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Endovascular Thoracic Aortic Stent Grafting 305
DISCUSSION AND COMMENTARY
Editor’s Counterpoint
(Based on Elefteriades J. “Endograft Therapy for Thoracic Aortic Aneurysms:
Wave of the Future or The Emperor’s New Clothes,” an invited editorial in press
in the Journal of Thoracic and Cardiovascular Surgery, by permission.)
As a profession, cardiothoracic surgeons owe a debt of gratitude to
Dr. Bavaria and colleagues for spearheading these exciting clinical investigations
into novel endovascular therapies for aneurysm disease.
It is important for medical science to evaluate endografting of aneurysms
with enthusiasm for this new modality, but, at the same time, a grain of skepti-
cism, or at least realism. Multiple reasons to be cautious can be cited.
Conceptual issues. First, some authorities question the very concept of
repair of an expanding cylindrical structure by means of a graft placed within its
lumen. Stents, it is pointed out, were developed to keep arteries from closing in
(as in coronary angioplasty), not to keep them from expanding outward. How can
a graft placed inside an enlarging aorta—and not attached to the aorta—prevent
the inexorable expansion of that aorta? Some say the graft would have to go out-
side, not inside, the aorta—a concept that was tried and failed many years ago.
To control a herd of cattle, the analogy goes, the wooden pen has to go outside
the cows; an internal endograft is like putting the pen inside the herd. The con-
cern is that the inexorable expansion of the aorta will ultimately leave the endog-
raft behind, “ignoring” it, so to speak. Another conceptual issue concerns
continued pressurization of the aneurysm sac by intercostal or lumbar vessels.
Yet another conceptual issue concerns the surgeon’s understanding that the
strength of the aorta resides in the adventitia, which is not incorporated in any
way by the endograft.
Short duration of follow-up of an indolent disease. This line of reasoning
leads to the second major concern: Thoracic aortic aneurysm, though ultimately
lethal, is an indolent disease. Many years are generally required from the time of
diagnosis to the time of aneurysm-related death, especially with small to moderate
size aneurysms (Fig. A) (2). To have patients alive at one or two years is not at all
reassuring. These patients would probably still be alive absent any directed ther-
apy whatsoever. As longer term follow-up becomes available through the
EUROSTAR investigation of endografting for abdominal aortic aneurysm, this
concern literally comes to life, with mortality and rupture rearing their ugly heads
as the aneurysm disease expresses its natural history, even after “successful”
endografting. The EUROSTAR study of endografting for abdominal aortic aneu-
rysms is much more “mature” than corresponding studies of thoracic aortic
aneurysm. In Figure B, it can be noted that endoleak becomes increasingly
common as duration of follow-up is extended (3). It appears that nearly half of
patients will suffer diagnosed endoleak as follow-up becomes extended toward
the five-year point. In this context, we need to keep in mind that the word
“endoleak” is itself a euphemism for failure of treatment. It has been demonstrated
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306 Brinster et al.
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
100%
012345
Years
3.5 to 3.9
4.0 to 4.9
5.0 to 5.9
> 6.0 cm
Survival prior to operative repair
Figure A Indolent nature of thoracic aortic aneurysm. Survival prior to operative repair is
shown, for different size classes. Note that years generally pass before the mortality risk
expresses itself, even for large aneurysms. Source: From Ref. 2.
Figure B Kaplan-Meier graph represents cumulative freedom from any endoleak in
patients operated for abdominal aortic aneurysm with endovascular aneurysm repair.
Source: From Ref. 3.
that endoleak predicts need for surgical conversion, rupture, and death, which in
one EUROSTAR publication affected respectively 14%, 13%, and 27% of
patients by five years post-procedure in patients presenting originally with large
aneurysms—sobering statistics after endograft therapy (4). Also concerning is the
emergence of substantial rates of aneurysm-related death after endograft therapy,
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Endovascular Thoracic Aortic Stent Grafting 307
when follow-up extends to four years, especially for large aneurysms (5). This is
shown vividly in Figure C; this figure suggests, in fact, that the aneurysm is indeed
“ignoring” the endograft and merely expressing its natural tendency to rupture. In
recognition of these sobering statistics, several major EUROSTAR publications
end with serious cautions about endograft therapy, calling attention to concerns
about the long-term effectiveness and safety:
● “The high incidence of late secondary interventions is a cause for con-
cern with regard to broad application of endovascular AAA repair, and
emphasizes the need for lifelong surveillance” (6).
● “Continuing need for surveillance for device related complications
remains necessary” (7).
● “… the durability of this technique is currently unknown, and contin-
ued use of registries should provide data from long-term follow-up… .
Only long-duration studies can tell us whether this type of therapy
really works—whether it prevents aneurysm growth and rupture and
patient death (8).
● The midterm outcome of large aneurysms after EVAR was associated
with increased rates of aneurysm related death, unrelated death, and
rupture … . This finding may justify reappraisal of currently accepted
management strategies (5).
The encyclopedic Health Services Technology Assessment Text of the
Guide to Clinical Preventive Services, 3rd Edition, issued the following conclud-
ing statement on endografting.
Figure C Cumulative freedom from aneurysm-related death. Note low attrition of
survival in first three years of follow-up and rapid attrition in fourth year. Gp, Group.
Groups represent increasing initial aneurysm size: Gp A = 4.0–5.4 cm, Gp B = 5.5–6.4,
Gp C > 6.5 cm. Source: From Ref. 5.
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308 Brinster et al.
● “Long-term complications, including AAA rupture … may result in
significant long-term morbidity and mortality” (9).
The pioneering investigations presented in this chapter should be viewed as
extended short-term evaluations of endograft therapy.
Despite these multiple concerns regarding endograft therapy, the work
described in this chapter represents a bold venture into new territory with a prom-
ising, albeit unproven; less invasive modality of therapy. We are indebted to the
investigators for this work. As the authors rightly point out, it is essential that each
patient who has received endograft therapy be followed vigilantly for possible
deterioration or complications as time passes. Moreover, it is incumbent on our
profession not only to follow individual patients closely, but also to evaluate the
durability of endograft therapy in general with a vigilant eye. We look forward to
longer and more complete follow-up of these specific patients and to randomized
studies in the future.
The authors of this chapter have done groundbreaking clinical work, forg-
ing a very important initial foray into endograft treatment of thoracic aortic
aneurysms and the evaluation of its early efficacy.
References
1. Cooley DA, DeBakey ME. Surgical considerations of intrathoracic aneurysms of the
aorta and great vessels. Ann Surg 1952; 135:660–680.
2. Coady MA, Rizzo JA, Hammond GL, et al. What is the appropriate size criterion for
resection of thoracic aortic aneurysms? J Thorac Cardiovasc Surg 1997; 113: 476–491.
3. Lange C, Leurs LJ, Buth J, et al. Endovascular repair of abdominal aortic aneurysm
in octogenarians: An analysis based on EUROSTAR data. J Vasc Surg 2005;
42:624–630.
4. Waasderp EJ, de Vries JP, Hobo R, et al. Aneurysm diameter and proximal aortic
neck diameter influence clinical outcome of endovascular abdominal aortic repair:
A 4-year EUORSTAR experience Ann Vasc Surg 2005; 19:757–759.
5. Peppelenbosch N, Buth J, Harris PL, et al. Diameter of abdominal aortic aneurysm
and outcome of endovascular aneurysm repair: Does size matter? A report from
EUROSTAR. J Vasc Surg 2004; 39:288–297.
6. Laheij RJ, Buth J, Harris PL, Moll FL, Stelter WJ, Verhoeven EL. Need for secondary
interventions after endovascular repair of abdominal aortic aneurysm. Intermediate-
term follow-up results of a European collaborative registry (EUROSTAR). Br J Surg
2000; 87:1666–1673.
7. Hobo R, Buth J, and the EUROSTAR investigators. Secondary interventions follow-
ing endovascular abdominal aortic aneurysm repair using current endografts.
A EUROSTAR report. J VascSurg 2006; 43:896–902.
8. Leurs LJ, Bell R, Degrieck Y, et al. Endovascular treatment of thoracic aortic dis-
eases: Combined experience from the EUROSTAR and United Kingdom Thoracic
Endograft registries. J Vasc Surg 2004; 40:670–680.
9. Health Services/Technology Assessment Text (HSTAT). Guide to Clinical Preventetive
Services, 3rd Ed. Evidence Syntheses, formerly Systematic Evidence Reviews.
National Library of Medicine and NCBI. hstat.nlm.nih.gov (accessed 9/24/06).
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309
17
Long-Term Suppressive Therapy:
Clinical Reality and Future Prospects
Amy E. Hackmann and Robert W. Thompson
Departments of Surgery (Section of Vascular Surgery), Radiology, and Cell
Biology and Physiology, Washington University School of
Medicine, St. Louis, Missouri, U.S.A.
Scott A. LeMaire
Division of Cardiothoracic Surgery, Michael E. DeBakey Department of
Surgery, Baylor College of Medicine, and Cardiovascular Surgery Service,
The Texas Heart Institute at St. Luke’s Episcopal Hospital, Houston, Texas, U.S.A.
INTRODUCTION
Progressive aortic dilatation and rupture are the inevitable consequences of untreated
aortic aneurysms and dissections. The only treatments that effectively eliminate the
risk of aortic rupture are surgical replacement of the diseased aortic segment with a
graft and intraluminal exclusion of the segment with an endovascular stent graft.
Because of the associated risks, aortic repair procedures are performed only in patients
who are at significant risk of aortic rupture. The decision of when to repair an aneurysm
is based primarily on the severity of aneurysmal disease—as indicated by symptoms,
aortic diameter, and aortic expansion rate—in the context of other factors that increase
the likelihood of rupture, such as connective tissue disorders or a family history of
ruptured aneurysm. Patients who have not reached the clinical threshold for aortic
repair receive nonoperative treatment and careful surveillance with imaging studies.
Current nonoperative treatment is rather unsophisticated and comprises
smoking cessation, avoidance of strenuous activity, and pharmacologic reduction of
hemodynamic stress. Although this regimen successfully halts aortic expansion in
some patients, aneurysms continue to enlarge and rupture in many patients, despite
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310 Hackmann et al.
treatment. New treatments are needed to stop aneurysm expansion and prevent rup-
ture. Recent experimental work has focused on improving our understanding of the
pathobiology of aortic aneurysms in hope of identifying new strategies for long-term
suppressive therapy.
PATHOBIOLOGY OF AORTIC ANEURYSMS
Over the last two decades, research on the pathobiology of aortic aneurysms has
greatly improved our understanding of the cellular and molecular mechanisms
involved in progressive aortic dilatation. Most studies have focused on abdominal
aortic aneurysm (AAA) formation. Until recently, most of the research regarding
thoracic aortic aneurysms (TAAs) has concentrated on those related to connective
tissue disorders, particularly Marfan syndrome (MFS). Relatively little is known
about the pathobiology of TAAs related to chronic medial degeneration or dissection
in patients without MFS. Studies in animals and human aortic tissue have shown
that the development of aneurysms results from a cascade of interacting cellular
and molecular processes, including matrix degeneration by elastin- and collagen-
degrading proteases, chronic inflammation, cytokine activity, and loss of smooth
muscle cells (SMCs) (Fig. 1) (1). Together, these processes undermine the mechan-
ical properties of the aortic wall, and lead to aneurysm expansion and rupture (2).
Matrix Proteolysis
The two proteins responsible for maintaining structural integrity of the aortic wall
are elastin and collagen, which respectively confer elasticity and tensile strength.
Figure 1 Diagram illustrating the overlapping cellular and molecular processes that
contribute to aortic aneurysm formation.
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Long-Term Suppressive Therapy 311
Medial destruction of the aortic wall by enzymes—especially matrix metallo-
proteinases (MMPs)—that degrade elastin and collagen is a critical component of
aneurysmal degeneration (3). Although each enzyme in the MMP family has some
specificity for certain substrates, all MMPs have several similarities, including a
zinc-binding active site, a propeptide domain at the amino terminus, and additional
variable domains (4). MMP production is regulated through gene transcription,
and each enzyme in this family is secreted as a zymogen (pro-MMP) that must be
activated. This activation step may be promoted by certain chemicals, decreased
pH, increased temperature, plasmin, nitric oxide, urokinase-type plasminogen
activator, or other activated MMPs (5–8). Activated MMPs are regulated by tissue
inhibitors of metalloproteinases (TIMPs).
MMP-9 has been a target of intense study because of its ability to degrade
insoluble elastin and because of increasing evidence that supports its role in
aneurysmal disease and other inflammatory conditions (9–11). Also known as
92-kDa type IV collagenase or gelatinase B, MMP-9 is produced by mononuclear
phagocytes and vascular SMCs after stimulation by inflammatory cytokines or
other factors (12,13). In addition to its elastolytic properties, MMP-9 promotes
the inflammatory response (14–17). For example, after being cleaved by MMP-9,
interleukin-8 potency as a neutrophil activator increases more than 10 times (18).
Several other members of the MMP family, including MMP-1, 2, 3, 12
(macrophage elastase), and MMP-13, as well as TIMPs, have been implicated in
the development of aneurysms. MMP-2 shares several properties with MMP-9,
including the ability to degrade elastin, and is secreted by vascular endothelium,
SMCs, fibroblasts, lymphocytes, and macrophages. Inflammation increases the
expression of MMP-2 in the aortic wall (13). Adding to its role in matrix
degradation, MMP-2 helps activate other proteinases along the cell surface (5).
Furthermore, MMP-2 promotes the migration of SMCs and inflammatory cells
through elastin-rich matrices (19). MMP-3 can activate MMP-9 in the extracellu-
lar matrix (20).
The contribution of MMPs to aneurysm formation has been studied in
animal models. In a mouse model of MFS, immunohistochemical studies showed
an inverse relationship between MMP-9 expression and elastic fiber number and
integrity (21). Genetically modified mice deficient in MMP-9 or MMP-2 do not
develop AAAs in either the elastase-induced or calcium chloride model, but
“normal” aneurysms develop in MMP-9 knockout mice transplanted with wild-
type macrophages (22,23). Doxycycline, a broad MMP inhibitor, prevents
aneurysm formation in animal models (22,24–26). These studies strongly support
the idea that MMP-9, probably secreted by activated macrophages, contributes to
an early critical step in aneurysm formation. The incidence of TAAs is increased
in TIMP-1 deficient mice but decreased in MMP-3 deficiency (27,28).
Several human studies indicate roles for MMP-1, 2, 3, 9, 12, and 13, and
TIMP-1 and 2 in aneurysm formation (29–33). Minimal, if any, MMP-9 is found
in normal aortic tissues; however, large quantities are secreted by macrophages in
AAAs (34). Levels of MMP-9 are significantly higher in organ cultures of AAA
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