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Jos C. van den Berg Chapter 1 Radio-Anatomy of the Thoracic Aorta. 3D Imaging of the Aorta (CT, MRI and 3D Rotational Angiography)
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ab
17
Fig. 1.14. a Sagittal oblique MIP from MRA; dissection flap (ar-
row) in the distal descending thoracic aorta.
MIP from MRA; extension of the intimal flap in the aortic arch
b Sagittal oblique
(arrowhead) and the left subclavian artery (arrow); patient
with type B dissection with secondary extension into type A
Volume-rendered imaging has become indispensable
for the evaluation of endovascular stent placement, by
demonstrating the spatial relationship between the aorta and major arch branches [1].
1.6 Conclusions
3D vascular imaging techniques offer a significant advantage over traditional imaging techniques. Using
these techniques, we can perform anatomical dissection
in vivo, thus helping in identifying disease, and helping
in preoperative planning of surgical and endovascular
procedures. Technical developments are rapidly evolving, and in the near future even more sophisticated
imaging systems will emerge.
Fig. 1.15. Sagittal MPR of a patient with aneurysm of the des-
cending thoracic aorta (asterisk); the absence of mural thrombus can be appreciated, as well as the relative position of the
aneurysm with respect to the supra-aortic vessels: left common
carotid artery (arrow) and left subclavian artery (arrowhead)
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abc
Fig. 1.16. a 3D-RA; cinefluoroscopic image (anterior±posterior
projection) of aneurysm of the descending thoracic aorta.
3D-RA; default reconstruction in same patient. c 3D-RA;
References
1. Lawler LP, Fishman EK. Multi-detector row CT of thoracic
disease with emphasis on 3D volume rendering and CT
angiography. Radiographics 2001; 21(5):1257±1273.
2. Kopp AF, Kuttner A, Trabold T, Heuschmid M, Schroder
S, Claussen CD. Contrast-enhanced MDCT of the thorax.
Eur Radiol 2003; 13(Suppl 3):N44±49.
3. Catalano C, Fraioli F, Danti M, Napoli A, Votta V, Lanciotti K, et al. MDCT of the abdominal aorta: basics, technical
improvements, and clinical applications. Eur Radiol 2003;
13(Suppl 3):N53±58.
4. Haage P, Schmitz-Rode T, Hubner D, Piroth W, Gunther
RW. Reduction of contrast material dose and artifacts by
a saline flush using a double power injector in helical CT
of the thorax. AJR Am J Roentgenol 2000; 174(4):1049±
1053.
5. Siegel MJ. Multiplanar and three-dimensional multi-detector row CT of thoracic vessels and airways in the pediatric
population. Radiology 2003; 229(3):641±650.
6. Lee EY, Siegel MJ, Hildebolt CF, Gutierrez FR, Bhalla S,
Fallah JH. MDCT evaluation of thoracic aortic anomalies
in pediatric patients and young adults: comparison of axial, multiplanar, and 3D images. AJR Am J Roentgenol
2004; 182(3):777±784.
7. Smith PA, Heath DG, Fishman EK. Virtual angioscopy
using spiral CT and real-time interactive volume-rendering techniques. J Comput Assist Tomogr 1998;22(2):212±
214.
8. Bartolozzi C, Neri E, Caramella D. CT in vascular pathologies. Eur Radiol 1998; 8(5):679±684.
9. Kunz RP, Oberholzer K, Kuroczynski W, Horstick G,
Krummenauer F, Thelen M, et al. Assessment of chronic
aortic dissection: contribution of different ECG-gated
breath-hold MRI techniques. AJR Am J Roentgenol 2004;
182(5):1319±1326.
10. Ho VB, Corse WR, Hood MN, Rowedder AM. MRA of the
thoracic vessels. Semin Ultrasound CT MR 2003; 24(4):
192±216.
11. Ho VB, Prince MR. Thoracic MR aortography: imaging
techniques and strategies. Radiographics 1998; 18(2):287±
309.
12. Merkle EM, Klein S, Wisianowsky C, Boll DT, Fleiter TR,
Pamler R, et al. Magnetic resonance imaging versus multislice computed tomography of thoracic aortic endografts.
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volume-rendered image with the cut plane chosen through the
longitudinal axis of the lumen, yielding an angioscopic view
b
13. Leung DA, Debatin JF. Three-dimensional contrast-enhanced magnetic resonance angiography of the thoracic
vasculature. Eur Radiol 1997; 7(7):981±989.
14. Holmqvist C, Larsson E-M, Stahlberg F, Laurin S. Contrast-enhanced thoracic 3D-MR angiography in infants
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15. Willinek WA, Gieseke J, Conrad R, Strunk H, Hoogeveen
R, von Falkenhausen M, et al. Randomly segmented central k-space ordering in high-spatial-resolution contrastenhanced MR angiography of the supraaortic arteries: initial experience. Radiology 2002; 225(2):583±588.
16. Wintersperger BJ, Huber A, Preissler G, Holzknecht N,
Helmberger T, Petsch R, et al. [MR angiography of the supraaortic vessels]. Radiologe 2000; 40(9):785±791.
17. Riederer SJ, Bernstein MA, Breen JF, Busse RF, Ehman
RL, Fain SB, et al. Three-dimensional contrast-enhanced
MR angiography with real-time fluoroscopic triggering:
design specifications and technical reliability in 330 patient studies. Radiology 2000; 215(2):584±593.
18. Arpasi PJ, Bis KG, Shetty AN, White RD, Simonetti OP.
MR angiography of the thoracic aorta with an electrocardiographically triggered breath-hold contrast-enhanced
sequence. Radiographics 2000; 20(1):107±120.
19. Klucznik RP. Current technology and clinical applications
of three-dimensional angiography 56. Radiol Clin North
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20. Unno N, Mitsuoka H, Takei Y, Igarashi T, Uchiyama T, Yamamoto N, et al. Virtual angioscopy using 3-dimensional
rotational digital subtraction angiography for endovascular assessment 52. J Endovasc Ther 2002; 9(4):529±534.
21. van den Berg JC. Three-dimensional rotational angiography. In: Wyatt MG, Watkinson AF, editors. Endovascular
intervention-current controversies. Shrewsbury: tfm; 2004;
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Using three-dimensional rotational angiography for sizing
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23. van den Berg JC, Moll FL. Three-dimensional rotational
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of distortion in a three-dimensional rotational angiography system 17. Br J Radiol 2002; 75(891):266±270.
25. Kersting-Sommerhoff BA, Sechtem UP, Schiller NB, Lipton
MJ, Higgins CB. MR imaging of the thoracic aorta in
Jos C. van den Berg Chapter 1 Radio-Anatomy of the Thoracic Aorta. 3D Imaging of the Aorta (CT, MRI and 3D Rotational Angiography)
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Marfan patients. J Comput Assist Tomogr 1987;
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arteries: principles, techniques, and anatomy. Radiographics 2003; 23(Spec No):S111±125.
27. Cademartiri F, Marano R, Luccichenti G, Mollet N, Nieman K, De Feyter PJ, et al. [Normal anatomy of the vessels of the heart with 16-row multislice computed tomography]. Radiol Med 2004; 107(1±2):11±21.
28. Maintz D, Aepfelbacher FC, Kissinger KV, Botnar RM, Danias PG, Heindel W, et al. Coronary MR angiography:
comparison of quantitative and qualitative data from four
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of the thoracic aorta. In: Kadir S, editor. Diagnostic angiography. Philadelphia: Saunders; 1986. p. 124±171.
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detected by using multi-detector row CT. AJNR Am J
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Sasaki M, et al. MR angiography and CT angiography of
the artery of Adamkiewicz: noninvasive preoperative assessment of thoracoabdominal aortic aneurysm. Radiographics 2003; 23(5):1215±1225.
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H, et al. Demonstration of the artery of Adamkiewicz at
multi-detector row helical CT. Radiology 2002; 223(1):39±
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K, Tanaka R. MRA of the Adamkiewicz artery: a preoperative study for thoracic aortic aneurysm. J Comput Assist Tomogr 2000; 4(3):362±368.
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Smolinsky A, et al. Giant right coronary aneurysm: CT
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Roentgenol 2001; 177(3):689±691.
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Spiral CT and 3D image reconstruction of vascular rings
and associated tracheobronchial anomalies. J Comput Assist Tomogr 1995; 19(4):564±568.
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J, Paul NS. Coarctation of the aorta before and after correction: the role of cardiovascular MRI. AJR Am J Roentgenol 2004; 182(5):1333±1339.
Embryology
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and Congenital Abnormalities
of the Aorta
Jean Philippe Guibaud and Xavier Roques
Chapter
2
Contents
2.1 Introduction .......................
2.2 Classification of Vascular Rings
andRelatedMalformations ...............
2.3 Description of Main Aortic Arch Abnormalities . . . 25
2.3.1 Coarctation of the Aorta ............ 25
2.3.2 Interrupted Aortic Arch (Group IV) ...... 25
2.3.3 Aberrant Right Subclavian Artery
or Arteria Lusoria (subgroup IIB1) ......
21
21
26
2.1 Introduction
The complex evolution of the vascular system from the
human embryo to the definitive pattern of the aortic
arch has been provided by Congdon [1] and by Barry
[2]. The ventral aortic root is in front of the oesophagus. It follows upon the conotroncus, last segment of
the primitive cardiac tube, and is prolonged by two vessels, the first aortic arches, which cross the intestine laterally, to join in the dorsal part of the embryo, the two
dorsal aortas. Six pairs of arches will develop, one for
each branchial cleft, connecting the ventral aorta with
the two dorsal aortas [3]. All are not present at any one
time, the first regresses when the following appears;
some disappear completely, others persist, but are notably modified [4]. The two dorsal aortas meet and merge
in a single vessel, on the median line at the inferior
part of the embryo. This fusion goes up until the seventh somite, at the level of the inferior part of the venous sinus (Fig. 2.1).
When the length of the embryo is 3 mm, the first
and second pairs of primitive aortic arches are the first
to be formed, and the first to disappear.
The third aortic arch is well developed when the
length of the embryo is 4 mm, and the fourth and sixth
arches are outlined. The fifth pair of arches makes only
a brief appearance and then disappears. At this same
stage, the dorsal aortic roots and dorsal aorta give off
intersegmental arteries which supply blood to spinal
cord and developing somites. The seventh intersegmen-
tal arteries enlarge to form the proximal portions of the
subclavian arteries, they migrate cephalad and in the
embryo of 5±6-mm length, they detach separately from
right and left dorsal aortas, upstream from fusion of
these two vessels.
In the embryo of 10-mm length, the third, fourth
and sixth arches are well formed. The primitive aorta is
now divided in trunks of aorta and pulmonary artery,
so that the third and fourth arches are detached from
the aorta, while the sixth one follows upon the trunk of
the pulmonary artery.
At stage of 15-mm length, the embryo has lost its
symmetrical aspect (Fig. 2.2). This transformation was
the result of interruption and displacement of segments
and the descent of the heart in the thorax. The proximal part of the third arch moved laterally, so that it
rose at the union of the fourth arch and the ventral aorta. The third arch forms the common carotid artery. At
this stage the dorsal aorta was interrupted between the
third and the fourth arch. Circulation occurs in two directions: to the head by the third arch and to the rest
of the body by the fourth arch. On the right side, the
distal part of the sixth arch disappears, while the proximal one forms the right pulmonary artery. On the left,
the proximal part of the sixth arch forms the left pulmonary artery, while its distal part persists until the
birth and forms the ductus arteriosus. With the regression of the eighth segment of the right dorsal root and
the right ductus arteriosus, the basic pattern of the normal left aortic arch is formed (Fig. 2.3).
2.2 Classification of Vascular Rings
and Related Malformations
After different attempts of classification (Krauss,
Rathke, Neuhauser, etc.), Stewart et al. [5] provided a
pertinent system explaining malformations.
Most vascular rings and related malformations of
the aortic arch result from either a lack of regression or
an abnormal regression of segments. The formation of
the normal aortic arch system is dependent primarily
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Fig. 2.1. Schematic diagram indicating the various components
of the embryonic aortic arch complex in the human embryo.
Those components which do not precisely persist in the adult
are indicated by broken outlines. The Arabic numbers indicate
the segments of each dorsal aorta. (From Barry [2] with permission)
Fig. 2.2. Diagrammatic view of the aortic
arch complex as it appears in the human
embryo of 15-mm crown±rump length.
The various components are indicated by
the same shading as was used in Fig. 2.1.
(From Barry [2] with permission)
J. P Guibaud and X. Roques Chapter 2 Embryology and Congenital Abnormalities of the Aorta
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Fig. 2.3. Diagrammatic ventral view
of the resultant normal aortic arch
complex. Scheme of identification
same as in Figs. 2.1 and 2.2. (From
Barry [2] with permission)
23
Fig. 2.4. Ventral view of Edwards` hypothetic double aortic arch
and bilateral ductus arteriosi. The ascending and descending
aorta are each depicted in midline positions. Arrows point to
the four key locations where regression occurs and are numbered from 1 to 4. Arrow 1 indicates the eighth segment of the
right dorsal aortic root, arrow 2 the right fourth arch, and ar-
rows 3 and 4 the corresponding two positions on the left [5]
on regression of the eight segment of the right dorsal
aortic root.
ªThe point of departure for this classification of malformation of the aortic arch is a hypothetic specimen
in which there is no regression at any of these sites.
This hypothetic form is a double aortic arch with bilateral ductus arteriosiº (Fig. 2.4). Some of the malformations were described before their discovery. The presence or the absence of one or both ductus arteriosi and
the upper descending aorta is pertinent to the classification.
When the separation of the proximal outflow tract
displaces the aorta and the pulmonary artery towards
the left, the upper descending aorta and ductus arteriosus will be at the left. When the separation displaces
these same vessels towards the right, the upper descending aorta and the ductus arteriosus will be at the
right.
Regression or development of a segment can be explained by the intensity of blood flow in the vessels [6].
When blood flow decreases, the segment regresses or
disappears.
Edwards described four main groups of malformations, and for each of them, there are subgroups:
l Group I is the group of the complete double aortic
arch; there is no interruption at any point in the
double aortic arch pattern. One or both arches may
be patent or not (subgroup A or B), associated with
the presence of left, right or bilateral ductus arteriosi
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Fig. 2.5. Subgroup IIA1. The normal aortic arch [5]
Fig. 2.7. The aberrant right subclavian artery arises from the
posterior of the uppermost part of the descending aorta and
ascends at an angle of about 708 from left to right behind the
oesophagus [5]
Fig. 2.6. Subgroup IIA1. The normal aortic arch system is
formed when the right dorsal aortic root (region 1) and the
right ductus arteriosus regress [5]
(subgroups 1, 2, 3). If one arch is not patent, the
atretic segment may be region 1 (eighth segment of
the right dorsal aortic root), region 2 (right fourth
arch), region 3 (eighth segment of the left dorsal
aortic root) or region 4 (left fourth arch).
l Group II is characterized by the presence of an in-
tact left aortic arch. There are three main subgroups
(A, B, C) according to the location of the interruption. The first subgroup (A) concerns normal
Fig. 2.8. Interruption at region 2 (right fourth arch) causes the
right subclavian artery to arise from the right dorsal aortic
root [5]
branching, the interruption occurs at region 1
(Figs. 2.5, 2.6). The second subgroup (B) concerns
the aberrant right subclavian artery and the interruption is at region 2 (Figs 2.7, 2.8). The third subgroup (C) concerns the isolation of the right subcla-
J. P Guibaud and X. Roques Chapter 2 Embryology and Congenital Abnormalities of the Aorta
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vian artery from the aorta; the interruption occurs
at both regions 1 and 2. Each of these subgroups
may be associated with the presence of a left, right
or bilateral ductus arteriosi (subgroups 1, 2, 3).
l Group III is characterized by the presence of a right
aortic arch. The anomalies of this group are the
mirror of the anomalies of group II: mirror-image
branching, aberrant left subclavian artery and isolation of the left subclavian artery from the aorta
(subgroups A, B, C).
l Group IV concerns unusual malformations explained
by complex combinations of interruptions at the four
sites.
2.3 Description of Main Aortic
Arch Abnormalities
2.3.1 Coarctation of the Aorta
25
Coarctation of the aorta is a congenital narrowing of
the upper descending thoracic aorta, adjacent to the site
of attachment of the ductus arteriosus [7]. Preductal or
postductal, this shelf is usually juxtaductal. Variability
in coarctation morphology, associated lesions, differences between neonatal, infant and adult coarctations,
and influence of the use of prostaglandin E1 in the preoperative management are many reasons underlying the
complexity of this abnormality. Two embryologic factors
will cause aortic obstruction at or near the isthmus.
One is the underdevelopment or hypoplasia of the aortic arch or the isthmus. If this is present, tubular hypoplasia will be important. In this case the amount of flow
across the distal aortic arch and the isthmus is an important factor of growth of this vascular structure [8].
Coarctation is usually most common when there are
proximal lesions which decrease ascending aortic flow
such as aortic stenosis or atresia, mitral stenosis or incompetence. The second factor is the presence of ectopic ductal tissue in the aorta at the aortic insertion of
the ductus. This ectopic tissue tends to develop when
ductal flow increases such as from an atrial or ventricular septal defect.
2.3.2 Interrupted Aortic Arch (Group IV)
Fig. 2.9. Group IV. Interruption of aortic arch type B in the
classification of Celeria and Patton. The ascending aorta terminates in the common carotid arteries. The descending aorta
arises from the pulmonary system by way of a large patent
ductus arteriosus. There is always an aberrant right subclavian
artery [5]
This is the complete luminal and anatomic discontinuity between two segments of the aortic arch. Three
types are described in the Celoria and Patton classification.
In type A interruption occurs at the level of the isthmus between the left subclavian artery and the ductus
arteriosus or between the fourth and the sixth left aortic arch after migration of the left subclavian artery.
Fig. 2.10. Group IV. Interruption of the aortic arch type B. Re-
gression at regions 2 and 4. The right ductus arteriosus disappears [5]
Type B (Figs. 2.9, 2.10) is the commonest type (55±
69%). The interruption occurs between the left common
artery and the left subclavian artery and concerns regression of the segment between the fourth and the
26
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I. State of the Art
sixth left aortic arches but in this case before migration
of the left subclavian artery. This type is often associated with an aberrant right subclavian artery.
Type C is extremely rare (less than 4%). The interruption occurs between the innominate artery and the
left common carotid.
2.3.3 Aberrant Right Subclavian Artery
or Arteria Lusoria (Subgroup IIB1)
The aberrant subclavian artery arises as the fourth
branch of the left aortic arch and passes behind the oesophagus to reach the right arm. In the abnormality the
interruption occurs at region 2 or the right fourth arch
and the right ductus disappears (Figs. 2.7, 2.8).
References
1. Congdon ED. Transformation of the aortic-arch system during the development of the human embryo. Contrib Embryo 1922; 14:47±110.
2. Barry A. Aortic arch derivatives in the human adult. Anat
Rec 1951; 111:221±238.
3. Bellot J. Embryologie des arcs aortiques. Nouv Presse Med
1972; 35:2321.
4. Mathey J, Binet JP, Denis B. Anomalies de dveloppement
des arcs aortiques. J Chir 1959; 77:505±527.
5. Stewart JR, Kincaid OW, Edwards JE. An atlas of vascular
rings and related malformations of the aortic arch system.
Springfield (IL): Thomas; 1964.
6. Rudolph AM, Heymann MA, Spitznas U. Hemodynamic
considerations in the development of narrowing of the aorta. Am J Cardiol 1972; 30:514±525.
7. Goor D, Lillehei CW. Congenital malformations of the
heart. Embryology, anatomy, and operative considerations.
New York: Grune and Stratton; 1975.
8. Shinebourne EA, Elseed AM. Relation between fetal flow
patterns, coarctation of the aorta, and pulmonary blood
flow. Br Heart J 1974; 36:492±498.
Hemodynamics
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of Aortic Dissection
Chris Elkins and Michael D. Dake
Chapter
3
Contents
3.1 Introduction and Background .............
3.2 Experiments on the Hemodynamics
of True-Lumen Collapse .................
3.3 Causative Factors in True-Lumen Collapse ...... 29
3.4 Effective Treatment for True-Lumen Collapse .... 30
3.5 Conclusions ........................ 31
27
28
3.1 Introduction and Background
Aortic dissection is the most frequent nontraumatic catastrophe that affects the aorta, with an annual incidence exceeding that of spontaneous rupture of aortic
aneurysms [1]. Aortic dissection occurs with a frequency of 10±20 cases per million population per year.
Approximately 30% (85 of 272 [2], 106 of 325 [3]) of
patients with aortic dissection have one or more ischemic complications of the peripheral vasculature,
including stroke, paraplegia, loss of peripheral pulses,
and compromised renal or mesenteric perfusion. The
surgical mortality rates for patients with acute aortic
dissection complicated by compromise of a peripheral
arterial branch exceed 50% [3]; visceral and renal ischemia are important independent predictors of death as
a result of surgery [2].
In the past, the direct propagation of a dissection
flap into an aortic branch with the resultant compromise or obstruction of the true lumen was considered
to be the basic mechanism for ischemic complications
in the peripheral vasculature. This understanding was
based on observations of cross-clamped or decompressed aortas without flow and on findings at necropsy.
Recently, collapse or obliteration of the true lumen
was proposed as another important mechanism for
compromise of the aortic branch in aortic dissection [4,
5]. This is based on antemortem cross-sectional imaging studies, including those performed with intravascu-
lar ultrasonography, that facilitate an appreciation of
the effects of flow on the anatomic relationships between the flap, aortic lumina, and branch vessels [4, 5].
In this setting, the plane of the dissection flap spares
the branch vessel. Instead, the flap is positioned in a
curtainlike fashion across the origin of the vessel, which
causes dynamic obstruction of the branch artery [5].
According to the report by Williams et al. [6], dynamic
obstruction due to true-lumen collapse was the cause of
the infradiaphragmatic organ or limb ischemia in 20 of
24 patients. Among the 20 patients, 14 had ischemia in
multiple organs that involved the mesenteric, renal, and
lower-limb circulations. Recently, percutaneous endovascular treatment with balloon fenestration and stent
placement was introduced to relieve true-lumen collapse
and showed promising results [1, 5, 6]. However, there
have been few clinical and experimental studies conducted to investigate the causes of true-lumen collapse
in aortic dissection and the possible treatment methods
to relieve true-lumen collapse or to determine the most
effective methods.
Patients with chronic dissection often develop late
complications mainly related to the patency of the false
lumen [7]. In these cases, there is progressive dilatation
of the false lumen that can lead to eventual rupture. An
acute aortic diameter of greater than 4 cm in type B
dissections has been found to be an indicator of possible future rupture [8, 9]. While some studies suggest
medically treating dissections with maximum diameters
less than 5 cm [10], others support surgery or placement of stent-grafts when the false lumen is greater
than 4 cm [8], 5 cm [11], or 6 cm [12] in order to avoid
certain rupture in the future. Obviously, there is considerable uncertainty about the critical diameter of the
false lumen and how to treat false lumen aneurysms.
While formation and development of dissections are
not well understood, it is generally accepted that hemodynamics plays a major role in the initiation, acute propagation, and chronic development of dissections. In all
three of these stages, hemodynamic effects couple with
mechanical and biological processes in the arterial
walls. It may be some time before the initiation and
propagation mechanics of dissection will be understood
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