wall shear stress level in TMHV because the incidence of blood hitting on the wall decreases due to the more
concentric streamlined flow of the TMHV.
Blood flow through mechanical prostheses can lead to high turbulent stresses that may damage and/or activate blood
elements and initiate platelet aggregation. Platelet aggregation can lead to thrombus formation with disastrous consequences for the patient. Thrombi may even detach from the valve and lodge in a downstream blood vessel, thus reducing or
even cutting off the blood supply to vital tissues. The hemodynamics of a BMHV differs significantly from that of natural
healthy heart valve. As such the use of a TMHV valve may yield a more physiological hemodynamics due to the central
orifice flow similar to that of native human valve.
EFFECT OF IMPLANTATION ANGLES OF MECHANICAL AORTIC VALVES ON FLOW
PATTERNS AND BLOOD SHEAR
To understand the flow through the TMHV further, the impact of the valve implantation angle on the downstream flow
was investigated. The trileaflet valve was positioned at different angles (0, 30, 60, and 90 degrees), as shown in Fig. 39.8,
in a curved downstream aortic arch model. The reference 0 degrees is the preferable orientation of aortic valve, known as
anatomic position as described earlier.
The flow field at peak systole (t = 0.115 s) was investigated for each case at the three different positions Z = 1D, 2D,
and 4D downstream along the centerline of the geometric model. Comparisons of the flow field velocity contours are
presented in Fig. 39.9.
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Z=1D
coronary
Z=2D
Z = 4D
º
60º
90º
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FIGURE 39.8 Four different valve orientations for trileaflet mechanical heart valve model.
Non
cusp
Right
coronary
cusp
Left
coronary
cusp
2.5
0
U m/s
2
1
Outer
Arch
Inner
Arch
2
0
U m/s
1
Outer
Arch
Inner
Arch
0
2
1
0º
30
U m/s
FIGURE 39.9 Velocity contours of four implantation angles of 0, 30, 60, and 90 degrees at positions Z = 1D, 2D, and 4D at peak systole (inlet view).
As described earlier for implantation angle 0 degrees, the flow profile through the TMHV at position Z = 1D was a bulk
flat profile. For the other two implantation angles (30 and 90 degrees), similar flat profiles were observed. The recirculation
regions were also similar with comparable velocity magnitude as shown in Fig. 39.10. On the other hand, the velocity profile for 60 degrees had a shorter flat profile and a bigger velocity magnitude for recirculation region at 1.7 m/s. This unusual
big recirculation region could be due to the position of the leaflets where the hinges were located along the centerline of the
sinus chamber at the noncoronary cusp. Meanwhile, at the downstream positions Z = 2D and 4D, similar flow profiles were
observed for all the valves implanted at the different angles.
Risk of Thrombosis in Downstream Flow of Mechanical Aortic Valves: A Computational Approach Chapter | 39 441
4
Radial Distance from centerline (m)
Velocity (m/s)
0.02
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3
2
1
0
–1
–2
–0.025 –0.02
Position Z= 1D
–0.015 –0.01 –0.005 0.005 0.01 0.015
Radial Distance from centerline (m)
2.5
2
1.5
1
Velocity (m/s)
0.5
0
0 degree
30 degree
60 degree
90 degree
Position Z = 4D
0.020
3.5
3
2.5
2
1.5
1
Velocity (m/s)
0.5
0
–0.5
–0.02
Position Z = 2D
–0.015 –0.01 –0.005 0
Radial Distance from centerline (m)
0 degree
30 degree
60 degree
90 degree
0 degree
30 degree
60 degree
90 degree
0.005 0.01 0.015
–0.5
–0.02 –0.015 –0.01 –0.005 0
0.005 0.01 0.015
0.02
FIGURE 39.10 Velocity profile comparison between the different implantation angles of trileaflet mechanical heart valve (0, 30, 60, and 90 degrees) at
position Z = 1D, 2D, and 4D at peak systole t = 0.115 s.
FIGURE 39.11 Wall shear stress distribution on the leaflet found to be higher at the inner edges of the valves.
The implantation angles of the TMHV have a limited effect on the downstream flow profile, especially at the immediate
downstream as seen at position Z = 1D. The difference further downstream at positions Z = 2D and 4D was not noticeable.
The simplified three-sinus aortic root model used in the simulation followed closely the natural anatomy of the aortic sinus
without the three aortic branches. The anatomic curvature of the downstream aorta resulted in an asymmetric flow condition, and the flow features were consistent among all the models in general despite the different valve implantation with a
more distributed flow profile.
The wall shear stress distributions of the valves in all implantation angles were similar. Fig. 39.11 shows the wall shear
stress distribution on the valve leaflets at orientation 0 degrees. As the valve leaflets opened, the blood was forced through
the valve leaflets, resulting in high velocity jets. These velocity jets will in turn cause high velocity gradients and induce
high shear stress. The shear stress may then cause hemolysis or platelet activation. It was seen from the contour plot that
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the shear stress was highest at valve leaflet edge, especially at the edge close to the inlet. This agreed with the CFD simulation results of the earlier study by Dumont et al. [6]. It was also observed that the wall shear stress was higher on the side
of the lateral orifice than the central orifice, which could be due to the tilting direction of the valve leaflet when the valve
was fully opened.
When the valves were fully opened, the external surfaces of the trileaflet valves had elevated wall shear stress values
compared to the inner surfaces. However, the trailing edges of the valves exhibited higher wall shear stresses at the inner
edges than at the outer edges.
The simulation results showed different flow fields at the downstream positions at Z = 1D and 2D for BMHV and
TMHV. At further downstream at Z = 4D, it was found that the flow field shared similarities in terms of the flow profile
and the velocity magnitude. The study also showed that implantation of the TMHVs in different angles did not affect the
downstream flow field as much compared to the BMHVs. In the simulations, it was observed that the flow profile through
the valve implanted at all the four locations shared similar flow structures, except for the valve implanted at 60 degrees, as
compared at position Z = 1D. Wall shear stress distribution on the leaflets was similar in all four cases.
SUMMARY
Artificial heart valve failures and complications arising from the implantation remain a crucial factor in determining the
quality of life for patients with heart valve diseases. When designing artificial heart valves, there is a need to look at the fundamentals involving hemodynamics and blood shear stress as a result of the interaction between the valve leaflets with the
flow. CFD provides a platform to study and identify areas, which cannot be captured experimentally, compared to in vivo
and in vitro experiments that are expensive and time consuming to setup. From a CFD perspective, the challenging task
ahead would be to model the dynamic interaction of the artificial heart valves with the surrounding blood and to calculate
the local deformations and stresses on the structure, as well as other hemodynamic properties.
The potential for this numerical model is that it can be used as a research and development tool to improve the design
of mechanical heart valves. This will help to simulate a more accurate flow in heart valves especially for TMHV design,
which is similar to the native aortic valve. This in turn enables clinicians and engineers to further develop superior artificial
heart valves.
REFERENCES
[1] Lefrak EA, Starr A. Cardiac valve prostheses. New York: Appleton-Century-Crofts; 1979. p. 67–118.
[2] Bourguignon T, Bergöend E, Mirza A, Ayegnon G, Neville P, Aupart MR, Marchand M. Risk Factors for valve-related complications after mechani-
cal heart valve replacement in 505 patients with long term follow up. J Heart Valve Dis 2011;20(6):673–80.
[3] Yin W, Alemu Y, Affeld K, Jetsy J, Bluestein D. Flow-induced platelet activation in bileaflet and monoleaflet mechanical heart valves. Ann Biomed
Eng 2004;32(8):1058–66.
[4] Sacks MS. Surface strains in the anterior leaflet of the functioning mitral valve. Ann Biomed Eng 2002;30(10):1281–90.
[5] Shahriari S, Maleki H, Hassan I, Kadem L. Evaluation of shear stress accumulation on blood components in normal and dysfunctional bileaflet
mechanical heart valves using smoothed particle hydrodynamics. J Biomech 2012;45(15):2637–44.
[6] Dumont K, Vierendeels J, Kaminsky R, Nooten GV, Verdonck P, Bluestein D. Comparison of the hemodynamic and thrombogenic performance of
two bileaflet mechanical heart valves using a CFD/FSI model. J Biomech Eng 2007;129(4):558–65.
[7] Nguyen V-T, Kuan YH, Chen P-Y, Ge L, Sotiropoulos F, Yoganathan AP, Leo HL. Experimentally validated hemodynamics simulations of mechan-
ical heart valves in three dimensions. Cardiovasc Eng Technol 2012;3(1):88–100.
[8] Kuan YH. 3-dimensional numerical and experimental studies to model artificial heart valves hemodynamics (Doctoral thesis). National University
of Singapore; 2014.
[9] Kuan YH, Nguyen V-T, Kabinejadian F, Leo HL. Computational hemodynamic investigation of bileaflet and trileaflet mechanical heart valves. J
Heart Valve Dis 2015;24(3):393–403.
[10] Kheradvar A, Pedrizzetti G. Effect of cardiac devices and surgery on vortex formation. Vortex formation in the cardiovascular system. London:
Springer; 2012. p. 81–124.
[11] Hager A, Kaemmerer H, Rapp-Bernhardt U, Blucher S, Rapp K, Bernhardt TM, Galanski M, Hess J. Diameters of the thoracic aorta throughout life
as measured with helical computed tomography. J Thorac Cardiovasc Surg 2002;123(6):1060–6.
[12] Pisani G, Scaffa R, Ieropoli O, Dell’ Amico EM, Maselli D, Morbiducci U, De Paulis R. Role of sinuses of Valsalva on the opening of the aortic
valve. J Thorac Cardiovasc Surg 2013;145(4):999–1003.
[13] Sallam AM, Hwang NH. Human red blood cell hemolysis in a turbulent shear flow: contribution of Reynolds shear stresses. Biorheology
1984;21(6):783–97.
[14] Hung TC, Hochmuth RM, Joist JH, Sutera SP. Shear-induced aggregation and lysis of platelets. Trans Am Soc Artif Intern Organs 1976;22:285–91.
[15] Ramstack JM, Zuckerman L, Mockros LF. Shear-induced activation of platelets. J Biomech 1979;12(2):113–25.
Risk of Thrombosis in Downstream Flow of Mechanical Aortic Valves: A Computational Approach Chapter | 39 443
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[16] Slack SM, Cui Y, Turitto VT. The effects of flow on blood coagulation and thrombosis. Thromb Haemost 1993;70(1):129–34.
[17] King MJ, David T, Fisher J. Three-dimensional study of the effect of two leaflet opening angles on the time-dependent flow through a bileaflet
mechanical heart valve. Med Eng Phys 1997;19(3):235–41.
[18] Cheng R, Lai Y, Chandran KB. Three-dimensional fluid-structure interaction simulation of bileaflet mechanical heart valve flow dynamics. Ann
Biomed Eng 2004;32(11):1471–83.
[19] Kiang-ia A, Chatpun S. Mechanical analysis of mechanical aortic heart valve: trileaflet versus bileaflet. IEEE; 2013.
[20] Yuan Q, Ngoi BK, Yeo TJ, Hwang NH. Dynamic impact stress analysis of a bileaflet mechanical heart valve. J Heart Valve Dis 2003;12:102–9.
[21] Walker PG, Yoganathan AP. In vitro pulsatile flow hemodynamics of five mechanical aortic heart valve prostheses. Eur J Cardiothorac Surg
1992;6(Suppl. 1):S113–23.
Chapter 40
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Thoracic Endovascular Aortic Repair
Debabrata Dash
1
Thumbay Hospital, Ajman, United Arab Emirates; 2Beijing Tiantan Hospital, Beijing, China; 3Tan Tao Medical School, Long An Province, Vietnam
1,2,3
Chapter Outline
Introduction 445
Developing a TEVAR Program 445
TEVAR for TAD 446
Stable Acute and Chronic B TAD 446
Unstable Acute Type B TAD 446
TEVAR for TAA 449
TEVAR for Traumatic Aortic Injury and Connective Tissue
Disorder 450
Current Technical Aspects of TEVAR 450
Vascular Access, Techniques, and Specifics 450
Stent Graft Selection 450
Preservation of Perfusion of Aortic Branches 451
Hybrid Procedure 451
Follow-Up 451
Complications 451
Vacular, Procedure, and Stent Graft–Related Complications 451
Endoleaks 451
Brain Injury 452
Spinal Cord Injury 452
Aortoesophageal or Aortobronchial Fistulation 452
Conclusion 452
Abbreviations 452
References 452
INTRODUCTION
Thoracic endovascular aortic repair (TEVAR) is a life-saving therapy embraced rapidly by clinicians treating thoracic aortic
disease [1–4]. By virtue of its lower mortality, morbidity, and paraplegia rates compared to open surgical repair, TEVAR is
a valid therapeutic option for thoracic aortic dissection (TAD) of the descending aorta (type B according to Stanford classification), thoracic aortic aneurysm (TAA), and thoracic aortic injury (AI). Rapid advances in endovascular technology
and procedural breakthroughs have resulted in dramatic transformation of entire field of thoracic aortic repair after the first
report of TEVAR in TAA [2]. This procedure can be technically challenging that demands seasoned endovascular experience and refined skills.
DEVELOPING A TEVAR PROGRAM
Symptoms of TAA and TAD of descending aorta are usually rare and nonspecific [5,6]. New onset hoarseness or dysphagia
may signal a developing aneurysm in distal aortic arch and proximal descending aorta. Most asymptomatic patients are
discovered incidentally. Patients of TAD are present with sudden onset chest pain, back pain, and signs of malperfusion.
Patients with focal penetrating ulcers in their thoracic aorta and progressive and complicated intramural hematoma are
another group in which TEVAR may prove beneficial.
Computed tomography angiography (CTA) [7] is the method of choice for preprocedure diagnosis and treatment planning.
Magnetic resonance imaging (MRI) [8] is not advisable in acute situation but may be used during follow-up. Positron emission
tomography in combination with CTA may be used an adjunct to detect signs of inflammation [9]. Transesophageal echocardiography (TEE) is useful as an adjunct imaging technique in aortic dissection [10]. Intravascular ultrasound and phased array
intracardiac ultrasound could play an important role in aortic dissection [11]. Prior to discharge CTA is advised to demonstrate
undetected complications during TEVAR. MRI could be used for follow-up but it lacks visualization of metallic stent struts
and is not compatible with stainless steel grafts [12]. A transthoracic echocardiogram is performed as a part of work-up in
elective cases to rule out structural and valvular heart disease. A stress test may not be necessary in asymptomatic patients.
Coronary angiography is recommended in patients with suspicion of coronary artery disease.
New Approaches to Aortic Diseases from Valve to Abdominal Bifurcation. http://dx.doi.org/10.1016/B978-0-12-809979-7.00040-7
Copyright © 2018 Elsevier Inc. All rights reserved.
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TEVAR FOR TAD
TEVAR abrogates impending ruptures and relieves static and dynamic malperfusion in acute phase. Later benefit is due to false
lumen (FL) thrombosis mitigating the risk of aneurysmal dilatation and subsequent rupture. The sealing of proximal entry tears
with customized stent graft is the most effective method to avoid enlarging FL (Fig. 40.1). It is mandatory to localize all tears
(with emphasis on primary entry tear), define extension of dissection and possible static, dynamic, or complex involvement of
supra-aortic, visceral, and pelvic vessels leading to malperfusion [7]. Refractory pain, rapidly expanding FL, extra-aortic blood
collection, and distal malperfusion syndromes are accepted indications of TEVAR (Table 40.1). Compared to OSR, this technique
has demonstrated lower morbidity and mortality rates, especially for complications pertaining to spinal cord ischemia [13].
Stable Acute and Chronic B TAD
With stabilization of blood pressure and symptom relief, patients with uncomplicated type B TAD can be discharged within
14 days on oral drugs with advice of clinical and imaging follow-up at 3 and 6 months and annually thereafter (Fig. 40.2).
However, despite adequate medical treatment, delayed aortic dilatation will develop in 20%–50% of cases of uncomplicated type B TAD leading to aortic rupture or long-term complications [14].
The Acute Dissection: Stent graft OR Best medical therapy trial suggested a benefit for TEVAR plus optimal medical therapy (OMT) over OMT alone for aortic remodeling outcomes 1 year postdissection [15]. The evolution of acute to
chronic type B TAD involves progressive thickening of intimal flap due to fibrosis. The growth of chronically dissected
aorta is estimated to be 0.10–0.74 cm per year depending upon initial aortic diameter and state of hypertension [16].
TEVAR should be recommended in patients with aortic diameter exceeding 55 mm, persistent thoracic pain, uncontrolled
hypertension, and rapid expansion of dissection (>1 cm/year). The data from the INSTEAD (Investigation of STEnt grafts
in Aortic Dissection) trial suggest that OMT and surveillance were associated with failure to prevent late complications,
including aneurysmal growth, rupture, and late conversion to emergent TEVAR, indicating a higher aorta-specific mortality [17]. Thus, initial clinical stability does not preclude emergent silent expansion and even rupture and both events might
be preventable by TEVAR in the early phase. Thus, TEVAR should be reserved for complicated cases of acute or chronic
type B TAD or for those in which OMT has failed. INSTEAD-XL (with extended length of follow-up) demonstrates that
TEVAR in addition to OMT is associated with improved 5-year aorta-specific survival and delayed disease progression. In
stable type B TAD with suitable anatomy, preemptive TEVAR (Fig. 40.3) should be considered to improve late outcome
[18]. Certain predictors of aortic growth and subsequent rupture have been identified (Table 40.2) [19].
Unstable Acute Type B TAD
TEVAR is the treatment of modality of choice in complicated acute type B TAD. The term “complicated” (Fig. 40.2) means
persisting or recurrent pain, uncontrolled hypertension despite full medication, malperfusion (ischemia that involves the
viscera, kidneys, spinal cord, or lower extremities), and evidence of aortic rupture (hemothorax, increasing periaortic, and
FIGURE 40.1 Thoracic endovascular aortic repair to seal the primary tear distal to left subclavian artery.
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