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202 Coady and Elefteriades
There is theoretical and limited clinical evidence that statin drugs, above
and beyond their lipid-lowering properties, have a beneficial effect on the aortic
wall, suppressing inflammation. It is possible that these drugs may have a role in
the treatment of thoracic aortic aneurysm. Further studies are warranted.
We and others have demonstrated a role for matrix metalloproteinases
(MMPs) in the pathogenesis of thoracic aortic aneurysm (7,8). It is clear that
MMP expression is elevated in patients with thoracic aortic aneurysm and
dissection, and that some of the tissue inhibitors of MMPs (TIMPs) are not upreg-
ulated, in patients with thoracic aortic aneurysm. This raises the possibility of
applying drugs that inhibit MMPs in the treatment of thoracic aortic aneurysms.
Doxycycline is an antibiotic that is used very widely in the treatment of gingivitis.
Preliminary studies of doxycycline in randomized trials for abdominal aortic
aneurysm have been equivocal. Many inhibitors of specific MMPs are in the drug
pipelines at several manufacturers.
All of these promising avenues will be explored in the next decade. There is
hope for viable medical treatments for thoracic aortic aneurysm, which may delay
or preclude aortic expansion, rupture, and dissection. At this time, no medications
can be said to be of proven benefit.
References
1. Shores J, Berger K, Murphy EA, Pyeritz PE. Progression of aortic dilatation and the
benefit of long-term beta-adrenergic blockade in Marfan’s syndrome. N Engl J Med
1994; 330:1335–1341.
2. Fuster V, Andrews P. Medical treatment of the aorta I. Cardiol Clin 1999; 17:697–715.
3. Propanolol Aneurysm Trial Investigators. Propanolol for small abdominal aortic
aneurysms: results of a randomized trial. J Vasc Surg 2002; 35:72–79.
4. Lindholt JS, Henneberg EW, Juul S, Fasting H. Impaired results of a randomized
double blinded clinical trial of propranolol versus placebo on the expansion rate of
small abdominal aortic aneurysm. Int Angiol 1999; 18:52–57.
5. Habashi JP, Judge DP, Holm TM, et al. Losartan, an AT1 antagonist, prevents aortic
aneurysm in a mouse model of Marfan syndrome. Science 2006; 312:117–121.
6. Liao S, Miralles M, Kelley BJ, Curci JA, Borhani M, Thompson RW. Suppression of
experimental abdominal aortic aneurysms in the rat by treatment with angiotensin-
converting enzyme inhibitors. J Vasc Surg 2001; 33:1057–1064.
7. Koullias GJ, Ravichandran P, Korkolis DP, Rimm DL, Elefteriades JA. Increased tissue
microarray matrix metalloproteinase expression favors proteolysis in thoracic aortic
aneurysms and dissections. Ann Thorac Surg 2004; 78:2106–2110.
8. Koullias GJ, Korkolis DP, Ravichandran P, Psyrri A, Hatzaras I, Elefteriades JA. Tissue
microarray detection of matrix metalloproteinases in diseased tricuspid and bicuspid
aortic valves with or without pathology of the ascending aorta. Eur J Cardiothorac
Surg 2004; 26:1098–2003.
Many cardiac specialists are aware of individual patients who have suffered
dissection of the aorta at a relatively small dimension, in the range of 4 cm. These
patients would not be selected for surgery based on the criteria enumerated in this
chapter. What response do the authors have to this point?
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Natural History of Thoracic Aortic Aneurysms 203
We have seen an abstract on this topic, but not a subsequent paper. There is no
question that dissection can occur at small sizes. In our studies of weight lifters
suffering aortic dissection (see Chapter 10), most young men dissected at a dimen-
sion between 4 and 5 cm. We feel these individuals imposed an extreme blood
pressure stress (likely above 300 mmHg) on their aortas. We know (see Chapter 7)
that wall stress depends on both aortic size and blood pressure. Aortic dissection
at small sizes does, additionally, occur in nonweight lifters. Here one must keep
in mind how huge is the denominator of patients with aortas in this size range.
If aortic dimension follows a bell curve, like most physical traits, the number of
patients must increase immensely as one comes back from the tails of the curve.
Our feeling is that there are so many (probably millions) of patients with aortas
of size 4 cm or more that the observed cases of dissection at these sizes represent
a very low percentage. This is certainly the case in our careful follow-up of patients
with known aortic size, whose percentage likelihood of dissection is represented
in the figures and tables in this chapter. The likelihood of dissection in this popula-
tion under direct observation is very low. In fact, once a patient has entered our
system, and a decision made for medical management because of lack of symp-
toms and small aortic size, we are not aware of any instances of aortic dissection
under such observation. We are now looking at this phenomenon from a heuristic,
decision-making standpoint, to determine precisely how many patients may
dissect when our recommended algorithms are applied. In short, we are not aware
of a means to apply clinically the observation that some patients dissect at very
small sizes. To operate prophylactic on all patients with minor enlargement of the
aorta (say those with aortas between 4 and 5 cm) would probably cause more
harm (surgical) than good.
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205
13
Treatment of Ruptured
Aortic Aneurysms
Ali Shahriari and Emily A. Farkas
Section of Cardiothoracic Surgery, Yale University,
New Haven, Connecticut, U.S.A.
INTRODUCTION
Despite advances in diagnostics, aortic surgical techniques, technology, and
perioperative medicine, ruptured aortic aneurysm remains one of the most lethal con-
ditions with which aortic surgeons are challenged. The perioperative mortality of
these conditions has remained unchanged over the past 20 years (1). In fact, mortality
from acute aortic syndromes, including ruptured aneurysms, ranks among the top 13
causes of death according to the National Center for Health Statistics (2). Since the
prevalence of aneurysmal disease increases with age, we can expect to encounter this
problem at an advancing rate as we face an expanded aging population.
The sobering statistics for ruptured aneurysm emphasize the importance of
rigorous screening programs for patients at risk for degenerative and hereditary
aneurysms. Such programs may translate into decreased incidence of rupture and
improved survival (3,4). Understanding the inheritance patterns and the molecular
biology (5) of this disease will be imperative for the development of genetic and
pharmacologic interventions to slow the progression to rupture.
PATHOLOGY
The most common pathology involving aortic aneurysms is degenerative athero-
sclerotic disease. The two most important protein fibers in the normal human
aorta are elastin and collagen, Types I and III. Elastin contributes to the viscoelastic
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206 Shahriari and Farkas
properties of the aorta, whereas collagen provides tensile strength. Histologic
examination of human aneurysmal aortic tissue has documented fragmentation
and decreased concentration of elastin. While this compromise in the quality and
quantity of the elastin contributes to the dilatation of the aorta (6–8), it does not
markedly decrease the tensile strength. As demonstrated in rodent experiments,
transgenic animals that do not produce elastin will form aortic aneurysms, yet will
not succumb to rupture. If there is degradation of the collagen in the same
elastin-deficient animal, however, susceptibility to rupture is demonstrated. The
loss of the elastic properties in the aortic wall seems to be compensated by an
increase in collagen synthesis during the early stages of aneurysm formation (9).
Later in the disease process, collagen degradation exceeds its synthesis and this
culminates in rupture (10).
Over the last decade, much research has been focused on the enzymes involved
in the degradation of elastin and collagen. The imbalance between proteases such as
matrix metalloproteinases (MMPs) and their inhibitors [e.g., tissue inhibitors of
metalloproteinases-2, Plasminogen activator inhibitor (PAI)] (11) has been sug-
gested as a possible mechanism (12–14). New insight into immunologic mecha-
nisms underlying aneurysm formation and rupture has resulted in emerging
hypotheses regarding the interactions between Th1/ Th2 cytokines (15–18).
Understanding these complex relationships may assist in altering the natural history
of aortic aneurysmal disease in the future.
EPIDEMIOLOGY
Thoracic Aortic Aneurysms
According to a Swedish study (19), the prevalence of asymptomatic thoracic
aortic aneurysms (TAAs) is highest in males 75 to 79 years of age, with a peak
incidence occurring 10 years later in females. Thirty-nine percent of the males
and 27% of the females have coexisting abdominal aortic aneurysms (AAA) or
iliac artery aneurysms. Bickersatff et al. (20) estimated the prevalence of TAA to
be 5.9/100,000 population per year. The incidence of rupture was calculated to
be 5.0/100,000 population per year (21). Our own institutional database outlining
the characteristics of over 1600 patients with TAA has previously shown (22)
a growth rate of 0.19 cm per year, and a mean annual rate of rupture or dissection
of 3% for aneurysms measuring 5.0 to 5.9 cm, and 7.0% for aneurysms greater
than 6.0 cm (Fig. 1) (23).
Risk factors for rupture include vascular disease, female gender, pulmonary
disease, hypertension, size of the aneurysm, chronic obstructive pulmonary dis-
ease, the presence of symptoms, and dissection within the aneurysm (21–23). In
one series (24) 12% of thoracic aortic ruptures were associated with dissection in
aortas less than 5.0 cm. Our institution addressed the impact of relative aortic size
by developing the “aortic size index,” which incorporates the patient’s body
surface area in the measurement (25). Increasing aortic size index was found to
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Treatment of Ruptured Aortic Aneurysms 207
be a significant predictor of increasing rates of rupture (P = 0.0014) as well as
the combined endpoint of rupture, death, or dissection (P = 0.0001). Using this
measurement, patients were able to be stratified into three risk groups: less
than 2.75 cm/m
2
were at low risk (~4% per year), 2.75 to 4.24 cm/m
2
were at
moderate risk (~8% per year), and those above 4.25 cm/m
2
were at high risk
(~20% per year).
Thoracoabdominal aortic aneurysms (TAAA) tend to follow the natural
history of their respective thoracic and abdominal components. Ruptured TAAA
represent approximately 15% of surgically treated TAAA in the United States, and
postoperative mortality for this condition ranges between 40% and 70% (26,27).
Crawford et al. (28) followed 94 patients who were poor surgical candidates or
refused surgical intervention. The two-year survival was 24%, with 50% of the
mortality related to rupture.
Abdominal Aortic Aneurysms
The most frequently ruptured segment of aorta involves the infrarenal location.
Rupture of AAA accounts for 1% to 3% of deaths in males between 65 to 85 years.
Bickerstaff et al. (29) found the incidence of AAA to be 36.5/100,000 population
per year, with 12% having ruptured aneurysms. The mortality for ruptured AAA
approaches 65% to 85% (30,31) and is responsible for 15,000 deaths annually in
the United States.
Figure 1 Average yearly rates of negative outcomes (rupture, dissection, and death).
Source: From Ref. 23.
18%
16%
14%
12%
10%
8%
6%
4%
2%
0%
Average Yearly Rate
Outcome
Rupture
Rupture or
Dissection
Rupture, Dissection
or Death
3.5 to 3.9 cm
3.7%
3.9%
6.9%
11.8%
15.6%
4.0 to 4.9 cm 5.0 to 5.9 cm
≥ 6.0 cm
Death
Dissection
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208 Shahriari and Farkas
The average yearly growth rate has been estimated to be 0.28 cm per year
(32). The incidence of rupture is 8/100,000 population per year, with an annual risk
of rupture that increases to 8% per year for aneurysms >5.0 cm (Fig. 2) (33,34).
The majority of patients who die from ruptured AAAs are asymptomatic prior to
their catastrophic event.
Familial Aneurysms
Familial aneurysms account for approximately 15% to 20% of all aneurysms,
both in the descending thoracic and abdominal aorta. Our knowledge and
understanding of the genetic etiology responsible for the presence of these
aneurysms continues to expand, as evidenced by the recent identification and
investigation of several loci responsible for their development. Familial TAAs
are inherited through Mendelian autosominal dominant traits with variable
expressivity and incomplete penetrance (35,36). Loci discovered to date
include thoracic aortic aneurysms and dissections 1 (TAAD1) (5q13-14),
TAAD2 (3p24-25), and familial aortic aneurysms (FAA) (11q) (37–42). A
recent nationwide Swedish study (40) revealed a biphasic distribution in the
incidence of familial aortic aneurysms, with an early peak between the ages of
20 and 40 and a late peak after the age of 60 (Fig. 3). There are also data to
suggest that patients with familial aneurysms rupture at a younger age than
those with degenerative pathology (39,40). Recommendations regarding the
optimal timing of surgical intervention specific to familial aortic aneurysms in
the abdomen lack robust data in the current literature. Our institution’s risk/
benefit analysis following review of 3000 serial images and 3000 patient-years
of follow up for TAAs suggests preemptive extirpation in asymptomatic
familial disease at 6.0 cm for the descending aorta. Close follow up of patients
and their family members with clinical evaluations and serial imaging
is mandatory.
Figure 2 Estimated risk of rupture for abdominal aortic aneurysms. Source: From Ref. 34.
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Treatment of Ruptured Aortic Aneurysms 209
PRESENTATION, DECISION-MAKING, AND
RESUSCITATIVE MANAGEMENT
True demographics of ruptured aortic aneurysms are speculative, since the majority
of patients do not survive long enough to pursue medical care. Most patients with
ruptured thoracic aortic aneurysm present with hypotension and sharp pain in
the back or interscapular region. A symptomatic thoracic aortic aneurysm may be
confused with many alternative disease processes including acute coronary syn-
drome, acute pulmonary embolism, esophageal perforation, and pneumothorax.
It is often a chest radiograph and computed tomography (CT) of the chest and
abdomen that will enable the diagnosis of the ruptured aneurysm (Fig. 4).
Figure 3 Age-specific incidence rates for familial (with sibling history) and sporadic
(without sibling history) aneurysms. The difference between the two curves gives an
approximation of the familial risk. Source: From Ref. 40.
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210 Shahriari and Farkas
Less than 15% of patients who present with ruptured AAAs carry a previous
diagnosis of aneurysm. The most common presentation associated with this
condition is abdominal and lower back pain associated with a tender and pulsatile
mass. Only one-third of patients present with the “classic triad” of pain, hypotension,
and pulsatile mass. Plain abdominal radiographs will reveal the calcified contour
of the aneurysm wall in approximately 75% of cases.
There has been much debate about the optimal preoperative management of
these patients. In particular regard to resuscitation, no randomized studies exist
evaluating different strategies. Crawford (43) published a series of 87 patients
with ruptured AAA with a 77% survival. Based on this experience, he recom-
mended the utilization of blood for resuscitation until surgery, while keeping the
systolic blood pressure less than 70 mmHg. Aggressive resuscitation with blood
and fresh frozen plasma was not recommended until after application of the aortic
cross clamp, and extensive evidence in the literature reinforces the danger of over-
vigorous volume resuscitation, which can exacerbate coagulopathy in patients
with ruptured AAA (44–49). However, this strategy has been criticized by other
authors who suggest that permissive hypotension may itself cause hypoperfusion
and multisystem organ failure leading to death (50).
The role of CT scans in the diagnosis of ruptured aortic aneurysms has been
discussed in the literature, and some authors have questioned its value in the
management of the patient. It is speculated that obtaining a CT scan may contrib-
ute to mortality by delaying the surgical therapy. For TAAs, most surgeons would
be reluctant to operate on a patient based only on suspicion. For abdominal aortic
aneurysm, because of the ability of the surgeon to diagnose the malady based on
the clinical presentation and the physical exam, some authors argue that time
should not be spent in the radiology department, but is better spent in the Operating
Room (OR). However over 40% of normotensive patients with known AAA and
Figure 4 Computed tomography image of a patient with contained rupture of the descend-
ing thoracic aneurysm.
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Treatment of Ruptured Aortic Aneurysms 211
abdominal pain do not suffer from ruptured AAA. In these situations CT scans can
be of utmost help in avoiding a negative laparotomy. The sensitivity and specificity
of CT scans for ruptured AAA have been estimated to be 79% and 78%, respec-
tively (51). Despite this there appears to be clinical advantage in judgmental use
of CT scanners for diagnosis. Kvilekval et al. (52) studied 65 hemodynamically
stable patients with AAA and abdominal and back pain. There were no deaths
related to the delay caused by obtaining the CT scan. The study provided useful
anatomic information in 28% of patients, and in 70% of patients, emergency
surgery was avoided.
Thus we recommend CT scans of the chest and abdomen with intravenous
contrast for all hemodynamically stable patients in whom there is a suspicion for
symptomatic or ruptured thoracic aortic aneurysm.
The CT scan should be obtained with and without intravenous contrast.
The noncontrast scans allow for detection of fresh hematomas, and the contrast
images permit accurate identification of the anatomy of the aneurysm. CT find-
ings suggestive of ruptured abdominal aortic aneurysm include obscuration of the
retroperitoneum and displacement of the aneurysm by an irregular high-density
collection. The kidneys may also be displaced anteriorly by a perinephric
fluid collection. Other signs include enlargement of the psoas muscle contour and
a crescent shaped area of high attenuation within the wall or mural thrombus of
the aneurysm (53–55). Rapid opacification of the inferior vena cava suggests an
aortocaval fistula.
MANAGEMENT OF RUPTURED AORTIC ANEURYSMS
General Considerations
While hemodynamic stability affords the opportunity to obtain imaging, the
converse requires expeditious transfer to the OR for emergency surgery. Successful
management of the unstable patient with ruptured aortic aneurysm requires a high
index of suspicion, an experienced surgical team, and a clear plan and pathway for
treatment.
Patients with ruptured aortic aneurysms should not be denied therapy on the
basis of any specific set of preoperative factors. According to Halpern et al. (56)
there is no correlation between preexisting medical comorbidities in ruptured
aortic abdominal aneurysm patients and the immediate perioperative outcome.
However, that series did find that hemoglobin level less than 10 mg/mL, loss of
consciousness, and creatinine >1.5 mg/mL were predictive of death.
Ruptured Thoracic Aortic Aneurysm and Thoracoabdominal
Aortic Aneurysm—Open Repair
Distal Arch/Proximal Descending Aortic Rupture
Efficient transfer of the patient to the operating suite is of paramount importance.
While there is no absolute requirement for selective ventilation, this may be
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