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Reduction of Left Ventricular Hypertrophy After Exercise and Weight Loss in Overweight Patients With Mild Hypertension
Alan Hinderliter, MD;
Andrew Sherwood, PhD;
Elizabeth C. D. Gullette, PhD;
Michael Babyak, PhD;
Robert Waugh, MD;
Anastasia Georgiades, PhD;
James A. Blumenthal, PhD
Arch Intern Med. 2002;162:1333-1339.
ABSTRACT
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Background Hypertrophy and concentric remodeling of the left ventricle are important
manifestations of hypertension that are associated with increased morbidity
and mortality. Although lifestyle interventions are efficacious in lowering
blood pressure, evidence that they have a beneficial effect on target organs
has been lacking.
Objective To assess the effects of regular aerobic exercise or exercise plus weight
management counseling on left ventricular mass and geometry in overweight,
sedentary men and women with high-normal or mildly elevated blood pressure.
Methods Eighty-two participants in a randomized, controlled trial were assigned
to supervised aerobic exercise only, a behavioral weight management program
that included exercise, or a waiting-list control group for 6 months. Blood
pressure and echocardiographic measures of left ventricular structure were
measured at baseline and at the conclusion of the treatment phase.
Results The 45 women and 37 men had a mean ± SD age of 47 ± 9
years and had a mean ± SD blood pressure of 140 ± 10/93 ±
5 mm Hg. Blood pressure fell by 7/6 mm Hg in the weight management group and
by 3/4 mm Hg in the aerobic exercise group. In association with these decreases
in blood pressure, participants in the intervention groups exhibited significant
decreases in left ventricular relative wall thickness (P = .003), posterior wall thickness (P = .05),
and septal thickness (P = .004) and a trend toward
a decrease in indexed left ventricular mass (P =
.08) relative to the control group.
Conclusions In a cohort of overweight, sedentary men and women, exercise and weight
loss reduced blood pressure and induced favorable changes in left ventricular
structure.
INTRODUCTION
HYPERTROPHY and concentric remodeling of the left ventricle are important
manifestations of hypertension that are associated with an enhanced risk for
morbidity and mortality. In the general population and in cohorts with hypertension
or coronary artery disease, increased left ventricular mass is a predictor
of cardiovascular events independent of blood pressure or other traditional
risk factors.1-4
The geometric pattern of hypertrophy is also of prognostic importance. Patients
with concentric remodeling, ie, an increase in the ratio of wall thickness
to chamber dimension but normal left ventricular mass, have a cardiovascular
risk intermediate between those with normal left ventricular structure and
those with concentric hypertrophy.5-6
Regression of hypertrophy is associated with a reduction in cardiovascular
risk.7-9
A number of studies have demonstrated that lowering blood pressure with
medication results in regression of left ventricular hypertrophy.10-11 Although lifestyle modifications
such as regular aerobic exercise are viewed as important elements of antihypertensive
therapy in patients with high-normal or mildly elevated blood pressure,12-13 the effects of nonpharmacologic measures
on left ventricular mass and structure have not been extensively evaluated.
Kokkinos et al14 demonstrated significant blood
pressure reduction and regression of left ventricular hypertrophy in severely
hypertensive African Americans who engaged in moderately intense aerobic exercise
training. However, several smaller studies in patients with milder hypertension
have yielded conflicting results.15-18
Published reports have not consistently demonstrated a beneficial effect of
weight loss or of weight loss combined with exercise on left ventricular structure.15, 19-23
A randomized, controlled trial recently reported by our group demonstrated
that exercise training is effective in lowering blood pressure in overweight,
sedentary patients with high-normal or mildly elevated blood pressure, and
that weight loss is of added benefit when combined with aerobic training.24 To assess the effect of these lifestyle modifications
on ventricular hypertrophy, we examined echocardiographic measures of left
ventricular structure in a substudy of this trial.
SUBJECTS AND METHODS
SUBJECTS
Participants were aged at least 29 years and were generally healthy,
with no history of cardiac disease, renal insufficiency, or diabetes mellitus
and no evidence of secondary hypertension. None had been treated with antihypertensives
for at least 6 weeks. Inclusion criterion consisted of a casual systolic blood
pressure of 130 to 180 mm Hg and/or diastolic blood pressure of 85 to 110
mm Hg, determined by averaging blood pressure measurements from 4 separate
visits during a 3-week period. All subjects were overweight or obese (body
mass index [BMI], 25-37) and sedentary (not performing regular aerobic exercise).
None were treated with medications that have hemodynamic effects, and none
had a history of abuse of alcohol or other drugs.
PROTOCOL
Details of the study protocol have been described previously.24 The protocol was approved by the institutional review
board at Duke University Medical Center, Durham, NC, and informed consent
was obtained from each subject before participation.
Subject eligibility for the study was established during a series of
screening visits that included a history and physical examination, measurement
of height and weight, determination of baseline casual blood pressure, and
assessment of dietary content. Exercise capacity was determined by treadmill
exercising testing, and left ventricular geometry and mass were measured by
echocardiography. Participants were than randomized in a 2:2:1 ratio, by sex,
to 1 of the following 6-month treatment conditions: (1) exercise, (2) exercise
plus a behavioral weight loss program, or (3) waiting-list control. In addition,
5 subjects who met all eligibility criteria but were unable to commit to regular
participation in the supervised exercise sessions were included in the control
group. At the conclusion of treatment, measurements of weight, blood pressure,
dietary content, exercise capacity, and left ventricular structure were repeated.
MEASUREMENTS
Blood Pressure
Blood pressure was measured by a trained technician using a random-zero
sphygmomanometer. On each visit, blood pressure was measured 4 times at 2-minute
intervals after an initial 5-minute rest. The last 3 measurements were averaged
to represent the blood pressure value for that visit, and the values for each
of 4 visits during a 3-week period were averaged to determine the casual blood
pressure. Blood pressure determinations were made in this standardized manner
at baseline and after the 6-month intervention.
Body Weight
Weight was measured in kilograms using a standard-balance scale, and
height was measured in meters. Body mass index was calculated as weight in
kilograms divided by the square of height in meters.
Exercise Capacity
Exercise capacity was assessed by measuring maximum oxygen consumption
using the Duke–Wake Forest Protocol.25
This protocol begins at 3.2 km/h (2.0 mph) and 0% grade, and the workload
is increased at a rate of 1 metabolic equivalent per minute. Expired gases
were collected for the determination of peak oxygen consumption using a metabolic
cart.
Dietary Content
Subjects recorded all food intake for 4 consecutive days in a diet diary
that was analyzed for energy and nutritional content.
Echocardiography
Echocardiography was performed with the use of an imaging system (Hewlett-Packard,
Palo Alto, Calif) equipped with a 2.5-MHz phased-array transducer. Images
were obtained with the patient in the partial left lateral decubitus position,
and were recorded on a Super-VHS videotape. The studies were subsequently
quantified by one of us (A.H.), who was masked to the subjects' identifying
information. Left ventricular end-diastolic diameter, posterior wall thickness,
and interventricular septal thickness were measured just distal to the mitral
valve tips at end diastole, using a leading edge–to–leading edge
convention. Left ventricular mass was estimated using a cube function model
with a correction factor.26 Relative wall thickness,
a measure of the ratio of the left ventricular wall thickness to the chamber
diameter, was calculated as the sum of the posterior wall thickness and the
interventricular septal thickness divided by the left ventricular end-diastolic
diameter. To adjust for variations in heart size due to differences in body
size, indexed left ventricular mass was calculated as ventricular mass (in
grams) divided by height (meters)2.7 (g/m2.7), as described
by de Simone et al.27
INTERVENTIONS
Exercise
Subjects in this group participated in supervised exercise sessions
3 to 4 times per week for 6 months. The exercise protocol consisted of 10
minutes of warm-up exercise; 35 minutes of bicycle ergometry, walking, or
jogging on a track to achieve a heart rate between 75% and 85% of the maximal
heart rate reserve; and 10 minutes of cool-down exercise. All training sessions
were supervised by an exercise physiologist, who monitored the heart rates
of each participant several times per session. Subjects in this treatment
group were instructed to maintain their usual diets.
Weight Management
Subjects randomized to this intervention exercised 3 to 4 times weekly
as described in the previous paragraph. In addition, they participated in
a behavioral modification program designed to facilitate weight loss. This
program consisted of 26 weekly group sessions. Sessions were based on the
LEARN program,28 which focuses on the following
5 elements: lifestyle, exercise, attitudes, relationships, and nutrition.
Topics of discussion included distinguishing cravings from hunger, planning
healthy meals, shopping for food, dealing with pressure to eat, eating away
from home, and coping with relapse. The primary goal of the intervention was
a weight loss of 0.5 to 1.0 kg/wk achieved by decreasing energy and fat intake
through permanent lifestyle changes. Initial dietary goals consisted of an
energy intake of approximately 1200 calories for women and 1500 calories for
men, with 15% to 20% of this energy from fat.
Waiting-List Control
Subjects in the waiting-list control group were contacted monthly and
encouraged to maintain their usual dietary and exercise habits until the second
evaluation after 6 months of observation. They were then offered the opportunity
to participate in either of the active treatment groups.
ANALYSIS OF DATA
Descriptive statistics of the study cohort and the participants in each
intervention were expressed as mean ± SD. We assessed baseline differences
among treatment groups using 1-way analysis of variance for continuous variables
and  2 tests for categorical variables. We evaluated the treatment
effects on weight, exercise duration, blood pressure, and left ventricular
dimensions using a general linear model, with the posttreatment value for
the measurement of interest serving as the dependent variable and treatment
group and baseline values for the measurement of interest serving as independent
variables. Because controlling for baseline values of the outcome variables
of interest has the effect of producing residualized change scores, the present
analyses can be interpreted as testing treatment group differences on the
change in outcome variables. Orthogonal contrasts were estimated by comparing
the weight management group with the exercise group and the combined treatment
groups with the control group. Tests for homogeneity of slopes (treatment
group x sex and treatment group x race) were conducted to exclude
an influence of sex or race on the treatment effects on measures of left ventricular
structure.
RESULTS
Echocardiograms of high technical quality were obtained before and after
treatment in 82 subjects. Of the 144 subjects originally enrolled, 4 (3%)
did not have baseline echocardiograms; 16 (11%) did not return for a follow-up
study; and 42 (29%) had studies in which left ventricular dimensions or wall
thicknesses could not be quantified with confidence. The subjects with interpretable
ultrasound studies tended to weigh less (91.7 ± 16.8 vs 97.6 ±
13.9 kg; P = .03) and have a lower BMI (31.4 ±
4.1 vs 34.2 ± 3.9; P<.001) than those with
unsatisfactory images; no differences were seen in age, sex, race, or baseline
clinic blood pressure. The results described in this manuscript refer to the
82 subjects for whom complete echocardiographic data were available.
Characteristics of the study population and subjects in each intervention
group are noted in Table 1. The
3 groups were comparable in all baseline clinical and demographic characteristics
except that the control group had more nonwhite subjects than the active treatment
groups (P = .03).
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Table 1. Baseline Characteristics of the Study Population by Intervention
Group*
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Echocardiographic characteristics of subjects in the 3 groups are shown
in Table 2. For the study group
as a whole, 25 participants (30%) had left ventricular hypertrophy, defined
as a left ventricular mass index exceeding the 95th percentile for a lean,
normotensive reference population previously studied in our laboratory (>53.9
g/m2.7). An additional 11 (13%) had concentric left ventricular
remodeling (ie, an increased relative wall thickness [>0.51] but normal left
ventricular mass). Participants in the 3 treatment groups were similar in
each measure of left ventricular structure.
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Table 2. Baseline Echocardiographic Characteristics of the Study Population
by Intervention Group*
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At the conclusion of the intervention phase of the study, subjects in
the weight management group consumed less energy than those in the exercise
and control groups (P<.001). The decrease in daily
energy intake from baseline averaged 717 calories in the weight management
group but only 120 and 109 calories in the exercise and control groups, respectively.
Similarly, those in the weight management group consumed less sodium after
the intervention (P<.001), averaging a decrease
of 1094 mg/d, compared with decreases of 568 mg/d in the exercise group and
217 mg/d in the control group. No significant differences were found between
groups in the consumption of potassium, calcium, or magnesium.
Figure 1 illustrates posttreatment
values for weight, BMI, peak oxygen consumption, and blood pressure, corrected
for baseline values, for subjects in each of the 3 groups. Significant group
differences were seen in postintervention weight and BMI (P<.001 for the exercise group vs the weight management group; P<.001 for both active treatment groups vs the control
group). Participants in the weight management group exhibited an average weight
loss of 7.4 kg, compared with a loss of 2.3 kg in the exercise group and a
gain of 0.2 kg in the control group. Both interventions also resulted in improved
exercise capacity, as demonstrated by increases in peak oxygen consumption
(P<.001 for the active treatment groups vs the
control group). Adjusted posttreatment diastolic blood pressure was significantly
lower (P<.001), and posttreatment systolic blood
pressure was marginally lower (P = .09) in the active
treatment groups relative to the control group. The average reductions in
blood presssure were 6.8/5.9 mm Hg and 3.2/4.4 mm Hg in the weight management
and exercise groups, respectively, compared with an increase of 0.1/0.8 mm
Hg in the control group.
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Figure 1. Weight, body mass index (BMI;
calculated as weight in kilograms divided by the square of height in meters),
peak oxygen consumption, and blood pressure (BP) after treatment, adjusted
for pretreatment levels. CT indicates waiting-list control group; EX, exercise
group; WM, weight management group; asterisk, a significant difference between
the combined WM and EX groups and the CT group (P<.05); and
dagger, a significant difference between the WM and EX groups (P<.05).
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The effects of the interventions on echocardiographic variables are
shown in Figure 2. Relative to the
control group, subjects in the active intervention groups had significantly
smaller adjusted posttreatment posterior wall (P
= .05) and septal (P = .004) thicknesses and a nonsignificant
trend toward a greater end-diastolic diameter. Subjects in the weight management
group exhibited 5% decreases in posterior wall and septal thicknesses and
a 3% increase in end-diastolic diameter. Those in the exercise group had similar
changes, with a 3% decrease in posterior wall thickness, a 5% decrease in
septal thickness, and a 2% increase in left ventricular chamber dimension.
No significant changes in these dimensions were noted in the control group.
In part due to the increase in chamber size associated with exercise training,
the adjusted decrease in left ventricular mass index in the intervention groups
was modest and not statistically significant (P =
.08). However, subjects in the active treatment groups had a significantly
smaller adjusted posttreatment relative wall thickness compared with those
in the control group (P = .003). During the intervention,
relative wall thickness decreased by 7% in the weight management group and
by 6% in the exercise group. This decrease in relative wall thickness in the
intervention groups remained significant when analyses controlled for baseline
differences in race (P = .01) and when the 5 nonrandomized
controls were excluded (P = .04). No significant
interactions were noted between treatment group and race or sex for any of
the measures of left ventricular structure.
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Figure 2. Echocardiographic variables after
treatment, adjusted for pretreatment values. LV indicates left ventricular;
asterisk, significant difference between the combined WM and EX groups and
the CT group (P<.05). Other abbreviations are described in
the legend to Figure 1.
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COMMENT
In our study of overweight, sedentary subjects with high-normal or mildly
elevated blood pressure, lifestyle interventions consisting of regular aerobic
exercise and weight management counseling resulted in improved exercise capacity,
weight loss, and decreases in blood pressure that were associated with ventricular
remodeling. Regular aerobic exercise with or without weight loss led to decreases
in posterior wall and septal thicknesses, a decrease in relative wall thickness,
and a trend toward a decrease in indexed left ventricular mass, independent
of sex or race.
LEFT VENTRICULAR ADAPTATIONS TO EXERCISE AND WEIGHT LOSS
Aerobic conditioning in normotensive individuals is associated with
an increase in the end-diastolic dimension of the left ventricle and a proportionate
increase in wall thickness.29 These adaptations
to exercise develop rapidly, with significant changes in left ventricular
architecture detectable by echocardiography within weeks of the initiation
of training.30 Cross-sectional studies document
that obesity is associated with eccentric hypertrophy, an increase in left
ventricular chamber size and wall thickness, at all levels of blood pressure.31-33 Most weight reduction
intervention trials that have used echocardiography have found that weight
loss leads to a decrease in left ventricular wall thickness but has little
effect on chamber size.19-20
EXERCISE AND WEIGHT LOSS INTERVENTIONS IN HYPERTENSION
Few studies have evaluated the effects of lifestyle modifications on
left ventricular structure in patients with hypertension. Kokkinos et al14 described the changes in left ventricular mass and
architecture observed in severely hypertensive, medically treated African
American men who completed a 12-week program of moderately intensive exercise.
Subjects participating in the exercise intervention exhibited a decrease in
diastolic blood pressure from 89 to 84 mm Hg, accompanied by decreases in
left ventricular mass and wall thickness but no significant change in end-diastolic
diameter. Previous studies in patients with mild hypertension have examined
smaller numbers of patients and have generally not included randomized control
groups. Reid et al15 described the effects
of 12 weeks of exercise, weight loss, or both in 23 obese individuals with
a mean baseline blood pressure of 131/84 mm Hg. Exercise and weight loss resulted
in significant blood pressure reduction, and the effects of these interventions
were additive. No significant changes were noted in left ventricular mass
or dimensions, however. Baglivo et al17 demonstrated
a decrease in blood pressure in 25 middle-aged hypertensive subjects after
endurance exercise training, with a marginally significant decrease in left
ventricular mass. Eleven older adults with mild to moderate hypertension were
studied by Turner et al.18 After 7 months of
regular aerobic exercise, resting systolic blood pressure, left ventricular
wall thickness, and the wall thickness-radius ratio were significantly decreased.
Finally, Zanettini et al16 described reductions
in left ventricular mass and wall thickness, with no significant change in
chamber diameter, in an uncontrolled trial of aerobic exercise in 14 patients
with mildly elevated diastolic blood pressure.
In our study, significant blood pressure reductions were observed in
both active intervention groups, but the amount of weight loss and the magnitude
of blood pressure lowering were greater in those who received weight management
counseling in addition to exercise training. Subjects in the 2 groups exhibited
similar changes in left ventricular structure, however. This observation suggests
that, in a relatively short 6-month intervention, exercise has a greater influence
on left ventricular architecture than does weight loss. Additional research
will be required to determine whether weight loss sustained over a longer
period results in incremental changes in left ventricular wall thickness and
mass.
CLINICAL SIGNIFICANCE OF THE FINDINGS
Previous observational studies using echocardiography have demonstrated
that left ventricular hypertrophy and remodeling are predictors of cardiovascular
morbidity and mortality, independent of blood pressure and other traditional
risk factors.1, 6 More recent data
suggest that favorable changes in left ventricular structure are associated
with a reduction in risk.7, 9 Lifestyle
interventions such as regular aerobic exercise and weight loss are recommended
as initial therapy in overweight patients with high-normal or mildly elevated
blood pressure. Although a number of studies have suggested that these interventions
are efficacious in reducing blood pressure, evidence that they minimize end-organ
damage or prevent cardiovascular events has been lacking. Our study demonstrates
that these nonpharmacologic measures not only reduce blood pressure but also
induce favorable changes in left ventricular structure. These findings support
a strategy of lifestyle modification as an initial approach in the management
of overweight, sedentary patients with high-normal or mildly elevated blood
pressure.
AUTHOR INFORMATION
Accepted for publication October 22, 2001.
This study was supported by grants HL 49572 and HL 59672 from the National
Institutes of Health, Bethesda, Md; and grant M01-RR-30 from the General Clinical
Research Center Program, National Center for Research Resources, National
Institutes of Health.
We thank Anne Middleton for her contribution in the preparation of the
manuscript.
Corresponding author and reprints: Alan L. Hinderliter, MD, Division
of Cardiology, University of North Carolina, CB 7075, 338 Burnett-Womack,
Chapel Hill, NC 27599-7075 (e-mail: hinderli{at}med.unc.edu).
From the Department of Medicine, University of North Carolina, Chapel
Hill (Dr Hinderliter), and the Departments of Psychiatry and Behavioral Sciences
(Drs Sherwood, Gullette, Babyak, Georgiades, and Blumenthal) and Medicine
(Dr Waugh), Duke University Medical Center, Durham, NC.
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