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222 Shahriari and Farkas
MEGS is deployed in position, the ipsilateral hypogastric artery is coil embol-
ized, and an occluder device is used to permanently occlude the contralateral
common iliac artery. To complete the procedure, a femoro-femoral bypass graft
is created (Fig. 11). If the patient does not meet criteria for eEVAR, an open
procedure is performed. Using this system, the authors have reduced their opera-
tive mortality for RAAAs to 10%.
Results achieved by other groups have not been so outstanding.
Using the Talent aorto-uni-iliac system (Medtronic, Minnesota, U.S.A.) in
the New ERA study (76), the investigators achieved 40% mortality in patients
treated with the Talent device versus 42% mortality in the open repair group.
Also, the group from Eindhoven (78) treating 24 patients with RAAAs achieved a
24% 30-day mortality with eEVAR.
Based on these feasibility studies, Mehta et al. (75) have established a
protocol to facilitate endovascular treatment of patients with RAAA. They treated
40 patients, using a variety of commercially available modular aorto-bi-iliac grafts,
with a mortality of 18% (Fig. 12).
Thus, eEVAR appears to be a promising treatment modality that may reduce
mortality in this difficult patient group. Although selected institutions have had
great success with eEVAR, the results have not been reproducible by others.
Lacking a well-designed prospective randomized trial, it is difficult to draw solid
conclusions for comparison of results between open and endovascular repair.
We should also keep in mind that the impressive results by the Montefiore
group (77) and Albany Medical Center (78) are also reflective of large clinical
experience with elective EVAR and a well-organized system that rapidly estab-
lishes a clinical pathway for treatment of the patient with ruptured abdominal
aortic aneurysm. Until most centers that offer treatment to patients with RAAA
have developed such organized multidisciplinary systems, open repair for ruptured
abdominal aneurysm remains the gold standard.
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Treatment of Ruptured Aortic Aneurysms 227
DISCUSSION AND COMMENTARY
Questions for the Authors
Do you think that endovascular repair of ruptured abdominal aortic aneurysm
will replace open repair in the setting of acute ruputure?
It is too early to tell. Traditional open repair can be extremely rewarding, but the
risk in the setting of acute rupture remains considerable. A few specialized centers
have reported excellent results with catheter-based management. The key advan-
tage is the potential to obtain near-immediate control of the rupture by passage of
a proximal occlusion balloon catheter. This controls the hemorrhage and sets the
stage for controlled stent-based aneurysm exclusion. However, the excellent
results in the small number of institutions with a special interest in interventional
treatment of ruptured AAA have not yet been widely duplicated. The next five to
ten years will probably show the proper place for endovascular therapy in the
setting of ruptured AAA.
Is it worthwhile to operate on ruptured thoracoabdominal aortic aneurysms?
The risk of mortality in ruptured thoracoabdominal aortic aneurysm is truly
daunting (73% in a recent series from Great Britain). We have a policy at our
institution that we operate for all ruptured aneurysms except thoracoabdominal
aneurysms, because of the very high acute risk (as well as a very poor long-term
survival for this particular group of patients). If the rupture is not frank, and the
patient is reasonably stable hemodynamically, then we do go forward with sur-
gery. Thoracoabdominal aneurysms can be operated quite safely electively, again
making the point that planned, pre-emptive surgical extirpation of these aneurysms
is optimal, preventing the difficult circumstance of a patient with a ruptured
thoracoabdominal aneurysm.
Reference
1. Gilling-Smith GI, Worswick I, Knight PF, et al. Surgical repair of thoracoabdominal
aortic aneurysm: 10 years’ experience. Br J Surg 1995; 82:624–629.
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229
14
Acute Aortic Dissection:
Anti-impulse Therapy
Javier Sanz, Andrew J. Einstein, and Valentin Fuster
The Zena and Michael A. Wiener Cardiovascular Institute and
Marie-Josee and Henry R. Kravis Center for Cardiovascular Health,
Mount Sinai School of Medicine, New York, New York, U.S.A.
INTRODUCTION
Acute aortic dissection is associated with extremely high mortality and morbidity.
Death rates are on the order of 1% to 2% per hour during the first 24 to 48 hours
after the onset of symptoms (1,2). Although today approximately 70% of those
receiving appropriate care survive the acute episode (3), it is important to realize
that up to 20% of subjects die before reaching the hospital (2).
Regardless of the definitive therapeutic option, most of these patients will
require intensive medical treatment at the time of presentation. In many instances,
the goal will be temporary clinical stabilization before surgical or percutaneous
repair is attempted. In other cases, depending on the location of the pathologic
process, the clinical course, and the presence of comorbidities, medical therapy
may be the preferred choice for long-term management.
In this chapter, we will review the most important principles of medical
therapy in the setting of acute aortic dissection. We will start with a brief overview
of the components of the aortic wall, focusing on their role in maintenance of
aortic structure and function. We will subsequently review those biomechanical
forces that trigger or contribute to the loss of integrity of the aortic wall, which
constitute the basis for the use of specific medications in this context. Finally, we
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230 Sanz et al.
will summarize current recommendations for the medical management in subjects
with acute aortic dissection, with special emphasis on drug therapy.
AORTIC WALL STRUCTURE
The aortic wall is composed of three layers: the intima, the media, and the adven-
titia (Fig. 1). The intima consists of a thin monolayer of endothelial cells resting
on a basal membrane and a variable amount of subendothelial space that contains
fibroblasts and connective tissue. The contribution of the endothelial layer to
modulation of wall tension is considered negligible (4).
The media is constituted by cellular elements (mostly smooth muscle cells)
and extracellular matrix that contains a variety of structural proteins, of which col-
lagen and elastin are the most important. Elastin forms fibers that organize in cir-
cumferential layers with interspersed cells and collagen, a structure known as a
Figure 1 Transverse section of the wall of a large elastic artery demonstrating the well-
developed tunica media containing elastic lamellae (pararosaniline–toluidine blue stain;
medium magnification). Source: From Ref. 97.
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Acute Aortic Dissection 231
lamellar unit (5). The number of lamellar units in a particular species is propor-
tional to the ambient arterial pressure and is similar among mammals, although it
is unexpectedly low in the infrarenal abdominal aorta in humans (6,7). Out of the
three aortic wall layers, the media plays the predominant role in bearing mechani-
cal stress (6). Elastin is very distensible and, under physiological conditions,
supports most of the tension derived from the arterial pulse, absorbs the systolic
impact of blood, and is responsible for the diastolic recoil of the arterial wall that
contributes to maintaining forward flow. On the other hand, collagen has very little
distensibility but provides most of the aortic wall’s mechanical resistance to rupture
or deformation (tensile strength). The distribution of elastic fibers and collagen is
such that, at low levels of dilatation, elastin will be stretched and deformation is
possible. When the vessel enlarges, nondistensible collagen fibers become stretched
and support most of the wall tension, preventing rupture and further dilatation
(4,8). In addition, elastic and collagen fibers have many interconnections that
ensure uniform distribution of tensile stress even in the presence of minor inhomo-
geneities of the aortic wall which may occur, for example, with aging (6).
Nonetheless, there is a transmural gradient of mechanical stress, more prominent
in the inner portions of the media (8). Smooth muscle cells regulate vascular tone
and stiffness through changes in their contraction status (9) and additionally have
significant metabolic functions that include the synthesis of collagen. Conversely,
the capability to synthesize elastin is lost early in life in humans (7).
The outer portion of the arterial wall, the adventitia, is composed of collagen,
elastin and few cells (mainly fibroblasts). Integrity of this layer seems to be an
important determinant of the maintenance of aortic diameter, and elastin degenera-
tion involving its inner portion may be necessary for aneurysmal dilatation to occur
(8,10). The adventitia is classically thought of by surgeons as the layer that has
strength for suturing and holds stitches well.
CONTRIBUTORS TO AORTIC WALL DISRUPTION
Structural Factors
The multiple abnormalities at the molecular and histological levels that occur in
conditions predisposing to aortic aneurysms or dissection are extensively reviewed
in other sections of this textbook. In brief, one of the common pathologic findings
is medial degeneration, characterized by the fragmentation of the lamellae and loss
of elastin fibers. In advanced cases, this is accompanied by reductions in the num-
bers of smooth muscle cells and multifocal accumulation of basophilic mucoid
material. Such medial degeneration is seen with aging, atherosclerotic disease,
arterial hypertension, and genetic diseases such as Marfan’s syndrome (11–13).
The loss of elastin fibers results in decreased arterial distensibility, leading to
increases in pulse pressure and systolic hypertension (14,15). Reduced distensi-
bility by itself may not influence the risk of rupture, independently of blood
pressure and aortic diameter; however, changes associated with medial degeneration
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