Background
Although it is widely accepted that obesity is related to increased aortic size, to
date, there is no large study assessing the effect of obesity, in the absence of co-morbidities,
on regional aortic diameter. In addition, despite the fact that magnetic resonance
imaging (MRI) is generally regarded as the gold standard technique for imaging the
aorta, the vast majority of data comes from 2D echo, which has marked limitations
in the setting of obesity. As a result, we aimed to use MRI to 1) establish a large
gender specific normal database of reference diameters for the aorta and 2) investigate
the effect of increasing body surface area (BSA) on aortic size.
Methods
484 subjects (230 male, 254 female), age 19-70 years without identifiable cardiac
risk factors (BMI range 15.7 - 52.6) underwent MRI to determine aortic diameter at
three levels namely; the ascending aorta (Ao) and proximal descending aorta (PDA,
pulmonary artery level), and the abdominal aorta (DDA, 12 cm below the PDA level).
In addition, 208 of the subjects had aortic root measurements performed at the aortic
valve annulus, aortic sinuses and sino-tubular junction.
Results
All subjects were normotensive (SBP 121±12, DBP 75±9 mmHg), normoglycaemic (4.8±0.5
mmol/l) and normocholesterolaemic (4.9±0.8 mmol/l) on the day of scanning. As expected,
with increasing BSA, aortic root diameter increased at all levels measured (AV annulus
♂+5.5, ♀+4.4 mm, Aortic Sinus ♂+5.1, ♀+4.2 mm, ST-junction ♂+5.7, ♀+4.4 mm all per
m2 (BSA) increase, Table 1, Figure 1). No gender difference in the degree of dilatation
with increasing BSA was seen (p>0.5). Aortic diameters at the more distal aortic levels
also increased with increasing BSA (Ao, ♂+6.5, ♀+6.1 mm, PDA ♂+4.4, +♀3.4, DDA ♂+3.2,
♀+3.3 mm, all per m2 BSA increase, Figure 1). Again, no gender differences in the
degree of dilatation were seen (p>0.5 for all analyses). However, the degree of regional
aortic dilatation in both male and female obesity without co-morbidities was minor
(AV annulus ♂+0.17, ♀+0.08 mm, ST junction ♂+0.16, ♀ +0.19 mm, Ao ♂+0.21, ♀+0.18 mm,
PDA ♂+0.16, ♀ +0.09 mm, DDA ♂+0.15, ♀+0.09 mm, per BMI point increase, p<0.05 for
all analyses).
Table 1
Gender Specific Effects of Obesity on Regional Aortic Diameter - Data Presented as
Mean With Normal Range (+/- 2SD)
Male
Aortic Diameter (mm)
Normal Weight
Overweight
Obese
ANOVA p
Aortic Valve Annulus
24.0 (18.8-29.2)
24.7 (19.5-29.9)
25.7 (20.7-30.7)
<0.05
Sinus of Valsalva
32.2 (24.6-39.8)
32.9 (25.3-40.5)
33.3 (25.3-31.3)
<0.05
Sino-tubular Junction
24.9 (18.1-31.7)
25.8 (17.0-34.6)
25.9 (19.1-32.7)
<0.05
Ascending Aorta
26.6 (18.2-35.0)
27.8 (18.8-36.8
28.6 (23.2-34.0)
<0.01
Proximal Descending Aorta
20.4 (14.6-26.2)
21.2 (15.6-26.8)
22.1 (16.5-27.7)
<0.01
Distal Descending Aorta
17.4 (12.0-22.8)
18.3 (12.7-23.9)
19.0 (14.8-23.2)
<0.01
BMI (kg/m2)
22 +/-1.7
27 +/-1.6
34 +/-4.8
<0.01
BSA (m2)
1.9 (+/-0.1)
2.0 (+/-0.1)
2.3 (+/-0.2)
<0.01
Female
Aortic Diameter (mm
Normal Weight
Overweight
Obese
ANOVA p
Aortic Valve Annulus
20.2 (17.0-23.4)
21.7 (18.5-23.9)
21.6 (17.6-25.6)
<0.01
Sinus of Valsalva
27.6 (22.0-33.2)
28.6 (21.6-35.6)
27.8 (22.2-33.4)
<0.05
Sino-tubular Junction
21.7 (16.7-26.7)
22.5 (16.5-28.5)
22.3 (16.5-28.1)
<0.05
Ascending Aorta
24.8 (17.6-32.0)
26.7 (19.3-34.1)
26.9 (19.3-34.5)
<0.01
Proximal Descending Aorta
18.6 (14.6-22.6)
19.5 (14.9-24.1)
20.1 (15.5-24.7)
<0.01
Distal Descending Aorta
16.1 (14.1-18.1)
16.9 (14.7-19.1)
17.6 (15.7-19.5)
<0.01
BMI (kg/m2)
22.0 (+/-1.6)
27.0 (+/-1.5)
37.0 (+/-4.8)
<0.01
BSA (m2)
1.7 (+/-0.1)
1.8 (+/-0.1)
2.0 (+/-0.2)
<0.01
Figure 1
The effect of gender on the relationship between regional aortic diameter and body
surface area.
Conclusions
Aortic diameters were larger in males than females at all levels measured. Across
both genders, obesity, in the absence of traditional cardiovascular risk factors,
is characterized by a minor degree of aortic dilatation. There are no significant
gender differences in the degree of dilatation with increasing obesity.
Funding
The study was supported by grants from the British Heart Foundation and Wellcome Trust
and by the Oxford Partnership Comprehensive Biomedical Research Centre with funding
from the Department of Health's NIHR Biomedical Research Centres funding scheme. SN
acknowledges support from the Oxford BHF Centre of Research Excellence