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Stability of Ascending Aortic Dilatation Following Aortic
Valve Replacement
Bruce W. Andrus, MD; Daniel J. O’Rourke, MD; MS;
Lawrence J. Dacey, MD, MS; Robert T. Palac, MD, MS
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Background—Replacement of the ascending aorta (Asc Ao) at the time of aortic valve replacement (AVR) is controversial
because the risk of progressive dilatation following valve replacement is uncertain. Our aim was to determine the natural
history of ascending aortic dilatation following AVR.
Methods and Results—We studied 185 patients undergoing AVR at our institution between 1992 and 1999. Clinical and
echocardiographic data were obtained by merging our institutional echocardiographic database with the DHMC
component of the Northern New England Cardiovascular Disease Study Group database. Baseline Asc Ao measurements obtained from intraoperative transesophageal echocardiograms or early (⬍8 weeks) postoperative transthoracic
echocardiograms were compared with late follow-up measurements (mean follow-up 30.0⫾23.4 months). During
follow-up, there was no increase in the mean Asc Ao diameter (3.6⫾0.6 cm versus 3.6⫾0.6 cm, p⫽NS). Progressive
aortic dilatation, defined as an increase in diameter ⬎0.3 cm, occurred in 27/185 patients (15%). Baseline Asc Ao
dilatation (ⱖ3.5 cm) was present in 107/185 patients (58%). In this subset of patients, there was no increase in mean
Asc Ao diameter (4.0⫾0.4 versus 3.9⫾0.6 cm, p⫽NS) and progressive aortic dilatation occurred in only 10 patients
(9.3%). No patients with baseline aortic dilatation (range, 3.5 to 5.3 cm) dilated beyond 5.5 cm on follow-up (range, 2.4
to 5.5 cm). There were no clinical or valvular characteristics that predicted progressive Asc Ao dilatation.
Conclusions—An increase in Asc Ao dilatation occurs infrequently following AVR and therefore, argues against routine
Asc Ao replacement at the time of AVR. (Circulation. 2003;108[suppl II]:II-295-II-299.)
Key Words:aneurysm 䡲 aorta 䡲 remodeling 䡲 valves
P
atients referred for aortic valve replacement (AVR) often have
accompanying ascending aortic (Asc Ao) dilatation. However,
the decision to extend the surgical procedure to include ascending
aortic replacement is difficult because of the increase in surgical risk
and the uncertain natural history of ascending aortic dilatation
following AVR. The existing body of literature regarding ascending
aortic dilatation focuses on patients who did not undergo valve
surgery. These studies have consistently documented progressive
aortic dilatation with expansion rates ranging from 0.12 cm to 0.42
cm/year. A frequently observed predictor of expansion rate is
baseline aortic diameter such that larger aneurysms grow more
rapidly than smaller ones.1–4
To date, there have been few studies addressing the natural
history of aortic dilatation following AVR.5,6 In some patients with
aortic valve disease, the pathogenesis of ascending aortic dilatation
likely involves an accompanying intrinsic defect in connective
tissue.7–11 However, in patients without apparent connective tissue
disease or congenital heart disease, the flow patterns of aortic valve
disease may play a role in the pathogenesis.12–15 Because AVR
often corrects these hemodynamic derangements, surgery may alter
the natural history of aortic dilatation.
The primary aim of this study was to examine the natural
history of ascending aortic dilatation following aortic valve
replacement. Additionally, we sought to identify predictors of
progressive aortic dilatation.
Methods
Study Population
The Northern New England Cardiovascular Disease Study Group
(NNE) database has been fully described elsewhere.16 Using this
database, we searched for patients who underwent AVR surgery
without ascending aortic replacement at Dartmouth Hitchcock Medical Center (DHMC) between January 1, 1992 and December 31,
1999. This search identified 696 patients. We next searched the
DHMC echocardiographic laboratory database to identify patients
who had an echocardiogram performed within the same time period
with referral diagnoses of “aortic stenosis,” “aortic insufficiency,”
and “aortic prosthesis follow-up.” This yielded 6362 echocardiograms of which 2312 were performed on patients in the surgical
registry.
The final study population consisted of 185 patients with technically adequate echocardiograms performed early after surgery (⬍8
weeks) and late after surgery (⬎8 weeks). When multiple follow-up
studies were available, the last complete study was selected. Of these
185 patients, 123 had Asc Ao measurements prospectively recorded
in the database. The remaining 62 patients were lacking either a
baseline and/or follow-up ascending aortic measurement (ie, the
sonographer did not enter a dimension in his or her report). The
missing information was obtained by reviewing the tapes and using
Received from the Cardiology Section, Cardiothoracic Surgery Section, Dartmouth Hitchcock Medical Center, Lebanon, NH, USA.
Correspondence to Bruce W. Andrus, MD, Dartmouth Hitchcock Medical Center, Cardiology Section, One Medical Center Drive, Lebanon, NH
03756-0001. Phone: 603-650-7840; Fax: 603-650-6164, E-mail: [email protected].
Circulation is available at http://www. circulationaha.org
DOI: 10.1161/01.cir.0000087385.63569.79
II-295
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Circulation
September 9, 2003
“off-line” digital calipers to measure the diameter of the ascending
aorta. The measurements were made by one of the investigators
(BWA) who was blinded to the comparison measurement (eg, the
follow-up diameter in the case of a missing baseline value).
Aortic Measurements
The ascending aortic diameter was measured 2 cm above the
sinotubular ridge in the parasternal long axis view in transthoracic
(TTE) studies. In transesophageal (TEE) exams, the ascending aortic
diameter was measured at the same location. Intraoperative TEE
measurements were validated by comparing them with preoperative
transthoracic measurements done less than 4 months earlier. There
was a close correlation between the preoperative and intraoperative
measurements of Asc Ao diameter (Pearson r⫽0.83).
TABLE 1.
Characteristics of Study Patients
Clinical
Mean age (years)
65.8
Gender (% male)
69.2
Smoking (%)
17
Hypertension (%)
43
Coronary artery disease (%)
52
Valvular
Valve type (%)
Carpentier
5
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Hancock
35
Statistical Analysis
Medtronic-Hall
43
All data are presented as mean⫾SD. Separate populations were
compared using the Student’s t-test for continuous variables and
Chi-square for nominal variables. Baseline and follow-up measurements were compared by the Student’s t-test for paired samples.
Associations between continuous variables were evaluated by linear
regression. Univariate analysis of clinical predictors of aortic dilatation was performed using the Student’s t-test for dichotomous
variables, ANOVA for categorical variables, and linear regression
for continuous variables. Probability values ⬍0.05 were considered
significant. Microsoft EXCEL 97® (Microsoft Corporation, Redmond, WA) and STATA (Release 6.0, Stata Corporation, College
Station, TX) software were used to perform statistical analyses.
St. Jude
15
Results
Baseline Characteristics
The characteristics of the study population are presented in
Table 1. The mean age of the population was 65.8⫾13.6
years and was predominately male (69.2%). While relatively
few patients were active smokers (17%), hypertension and
coronary artery disease (CAD) were frequent comorbidities
(43% and 52%, respectively). Moderate to severe aortic valve
stenosis was the most common valve lesion (79%), most
often secondary to calcific or degenerative valve disease
(87%). Most patients received mechanical prostheses (58%).
At baseline, Asc Ao diameters ranged from 2.2 to 5.3 cm with
a mean of 3.6⫾0.6. There were 58% (107/185) of the patients
who had an Asc Ao diameter ⱖ3.5 cm at baseline (Figure 1).
Change in Asc Ao Diameter
The mean duration of follow-up was 30.0⫾23.4 months.
There was no significant difference between mean Asc Ao
diameter at baseline and at follow-up (3.6 cm ⫾0.6 versus 3.6
cm ⫾0.6). The distribution of change in Asc Ao diameter is
displayed in Figure 2. There were 15% (27/185) of the
patients who demonstrated a postoperative increase in aortic
dilatation ⬎0.3 cm. The mean Asc Ao expansion rate in the
entire study population was ⫺0.03⫾1.09 cm/year.
Limiting analysis to those patients with more than 1 year
(N⫽131) and more than 3 years follow-up (N⫽67) yielded
expansion rates similar to the entire study population (Table 2).
Other
2
Valve pathology (%)
Congenital
13
Degenerative
69
Endocarditis
5
Rheumatic
10
Other
3
Valve pathology (%)
Noncongenital
87
Congenital
13
Aortic stenosis (%)
None or mild
18
Moderate or severe
79
Aortic regurgitation (%)
None or mild
57
Moderate or severe
43
patients is displayed in Figure 3. The characteristics of these
patients are displayed in Table 3. Only 10/107 (9.3%)
displayed an increase in diameter exceeding 0.3 cm. No
patients with baseline aortic dilatation (range 3.5 to 5.3 cm)
dilated beyond 5.5 cm on follow-up (range 2.4 to 5.5 cm).
The mean Asc Ao expansion rate in patients with baseline
dilatation was ⫺0.10⫾0.70 cm/year.
Clinical Predictors of Aortic Dilatation
No statistically significant univariate association was found
between Asc Ao dilatation and any of the clinical variables
Subgroup Analysis: Patients With Baseline Asc
Ao Dilatation
In the population of patients with baseline Asc Ao diameter
ⱖ3.5 cm, aortic size remained stable over a mean follow-up
period of 33.6 months (4.0⫾0.4 cm versus 3.9⫾0.5 cm). The
distribution of change in Asc Ao diameter among these
Figure 1. Frequency distribution of ascending aortic diameter at
baseline. The black bars represent patients with ascending aortic dilatation at baseline.
Andrus et al
Ascending Aortic Dilatation and AVR
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TABLE 2. Comparison of Expansion Rate Stratified by
Follow-up Duration
Length of Follow-up
(months)
Expansion Rate
(cm/year)
All patients (n⫽185)
30.0 (⫾23.4)
⫺0.03 (⫾1.09)
Patients with ⬎1 year
follow-up (n⫽131)
39.6 (⫾20.9)
⫺0.02 (⫾0.16)
Patients with ⬎3 years
follow-up (n⫽67)
56.7 (⫾14.2)
0.01 (⫾0.08)
Study Cohort
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examined. These included age, gender, smoking, hypertension, and coronary artery disease. Likewise, no significant
association was found between any valvular characteristic
and Asc Ao dilatation. These characteristics included the
presence of moderate/severe AS, moderate/severe AR, valve
pathology (congenital, degenerative, endocarditis, rheumatic,
and other), and prosthesis type (Carpentier, Hancock,
Medtronic-Hall, St. Jude, and other). The difference in
expansion rate between mono- and bicuspid valves (n⫽21)
and that of trileaflet valves (n⫽164) nearly reached statistical
significance (⫹0.14⫾0.36 cm/year versus ⫺0.05⫾1.16 cm/
year, P⫽0.06 for one tailed t-test). There was no statistically
significant association between the baseline Asc Ao diameter
and the annual rate of expansion (r⫽0.14).
Discussion
Our findings suggest that Asc Ao dilatation is prevalent in
patients who undergo AVR. Furthermore, our study documents that Asc Ao dilatation rarely progresses following
AVR. We noted no increase in mean Asc Ao diameter during
a mean follow-up interval of 30.0 months. In the subpopulation with baseline aortic dilatation, we observed stability in
mean aortic diameter with a mean expansion rate of
⫺0.10⫾0.70 cm/year during a follow-up period of 33.6
months. An absolute increase in Asc Ao diameter exceeding
0.3 cm was infrequent, seen in 15% of the entire study
population and in 9.3% of the population with baseline Asc
Ao dilatation.
Other investigators have noted a similar prevalence of Asc
Ao dilatation in association with aortic valve disease. Hahn et
al10 reported on 83 patients with bicuspid aortic valves. In this
diverse population comprised of patients with varying degrees of valvular dysfunction, the overall prevalence of aortic
dilatation was 60%. Among patients with mild to moderate
Figure 3. Frequency distribution of absolute change in ascending aortic diameter in patients who had ascending aortic dilatation at baseline. The black bars represent patients with ascending aortic dilatation exceeding 0.3 cm.
AS, the prevalence was 63%. Crawford and Roldan14 compared the Asc Ao diameter of 118 patients with AS to 108
age-matched controls with normal or sclerotic valves. They
reported a significant difference in sinotubular diameter in
patients with all degrees of AS (mean diameter 3.5 to 3.6 cm)
compared with those with normal (3.0 cm) or sclerotic valves
(3.2 cm) (P⬍0.001).
Several studies have evaluated the natural history of Asc
Ao dilatation in the absence of AVR. Coady1 reported a rate
of 0.12 cm/year in a cohort of 79 patients followed for a mean
of 25.9 months. Hirose3 reported a mean growth rate of 0.28
cm/year based on a sample of 11 patients with ascending
TABLE 3. Comparison of Baseline Characteristics of Patients
With Baseline Ascending Aortic Dilatation
Expanders
(n⫽10)
Nonexpanders*
(n⫽97)
Mean age (years)
65.7
64.6
Gender (% male)
90
77
Smoking (%)
10
19
Clinical
Hypertension (%)
50
44
Coronary artery disease (%)
60
45
Aortic
Baseline ascending aortic
diameter (cm, ⫾SD)
3.8⫾0.4
4.1⫾0.4
Valvular
Valve type (%)
Carpentier
10.0
5.2
Hancock
30.0
29.9
Medtronic-Hall
60.0
50.5
St. Jude
0.0
13.4
Other
0.0
1.0
Congenital
30.0
14.4
Degenerative
70.0
63.9
Endocarditis
0.0
6.2
Rheumatic
0.0
13.4
Valve pathology (%)
Other
Figure 2. Frequency distribution of absolute change in
ascending aortic diameter during the time of follow-up. The
black bars represent patients with ascending aortic dilatation
exceeding 0.3 cm.
0.0
0.0
Moderate or severe AS† (%)
80.0
14.4
Moderate or severe AR‡ (%)
40.0
71.1
*P⫽NS for all comparisons. †AS⫽aortic stenosis. ‡AR⫽aortic regurgitation.
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TABLE 4.
Comparison With Previous Studies of Ascending Aortic Aneurysm
Affiliation
Study Size
(n)
Follow-up
(months)
Expansion Rate
(cm/year)
Coady et al
Yale
109
29.4
⫹0.10
Dapunt et al
Mt Sinai
67
18.0
⫹0.43
Investigator
Natural history studies
Masuda et al
Chiba
14
36.0
⫹0.13
Hirose et al
Osaka
11
36.0
⫹0.42
Dartmouth
107
33.6
⫺0.10
Aortic valve replacement series
Andrus et al
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aortic aneurysm followed for a mean of 34 months. Masuda2
described another nonoperative series of 14 patients with
ascending aortic aneurysm followed by computed tomography (CT) scan for a mean of 36 months. The mean expansion
rate was 0.13 cm/year with no significant differences between
the ascending, transverse, and descending aorta. Finally,
Dapunt4 reported a rate of 0.43 cm/year for a series of 67
patients with thoracic or thoracoabdominal aneurysm followed by 3-D reconstruction of CT scans. These studies are
summarized in Table 4. In contrast to these studies, we found
an expansion rate of ⫺0.10 cm/year. We suspect that in
patients without congenital heart disease or abnormal connective tissue, the hemodynamic effects of AS and AR may
contribute to progressive ascending aortic dilatation. We
further speculate that by correcting these flow patterns, AVR
may modify the natural history of ascending aortic dilatation.
Further investigation to test this hypothesis is required.
Previous studies have identified several different predictors
of progressive dilatation. Dapunt4 identified initial aortic size
and smoking as independent predictors. Masuda2 found
diastolic blood pressure, renal failure and initial aortic size to
be predictors of expansion by univariate analysis. However,
after adjusting for differences by multivariate analysis, only
initial aortic size was predictive. Using logistic regression,
Palmieri15 reported male gender, fibrocalcific changes in the
aortic valve, and left ventricular wall motion abnormalities to
be correlated with aortic root dilatation. Other investigators
have noted that ascending aortic dilatation is over-represented
in patients with bicuspid valves and in those with Marfan’s
syndrome7–11 leading to speculation that these conditions may
be manifestations of a common developmental defect. In our
study, we did not identify any variables associated with Asc
Ao expansion, though there was a trend toward more rapid
expansion in patients with mono- and bicuspid aortic valves.
It is tempting to speculate that with a larger study population
or a longer period of follow-up this difference would have
reached statistical significance. This trend is consistent with
the previously cited studies which have linked aortic dilatation to structural abnormalities in the connective tissue of
congenitally abnormal valves.7–11 Other explanations for the
absence of clinical or valvular predictors include the possibility that the impact of correcting abnormal flow patterns
outweighed their comparatively minor effect or that we did
not specifically evaluate the relevant variables.
Our study has potential limitations. First, there is the
possibility that selection bias exists because our study popu-
lation was not a consecutive series or a randomly selected
population. However, comparing the study population with
the total surgical population revealed only minor differences
in age and gender distribution. The study population was
younger (65.8 versus 69.8 years, P⫽0.001) and more often
male (69.2% versus 57.1%, P⫽0.003). There were no other
statistically significant differences between the populations.
Second, the possibility exists that there was observer bias
resulting from the need to perform retrospective echocardiographic measurements in 81 study patients. However, all
measurements were blinded to the comparison value. In
addition, the mean change in Asc Ao diameter was similar in
prospectively and retrospectively measured aortas (⫺0.028
cm and ⫺0.003 cm, respectively).
In summary, our findings have important clinical implications. In patients requiring aortic valve replacement who have
accompanying mild or moderate ascending aortic dilatation
(3.5 to 4.9 cm), aortic valve replacement alone may be
reasonable. Exceptions to this would include patients with a
mono- or bicuspid aortic valve, an underlying connective
tissue disease, endocarditis, a family history of ascending
aortic aneurysm, or a rapidly dilating aorta.
Acknowledgments
The authors would like to thank Brenda Arbuckle, RDCS, Patrick
Nestor, BS, and Kathryn A. Sabadosa, MS, for their assistance with
the project.
References
1. 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.
2. Masuda Y, Kazunori T, Takasu J, Morooka N, et al. Expansion rate of
thoracic aortic aneurysms and influencing factors. Chest. 1992;102:
461– 466.
3. Hirose Y, Hamada S, Takamiya M, et al. Aortic Aneurysm: growth rates
measured with CT. Radiology. 1992;185:249 –252.
4. Dapunt OE, Galla JD, Sadeghi AM, et al. The natural history of thoracic
aortic aneurysms. J Thorac Cardiovasc Surg. 1994;107:1323–1333.
5. Nancarow PA, Higgins CB. Progressive thoracic aortic dilatation after
aortic valve replacement. Am J Roentgenol. 1984;142(4):669 –772.
6. Natsuaki M, Itoh T, Rikitake K, Okazaki Y, Naitoh K. Aortic complications after aortic valve replacement in patients with dilated ascending
aorta and aortic regurgitation. J Heart Valve Dis. 1998;7(5):50 –509.
7. Keane MG, Wiegers SE, Plapppert T, Pochettino A, Bavaria JE, St. John
Sutton MG. Bicuspid aortic valves are associated with aortic dilatation
out of proportion to coexistent valvular lesions. Circulation. 2000;
102(suppl III):III35–III39.
8. Niwa K, Perloff JK, Bhuta, Laks H, Drinkwater DC, Child JS, Miner PD.
Structural abnormalities of great arterial walls in congenital heart disease:
light and electron microscopic anlyses. Circulation. 2001;103:393– 400.
Andrus et al
9. Nkomo VT, Enriquez-Sarano M, Amash NM, Melton LJ 3rd, Bailey KR,
Desjardins V, Horn RA, Tajik AJ. Biscuspid aortic valve associated with
aortic dilatation: a community-based approach. Arterio Thromb Vasc Bio.
2003;23(2):351–356.
10. Hahn RT, Roman MJ, Mogtader AH, et al. Association of aortic dilation
with regurgitant, stenotic and functionally normal bicuspid aortic valves.
J Am Coll Cardiol. 1992;19:283–288.
11. Nistri S, Sorbo MD, Marin M, et al. Aortic root dilatation in young men
with normally functioning bicuspid aortic valves. Heart. 1999;82(1):
19 –22.
12. Holman E. The obscure physiology of poststenotic dilatation: its relation
to the development of aneurysms. J Thorac Surgery. 1954;28(2):
109 –133.
13. Tandon PN, Rana UV, Kawahara M, Katiyar VK. A model for blood flow
through a stenotic tube. Int J Bio Med Comp. 1993;32(1):61–78.
Ascending Aortic Dilatation and AVR
II-299
14. Crawford MH, Roldan CA. Prevalence of aortic root dilatation and small
aortic roots in valvular aortic stenosis. Am J Cardiol. 2001;87:1311–1312.
15. Palmieri V, Bella JN, Arnett DK, et al. Aortic root dilatation at sinuses of
Valsalva and aortic regurgitation in hypertensive and normotensive subjects: The hypertension genetic epidemiology network study. Hypertension. 2001;37:1229 –1235.
16. Niles NW, McGrath PD, Malenka D, et al. Survival of patients with
diabetes and multivessel coronary artery disease after surgical or percutaneous coronary revascularization: results of a large regional prospective
study. J Am Coll Cardiol. 37(4):1008 –1015.
17. Ward C. Clinical significance of the bicuspid aortic valve. Heart. 2000;
83(3):81– 85.
18. Child AH. Marfan syndrome: current medical and genetic knowledge:
how to treat and when. J Card Surg. 1997;12(suppl 2):131–136.
Downloaded from http://circ.ahajournals.org/ by guest on June 15, 2017
Stability of Ascending Aortic Dilatation Following Aortic Valve Replacement
Bruce W. Andrus, Daniel J. O'Rourke, Lawrence J. Dacey and Robert T. Palac
Circulation. 2003;108:II-295-II-299
doi: 10.1161/01.cir.0000087385.63569.79
Downloaded from http://circ.ahajournals.org/ by guest on June 15, 2017
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