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Bariatric surgery
The Effect of Surgical Weight Reduction
on Left Ventricular Structure and Function
in Severe Obesity
Chin-Feng Hsuan1,2, Chih-Kun Huang2,3, Jou-Wei Lin4, Lung-Chun Lin5, Thung-Lip Lee1,
Chi-Ming Tai1, Wei-Hsian Yin6, Wei-Kung Tseng1,7, Kwan-Lih Hsu1 and Chau-Chung Wu5
The aim of this study was to examine the effect of surgical weight reduction on cardiac structure and function and
to seek the determinants of these changes. Sixty-six severely obese adults (BMI ≥35 kg/m2) who received bariatric
surgery underwent echocardiographic examination before and 3 months after surgery. At 3 months after surgery, BMI
and systolic blood pressure (BP) decreased (43.3 ± 6.3 to 34.1 ± 5.6 kg/m2, P < 0.001, and 146 ± 12 to 130 ± 14 mm Hg,
P < 0.001, respectively). In left ventricular (LV) geometry, the relative wall thickness (RWT) and LV mass index
decreased significantly (0.43 ± 0.05 to 0.35 ± 0.05, P < 0.001, and 50 ± 11 to 39 ± 11 g/m2.7, P < 0.001, respectively)
without changes in chamber size. Multivariate analyses showed change in systolic BP to be an independent predictor
for the changes in RWT and LV mass index. In myocardial performance, peak systolic mitral annular velocity and all
diastolic indexes showed significant improvements. We concluded that LV hypertrophy and function improved rapidly
after bariatric surgery in severely obese adults. BP reduction was the major determinant for the regression of LV
hypertrophy in the early stage of surgical weight reduction.
Obesity (2010) doi:10.1038/oby.2010.42
Introduction
Obesity is associated with abnormalities in cardiac structure
and function, including increased left ventricular (LV) wall
thickness, chamber size, LV mass, and systolic and diastolic
dysfunction (1–5). These structural and functional changes,
especially LV hypertrophy, are independent risk factors for cardiovascular disease (6). Studies have shown that weight reduction by diet and exercise programs may induce regression of LV
mass; however, the magnitude of weight reduction and changes
in cardiac structure and function were subtle (7). Bariatric surgery is a more effective and rapid method for weight reduction
(8,9). Studies evaluating the effect of surgical weight reduction
demonstrated significant improvements in LV mass and some
demonstrated improvements on diastolic function (10–15).
Nonetheless, little is known about the determinants for improvement in LV structure and function after this procedure.
We, therefore, conducted a prospective study in severely obese
patients receiving bariatric surgery to evaluate the effect of surgical weight reduction on LV structure, systolic and diastolic
function, to examine the association of weight reduction with
changes in hemodynamics, LV geometry and function, and,
most importantly, to seek the predictors of these changes.
Methods and Procedures
Study population
From May 2007 to August 2008, all severely obese (BMI ≥40 kg/m2 or
≥35 kg/m2 with comorbidities) adults (≥20 years of age), being scheduled for bariatric surgery (laparoscopic Roux-en-Y gastric bypass
or laparoscopic sleeve gastrectomy) at a single medical center in the
southern part of Taiwan after evaluation by a multidisciplinary team,
were assessed for eligibility. Studied patients received echocardiographic evaluations before and 3 months after surgery. Patients with
heart failure, valvular heart disease, coronary artery disease, regional
wall motion abnormality, congenital heart disease, left bundle branch
block or atrial fibrillation determined on the basis of previous ­history,
physical examination, electrocardiography, and echocardiography
were excluded from this study. Patients with an image inadequate
for analysis were also excluded. The study protocol was approved by
the hospital ethics committee, and all studied patients gave informed
consent.
Clinical and demographic data
Before surgery, studied patients’ age, sex, and medical history
were obtained. A detailed physical examination and 12-lead
­electrocardiography were performed. Weight, height, waist circumference, and blood pressure (BP) were measured before and 3 months
after surgery by a well‑trained nurse. BMI was calculated as weight
(Kg)/height × height (m2). Percent of excess BMI lost was ­calculated
as (preoperative BMI−current BMI)/(preoperative BMI−23) × 100
1
Department of Internal medicine, E-Da Hospital, Kaohsiung, Taiwan; 2Institute of Biotechnology and Chemical Engineering, I-Shou University, Kaohsiung,
Taiwan; 3Department of Surgery, E-Da Hospital, Kaohsiung, Taiwan; 4Cardiovascular Center, National Taiwan University Hospital Yun-Lin Branch, Yun-Lin, Taiwan;
5
Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan; 6Division of Cardiology, Cheng-Hsin General Hospital, Taipei, Taiwan;
7
Department of Medical Imaging and Radiological Sciences, I-Shou University, Kaohsiung, Taiwan. Correspondence: Wei-Kung Tseng ([email protected])
Received 18 October 2009; accepted 5 February 2010; advance online publication 18 March 2010. doi:10.1038/oby.2010.42
obesity
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Bariatric surgery
(16,17). BP was measured according to the recommendations
described by Chobanian et al. (18).
Echocardiography
Echocardiographic studies were performed using a Sonos 7500
(Philips Ultrasound, Bothell, WA) ultrasound system equipped
with a 1.6-3.2 MHz phased-array transducer. All echocardiographic
images were digitally stored on optical discs for off-line analysis.
Each parameter was measured off-line and quantified with the average of measurements of three consecutive cardiac cycles by a single
experienced sonographer who was blinded to the patients’ clinical
information.
Two-dimensional guided M-mode echocardiographic tracings in
the parasternal long axis view were performed to measure the left atrial
(LA) diameter and the parameters of the LV geometry, including the LV
end-diastolic dimension (LVEDD), end-diastolic interventricular ­septal
thickness (IVSd) and LV posterior wall thickness (LVPWd) (19). LV
endocardial fractional shortening was calculated as (LVEDD−LVESD)/
LVEDD. The relative wall thickness (RWT) was calculated as (IVSd +
LVPWd)/LVEDD. LV mass was calculated using the corrected American
Society of Echocardiography convention proposed by Devereux et al.: LV
mass (g) = 0.8 × 1.04 × ((LVEDD + LVPWd + IVSd)3−LVEDD3) + 0.6
(20). For more appropriate normalization of LV mass in obese patients,
LV mass was indexed by dividing by height2.7 (21). LV hypertrophy was
defined as LV mass index >51 g/m2.7 (22), and LV concentricity was determined using RWT >0.45 as a cutoff point (23). The LV geometries of
the studied patients were categorized into four groups: concentric LV
hypertrophy, eccentric LV hypertrophy, concentric LV remodeling, and
normal.
Using pulsed-wave Doppler, early diastolic mitral inflow velocity
(E-wave), late diastolic mitral inflow velocity (A-wave) and isovolumetric
relaxation time were measured in apical 4-chamber and 5-chamber view,
and an E/A ratio was calculated. Myocardial velocities was measured
through the apical 4-chamber view with the Doppler beam parallel to the
motion of the part of the LV of interest. Peak systolic and early diastolic
tissue velocities were recorded over the septal and lateral mitral annulus.
Representative values of peak systolic (Sa) and early (Ea) diastolic mitral
annular velocities were obtained from the average of measurements of
septal and lateral annulus. An E/Ea ratio was applied to estimate the LV
filling pressure (24).
Statistical analysis
Statistical analyses were performed with SPSS, version 11.0 (SPSS,
Cary, NC). All continuous variables were expressed as mean ± s.d.
Differences in variables before and after surgery were assessed using
the paired t-test. Pearson’s correlation analysis was used to estimate
the relationships between BMI, waist circumference, hemodynamics,
and echocardiographic variables preoperatively and, also, to determine
the relationships between changes in these variables after surgery. At
baseline, age, sex, and systolic BP were entered in the multiple linear
regression analyses for adjustment of the possible relationship with the
examined dependent variables. Hierarchical multiple linear regression
analyses were also applied to examine the association between dependent variables, including the change in measurements of LV geometry
and the indexes of systolic and diastolic function, and independent
variables. The independent variables were selected if a significant correlation with the dependent variable was found in univariate analysis;
and factors such as age, sex, and other clinically important baseline data
were forced to remain in the model. A P value <0.05 was considered
significant.
Results
Patient characteristics and echocardiographic
measurements at baseline
Sixty-six consecutive patients (23 men and 43 women; mean
age 31 ± 9 years, range 20–58 years) were studied. All were
2
of Chinese ethnicity. Fifty-four patients received laparoscopic
Roux-en-Y gastric bypass, and the other 12 patients received
laparoscopic sleeve gastrectomy. Preoperative characteristics and echocardiographic measurements are summarized
in Table 1. BMI ranged from 35 to 65.3 kg/m2 with a mean
of 43.3 ± 6.3 kg/m2. Regarding LV geometry, the LV mass, LV
mass index, and LVEDD correlated with BMI and waist circumference in all patients (Table 2), and in those with or without hypertension (systolic BP ≥ 140 mm Hg as a cutoff point)
(data not shown). The RWT and LV mass, but not the LVEDD,
correlated with systolic BP, and the LV mass index showed
Table 1 Clinical characteristics and echocardiographic
parameters of the study population at baseline and 3-month
follow-up
Preoperative
Age (years)
Postoperative
P value
95 ± 18
<0.001
31 ± 9
Sex (male:female)
23: 43
Weight (kg)
121 ± 21
43.3 ± 6.3
34.1 ± 5.6
<0.001
Waist
circumference (cm)
BMI (kg/m )
123.4 ± 14.2
106.9 ± 13.3
<0.001
Systolic BP (mm Hg)
146 ± 12
130 ± 14
<0.001
Diastolic BP (mm Hg)
90 ± 10
81 ± 13
<0.001
<0.001
2
Heart rate (beats/min)
86 ± 11
76 ± 13
LVEDD (cm)
5.00 ± 0.37
5.00 ± 0.37
0.869
IVSd (cm)
1.09 ± 0.15
0.89 ± 0.15
<0.001
LVPWd (cm)
1.04 ± 0.13
0.87 ± 0.13
<0.001
RWT
0.43 ± 0.05
0.35 ± 0.05
<0.001
LV mass (g)
201 ± 51
157 ± 45
<0.001
50 ± 11
39 ±11
<0.001
Concentric
hypertrophy
19.7%
3.0%
Eccentric
hypertrophy
24.2%
13.6%
Concentric
remodeling
15.2%
1.5%
Normal
40.9%
81.8%
LV mass index (g/m )
2.7
LV concentricity
FS (%)
40.4 ± 2.8
40.1 ± 3.4
0.492
LA diameter (cm)
4.11 ± 0.41
4.02 ± 0.43
0.02
E/A ratio
1.32 ± 0.38
1.62 ± 0.45
<0.001
IVRT (ms)
93 ± 14
82 ± 15
<0.001
Ea (cm/s)
10.5 ± 2.4
12.6 ± 2.3
<0.001
Sa (cm/s)
8.1 ± 1.2
8.6 ± 1.3
0.001
E/Ea ratio
8.6 ± 1.9
7.6 ± 1.6
<0.001
Values are mean ± s.d.
BP, blood pressure; E/A ratio, the ratio of early to late diastolic mitral inflow
­velocity; Ea, early diastolic mitral annular velocity; FS, endocardial fractional
shortening; IVRT, isovolumetric relaxation time; IVSd, end-diastolic interventricular septal thickness; LA, left atrial; LV, left ventricular; LVEDD, left ventricular end­diastolic dimension; LVPWd, end-diastolic left ventricular posterior wall thickness;
RWT, relative wall thickness; Sa, peak systolic mitral annular velocity.
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Table 2 Correlations of age, systolic BP, BMI, waist circumference with LV geometry and diastolic function at baseline
Age
Systolic BP
BMI
Waist
circumference
RWT
0.23
0.26*
0.06
0.21
LV mass
0.13
0.32*
0.46**
0.54**
0.21
0.23
0.55**
0.45**
−0.01
0.18
0.46**
0.42**
LV mass index
LVEDD
RWT
LV mass index
E/A ratio
−0.64**
−0.05
0.18
−0.01
−0.42**
−0.21
Ea
−0.48**
−0.09
0.05
−0.12
−0.44**
−0.37*
IVRT
0.24
−0.07
0.15
0.17
−0.03
0.29*
E/Ea ratio
0.01
0.07
0.31*
0.26*
0.14
0.39**
−0.16
0.13
0.38**
0.35*
0.20
0.36**
LA diameter
Values are Pearson’s coefficient; *P < 0.05; **P < 0.001.
BP, blood pressure; E/A ratio, the ratio of early to late diastolic mitral inflow velocity; Ea, early diastolic mitral annular velocity; IVRT, isovolumetric relaxation time; LA, left
atrial; LV, left ventricular; LVEDD, left ventricular end-diastolic dimension; RWT, relative wall thickness.
Weight, BP, and heart rate changes after bariatric surgery
Weight, BMI, and waist circumference showed significant
reductions 3 months after bariatric surgery (121 ± 21 to
95 ± 18 kg, 43.3 ± 6.3 to 34.1 ± 5.6 kg/m2, and 123.4 ± 14.2
to 106.9 ± 13.3 cm, respectively). The percent of excess BMI
lost was 45.1% at 3 months. Systolic, diastolic BP, and heart
rate decreased ­significantly after bariatric surgery (Table 1).
Changes in systolic BP correlated with the percent change in
BMI and percent of excess BMI lost (r = 0.28, P = 0.025 and r =
0.33, P = 0.007, respectively).
Changes in LV mass and geometry after bariatric surgery
The effects of weight reduction on LV mass and the para­meters
of LV geometry are listed in Table 1. Three months after baria­
tric surgery, except LVEDD, there were significant reductions in IVSd, LVPWd, RWT, LV mass, and LV mass index.
The results remained the same in subgroup analyses (either in
patients with or without hypertension, and either in patients
with concentric or eccentric LV geometry) (data not shown).
Univariate analysis revealed the changes in RWT and LV mass
index correlated with change in systolic BP (r = 0.49, P < 0.001;
obesity
a
0.15
r = 0.49
P < 0.001
Change in RWT
0.05
–0.05
–0.15
–0.25
–50
–25
0
25
50
Change in systolic BP (mm Hg)
b
15
Change in LV maa index (g/m2.7)
a trend toward correlation with systolic BP (Table 2). The
­observation was similar in patients with hypertension, but not
in those without hypertension. The associations of LV mass,
LV mass index, and LVEDD with BMI and waist circumference persisted even after adjustment for age, sex, and systolic
BP (regression coefficient (B) = 0.51, P < 0.001; B = 0.63, P <
0.001; B = 0.48, P < 0.001, respectively, for BMI and B = 0.44,
P < 0.001; B = 0.46, P < 0.001; B = 0.38, P = 0.003, respectively,
for waist circumference).
In diastolic indexes, the E/A ratio and Ea correlated well with
RWT (Table 2), even after adjustment for age, sex, and systolic
BP. On the other hand, Ea and isovolumetric relaxation time
correlated with LV mass index. LA diameter and the E/Ea ratio,
representing LV filling pressure, correlated with BMI and waist
circumference. There was no correlation between the hemo­
dynamic measurements (systolic, diastolic, mean BP, and heart
rate) and systolic or diastolic function.
r = 0.38
P < 0.001
5
–5
–15
–25
–35
–50
–25
0
25
50
Change in systolic BP (mm Hg)
Figure 1 Correlation between (a) change in relative wall thickness
(RWT) and change in systolic blood pressure (BP), and (b) change in
left ventricular (LV) mass index and change in systolic BP after weight
reduction induced by bariatric surgery.
r = 0.38, P = 0.001, respectively) (Figure 1). There were no
associations among change in BMI, the percent of excess BMI
lost, or change in waist circumference and changes in LV mass,
LV mass index, RWT, or LVEDD. Multivariate linear regression analyses showed changes in systolic BP and baseline RWT
to be independent predictors for the change in RWT, and
changes in systolic BP and baseline LV mass index were independent predictors for the change in LV mass index (Table 3).
In subgroup analysis, regardless of the existence of hypertension at baseline, the most powerful predictor for changes in
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RWT and LV mass index was still the change in systolic BP
(Supplementary Table S1 online).
Changes in systolic and diastolic function
after bariatric surgery
The fractional shortening remained stable 3 months after baria­
tric surgery. Nonetheless, Sa increased significantly (Table 1),
and the magnitude of Sa increase correlated with the magnitude of BMI decrease (r = −0.36, P = 0.003) and the percent of
excess BMI lost (r = −0.29, P = 0.017). Regarding LV diastolic function, the E/A ratio and Ea increased significantly after
surgery. Isovolumetric relaxation time, LA size, and LV filling
pressure (E/Ea ratio) also decreased significantly (Table 1).
These changes represented improvements in diastolic function
3 months after bariatric surgery. Univariate analysis revealed
that the change in the E/A ratio correlated with percent of
excess BMI lost and change in waist circumference (r = −0.34,
P = 0.005 and r = −0.26, P = 0.035, respectively), and the change
in Ea correlated with percent of excess BMI lost (r = −0.26, P =
0.039) (Table 4).
Discussion
The results of the present study are consistent with previous
reports that weight reduction after bariatric surgery could
significantly improve LV hypertrophy and hemodynamics.
Table 3 Multivariate analysis for determinants of changes in
RWT and LV mass index
Change in RWT
R2 = 0.509
B
P value
Age
0.2
0.039
Sex
−0.09
0.377
Baseline LV mass
index
Baseline RWT
Change in LV mass
index R2 = 0.327
B
−0.01
P value
0.902
0.07
0.566
−0.363
0.004
−0.56
<0.001
Change in
systolic BP
0.43
<0.001
0.51
<0.001
Percent of excess
BMI lost
0.02
0.843
−0.16
0.202
B, regression coefficient; BP, blood pressure; LV, left ventricular; RWT, relative
wall thickness.
However, it provides some new information in addition to
previous ones. It was the first study to show that subclinically
impaired LV systolic function can be reversed after weight
reduction. We also demonstrated that all diastolic indexes were
improved after surgical weight reduction. Most importantly,
our results indicated that, shortly after bariatric surgery, systolic BP reduction was the major determinant for the improvements in RWT and LV mass index.
LV hypertrophy, especially the concentric type, has been
demonstrated to be an important predictor for cardiovascular
disease, heart failure or sudden death, even though an ­obesity
paradox exists (6,25–27). Earlier studies reported ­obesity
is related to eccentric hypertrophy, a compensatory hypertrophy to volume overload (28,29). Recent studies involving
cardiac remodeling in obesity have shown that LV wall thickness appeared to increase to a greater extent than the internal
dimension, which implies that LV hypertrophy in obesity may
represent more than simple volume compensation (1–4,30).
In agreement with most of the previous studies, the present
results showed BMI was independently correlated with LV
mass, LV mass index, and chamber size. An increase in RWT
and a substantial percentage of concentric hypertrophy or
remodeling of LV were also found in obese patients (Table 1),
regardless of the existence of hypertension. This observation
further confirmed that LV hypertrophy in obesity is not always
of the eccentric type.
The effect of weight reduction on LV geometry and mass
through diet control and exercise programs was reported to
be minor and even variable (7,31). The relatively small magnitude of weight loss in these programs may explain this result.
Bariatric surgery offers an intervention that induces more
vigorous and rapid weight reduction (8,9), and significantly
improves the LV structure (11–15). However, there were few
data from these reports to define the determinants for improving LV mass and geometry after bariatric surgery.
Clinical trials have documented that weight loss could
result in reduction of BP (32). On the other hand, reduction
of BP by antihypertensive agents may induce regression of LV
hypertrophy (33). Whether the regression of LV hypertrophy after bariatric surgery in severe obesity occurs because
of reduction of BP, weight reduction itself, or other mechanism is unclear. Karason et al. and Ippisch et al. found that
the regression of LV mass was better predicted by the weight
Table 4 Correlations of changes in systolic BP, BMI, waist circumference, and LV geometry with changes in diastolic function
Δ Systolic BP
Δ BMI
%EBL
Δ Waist
circumference
Δ RWT
Δ LV mass index
Δ E/A ratio
−0.24
−0.14
−0.34*
−0.26*
−0.19
−0.09
Δ Ea
−0.08
−0.15
−0.26*
−0.20
−0.07
0.11
0.10
0.11
−0.06
0.07
0.09
0.11
−0.10
0.02
−0.09
0.04
−0.04
−0.07
0.02
0.08
0.08
0.15
0.06
Δ IVRT
Δ E/Ea ratio
Δ LA diameter
0.27*
Values are Pearson’s coefficient; *P < 0.05.
BP, blood pressure; E/A ratio, the ratio of early to late diastolic mitral inflow velocity; Ea, early diastolic mitral annular velocity; IVRT, isovolumetric relaxation time; LA, left
atrial; LV, left ventricular; RWT, relative wall thickness; Δ, change in; %EBL, percent of excess BMI loss.
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loss than by the reduction of BP (11,15). Both studies had a
­relatively longer follow-up period (10–12 months). Another
study with a shorter follow-up period after bariatric surgery
(mean 4.6 ± 1.1 months) showed that change in LV mass
index was positively correlated with change in systolic BP and
percent ­overweight (10).
The present study with 3 months of follow-up after baria­
tric surgery demonstrated significant BP reduction. Also, our
results showed that the short-term effect of bariatric surgery
on the LV structure was prominent except for that on the
chamber size regardless of the baseline LV geometry. No sufficient time for remodeling might be the reason for no change in
LV chamber size. Therefore, the improvements in LV mass, LV
mass index, and RWT in this early stage after bariatric surgery
resulted mainly from the improvement in LV wall thickness.
Furthermore, this study found that the magnitude of systolic BP
reduction had the strongest correlation with the improvements
in LV mass index and RWT 3 months after bariatric surgery.
These findings implied that BP reduction play an important
role in the regression of LV mass and improvement of concentricity in the early stage of weight reduction after baria­tric
surgery. A regain of BP was observed 1 year after baria­tric
surgery (34), which may be a possible reason to explain why
BP reduction becomes less important in the regression of LV
hypertrophy in the long-term after bariatric surgery.
Results of studies evaluating LV systolic function in obesity were variable. Most studies reported that LV ejection fraction or fraction shortening is preserved in obese patients.
Nonetheless, increased endocardial shortening in LV hypertrophy may overestimate the LV systolic function in obesity (35).
Several recent studies using newer and more sensitive methods, such as midwall fractional shortening or systolic myocardial velocity, detected subclinical depression of LV systolic
function in obese patients (2,3). Some studies of the results of
depressed LV systolic function in obese patients showed that
duration of obesity was a determinant for LV systolic dysfunction (33,37). These findings suggested that obesity may have an
impact on LV systolic function that may be subtle in the early
stage of obesity. The results of our study further demonstrated
that, after weight reduction, the subtle and possibly preclinical
depressed LV systolic function can be reversed to avoid future
deterioration.
As with the findings for systolic function, studies on
assessing LV diastolic function in obese patients with conventional Doppler methods to measure mitral inflow velocities showed inconsistent results (38–41). Recently, a newer
echocardiographic technique using tissue Doppler imaging
to measure myocardial velocity offers a more sensitive and
load-­independent method to assess LV diastolic function (42).
Three recent studies applying this method consistently found
decreased early diastolic mitral annular velocity (Ea) in obese
patients (2,4,43). In the present study, we observed that Ea and
the E/A ratio were independently associated with RWT rather
than BMI, suggesting that the LV concentric geometry related
to obesity, not obesity itself, had an influence on ventricular
diastolic function, causing abnormal ventricular relaxation.
obesity
The E/Ea ratio has been widely used to estimate the LV ­filling
pressure (24). Also, LA enlargement reflects chronic elevation
of LV filling pressure (44,45). Elevation of the E/Ea ratio and
LA enlargement in obese patients has been reported previously (2–4,40). A positive correlation between BMI and the
E/­Ea ratio and LA diameter in the present study indicated that
elevated LV filling pressure may be related to volume expansion in obese patients.
Importantly, the present study demonstrated that all diastolic indexes, including the E/A ratio, Ea, isovolumetric relaxation time, E/Ea ratio, and LA size, significantly improved after
bariatric surgery, representing improvement in LV relaxation
and decrease in LV filling pressure. However, only the changes
in E/A ratio and Ea showed weak correlations with the percent
of excess BMI lost. Further investigation is needed to clarify
the mechanism of the improvement of diastolic dysfunction.
Our study had several limitations. First, other comorbidities
accompanying obesity, including insulin resistance, and some
factors such as the duration of obesity, that may affect cardiac
performance were not evaluated. Second, we used office BP in
this study, which is inferior to 24-h average BP in the assessment of LV hypertrophy or dysfunction (46). Finally, this
study demonstrated the improvements in cardiac structure
and function echocardiographically without investigating the
long-term benefit on survival or major adverse cardiac events.
Further studies addressing these issues are needed.
In conclusion, obesity was associated with increased LV
mass, wall thickness and impaired LV function. Rapid weight
reduction after bariatric surgery could induce a dramatic and
rapid regression of LV mass and wall thickness, and improve
not only diastolic but also systolic function of the heart in
severely obese patients. More importantly, the present study
indicated that BP was the major determinant for the regression
of LV hypertrophy in the early stage of rapid weight reduction
after bariatric surgery.
SUPPLEMENTARY MATERIAL
Supplementary material is linked to the online version of the paper at
http://www.nature.com/oby
Disclosure
The authors declared no conflict of interest.
© 2010 The Obesity Society
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