JACC: CARDIOVASCULAR IMAGING
VOL. 6, NO. 12, 2013
ª 2013 BY THE AMERICAN COLLEGE OF CARDIOLOGY FOUNDATION
PUBLISHED BY ELSEVIER INC.
ISSN 1936-878X/$36.00
http://dx.doi.org/10.1016/j.jcmg.2013.08.009
iFORUM
DEBATES IN IMAGING
Aortic Surgery for Ascending Aortic
Aneurysms Under 5.0 cm in Diameter
in the Presence of Bicuspid Aortic Valve
Klaus Kallenbach, MD, PHD,* Thoralf M. Sundt, MD,y
Thomas H. Marwick, MD, PHD, MPHz
ANEURYSM OF THE ASCENDING AORTA MAY CAUSE ACUTE TYPE A AORTIC
D I S S E C T I O N , and the primary aim of a prophylactic operation is avoidance of this life-threatening
complication. Current guidelines recommend prophylactic replacement of the aneurysmal ascending
aorta at a diameter of $5.5 cm. However, several reports have shown that nearly 50% of patients with an
acute type A aortic dissection present with an aortic diameter <5.5 cm. It is controversial how to best
respond to these observations. Because surgical advances have led to a reduction of early surgical
mortality between 1% and 3%, many clinicians believe that surgery is warranted in smaller aortas. Given
the frequency of a bicuspid aortic valve (BAV), such a strategy has health implications for this population.
Under 5.0 cm in Diameter
Klaus Kallenbach, MD, PhD*
At first glance, it seems
there is no doubt: the guidelines recommend
prophylactic surgical replacement of the ascending
aorta in non-Marfan patients at an aneurysm
diameter of $5.5 cm to avoid an acute type A
aortic dissection (1). This is a class I quoted recommendation with general agreement of the
writing committee, but the level of evidence is
weak (grade C), based on expert opinion rather
than randomized clinical trials or meta-analyses.
On closer evaluation, it is apparent that the recommendation is based only on a 1997 study by
Coady et al. (2), which defines an inflexion in the
risk of dissection at an ascending aortic aneurysm
diameter of 6.0 cm; an illustration of this is even
displayed in the guidelines. Less widely known is
that the resulting recommendation of surgery at
5.5 cm is based on the analysis of a heterogeneous
cohort of only 54 patients with aneurysms of the
ascending aorta or aortic arch, including both
connective tissue disease and degenerative etiology. Analysis of the aneurysmal growth rate and
aortic diameter at the time of dissection showed
Current guidelines.
that the incidence of rupture or dissection was
45.2% at an aortic size of >6.0 cm. However, some
additional information is pertinent. Acute dissections or ruptures occurred in this cohort at
diameters <6.0 cm: in 7.1% of those with an aortic
diameter <4.0 cm, 8.5% of those with a diameter
of 4.0 to 4.9 cm, and 12.8% with a diameter of 5.0
to 5.9 cm (2). Thus, rupture or dissection occurred
at an aortic diameter <5.5 cm in 22% of investigated patients. On the basis of this information,
pursuit of the current recommendations of surgery
at a diameter of $5.5 cm would lead to nearly onefourth of patients with an ascending aneurysm
experiencing an acute type A aortic dissection or
aortic rupture, which is a devastating disease with
a poor outcome (3). This is surprising, because the
primary aim of aortic aneurysm surgery is the
avoidance of these complications!
There is further evidence that the recommended
cutoff of 5.5 cm may be of harm for a number of
patients with moderate-sized aneurysms of the
ascending aorta. Neri et al. (4) measured the
internal diameter of the ascending aorta by analyzing aortic samples from 220 patients who
underwent surgery for an acute type A aortic dissection. They found that the median aortic diameter was only 41.3 mm for patients with an acute
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Surgery for Ascending Aortic Aneurysm
type A aortic dissection without connective tissue disease. Thus, only 4.7% of
patients with an acute type A aortic dissection had an aneurysm of the ascending
aorta using the definition of a 50% increase
in diameter compared with the expected
normal aortic diameter. In the International Registry of Acute Aortic Dissection, 59% of 591 patients presenting
with an acute type A aortic dissection had
an ascending aortic diameter <5.5 cm and
40% had a diameter <5.0 cm (5). Independent predictors of the occurrence of an
acute type A aortic dissection at a diameter
<5.5 cm included history of hypertension,
radiating pain, and increasing age. Aortic
size at presentation was unrelated to
mortality. Transesophageal echocardiography measurements of the aortic annulus,
sinus segment, sinotubular junction, and
ascending aorta in 177 non-Marfan
patients with tricuspid aortic valves who
presented with an acute type A aortic
dissection showed that 62% had a maximal aortic diameter of <5.5 cm, 42% had
a maximal aortic diameter <5.0 cm, and
>20% had maximal aortic dimensions
<4.5 cm (6).
Thus, these studies show that acute
type A aortic dissection occurs in many
patients at less than the recommended
diameter of 5.5 cm for surgical intervention, so the current aortic diameter
threshold excludes approximately 50%
of patients with an acute type A aortic
dissection from prophylactic replacement of the ascending aorta. Moreover,
risk factors other than the diameter of
the ascending aorta influence the
development of an acute type A aortic
dissection and must be identified.
However, the law of Laplace cannot be
ignored; aneurysmal diameter is definitively a risk factor for acute type A aortic
dissection, and the incidence of dissection and rupture increases with
increasing size of the ascending aortic
aneurysm (7). The important question
remains: is a diameter of 5.5 cm the right
indication for prophylactic surgery, or
must we readjust to a smaller diameter?
Outcome of prophylactic replacement of
ascending aortic aneurysm. The pri-
mary aim of replacement of the dilated
JACC: CARDIOVASCULAR IMAGING, VOL. 6, NO. 12, 2013
DECEMBER 2013:1321–6
ascending aorta in asymptomatic patients is the avoidance of an acute type
A aortic dissection; this is truly a prophylactic indication. In patients with
chest pain, immediate surgery is indicated and may be warranted for significant valve disease. Various operative
techniques are available for replacement
of the ascending aorta; supracoronary
tube graft replacement is a straightforward operation indicated for patients
without aneurysmal involvement of
the aortic root. Additional aortic valve
replacement is possible. In cases with
root dilation, the modified Bentall
operation, in which a vascular tube graft
incorporating a biological or mechanical
aortic valve prosthesis is used to replace
the root after reinsertion of the coronary
ostia, has been the gold standard for
3 decades. Since the 1990s, valvepreserving techniques for root replacement have become the operation of
choice when the native aortic valve is
structurally intact.
In cardiac surgical centers experienced in aortic surgery, the results of
these techniques are excellent. Today,
the ascending aorta can be replaced
with very low operative mortality and
morbidity. Garrido-Olivares et al. (8)
reported on combined aortic valve replacement and supracoronary ascending
aortic replacement in 89 patients with
an operative mortality rate of 2.3%. In a
series of 597 patients reported from
New York, the early mortality rate in
elective patients undergoing the Bentall
procedure was 1.4% for composite grafts
with mechanical valves and 3.7% with
biological valves (9). A group from
South Korea reported an operative
mortality rate of 2.6% in 195 patients,
including 24 urgent patients with an
acute type A aortic dissection (10). For
the valve-sparing reimplantation technique, the Hannover group reported a
30-day mortality rate of 1.3% in 230
elective patients (11), and the Leipzig
group reported a 0% mortality rate in
151 patients who underwent the David
operation (12). Similar results have
been achieved with the remodeling
technique, with 1% to 3% early deaths
in elective patients (13,14). At the
University Hospital Heidelberg, an
analysis of 548 consecutive patients who
underwent surgery for an ascending
aortic aneurysm over a period of 17
years had an average early mortality rate
of 4.8%. However, during the last 5
years, the average mortality rate was
1.6% in 381 patients (including 0%
mortality in the David group), reflecting
technical advances in cardiac surgery
and the effect of a large caseload (15).
Encouraged by these results and in
contrast to the current guidelines, we
recommend surgery for an ascending
aortic aneurysm in patients without
connective tissue disease or a BAV at
5.0 cm and less in selected cases.
The balance between the risk of acute
aortic dissection and operative risk. We
must balance the reduced incidence
of acute type A aortic dissection as a
result of earlier surgery against the
operative risk of prophylactic surgery in
an asymptomatic patient. Because the
occurrence of an acute type A aortic
dissection is potentially life threatening
but elective surgical replacement of the
ascending aorta carries relatively low
operative risk, the balance moves toward
earlier surgery; the harm of an acute type
A aortic dissection is greater than the
risk of surgery. Consequently, patients
should undergo surgery at a diameter of
<5.0 cm because many patients experience dissection at a smaller diameter,
as explained in the preceding text. The
development of an acute type A aortic
dissection is not only triggered by the
size of the aneurysm; factors such as
connective tissue disease (e.g., Marfan
or Loeys-Dietz syndrome), pregnancy,
BAV, familial history of thoracic aortic
aneurysm and dissection, hypertension,
aortic stiffness (measured noninvasive),
normative data instead of absolute aortic
size (such as the Z-score), sex, and
aortic growth may influence the timing
of the operation, and several of these
factors are already considered in the
effective guidelines (16). Individual
judgment of any patient is pivotal when
calculating operative risk versus the
likelihood of development of an acute
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DECEMBER 2013:1321–6
type A aortic dissection. However, as
long as the size of the aneurysm is
believed to be the most important predictor for the development of an acute
type A aortic dissection, operation
for aneurysms of the ascending aorta
<5.0 cm in diameter is justified not only
in high-risk patients for acute type A
aortic dissection. Many centers that
specialize in aortic surgery already
operate on ascending aortic aneurysms
<5.0 cm in diameter, and it is time to
reappraise the guidelines.
No, Not Under 5.0 cm
in the Absence of
Connective Tissue
Disease
Thoralf M. Sundt, MDy
No surgeon should approach the victim
of his operation without a sacred dread
and reluctance
dJohn Hunter (17)
Remarkable technological advances in
recent decades have made highresolution imaging widely available.
With their broader application, physicians are increasingly confronted with
management of the asymptomatic, and
often incidentally discovered, anatomic
“abnormality.” Gratifying advances in
surgical care have also reduced the
mortality and morbidity of many elective
operative interventions, and surgeons
are, in turn, increasingly asked to consider “prophylactic” procedures. Because
the risks associated with both the natural
history of these incidentally discovered
abnormalities and the interventions to
“fix them” lie at the low extreme of the
bell-shaped curve, decision making on
the basis of risk/benefit analysis is increasingly challenging. Nowhere is this
dilemma more apparent than in the
debate over management of moderate
nonsyndromic aortic dilation.
The drivers to early aortic intervention are strong. Aortic dissection is
the most common fatal aortic complication by a factor of 2 or 3, with
abdominal aneurysms more frequent
but less often lethal. Of those with
dissection involving the ascending aorta
who make it to the hospital, one-fourth
will die before discharge; an unknown
number die before diagnosis (18). On
long-term follow up, 10% to 30% of
patients with involvement of the entire
aorta (DeBakey type I) will require late
operation on the distal segments (19)
and late survival falls far below expected (20). Perhaps a contributing factor
to the operative risk is the likelihood, at
least in the United States, that the
emergent repair will be conducted by a
surgeon performing fewer than 2
operations for acute dissection each year
(21). Add to this the emotional strain
associated with the risk of a catastrophic
event occurring at an uncertain time,
and it is clear why the trend to recommend elective surgery for aortic
enlargement in a “center of excellence”
has grown over time.
Are we asking the right questions?
How solid are the data? How rational
are our recommendations?
There is no question that aortic dissection is a dreaded disease for all of
the reasons stated in the preceding
text, but this alone is not an argument
for indiscriminant aortic replacement.
Diseases of other organs, such as cancer
of the pancreas, have a dismal prognosis
but are not themselves arguments for
prophylactic extirpation of the susceptible site. This is true regardless of the
skill of the surgeon and how close his
or her rate of operative complications is believed to approach zero. Of
course, with regard to this estimate of
operative outcomes, surgeons (like all
other humans) are subject to illusory
superiority or “the Lake Wobegon
effect” and the literature is flawed by
publication bias, but that is another
discussion (22). Suffice it to note that,
according to the Society of Thoracic
Surgeons database, the operative risk
associated with replacement of the
proximal aorta under elective circumstances is 3.4% (23).
The question at hand is “What is
the risk that any individual, specifically
the one sitting across from me in my
Kallenbach et al.
Surgery for Ascending Aortic Aneurysm
1323
office, will get the dreaded disease?”
and not merely the risk of death should
the patient develop the condition. To
determine this risk, accurate assessment
of both the numerator and the denominator is needed for the given clinical
parameter (risk factor) of interest.
Unfortunately, in most cases, we have
only a global picture of the condition
with very imprecise information on
specific subsets of patients at risk,
derived in most instances from study of
those experiencing the complication
(the numerator) rather than from the
total population (the denominator).
Specifically with regard to aortic dissection, we have a growing understanding of the spectrum of aortic
diameter before dissection among those
experiencing dissection. What we need
to inform our discussion of prophylactic
surgery with our patient in the office,
however, is knowledge of the risk of
dissection among those with a given
aortic diameter. The 2 questions yield
dramatically different results; for example, the likelihood of female sex with
breast cancer is approximately 99%, but
the likelihood of breast cancer with
female sex is one-fifth that number.
Fortunately, Bayesian analysis can suggest answers to these questions;
unfortunately, it is not always intuitive.
What of the quality of the data that
we do have at hand? One of the first
studies concerning the natural history
of thoracic aortic aneurysmal disease
was performed in the early 1960s by
Dr. John Joyce at the Mayo Clinic. In
that study, which was inspired by surgical progress that made intervention
on the dilated aorta a realistic therapeutic option, he identified the 6.0-cm
mark as a particularly important risk
factor for significant aortic complications (24). Subsequent studies, particularly those performed by Dr. John
Elefteriades and his collaborators at
Yale University, have confirmed that,
for the ascending aorta, the incidence of
complications rises dramatically at a
diameter of 6.0 cm (25). It is largely on
the basis of these studies that it is reasonable and prudent to replace the
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Kallenbach et al.
Surgery for Ascending Aortic Aneurysm
ascending aorta at 5.5 cm in the interest
of providing a bit of a safety margin.
Although it is comforting that a
number of studies by different investigators point roughly to the same critical diameter, it should also be noted
that these studies are subject to entry
bias. Far from a population-based
dataset, surgical databases at any large
academic center located in a dense
population and surrounded by multiple
community providers are likely to be
enriched for those patients who experience complications. I would argue that
the implication is that the risks will
be overestimated even for dilation to 5.5
or 6.0 cm, but what about the mounting
evidence that dissection can occur at
aortic diameters <5.0 cm? Data on
aortic diameter from 591 patients with
type A dissection were reported from the
International Registry of Acute Dissection in 2007 (5). The average
ascending aortic diameter was 5.3 cm,
and 40% of patients had an aortic
diameter <5 cm! Surely this argues for
aggressive intervention at lower and
lower diameters.
There are at least 2 problems with
this line of thinking. Given the aforementioned
“numerator/denominator
problem,” we cannot make a statement
about the risk of dissection among
patients with aortic diameters <5.0 cm
without considering the denominator,
which in this case is enormous because
most humans have aortas <5.0 cm in
diameter. The second problem is that
the dataset itself includes only those
patients who made it to the hospital.
An unknown number likely died before
entry into the dataset, and their aortic
diameters are unknowable.
I would argue that it is not a surprise
that aortic size alone is a poor predictor
of the risk of aortic complications.
Aortic dissection represents a mechanical failure of the aortic wall. That
failure can be expected when wall stress
exceeds wall strength. The law of
Laplace certainly predicts higher wall
tension with greater aortic radius, but
there is more to the equation than
radius; intraluminal pressure is equally
JACC: CARDIOVASCULAR IMAGING, VOL. 6, NO. 12, 2013
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important (law of Laplace: T ¼ PR).
We have no direct assessment of
material strength in clinical practice
today. The presence of a known connective tissue disorder characterized by
medial degeneration suggests reduced
wall strength, as does the dilation itself
in most instances. Incidentally, in the
special case of the BAV, it could be
argued that moderate aortic dilation is
“normal” and not evidence of medial
degeneration. I am not aware of any
data that support greater susceptibility
to dissection or rupture at any given
diameter compared with patients with a
tricuspid valve.
Where does that leave the concerned
clinician anxious to prevent aortic catastrophe? Surely the ideal solution to
the problem is a patient-specific assessment of the risk of aortic complications on the basis of noninvasive
imaging assessments of material properties of the aortic wall and calculation of
wall stress. A similarly patient-specific
determination of the risks associated
with prophylactic surgery of this type
can now be calculated for coronary
bypass or aortic valve replacement
on the Society of Thoracic Surgeons
website (http://sts.org/quality-researchpatient-safety/quality/risk-calculator-andmodels). In the meantime, our clinical
decision making is likely to be as much
anecdote driven as evidence based. Both
the physician and the patient will be
subject to the decision-making biases
that form the basis for the entire field of
behavioral economics (26). The valence
effect will influence our thinking in
favor of a greater likelihood of a positive
than negative outcome of the surgical
procedure, while the impact of vividly
framing the risk associated with aortic
enlargement as a “time-bomb in my
chest” will push us toward intervention.
Additionally, the certainty effect will
favor a decision to take definitive action
to eliminate even a small risk of an
event occurring at an unknown time.
This all adds up to a busy operative
schedule, particularly when considering
that 30% to 50% of the approximately
3 million patients in the United States
with a BAV will have some aortic
enlargement, as noted in the preceding
text. Still, it is worth remembering John
Hunter’s admonition and recognizing
that at some point the lines describing
risk and benefit will cross; with an
overly aggressive approach, we will
surely hurt more people than we help.
We don’t know where that point is, but
it exists.
Moving Imaging
From Part of the
Problem to Part of
the Solution
Thomas H. Marwick, MD, PhD, MPHz
Current surgical decision making
regarding aortopathy is almost completely based on the aortic dimension
and surgical plans for the aortic valve.
However, as discussed in the preceding
text, aortic dissections are quite commonly reported in vessels that are
smaller than the recommended threshold. Controversy about the appropriate
threshold will be informed by clinical
trials or decision models, but imaging
may be able to inform this better than
simply by provision of aortic dimensions. Indeed, there is nascent evidence
that a number of other observations
may be of value.
In patients with a BAV, leaflet morphology may be an important consideration. In a study of 581 patients with
a BAV, a “type 1” morphology (fusion of
the right and left cusps with opening in
an anterior-posterior direction) was
present in 71% of bicuspid valves and
was associated with annulus and sinus
enlargement (27). In a separate study,
this morphology was associated with
aortic regurgitation, whereas fusion of
the right or left cusp with the noncoronary cusp was associated with aortic
stenosis and enlargement extending into
the aortic arch (28). Indeed, aortic
stenosis has an important association
with aortopathy, with aortic dilation
rates increased similarly in stenotic
Kallenbach et al.
Surgery for Ascending Aortic Aneurysm
JACC: CARDIOVASCULAR IMAGING, VOL. 6, NO. 12, 2013
DECEMBER 2013:1321–6
bicuspid and tricuspid valves (29). Although the previous teleologic explanation of aortopathy on the basis
of post-stenotic dilation has fallen into
disfavor, there is evidence to show
increased aortic wall stress in the setting
of a right-left fusion of the bicuspid
valve, independent of the severity of
stenosis (30). In this setting, the stenotic
jet is directed anteriorly and to the right,
and this is associated with asymmetric
enlargement of the aortic root, most
commonly on the convexity of the vessel
(31). The resulting inhomogeneity of
circumferential aortic strain has been
associated with the degree of reduced
cusp motion (32). The measurement of
flow direction may be helpful in understanding the risk of dissection, given
that most patients with a BAV have
neither symmetrical nor markedly
asymmetrical valves (33). In this issue
of iJACC, Della Corte et al. (34)
describe the importance of aortic morphology to disease progression. In a
study of 133 adult outpatients with a
BAV at baseline, 69% showed fusion on
the right and left aortic cusps, ascending
aortic dilation was present in 57%, and
root dilation was present in 13.5%.
Over an average follow-up of 4 years,
the mean growth rate was 0.3 mm/year
at the sinuses and 0.6 mm/year at
the ascending level. Root phenotype
at presentation, rather than absolute
baseline diameter, was an independent predictor of rapid progression
(>0.9 mm/year) for the ascending aorta.
In contrast, the more common ascend-
1325
The current guidelines for surgery in
aortopathy are heavily dependent on
measurement of aortic dimension.
However, these measurements have a
number of limitations, not the least of
which is how best (or whether at all) to
index the measurement for size. A more
sophisticated risk evaluation approach
should be considered, incorporating the
morphology of the aorta, the severity of
aortic stenosis, the morphology of the
aortic valve, and perhaps also the
characteristics of the aortic wall tissue.
ing phenotype proved a more stable
disease entity, generally with slower
progression. Aortic morphology might
therefore warrant closer surveillance and
earlier treatment of aortopathy, and
indeed a variety of other factors might
also be helpful for decision making.
The nature of the aortic tissue is
another aspect that may be important
in understanding the risk of events.
Measurements of stiffness index and
pulse-wave velocity in patients with a
BAV and hereditary thoracic aneurysms
have shown a relationship between
stiffness and progression, but unfortunately the negative predictive value
of abnormal stiffness and pulse-wave
velocity has been only modest, with a
large overlap between patients with
Marfan syndrome, BAV, and familial
aneurysm (35). Thus, current techniques for measurement of aortic tissue
appear insufficiently sensitive to play a
role in surgical decision making. However, evidence of activation of molecular
pathways by hemodynamic and jetrelated stimuli may control extracellular
matrix regulation and thereby link to
aortic thinning and dilation (36–38).
Therefore, tissue measurements may
not provide substantial incremental
information to that provided by jet
characteristics. Nonetheless, although
aortic thickness does not differ between
patients undergoing aortic surgery with
bicuspid and tricuspid valves, patients
with BAV are reported to have thinner
elastic lamellae and a greater distance
between lamellae (39).
Reprint requests and correspondence: Dr.
Klaus Kallenbach, University of Heidelberg,
INF 110, Heidelberg D-69120, Germany.
E-mail: [email protected].
OR Dr. Thoralf Sundt, Massachusetts
General Hospital, Cardiac Surgery, 55 Fruit
Street, Boston, Massachusetts 02114-2696.
E-mail: [email protected]. OR Dr. Thomas
H. Marwick, Menzies Research Institute
Tasmania, 17 Liverpool Street, Hobart, TAS
7000, Australia. E-mail: Tom.Marwick@utas.
edu.au.
4. Neri E, Barabesi L, Buklas D, et al. Limited
role of aortic size in the genesis of acute type
A aortic dissection. Eur J Cardiothorac Surg
2005;28:857–63.
5. Pape LA, Tsai TT, Isselbacher EM, et al.
Aortic diameter $5.5 cm is not a good predictor of type A aortic dissection: observations
from the international registry of acute aortic
dissection (IRAD). Circulation 2007;116:
1120–7.
6. Parish LM, Gorman JH, Kahn S, et al. Aortic
size in acute type A dissection:
implications for preventive ascending aortic
replacement. Eur J Cardiothorac Surg 2009;
35:941–6.
7. Davies RR, Lee JG, Coady MA, et al.
Yearly rupture or dissection rates for thoracic
aortic aneurysms: simple prediction based on
size. Ann Thorac Surg 2002;73:17–28.
8. Garrido-Olivares L, Maganti M, Armstrong S,
et al. Aortic valve replacement with Hancock II
bioprothesis with and without replacement
of the ascending aorta. Ann Thorac Surg 2011;
92:541–7.
9. Etz CD, Bischoff MS, Bodian C, et al. The
Bentall procedure: is it the gold standard? A
Author disclosures
The authors have reported that they
have no relationships relevant to the
contents of this paper to disclose.
From the *Department of Cardiac
Surgery, University Hospital Heidelberg, Heidelberg, Germany; yDivision
of Cardiac Surgery, Massachusetts
General Hospital, Harvard Medical
School, Boston, Massachusetts; and the
zMenzies Research Institute Tasmania,
Hobart, Australia.
REFERENCES
1. Hiratzka LF, Bakris GL, Beckmann JA, et al.
ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/
SIR/STS/SVM guidelines for the diagnosis
and management of patients with thoracic
aortic disease. J Am Coll Cardiol 2010;55:
e27–129.
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;113:476–91.
3. Meszaros I, Morocz J, Szlavi J, et al. Epidemiology and clinicopathology of aortic dissection. Chest 2000;117:1271–8.
1326
Kallenbach et al.
Surgery for Ascending Aortic Aneurysm
series of 597 consecutive cases. J Thorac
Cardiovasc Surg 2010;140 Suppl:S64–70.
10. Kim TS, Na CY, Oh SS, et al. Long-term
mortality and morbidity after button Bentall
operation. J Card Surg 2013;28:280–4.
11. Kallenbach K, Karck M, Pak D, et al. Decade
of aortic valve sparing reimplantation: are we
pushing the limits too far? Circulation 2005;
112:I253–9.
12. Leontyev S, Trommer C, Subramanian S,
et al. The outcome after aortic valve sparing
(David) operation in 179 patients: a singlecentre experience. Eur J Cardiothorac Surg
2012;42:261–6.
13. Yacoub MH, Gehle P, Chandrasekaran V,
et al. Late results of a valve-preserving operation in patients with aneurysms of the
ascending aorta and root. J Thorac Cardiovasc
Surg 1998;115:1080–90.
14. Aicher D, Langer F, Lausberg H, et al. Aortic
root remodeling: ten-year experience with274
patients. J Thorac Cardiovasc Surg 2007;134:
909–15.
15. Kallenbach K, Kojic D, Oezsoez M, et al.
Treatment of ascending aortic aneurysms
using different surgical techniques: a singlecentre experience of 548 patients. Eur J Cardiothorac Surg 2013;44:337–45.
16. Von Kodolisch Y, Robinson PN, Berger J.
When should surgery be performed in Marfan
syndrome and other connective tissue disorders to protect against type A dissection?
In: Bonser RS, Haverich A, Mascaro J,
Pagano D, editors. Controversies in Aortic
Dissection and Aneurysmal Disease. London,
United Kingdom: Springer, in press.
17. Palmer JF, editor. Lectures on the Principles
of Surgery in the Surgical Works of John
Hunter, FRS. London, England: Longman,
Rees, Orme, Brown, Green, and Longman,
1835.
18. Hagan PG, Nienaber CA, Isselbacher EM,
et al. The International Registry of Acute
Aortic Dissection (IRAD): new insights into
an old disease. JAMA 2000;283:897–903.
19. Geirsson A, Bavaria JE, Swarr D, et al. Fate
of the residual distal and proximal aorta after
acute type A dissection repair using a
JACC: CARDIOVASCULAR IMAGING, VOL. 6, NO. 12, 2013
DECEMBER 2013:1321–6
contemporary surgical reconstruction algorithm. Ann Thorac Surg 2007;84:1955–64.
20. Olsson C, Hillebrant CG, Liska J,
Lockowandt U, Eriksson P, Franco-Cereceda A.
Mortality and reoperations in survivors operated on for acute type A aortic dissection and
implications for catheter-based or hybrid
interventions. J Vasc Surg 2013;58:333–9.
21. Chikwe J, Cavallaro P, Itagaki S, Seigerman M,
Diluozzo G, Adams DH. National outcomes
in acute aortic dissection: influence of surgeon
and institutional volume on operative mortality.
Ann Thorac Surg 2013;95:1563–9.
22. Hoorens V. Self-enhancement and superiority
biases in social comparison. Eur Rev Soc
Psychol 1993;4:113–39.
23. Williams JB, Peterson ED, Zhao Y, et al.
Contemporary results for proximal aortic
replacement in North America. J Am Coll
Cardiol 2012;60:1156–62.
24. Joyce JW, Fairbairn JF II, Kincaid OW,
Juergen JL. Aneurysms of the thoracic aorta.
a clinical study with special reference to
prognosis. Circulation 1964;29:176–81.
25. Elefteriades JA. Indications for aortic
replacement. J Thorac Cardiovasc Surg 2010;
140 Suppl:S5–9.
26. Tversky A, Kahneman D. Certainty part of
prospect theory. Rational choice and the
framing of decisions. J Business 1986;59:
S251–78.
27. Khoo C, Cheung C, Jue J. Patterns of aortic
dilatation in bicuspid aortic valve associated
aortopathy. J Am Soc Echocardiogr 2013;26:
600–5.
28. Kang JW, Song HG, Yang DH, et al.
Association between bicuspid aortic valve
phenotype and patterns of valvular dysfunction and bicuspid aortopathy. J Am Coll
Cardiol 2013;6:150–61.
29. Kim YG, Sun BJ, Park GM, et al. Aortopathy
and bicuspid aortic valve: haemodynamic
burden is main contributor to aortic dilatation. Heart 2012;98:1822–7.
30. Barker AJ, Markl M, Burk J, et al. Bicuspid
aortic valve is associated with altered shear
wall stress in the ascending aorta. Circ Cardiovasc Imaging 2012;5:457–66.
31. Bauer M, Gliech V, Siniawski H, Hetzer R.
Configuration of the ascending aorta in
patients with bicuspid and tricuspid aortic
valve disease undergoing aortic valve replacement with or without reduction aortoplasty.
J Heart Valve Dis 2006;15:594–600.
32. Della Corte A, Bancone C, Conti CA, et al.
Restricted cusp motion in right-left type of
bicuspid aortic valves: a new risk marker for
aortopathy. J Thorac Cardiovasc Surg 2012;
144:360–9.
33. Sabet HY, Edwards WD, Tazelaar HD,
Daly RC. Congenitally bicuspid aortic valves: a
surgical pathology study of 542 cases (1991
through 1996) and a literature review of 2,715
additional cases. Mayo Clin Proc 1999;74:14–26.
34. Della Corte A, Bancone C, Buonocore M,
et al. The pattern of ascending aortic dimensions predicts the growth rate of the aorta in
bicuspid aortic valve patients. J Am Coll
Cardiol Img 2013;6:1301–10.
35. De Wit A, Vis K, Jeremy R. Aortic stiffness in
hereditable aortopathies: relationship to aneurysm growth rate. Heart Lung Circ 2013;22:3–11.
36. Ikonomidis JS, Jones JA, Barbour JR, et al.
Expression of matrix metalloproteinases and
endogenous inhibitors within ascending aortic
aneurysms of patients with bicuspid or tricuspid aortic valves. J Thorac Cardiovasc Surg
2007;133:1028–36.
37. Fedak PW, de Sa MP, Verma S, et al. Vascular matrix remodeling in patients with
bicuspid aortic valve malformations: implications for aortic dilatation. J Thorac Cardiovasc
Surg 2003;126:797–806.
38. Malecki S, Bjorck HM, Folkersen L, et al.
Identification of a novel flow-mediated gene
expression signature in patients with bicuspid
aortic valve. J Mol Med 2013;92:129–39.
39. Bauer M, Pasic M, Meyer R, et al. Morphometric analysis of aortic media in patients
with bicuspid and tricuspid aortic valve. Ann
Thorac Surg 2002;74:58–62.
Key Words: aortic aneurysm bicuspid aortic valve - surgery.