Intracranial Aneurysm Enlargement on Serial Magnetic
Resonance Angiography
Frequency and Risk Factors
Joseph D. Burns, MD; John Huston, III, MD; Kennith F. Layton, MD;
David G. Piepgras, MD; Robert D. Brown, Jr, MD
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Background and Purpose—Size of an unruptured intracranial aneurysm (UIA) may be an important risk factor for rupture.
Accordingly, serial noninvasive imaging is commonly used to assess untreated UIA for enlargement. Few data exist
regarding the frequency and predictors of enlargement. We obtained this information from a group of patients followed
with serial MR angiography (MRA).
Methods—We retrospectively identified 165 patients with 191 UIA followed with serial MRA. Fusiform aneurysms, UIA
⬍2 mm, and UIA that were surgically or endovascularly treated before the first MRA were excluded. MRA was
performed using 1.5-T and 3-T MRI. Maximal diameter was determined on MRA source images. Multivariate
regression analysis was used to determine independent risk factors for growth.
Results—Twenty aneurysms (10%) grew over a median follow-up period of 47 months. Frequency of enlargement was
6.9%, 25%, and 83% for aneurysms ⬍8 mm, 8 to 12 mm, and ⱖ13 mm, respectively (P⬍0.001 for trend). Of the
variables we evaluated, original aneurysm diameter (OR, 1.28 per mm; 95% CI, 1.07 to 1.58) was the only independent
predictor of enlargement. Aneurysms ⱖ8 mm in diameter were at highest risk for enlargement (OR, 7.25; 95% CI, 1.96
to 27.1). There was a trend toward increased risk of enlargement in patients with multiple aneurysms (OR, 2.50; 95%
CI, 0.86 to 7.53).
Conclusions—Over a median follow-up period of 47 months, 10% of UIA enlarged. Larger aneurysms had a significantly
increased risk of enlargement. The likelihood of enlargement was highest in aneurysms with diameters ⱖ8 mm.
However, a clinically significant proportion of small aneurysms grow, and this growth can be detected by serial MRA.
(Stroke. 2009;40:406-411.)
Key Words: enlargement 䡲 magnetic resonance angiography 䡲 risk factors 䡲 unruptured intracranial aneurysm
I
ntracranial aneurysms are common, with autopsy and
imaging studies reporting frequencies of aneurysm detection of 1% to 9%1,2 and 0.5% to 2%,3,4 respectively. In a
population-based study, the prevalence of intracranial aneurysms was 83.4 per 100 000 persons.5 On the basis of these
data, it can be estimated that at least 3 to 6 million people in
the United States have an intracranial aneurysm.
Because a subset of these aneurysms cause approximately
80% of subarachnoid hemorrhage cases,6 selected unruptured
intracranial aneurysms (UIAs) are often treated using surgical
and endovascular techniques. These treatments, however, are
associated with a significant degree of morbidity and mortality.7 Ideally then, only aneurysms with a high risk of
rupture that outweighs the risk of treatment would undergo
a corrective procedure. For those patients selected for
conservative management, questions arise regarding the
need for repeat imaging during follow-up. The decision to
repeat imaging is typically driven by concern that the
aneurysm might enlarge or otherwise change in appearance, thus potentially portending an increased risk of
future rupture. This strategy raises important questions
regarding aneurysm enlargement. What is the frequency of
enlargement for UIA? What characteristics of patient and
aneurysm affect this frequency?
Relatively few data are available to answer these questions,
leaving clinicians with little guidance in determining the
optimal surveillance strategy in patients with UIA. Four
existing studies have used noninvasive imaging techniques to
address these questions.8 –11 Of these, only 2,9,10 including an
earlier study from our institution, have exclusively used MR
angiography (MRA), and only one has used multivariate
analysis in the identification of risk factors for enlargement.9
We sought to provide further information about the frequency
and predictors of enlargement of conservatively managed
Received March 6, 2008; final revision received June 18, 2008; accepted June 19, 2008.
From the Departments of Neurology (J.D.B., R.D.B.), Diagnostic Radiology (J.H.), and Neurosurgery (D.G.P.), Mayo Clinic, Rochester, Minn; and
the Department of Diagnostic Radiology (K.F.L.), Baylor University Medical Center, Dallas, Tex.
Correspondence to John Huston, III, MD, Department of Diagnostic Radiology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905. E-mail
[email protected]
© 2009 American Heart Association, Inc.
Stroke is available at http://stroke.ahajournals.org
DOI: 10.1161/STROKEAHA.108.519165
406
Burns et al
Table 1.
Intracranial Aneurysm Enlargement on MRA
407
Summary of Patient-Specific Data
Patients With Aneurysm Enlargement
(n⫽17)
Variable
Patients Without Aneurysm Enlargement
(n⫽148)
All Patients
(n⫽165)
Age, years, mean⫾SD
69⫾8.9
63⫾13
64⫾13
Female gender
14 (82%)
106 (72%)
120 (73%)
8/16 (50%)
83/144 (58%)
91/160 (57%)
12 (71%)
104 (70%)
116 (70%)
Smoking, past or current*
Hypertension
History of aneurysm rupture
1 (5.9%)
11 (7.4%)
12 (7.3%)
4/16 (25%)
16/147 (11%)
20/163 (12%)
Coronary artery disease
3 (18%)
19 (13%)
22 (13%)
ADPKD
1 (5.9%)
16 (11%)
17 (10%)
Family history of SAH*
Coarctation of the aorta
Multiple aneurysms
8 (5.4%)
8 (4.8%)
10 (59%)
0
36 (24%)
46 (28%)
2, 1–2
1, 1–2
1, 1–1
1–4
1–8
1–8
No. of aneurysms
Median, IQR
Range
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*Data concerning these variables were unavailable for some patients.
SAH indicates subarachnoid hemorrhage; ADPKD, autosomal-dominant polycystic kidney disease; IQR, interquartile range.
aneurysms by retrospectively analyzing serial MRA and
clinical data in 165 patients with UIA.
Methods
We retrospectively identified 165 patients with 191 unruptured
intracranial saccular aneurysms who were followed with serial MRA
between 1987 and 2006. Fifty-seven of these patients (62 aneurysms)
were included in the earlier study of similar design.10 Fusiform,
mycotic, and traumatic aneurysms and UIA that were surgically or
endovascularly treated before the first MRA were excluded. UIA
⬍2 mm in diameter were considered beyond the capabilities of MRA
and were therefore also excluded. All included patients had at least
2 MRA examinations separated by at least 12 months. The study was
approved by the Mayo Foundation Institutional Review Board.
Clinical Data
Clinical data were obtained by a review of medical records performed by one of the authors (J.D.B.). Collected data included
demographic information such as date of birth, gender, and race. We
also recorded putative risk factors for subarachnoid hemorrhage and
aneurysm formation: personal history of subarachnoid hemorrhage,
history of subarachnoid hemorrhage in a first-degree relative, total
number of known intracranial aneurysms at the time of the first MRA
included in the study (including those that had previously ruptured
and those that had previously been treated), past or current cigarette
smoking, hypertension, coronary artery disease, autosomal-dominant
polycystic kidney disease, and coarctation of the aorta. Finally, we
noted any treatment and/or rupture of an aneurysm included in this
analysis that took place after the date of the second MRA.
Aneurysm Measurement Technique
MRA was used to determine aneurysm number, location, and size.
All MRA interpretations were performed by 2 neuroradiologists
(J.H., K.F.L.). The location of an aneurysm was defined as extradural
or intradural on the basis of its relationship to the ophthalmic artery.
The name used to describe the aneurysm was based on the junction
of the secondary artery arising from the parent artery. The aneurysms
were independently measured on a workstation (Advantage Windows; General Electric Medical Systems) to the nearest 0.1 mm and
the average between the 2 readers used for analysis. Aneurysm size
was determined in the transverse plane on the axial source images to
be the largest diagonal measurement, including any appendages. The
superior–inferior dimension was determined by the number of axial
source images that included the aneurysm multiplied by 0.7 mm (the
reconstructed axial slice thickness). Final aneurysm size was defined
as the larger of the transverse or superior–inferior measurements.
Results that differed by 1 mm or more were adjudicated by
consensus. The investigators who performed the interpretations were
blinded to previous measurements of the lesion, clinical history of
the patient, and any available conventional angiography findings.
Aneurysms ⬍5 mm in diameter were considered to have enlarged if
the maximum transverse measurement had increased by ⱖ1 mm on
a follow-up MRA. Aneurysms ⱖ5 mm were considered to have
enlarged if the maximum transverse measurement had increased by
ⱖ2 mm on a follow-up MRA.
MR Angiography Technique
Time of flight MRA was performed on 1.5- and 3.0-T MR imagers
(General Electric Medical Systems). The sequences included 3 axial
slabs of 32 sections per slab with 1.4-mm thick sections yielding an
imaging volume extending from the posterior inferior cerebellar
arteries to the bifurcation of the pericallosal and callosal marginal
arteries. Imaging parameters for 1.5 T included: TE 6.9 ms, TR 38
ms, flip angle 25°, matrix 256⫻224, and field of view 18 cm.
Imaging parameters for 3.0 T included: TE 38 ms, TE 3.4 ms, flip
angle 25°, matrix 288⫻224, and field of view 18 cm. For both the
1.5- and 3.0-T acquisitions, a ramped radiofrequency pulse and
3-directional zero-filling were used.
Statistical Analysis
Clinical and MRA variables were described statistically as appropriate for the data. Mean diameters of cavernous and intradural
aneurysms were compared using the Wilcoxon rank sum test.
Univariate logistic regression analysis was performed to investigate
potential associations between these variables and UIA enlargement.
Those parameters that yielded a probability value ⬍0.2 in the
univariate analysis were combined with duration of follow-up in a
multivariate logistic regression analysis. All analyses were carried
out using individual aneurysms as the unit of observation. Although
this could lead to confounded results in the logistic regression
analyses by oversampling data from patients with multiple aneurysms, we chose this method because our central question concerned
the likelihood of growth of individual aneurysms. A 2-sided probability value of ⬍0.05 was considered statistically significant. All
analyses were performed using JMP version 6.0 (SAS Institute Inc,
Cary, NC).
Results
Patient and aneurysm characteristics are summarized in
Tables 1 and 2, respectively.
408
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February 2009
Table 2.
Summary of Aneurysm-Specific Data
Variable
Aneurysms With Enlargement
(n⫽20)
Aneurysms Without Enlargement
(n⫽171)
All Aneurysms
(n⫽191)
47, 25–73
47, 25–74
12–171
12–171
4.8, 3.2–6.0
4.9, 3.4–6.0
Follow-up time, months
Median, IQR
Range
56.0, 39.3–88.5
14–126
Aneurysm diameter, mm
Median, IQR
5.5, 3.9–12.2
Range
2.75–18.4
2–13.5
2.0–18.4
12 (60%)
161 (94%)
173 (91%)
Original diameter 8–12 mm
3 (15%)
9 (5.2%)
12 (6.3%)
Original diameter ⱖ13 mm
5 (25%)
1 (0.6%)
6 (3.1%)
Original diameter ⬍8 mm
Location
Cavernous carotid artery
Anterior circulation
6 (30%)
13 (7.6%)
19 (9.9%)
10 (50%)
139 (81%)
149 (78%)
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ACA
0
ICA
1 (5%)
6 (3.5%)
47 (27%)
6 (3%)
48 (25%)
MCA
7 (35%)
49 (29%)
56 (29%)
ACom
1 (5%)
23 (13%)
24 (13%)
PCom
1 (5%)
14 (8.1%)
15 (7.9%)
4 (20%)
19 (11%)
23 (12%)
Posterior circulation
PCA
1 (5%)
5 (2.9%)
BA
3 (15%)
9 (5%)
6 (3%)
12 (6.3%)
SCA
0
3 (1.8%)
3 (1.6%)
PICA
0
2 (1.2%)
2 (1.0%)
IQR indicates interquartile range; ACA, anterior cerebral artery; ICA, internal carotid artery; MCA, middle cerebral artery; ACom,
anterior communicating artery; PCom, posterior communicating artery; PCA, posterior cerebral artery; BA, basilar artery; PICA,
posterior inferior cerebellar artery.
Interobserver agreement for the determination of growth
was excellent (␬⫽0.942). The occurrence of aneurysm enlargement for all aneurysms was 10% (20 of 191). When
cavernous carotid aneurysms were excluded, thus restricting
the analysis to only intradural aneurysms, the occurrence of
enlargement over the study period was 8% (14 of 172). There
was a trend toward larger original diameters for cavernous
carotid aneurysms compared with aneurysms in all other
locations (mean⫾SD, 7.1⫾4.6 mm versus 4.9⫾2.0 mm;
P⫽0.07).
The likelihood of enlargement increased with larger original diameter: enlargement was noted in 6.9% (12 of 173;
95% CI, 4.0% to 12%) of aneurysms with original diameter
⬍8 mm, 25% (3 of 12; 95% CI, 8.9% to 53%) in the 8- to
12-mm group, and 83% (5 of 6; 95% CI, 44% to 97%) for
aneurysms ⱖ13 mm in diameter. This trend was statistically
significant (P⬍0.001). In addition, although 17% (12 of 69;
95% CI, 10% to 28%) of aneurysms in patients with a history
of multiple aneurysms enlarged, this was noted in only 6.6%
(8 of 122; 95% CI, 3.4% to 12%) of aneurysms in patients
with a single aneurysm (P⫽0.02). Examples of aneurysm
enlargement as seen on MRA are shown in the Figure.
We performed univariate analyses of potential predictors
of aneurysm enlargement using individual aneurysms as the
unit of observation (Table 3). Predictors of aneurysm enlargement identified by this method included increasing age, the
presence of multiple aneurysms, increasing original diameter,
and location on the cavernous carotid artery; aneurysms in the
intradural anterior circulation were significantly less likely to
grow. We also performed an analysis of patient-specific risk
factors using individual patients as the unit of observation to
determine if oversampling from patients with multiple aneurysms in the by-aneurysm analysis led to false associations
between these variables and enlargement. Age was statistically insignificant in this analysis. Otherwise, results for all
other variables were similar to those obtained in the by-aneurysm analysis.
In a multivariate logistic regression analysis (Table 4), the
only independent predictor of aneurysm enlargement was
original diameter (OR, 1.27 per mm; 95% CI, 1.05 to 1.57;
P⫽0.01). By substituting diameter as a dichotomous variable
in place of diameter as a continuous variable into this model
and sequentially increasing the cutoff size by 1 mm, we found
that a diameter of ⱖ8 mm was a strong independent predictor
of growth (OR, 6.13; 95% CI, 1.63 to 23.0; P⫽0.003). This
substitution did not significantly change the results for the
remainder of the variables in the model. In the multivariate
model, there was a trend toward an increased risk of enlargement in patients with multiple aneurysms (OR, 2.50; 95% CI,
0.86 to 7.53; P⫽0.09).
Ten aneurysms in 8 patients were treated by surgical or
endovascular methods after the second MRA examination. Of
these, 8 had demonstrated enlargement before treatment. The
median size of these aneurysms was 7.7 mm. One aneurysm
Burns et al
Intracranial Aneurysm Enlargement on MRA
409
Table 3. Univariate Analysis (by aneurysm) of Potential Risk
Factors for Aneurysm Enlargement
Variable
OR
95% CI
P Value
Age per year
1.06
1.01–1.11
0.02*
Gender, male
0.45
0.10–4.42
0.22
Smoking, past or current
0.54
0.20–1.39
0.20
Smoking, current
0.60
0.09–2.27
0.51
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Hypertension
1.27
0.47–4.09
0.65
History of aneurysm rupture
0.70
0.04–3.85
0.74
Family history of SAH
2.10
0.56–6.53
0.22
Coronary artery disease
1.60
0.43–4.86
0.43
ADPKD
0.42
0.02–2.22
0.41
Coarctation of the aorta
0.95
0.05–5.47
0.96
Follow-up time per month
1.01
0.99–1.02
0.25
Multiple aneurysms
3.00
1.17–8.05
0.02*
No. of aneurysms
1.23
0.79–1.76
0.28
Diameter per mm
1.40
1.20–1.67
⬍0.0001*
Original diameter ⱖ8 mm
10.7
3.54–32.7
⬍0.0001*
Original diameter ⱖ13 mm
56.7
8.45–1120
0.0003*
Cavernous carotid artery†
5.20
1.63–15.5
0.004*
Anterior circulation†‡
0.23
0.09–0.60
0.003*
Posterior circulation†‡
2.00
0.53–6.15
0.26
*P value statistically significant.
†Exploratory analyses considering each specific location by parent artery as
well as various combinations thereof did not reveal any statistically significant
relationships to enlargement.
‡Anterior circulation and posterior circulation as defined in Table 2.
SAH indicates subarachnoid hemorrhage; ADPKD, autosomal-dominant
polycystic kidney disease.
Discussion
Figure. Growth of 2 aneurysms in a single study patient over
approximately 33 months on MRA. Maximum intensity projection (MIP; A–B) and source images (C–D) showing enlargement
of a left intracavernous aneurysm from 12.6 mm to 20 mm. MIP
(E–F) and source images (G–H) demonstrating a basilar tip aneurysm, which enlarged from 2.8 to 5.4 mm.
from the cohort ruptured. It was located on the posterior
communicating artery and had enlarged from 6 mm to
9.4 mm over 100 months. Before rupture, this patient developed an ipsilateral posterior cerebral artery aneurysm that
grew from 4.9 mm to 5.6 mm over 62 months. Our follow-up
information regarding aneurysm rupture is, however, incomplete. Many of the patients included in this study were
referred from geographically distant locations. Because our
clinical data were obtained by reviewing medical records at
only our institution, it is possible that other aneurysms
ruptured and were either treated locally or led to the patient’s
death.
We report on the frequency of and risk factors for enlargement as measured by serial MRA in the largest collection of
aneurysms evaluated for this purpose to date in the English
language literature. Strengths of our study include the large
number of patients and aneurysms, rigorous measurement
techniques applied by neuroradiologists, strictly and clearly
defined criteria for enlargement, and the use of multivariate
logistic regression models. We found that aneurysm enlargement occurred in one in 10 aneurysms and that larger size,
particularly a diameter ⱖ8 mm, was predictive of future
enlargement. We also showed that even small aneurysms
Table 4. Multivariate Analysis (by aneurysm) of Selected Risk
Factors for Aneurysm Enlargement
Variable
Age per year
OR
95% CI
1.04
0.99–1.11
P Value
0.12
Follow-up time per month
1.01
0.99–1.02
0.20
Multiple aneurysms
2.50
0.86–7.53
0.09
Original diameter per mm
1.28
1.07–1.58
0.01*
Original diameter ⱖ8 mm
7.25
1.96–27.1
0.003*
Cavernous carotid artery
1.71
0.27–10.7
0.56
Anterior circulation†
0.46
0.12–2.10
0.28
*P value statistically significant.
†Anterior circulation as defined in Table 2.
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February 2009
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carry a clinically relevant risk of enlargement. As well, there
was a statistically nonsignificant trend toward increased risk
of enlargement in patients with multiple aneurysms. These
data suggest that serial MRA monitoring of aneurysms should
be considered for all patients with conservatively managed
UIA and that those with larger and perhaps multiple aneurysms should be imaged more frequently.
In our cohort, the proportion of aneurysms that enlarged
over a median follow-up period of 47 months was one in 10.
This is almost identical to the 10.8% frequency of enlargement over a mean of 29.3 months reported by Miyazawa et
al.9 Wermer et al found a lower frequency of enlargement of
3.2%, but their study included only aneurysms with diameters
⬍5 mm and had a shorter medial follow-up time of only 1.3
years.11 In a study that used serial CT angiography to assess
aneurysm growth, Matsubara et al described a frequency of
enlargement of 6.4% over a mean of 17.7 months.8 Bleb
formation was included in their definition of enlargement,
making comparison of these results to those of the present
study problematic.
The most striking finding from the current study is the
independent effect of size on an aneurysm’s risk for future
enlargement (OR, 1.27 per mm; 95% CI, 1.05 to 1.57).
Aneurysms ⱖ8 mm in diameter were particularly likely to
enlarge with an OR of 6.13 (95% CI, 1.63 to 23.0). Aneurysm
diameters of ⱖ5 mm9 and ⱖ10 mm8 have been shown to be
predictive of enlargement in 2 studies from other centers that
have examined this relationship.
In a previous study of this topic from our institution that
included 57 of the patients (62 aneurysms) included in the
present study, we reported a frequency of enlargement of 7%
over a median duration of follow-up of 47 months and that
diameter ⱖ9 mm was a significant risk factor for growth.10
These findings are similar to those of the present study.
However, whereas no aneurysm ⬍9 mm enlarged in the
earlier study, we found in the present group that 6.9% of
aneurysms ⬍8 mm enlarged. This difference possibly stems
from a combination of the inclusion of more patients in the
present study as well as improvement in MRA technology
since the first study, which might have better allowed for
detection of enlargement. Other studies have also shown that
an important proportion of small aneurysms grow.8,11 This
suggests that even small aneurysms should be carefully
followed with serial noninvasive imaging.
Miyazawa et al found that the presence of multiple aneurysms was a strong independent risk factor for aneurysm
enlargement,9 whereas Wermer et al found a significant
association between these factors on univariate analysis.11
There was a trend toward statistical significance for the
presence of multiple aneurysms at the time of first MRA as an
independent predictor for future enlargement in the current
study (P⫽0.09). Interestingly, when our definition of multiple aneurysms is changed to include all aneurysms noted at
any time during the study period, this variable becomes
strongly and independently associated with enlargement (OR,
4.24; 95% CI, 1.42 to 14.5; P⫽0.01) without otherwise
affecting the multivariate model. Another study, however, did
not found a history of multiple aneurysms to be predictive of
enlargement.8 Accordingly, the usefulness of a history of
multiple aneurysms in predicting aneurysm enlargement is
uncertain and deserves further study.
In contrast to some earlier studies, we did not find
aneurysm location to be an important predictor of enlargement. Location at the tip of the basilar artery was predictive
of enlargement in the study by Matsubara et al.8 However,
because multivariate analysis was not performed, it is not
clear if this effect is independent of other variables, most
notably size. Miyazawa et al reported location on the middle
cerebral artery to be a risk factor for growth.9 Although we
found that location on the cavernous carotid artery and in the
anterior circulation were correlated positively and negatively,
respectively, with enlargement in the univariate analysis,
location was not a significant predictor in the multivariate
analysis. This might be because size and location are confounded variables in this selected group of conservatively
managed patients.
We found that traditional risk factors for aneurysm formation and rupture such as female gender, smoking, and
hypertension were not associated with enlargement.13,14
These findings are in agreement with other studies that have
investigated the topic8,9,11 and suggest, as pointed out by
Matsubara,8 that aneurysm growth might be a separate
process from formation and rupture.
Although conventional angiography remains the gold standard for aneurysm detection, the risks associated with it make
it undesirable for use in serial observation.15 Thus, noninvasive techniques are often used to follow UIA. The present
study shows that MRA is an effective tool for this purpose.
The sensitivity of 1.5-T MRA in the detection of intracranial
aneurysms has been demonstrated to be between 79% and
97%.16 –18 Its sensitivity is equivalent to that of CT angiography and is dependent on aneurysm size with one study
suggesting a minimum size of 5 mm for a clinically useful
degree of sensitivity for both techniques.18 Three-Tesla MRA
is becoming more widely available and has been shown to be
superior to 1.5 T in depiction of intracranial aneurysms.19
This might increase the sensitivity of detection of small
aneurysms as well as the accuracy of the determination of size
and enlargement.
Several potential limitations of the present study should be
noted. This is a retrospective analysis, which could have
caused biased selection of patients who underwent follow-up
MRA. Specifically, in this group of patients with small
aneurysms that went largely untreated, we might have underestimated the risk of enlargement in all patients with aneurysms. However, this group is probably representative of the
population of patients to whom this study’s findings are most
applicable. A second limitation is the inclusion of patientspecific data in analyses that used aneurysms as the unit of
observation. This could confound the univariate and multivariate analyses by oversampling patient-specific data from
patients with multiple aneurysms. As demonstrated by the
similar results in the by-aneurysm and by-patient univariate
analyses, however, this effect is likely minimal. Our study is
also limited by variable duration of follow-up. However, this
measurement was not significantly associated with enlargement in either the univariate or multivariate analysis. Finally,
the small number of aneurysms with enlargement included in
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our study relative to the large number of risk factors for
enlargement that we examined renders our risk factor analysis
exploratory and the conclusions drawn from it hypothesisgenerating in nature rather than decisive clinical evidence.
Many of these limitations could be addressed in a prospective
study.
In conclusion, we have shown that 10% of UIA followed
by serial MRA will enlarge over a period of approximately 4
years and that original aneurysm diameter as measured from
MRA source images is an independent predictor for enlargement. Our data also suggest that even small aneurysms can
enlarge during follow-up and that aneurysms in patients with
multiple aneurysms might be at increased risk of enlargement. Although it is not presently known if aneurysm
enlargement is predictive of a heightened risk of future
rupture, because of the concern that the walls of growing
aneurysms have not reached a steady state, enlarging aneurysms are more likely to be aggressively treated.20 Taking this
into consideration, this study suggests that when a UIA is
managed without surgical or endovascular treatment, intermittent imaging using MRA should be considered for all
patients with more frequent imaging in patients with aneurysms ⱖ8 mm.
Sources of Funding
This project was supported by the Mayo Foundation for Medical
Education and Research and Grant Number 1 UL1 RR024150-01 from
the National Center for Research Resources (NCRR), a component of the National Institutes of Health (NIH), and the NIH
Roadmap for Medical Research. Its contents are solely the
responsibility of the authors and do not necessarily represent the
official view of NCRR or NIH. Information on NCRR is available
at www.ncrr.nih.gov/. Information on Reengineering the Clinical
Research Enterprise can be obtained from http://nihroadmap.nih.
gov/clinicalresearch/overviewtranslational.asp.
Disclosures
None.
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Intracranial Aneurysm Enlargement on Serial Magnetic Resonance Angiography:
Frequency and Risk Factors
Joseph D. Burns, John Huston III, Kennith F. Layton, David G. Piepgras and Robert D. Brown,
Jr
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Stroke. 2009;40:406-411; originally published online November 20, 2008;
doi: 10.1161/STROKEAHA.108.519165
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