BMJ No 7113 Volume 315
Papers Saturday 11 October 1997
Effects of obesity and weight loss on left ventricular mass and relative wall thickness: survey and intervention study
Kristjan Karason, Ingemar Wallentin, Bo Larsson, Lars Sjöström
Abstract
Objectives: To investigate the consequences of longstanding obesity on left ventricular mass and structure and to examine the effects of weight loss on these variables.Design: Cross sectional survey and controlled intervention study.
Setting: City of Gothenburg and surrounding areas, Sweden.
Subjects: 41 obese patients treated with weight reducing gastric surgery, 31 obese patients treated conventionally, and 43 non-obese subjects.
Main outcome measures: Changes in left ventricular mass and relative wall thickness.
Results: Obese patients had higher blood pressure, greater left ventricular mass, and increased relative wall thickness than did matched non-obese control subjects. Obese subjects treated with gastric surgery had a substantial weight loss and a significant reduction in all variables when compared with conventionally treated obese subjects. Univariate and multivariate analysis of pooled data from the two groups of obese subjects showed that changes in relative wall thickness and left ventricular mass were more closely related to the change in weight than to the concomitant change in blood pressure.
Conclusions: Structural heart abnormalities occurring in conjunction with obesity diminish after weight loss. The regression in these structural aberrations is better predicted by the weight loss than by the accompanying reduction in blood pressure. To prevent or improve abnormalities of heart structure in obese people, weight control should be the primary goal; it should be regarded as at least as important as regulating blood pressure.
Introduction
Obesity is related to several disturbances in cardiac structure.(1) Obese people have greater left ventricular mass, greater wall thickness, and larger chamber size than those who are not obese,(2-3) and the ratio between wall thickness and chamber radius (the relative wall thickness) is larger in obese people than in lean people.(1)(4) These aberrations in left ventricular mass and structure are of great importance. Left ventricular hypertrophy is one of the strongest risk factors for cardiovascular morbidity and mortality,(5) and an increase in relative wall thickness has been shown to increase cardiovascular risk.(6-7)
The changes in left ventricular mass and structure with increasing body weight can be partially explained by the haemodynamic changes that accompany obesity.(8-9) As body weight increases, total blood volume and cardiac output rise. This leads to a volume overload that causes left ventricular dilatation and a parallel thickening of the ventricular wall (eccentric left ventricular hypertrophy). Obesity is also closely related to arterial hypertension,(10-11) a form of pressure overload that is followed by increased wall thickness without chamber dilatation (concentric left ventricular hypertrophy). Metabolic and hormonal factors can also influence the heart structure of obese people.(12)
Though it is well known that the medical treatment of hypertension can induce a regression in left ventricular hypertrophy,(13) little is known about the effect of weight reduction on left ventricular mass. The few studies on the subject have produced contradictory results.(14-17) The importance of relative wall thickness for estimating cardiovascular risk has only recently been spotlighted and is still under debate.(18) The effect of weight reduction on relative wall thickness has not previously been investigated. We investigated the consequences of longstanding obesity on left ventricular mass and structure and examined the effects of weight loss on these variables.
Subjects and methods
In total, 119 subjects from the city of Gothenburg and the surrounding areas were enrolled, comprising 61 men and 58 women with ages ranging from 37 to 61 years. The study population consisted of two groups of obese patients (body mass index 30-47 kg/m2) and one group of non-obese subjects (body mass index 18-27 kg/m2). The obese subjects were recruited from the ongoing Swedish obese subjects study, which is a nationwide trial designed to determine whether the mortality and morbidity among obese people who lose weight by surgical means differs from that in an obese reference group.(11) The non-obese subjects were recruited from a randomly selected sample of adults living in the municipality of Mölndal.
The two groups of obese subjects comprised 41 consecutive patients referred for weight reducing gastric surgery (the "obese operation" group) and 35 matched control subjects who were treated with conventional dietary recommendations ("obese control" group). The non-obese group consisted of 43 subjects matched with the obese groups for sex, age, and height. Subjects in all three study groups were examined at baseline and those in the two obese groups were examined again after one year. Four of the obese control patients were excluded from the study as they did not participate in the follow up, leaving 31 subjects in the obese control group. Table 1 shows the clinical characteristics of the three study groups (115 subjects).
| Table 1 - Clinical characteristics of study groups at baseline and one year follow up. Values are means (SD) unless specified otherwise | |||||
|---|---|---|---|---|---|
| Obese subjects (n=72) | Non-obese subjects (n=43) | Difference between non-obese and obese (95% CI) | |||
| Operation (n=41) | Control (n=31) | Difference (95% CI) | |||
| No of men | 21 | 16 | NS | 23 | NS |
| Age (years) | 48 (6) | 49 (6) | NS | 49 (7) | NS |
| Height (cm) | 173 (10) | 171 (9) | NS | 173 (9) | NS |
| No (%) current smoker | 11 (27) | 6 (19) | NS | 8 (19) | NS |
| No (%) receiving antihypertensive treatment | 9 (22) | 8 (26) | NS | 1 (2) | P=0.002 |
| Weight (kg): | |||||
| Baseline | 117 (15) | 112 (14) | -5 (-12 to 2) | 70 (11) | 45 (40 to 50)** |
| One year follow up† | 84 (14) | 115 (14) | 31 (26 to 36)** | ||
| Body mass index (kg/m2): | |||||
| Baseline | 39 (4) | 39 (5) | 0 (-2 to 2) | 23 (2) | 16 (14 to 18)** |
| One year follow up† | 29 (3) | 39 (3) | 10 (8 to 12)** | ||
| Systolic blood pressure (mm Hg): | |||||
| Baseline | 143 (18) | 139 (18) | -4 (-12 to 4) | 116 (14) | 25 (19 to 31)** |
| One year follow up† | 125 (14) | 141 (14) | 16 (10 to 22)** | ||
| Diastolic blood pressure (mm Hg): | |||||
| Baseline | 88 (11) | 83 (12) | -5 (-11 to 1) | 72 (11) | 14 (10 to 18)** |
| One year follow up† | 75 (9) | 85 (9) | 10 (6 to 14)** | ||
| **P<0.001. †Adjusted mean (SD). | |||||
Body weight was measured with the subjects wearing light clothing and no shoes and was rounded to the nearest 0.1 kg. Height measurements were rounded to the nearest 0.01 m, and body mass index was calculated as the weight in kilograms divided by the height in metres squared.
Systolic and diastolic (phase V) blood pressure was measured in
the right arm using a mercury sphygmomanometer with the subject in
the supine position after 10 minutes of rest. An appropriate cuff was
used, with a width of at least 40% of the circumference of the arm.
Echocardiography was performed on each subject in the left lateral
decubitus position, using a commercially available ultrasound system
(Accuson 128 XP; Mountain View, CA) with 2.0-2.5 MHZ transducers. Two
dimensional echocardiography registrations were obtained with short
axis and four chamber views. From the left ventricular short axis view,
epicardial and endocardial perimeters were traced and mean wall
thickness and cavity radius were calculated. Relative wall thickness
was defined as the ratio of mean wall thickness to chamber radius. Left
ventricular mass was calculated according to the truncated ellipsoid
algorithm from Byrd et al.(19) Left ventricular diastolic
volumes were e All recordings were performed by doctors experienced in
echocardiography, and 75% of the registrations were made by one
investigator (IW). Each reading was assessed before statistical
analyses took place, and only subjects with recordings of excellent or
good quality were included in data analyses. As a result, 9 (13%) of
the obese patients were excluded from the analyses of left ventricular
wall thickness and mass and 20 (28%) from the estimations of left
ventricular volumes. Only 1 (2%) of the lean subjects was excluded
from data analyses because of deficient registrations. The standard
error of a single determination of left ventricular mass among obese
subjects was 17%, assessed by a double determination in nine patients.
Statistical analyses were performed with the Statview (Abacus Concepts;
Berkeley, CA) and SAS (SAS Institute, Cary, NC) statistical software
packages. The data are summarised as means (SD). At baseline,
differences between non-obese and obese groups were assessed with
chi2 or unpaired t tests, and at the one
year follow up, differences between the obese operation and the obese
control groups were investigated with analyses of covariance with
adjustment for baseline values. After data in the obese groups were
pooled, associations between changes in body weight and blood pressure
and changes in left ventricular measurements were evaluated with
univariate and multivariate regression analyses. All probability values
were derived from two tailed tests, and a P value <0.05 was considered
significant. At baseline, there were no differences in sex ratio, age, height,
or smoking habits between obese and non-obese subjects. By definition,
obese subjects had a significantly higher body weight and body mass
index than lean ones; they also had higher blood pressure, and a
greater proportion were receiving antihypertensive treatment (table 1).
At baseline, clinical and echocardiographic variables were similar in
the two obese groups (tables 1 and
2).
Although short axis measurements at baseline showed no difference
in chamber radius between obese and non-obese subjects, measurements
from the four chamber view showed that obese subjects had a larger left
ventricular volume than lean ones (table 2). Moreover, in
comparison to non-obese subjects, obese patients had increased wall
thickness, increased relative wall thickness, and a greater left
ventricular mass (table 2).
At the one year follow up, the surgically treated obese patients showed
substantial reductions in weight and body mass index and significant
decreases in systolic and diastolic blood pressure in comparison to
conventionally treated obese patients (table 1). They also had
significant reductions in wall thickness, relative wall thickness, and
left ventricular mass. Left ventricular dimension and volume were
similar in the two groups of obese patients (table 2).
The Framingham heart study has clearly shown that both obesity and
hypertension are associated with increased left ventricular mass and
that left ventricular hypertrophy is one of the strongest risk factors
for cardiovascular morbidity and mortality.(5)(20) Several
studies have shown that left ventricular hypertrophy is reduced after
the pharmacological treatment of hypertension,(21) but
results of studies on the effect of weight loss on left ventricular
mass have been scarce and inconsistent.
In 1972 Alexander and Peterson reported that raised left ventricular
filling pressure in obese subjects persisted three years after weight
loss and concluded that myocardial hypertrophy did not regress after
weight reduction.(14) Likewise, Alpert et al reported that
surgically induced weight loss (mean 56 kg) in a group of obese
patients had no effect on septal or posterior wall
thickness.(15) In contrast, MacMahon et al found that a
weight loss of only 8 kg in mildly obese patients with hypertension
was associated with a significant decrease in left ventricular
mass,(16) and more recently, Alpert et al observed a
reduction in left ventricular mass after weight loss in obese subjects
with pre-existing left ventricular hypertrophy.(17)
To explain the discrepancy in these studies it has been suggested
that the effects of weight loss on left ventricular measurements occur
only if obesity is mild or of short duration.(22) However,
our results show that weight loss in subjects with long term morbid
obesity is associated with reduced left ventricular wall thickness and
left ventricular mass. Moreover, we conclude that improvements in left
ventricular structure after weight loss are related to both the
magnitude of weight reduction and the initial degree of left
ventricular hypertrophy.
Left ventricular chamber size is known to be larger in obese subjects
than in lean ones, as a result of the volume overload that occurs with
obesity.(23) In our group of obese patients the increased
chamber volume did not regress significantly in conjunction with weight
loss, which indicates that chamber dilatation related to obesity may be
less reversible than left ventricular wall thickening.
Recent trials have shown that a high relative wall thickness
(concentric left ventricular pattern) is associated with increased
cardiovascular risk.(6-7) Relative wall thickness was
higher in our obese subjects than in lean subjects and, because wall
thickness decreased more than cavity dimension after weight loss,
relative wall thickness also decreased significantly. To our knowledge,
this has not been reported previously.
It has been suggested that hypertension in obesity is a result of
complex interactions between weight related volume overload and changes
in hormonal factors.(24-25) In addition to
promoting hypertension, v Limitations of the study Conclusion
We thank Lauren Lissner for her help in recruiting study
subjects form the municipality of Mölndal.
Funding: Swedish Medical Research Council (grant No 05239),
Sahlgrenska University Hospital, Gothenburg Medical Society, Volvo
Research Foundation, Hoffmann-La Roche.
Department of Cardiology, Department of
Clinical Physiology, Department of
Medicine,
Correspondence to: Dr Karason
email:
kristjan.karason@medfak.gu.se
References
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Results
Table 2 - Mean (SD) echocardiographic measurements at
baseline and one year follow up
Obese
subjects Non-obese
subjects Difference between non-obese and obese
subjects (95% CI)
Operation Control Difference (95% CI) Truncated ellipsoid
model (n=38) (n=25) (n=42) Chamber
radius
(mm): Baseline 22.4
(2.5) 23.0 (3.3) 0.6 (-0.9 to 2.1)
21.9 (2.9) 0.8 (-0.3 to 1.9) One
year follow up† 24.1 (2.2) 23.3
(2.2) -0.8 (-1.9 to 0.3)
Average wall thickness
(mm): Baseline 13.2
(2.3) 12.6 (2.3) -0.6 (-1.8 to
0.6) 10.8 (0.19) 2.2 (1.4 to
3.0)(P< 0.001) One year follow up† 11.1
(2.1) 12.7 (2.1) 1.6 (0.6 to 2.6)
(P=0.005) Relative wall
thickness: Baseline 0.60
(0.13) 0.57 (0.16) -0.03 (-0.10 to
0.04) 0.50 (0.10) 0.09 (0.04 to 0.14)
(P=0.001) One year follow up† 0.47
(0.12) 0.55 (0.12) 0.08 (0.02 to 0.14)
(P=0.01) Left ventricualr mass
(g): Baseline 193
(57) 188 (44) -5 (-31 to
23) 138 (40) 53 (34 to 72) (P<
0.001) One year follow up† 165
(41) 189 (41) 24 (3 to
45)(P=0.03) Apical
four chamber
view (n=29) (n=23) (n=42) Left
ventricular volume diastole
(ml): Baseline 104
(27) 97 (23) -7 (-23 to
9) 80 (20) 21 (11 to 31) (P<
0.001) One year follow up† 93
(23) 96 (23) 3 (-11 to
17) †Adjusted mean (SD).
Analyses of pooled data from the obese operation and obese
control groups showed that changes in weight and changes in relative
wall thickness and left ventricular mass were significantly correlated
(figure). Changes in blood pressure correlated significantly with
changes in relative wall thickness (r=0.33; P<0.05) but
not with changes in left ventricular mass. Multiple regression analysis
showed that changes in relative wall thickness and left ventricular
structure were predicted by baseline relative wall thickness and
baseline left ventricular mass respectively, as well as by changes in
body weight. Changes in blood pressure did not contribute to the
variation of left ventricular structure explained by these analyses
(table 3). The findings persisted even after adjustment for age, sex,
and antihypertensive
treatment. 
Fig 1: Mean (SEM) changes in relative wall thickness and left
ventricular mass as a function of weight change (in fifths) in obese
subjects. Correlation coefficients are based on all individual
observations (n=63). Table 3 - Multiple regression analyses of changes in
relative wall thickness and left ventricular mass on changes in weight
and systolic blood pressure after adjustment for baseline values*
Independent variables Dependent
variables Change in relative wall
thickness Change in left
ventricular mass Standardised regression
coefficient P value Standardised regression
coefficient P value Baseline relative wall
thickness -0.62 <0.001 Baseline
left ventricular
mass -0.68 <0.001
Baseline
weight 0.17 0.10 0.31 0.004
Baseline systolic blood
pressure 0.19 0.12 0.27 0.04
Change in
weight 0.32 0.007 0.37 0.002
Change in systolic blood
pressure 0.07 0.63 0.10 0.49
P value for
model <0.001 <0.001
Adjusted R2
(%) 48 47 *Data from the obese operation and obese control groups are
pooled in these analyses. Discussion
Before generalising the results of this study, certain limitations
in the design and methods should be taken into account. Firstly, the
study was neither randomised nor blinded; this was not possible for
practical and ethical reasons. However, the subjects in each group were
carefully matched for clinical variables, thereby improving the
credibility of the results. Secondly, it was difficult to evaluate
obese subjects echocardiographically, leading to missing data,
especially with respect to measurements of left ventricular volumes.
Nevertheless, the exclusion rate was similar in both obese groups, and
patients with unacceptable readings had similar clinical
characteristics to those of the remaining obese patients. Furthermore,
the main effect of missing data is in cross sectional data analyses;
longitudinal analyses are less sensitive. A third limitation is the
problem of measuring blood pressure precisely in obese subjects, as
well as the assumption that single measurements are representative of
blood pressure over time. These factors could explain the relatively
weak association between the changes in blood pressure and the changes
in left ventricular structure observed in our study. Even so, optimal
measurement techniques were used in all study subjects, and average 24
hour ambulatory blood pressure registrations have not been shown to
correlate much more strongly with left ventricular mass than one-off
blood pressure measurements.(28) Our study included an obese
control group,which strengthens our conclusions.
We have confirmed that obese people have abnormalities of heart
structure which are associated with increased cardiovascular risk, and
we have shown that these structural aberrations diminish after weight
loss. The regression of abnormal heart structure should be regarded as
favourable, even though the question of whether it can reduce morbidity
and mortality remains unanswered. One important finding in this study
is that the regression in abnormalities of heart structure is better
predicted by weight loss than by reduction in blood pressure. To
prevent or improve abnormal heart structure in obese subjects, weight
control should be the primary goal and should be regarded as being at
least as important as regulating blood pressure.
Key Messages
Obesity and hypertension often coexist, leading to various
degrees of eccentric and concentric left ventricular hypertrophy These structural heart changes are in turn powerful risk
factors for cardiovascular morbidity and mortality Weight loss is followed by a reduction in left ventricular
mass and relative wall thickness Changes in left ventricular structure are better predicted by
the weight loss than by the accompanying reduction in blood pressure
To prevent or improve abnormal heart structure in obese
people, weight control should be the primary goal and should be
regarded as at least as important as regulating blood pressure
Conflict of interest: None.
(Accepted 11 June 1997)
Sahlgrenska
University Hospital,
Gothenburg,
S-413 45 Sweden
Kristjan
Karason, consultant cardiologist
Sahlgrenska University Hospital
Ingemar
Wallentin, associate
professor
Sahlgrenska University Hospital
Bo Larsson,
associate professor
Lars Sjöström,
professor
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