Obesity and Cardiac Function
ORESTE DE DIVITIIS, M.D., SERAFINO FAZIO, M.D., MAURIZIO PETITTO, M.D.,
GIOVANNI MADDALENA, M.D., FRANCO CONTALDO, M.D., AND MARIO MANCINI, M.D.
SUMMARY We studied 10 obese volunteers, mean age 36.5 ± 10.3 years, who weighed 123.56 ± 28.7 kg
and were 69.96 ± 22.5 kg overweight. The subjects did not have diabetes, arterial hypertension or signs of cardiac and respiratory failure or disease and all underwent right- and left-heart catheterization. Cardiac output
and stroke volume were high, according to increased oxygen consumption and to the degree of obesity. Ventricular end-diastolic and atrial pressures ranged from normal to high and correlated with body weight, signs of
volume overloading and reduced left ventricular (LV) compliance. The mean pulmonary artery pressure was
elevated and correlated well with weight, pulmonary resistance being normal; mean aortic pressure did not correlate with weight, and systemic arterial resistance tended to have a negative correlation. The LV function
curve showed impaired ventricular function, particularly for the heaviest subjects, in whom Vma, and the ratio
of the stroke work index to LV end-diastolic pressure were reduced. These indexes correlated well with each
other and both correlated negatively with the degree of obesity. In contrast, maximal dP/dt was normal and
did not correlate with excess weight. These observations show that depressed LV function is already present in
relatively young obese people, even if they are free from signs of cardiopathy and other associate diseases. The
degree of impairment of heart function seems to parallel the degree of obesity.
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HEART FAILURE occurs frequently in obese patients and appears to be the predominant cause of
death in grossly obese subjects.1`3 Hemodynamic
features contributing to the development of cardiac
failure have been identified; particularly in obese people, changes in the factors that determine the preload
and afterload stresses of the heart are present before
cardiac failure occurs.3"- Few studies on the contractile function of the ventricle have been done.3
However, many features that depend on conditions
that are often associated with contractile function, including arterial hypertension, diabetes, arteriosclerotic changes and respiratory disease, can interfere
directly or indirectly with cardiac function, adding
their own variations to those deriving from obesity.
Therefore, we studied the changes of cardiac function
in 10 relatively young volunteers who had varying
degrees of obesity and were free from such pathologic
conditions.
significant ECG changes, x-ray cardiothoracic ratio
exceeding 0.55 and stable arterial diastolic hypertension (diastolic arterial pressure > 100 mm Hg). None
of the patients had treatment with digitalis or antihypertensive or diuretic drugs. These subjects underwent both right- and left-heart catheterization. Ten
patients gave informed consent for the procedure.
Left-heart catheterization was performed through a
brachial arteriotomy. The first derivative of left ventricular pressure was obtained simultaneously with the
pressure curve by Millar microtip transducer catheter
and was recorded at a paper speed of 500 mm/sec with
time lines of 0.01 second. Oxygen consumption (V02)
was determined by a spirograph metabolimeter
(Helite/CV). Hemoglobin and oxygen saturations
were obtained by Hb-Oximeter (Philips XO-1000/00).
The cardiac output (CO) was measured by the Fick
technique.
From the basic data, the hemodynamic variables
were calculated as follows: CO (I/min) = VO2/AV02; CI (I/min/2) = CO/BSA; SV (ml/beat) =
CO/HR; SI (ml/beat/m2) = SV/BSA; LVSW (gm/beat) = SV (aortic mean pressure - LVEDP)
X 0.0136; LVSWI (g-m/beat/m2) = SI (aortic mean
pressure - LVEDP) X 0.0136; TPR (dyn-sec-cm- ) =
PA mean pressure X 80/CO; APR (dyn-sec-cm-3) =
(PA mean pressure -PA wedge mean pressure) X
80/CO; SVR = (dyn-sec-cm-5) = (aortic mean
pressure - RA mean pressure) X 80/CO. (See legend
to table 1 for abbreviations.)
Contractile element velocity (VCE) was calculated
every 10 msec as the ratio of dP/dt to its instantaneous isovolumic total pressure, assuming a fixed
series elastic constant of 32.10 The C constant, or zero
intercept, for the series elastic element was considered
to be negligible. VCE at zero load (Vmax) was linearly
extrapolated by hand from total pressure/VcE curve.
The isovolumic indexes (dP/dt max and Vmax) represent the average of five beats. Normal values of the
isovolumic indexes were obtained in our laboratory in
10 patients, ages 17-45 years (mean 31 years), with
normal body weight (overweight 0-19 kg, mean 10.5
Methods
The 10 obese subjects (table 1) included seven
women and three men who were 20-55 years old
(mean 36.5 ± 10.3 years) and weighed 81-183 kg
(mean 123.56 ± 28.7 kg). Their overweight ranged
from 29-100 kg (mean 69.96 ± 22.5 kg). Ideal
weights, corresponding to the longest life expectancy,
were established according to the tables developed by
life insurance companies and converted to metric
units.
We excluded subjects who had diabetes, valvular
heart disease, signs of cardiac or respiratory failure,
From the Sezione Autonoma di Cardioangiologia, Clinica
Medica and Semeiotica Medica, Second Faculty of Medicine,
University of Naples, Italy.
Address for correspondence: Prof. Oreste de Divitiis, Sezione
Autonoma di Cardioangiologia, c/o Clinica Medica, 2a Facolta di
Medicina et Chirurgia (Nuovo Policlinico), Via Sergio Pansini,
80131 Napoli, Italia.
Received June 11, 1980; revision accepted December 24, 1980.
Circulation 64, No. 3, 1981.
477
478
CIRCULATION
VOL 64, No 3, SEPTEMBER 1981
TABLE 1. Clinical and Hemodynamic Data in Obese Subjects
Pressures (mm Hg)
OverAge
Height Weight weight
(years) Sex (cm) (kg) (kg)
F
81
20
155
29
M 170 119
23
56
34
F
161 112
53
55
F
149 150
97
40
M 173 183
100
F
50
45
153 103
PA
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BSA
RA
Mean Wedge
Aorta
Pt
(m2) Mean a-waveRVEDP Mean wedge a-wave LVEDP S
D
M
1
8
11
1.8
8
15
10
16
5
138
95 110
2
2.3
22
20
14
8.5
12
10
13
132
87 105
3
7
14
2.1
7
20
22
18
150
18
90 110
4
2.3
10
16
11
25.5 14
23
18
145
85 110
5
2.7
15
22
37
28
18
31
28
135
95 110
6
7
10
19
1.9
8
13
20
13
138
88
99
7
F
41
152 113
60
2.0
9
12
10
22
16
18
14
155 100 115
F
8
41
32
25
156 134
78
2.2
13
21
15
30
22.5
170
95 125
F
9
35
6
14
156 103.6 49.6 2.0
17
10
12.5
15
14
135
95 110
M 164 137
10
31
77
2.3
8
10
10
25
18
21
20
158
98 118
Abbreviations: HR = heart rate; V02 oxygen consumption; A-V02 = arteriovenous oxygen difference; CO = cardiac
output; BSA = body surface area; CI = cardiac index; SV = stroke volume; SI = stroke index; RA = right atrium; RVEDP =
right ventricular end-diastolic pressure; PA = pulmonary artery; LVEDP = left ventricular end-diastolic pressure; TPR =
total pulmonary resistance; APR = arteriolar pulmonary resistance; SVR = systemic vascular resistance; LVSW - left
ventricular stroke work; LVSWI = left ventricular stroke work index; Max dp/dt = peak of the rate of change of pressure with
respect to time during early systole; Vmax - maximal velocity of the contractile element VCE derived by extrapolation of VCE
to zero load from the plot of VCE and total left ventricle pressure during isovolumic phase.
kg), affected by idiopathic pulmonary dilatation
(three), benign murmurs (three), very mild mitral
stenosis (two), mild pulmonary stenosis (one), and
small atrial septal defect (one). The normal range for
dP/dt max is 903-2060 mm Hg/sec (mean 1424 mm
Hg/sec) and for Vmax 1.27-1.78 muscle lengths
(ML)/sec (mean 1.49 ML/sec). Body surface area
was calculated according to the formula of Du Bois
and Du Bois.11 The ventricular function curve was obtained by plotting LVSWI against LVEDP.12-14
Variables were correlated with weight and with the
amount of overweight, and Vmax was correlated with
the LVSWI/LVEDP ratio.
below Ross and Braunwald's range of normal variability of left ventricular function,"' and the curve was
shifted to the right (fig. 1). Further, the SWI/ LVEDP
ratio showed a significant negative correlation with
weight and overweight (fig. 2). The peak value of first
derivative (dP/dt max) of the left ventricular pressure
curve was normal. Vmax was low to normal. Although
dP/dt max did not correlate with the degree of
obesity, Vmax correlated negatively with weight
(fig. 3). An excellent correlation (y = 3.878x + 0.088,
r = 0.821, p < 0.01) was found between Vmax and
LVSWI/LVEDP (fig. 4).
Results
The hemodynamic data are summarized in table 2.
VO2, CO and SV were elevated and positively correlated with weight and with amount of overweight.
A-VO2 was normal, but correlated positively with
weight and overweight. Mean and a-wave right atrial,
right ventricular end-diastolic and mean pulmonary
artery pressures were high and correlated positively
with weight and overweight; also mean pulmonary
capillary wedge pressures, with evident "a" wave, and
LVEDP were generally high and correlated
significantly with weight and overweight. Systolic,
diastolic and mean aortic pressures were normal and
did not correlate significantly with the degree of
obesity. Total and arteriolar pulmonary resistances
were also normal but did not correlate with weights.
Systemic vascular resistance was low to normal and
showed a significant negative correlation with weight.
Left ventricular stroke work was increased in relation
to the degree of obesity. The left ventricular function
curve showed that ventricular function was impaired
in the eight heaviest subjects. In fact, their points lay
Discussion
Our results indicate that cardiac performance is
reduced in obese subjects despite increased cardiac
output. This increased cardiac output depends on
VO2, which was also elevated and correlated with
weight and overweight. However, the A-VO2 was normal in each subject, which confirms the absence of
clinically evident cardiac failure. However, the A-VO2
values correlated significantly with the degree of
obesity. This tendency of A-VO2 to increase with
weight could be explained by increased oxygen uptake
as a consequence of an inadequate CO, which was
found at the highest degree of body weight excess.
Alexander and Peterson7 reported that A-VO2,
although normal, tends to decrease with weight loss.
Further, the increased CO was in turn produced
primarily by the increased SV, which was correlated
with CO and with weight and overweight, while heart
rate remained normal. Such increases in CO and SV
were described by Alexander and co-workers and were
attributed to increased preload due to increased blood
volume.2 7 Also, the increased right ventricular enddiastolic pressure, LVEDP and the large a-wave in the
OBESITY AND CARDIAC FUNCTION/de Divitiis et al.
479
TABLE 1. (Continued)
HR
V02
(beats/ (ml/
min) min)
170
109
340
72
86
280
370
66
425
86
250
72
94
270
300
78
300
95
410
88
SI
Max
SV (ml/ LVSWI LVSW LVSWI/ dp/dt
(ml/ beat/ (g-m/m2/ (g-m/ LVEDP (mm Hg/
sec)
beat) m2)
beat) beat) ratio
2002
39.55
71.4 7.91
27.7
50
887.5
56.43 128.7 4.03
45.6
104
1145
2.94
53.05
112.6
42.4
90
1545
62.93 148.9 3.49
50.3
119
858.7
46.02 124.9 1.64
112
41.3
1178
46.02
95.9 3.54
41.8
82
1229
62.67 127.7 4.47
93
45.6
1423
51.52 115.4 2.28
82.8 36.9
1818
52.55 105.1 3.75
80.5 40.2
1165
99.5 42.5
56.68 132.6 2.83
CI
A-V02
CO (l/min/
(vol%) (1/min) m2)
5.46
3.03
3.11
7.48
3.28
4.54
7.75
3.61
3.65
4.71
7.85
3.32
3.55
4.42
9.60
5.92
3.01
4.22
8.76
4.29
3.08
4.64
6.46
2.88
7.65
3.82
3.32
3.74
4.68
8.76
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TABLE 2. Summary of Hemodynamic Data in Obese Subjects
Weight
r
Mean
SD Regression equation
p
-0.441 NS
HR (beats/min)
84.6
12.97 y = -0.199x + 109
311.5
77.10 y = 2.383x + 17.00
0.886 0.001
V02 (ml/min)
=
y
+
4.09
0.63
0.014x 2.32
0.650 0.05
A-V02 (vol%)
CO (1/min)
7.56
1.30 y = 0.032x + 3.56
0.708 0.05
0.40 y = 0.001x + 3.29
0.084 NS
CI (1/min/m2)
3.45
0.812 0.01
91.28 19.40 y = 0.550x + 23.20
SV (ml/beat)
=
y
0.462 NS
41.44
+
0.096x
29.47
6.00
SI (ml/beat/M2)
RA mean pressure
(mm Hg)
RA a-wave (mm Hg)
RVEDP (mm Hg)
PA mean pressure
(mm Hg)
PA wedge mean
pressure (mm Hg)
PA wedge a-wave
(mm Hg)
LVEDP (mm Hg)
Aortic mean pressure
(mm Hg)
Aortic systolic pressure
0.079x - 0.51
0.106x + 1.08
y = 0.096x - 1.20
TPR APR SVR
(dyn- (dyn- (dynsec- sec- secsec) cm5) cm5) cm5)
73 1611
1.76 219
96 1032
0.68 235
21 1063
0.72 206
0.88 260 117 1019
791
75
0.46 308
81 1243
0.66 257
55
968
0.98 201
87 1387
0.99 396
47 1087
1.20 178
64 1004
0.95 228
Vm.,
(ml/
Overweight
r
p
Regression equation
y = -0.304x + 104.37
-0.528 NS
y = 2.930x + 121.03
0.856 0.01
y = 0.001x + 3.36
y = 0.718x + 44.59
y = 0.145x + 31.96
0.688 0.05
0.646 0.05
0.071 NS
0.831 0.01
0.549 NS
0.752 0.05
0.710 0.05
0.821 0.01
y = 0.092x + 3.14
y = 0.127x + 5.91
y = 0.112x + 3.37
0.736 0.05
0.670 0.05
0.754 0.05
y = 0.019x + 2.83
y = 0.037x + 5.12
9.10
14.20
10.70
2.82
4.28
3.30
y=
23.45
6.70
y
=
0.217x - 3.38
0.921 0.001
y=
16.75
5.70
y
=
0.156x - 2.54
0.779 0.01
y=0.178x+5.16
0.698 0.05
21.60
16.65
5.31
6.20
y
0.814 0.01
0.911 0.001
y =
y=
0.181x + 9.79
0.239x + 1.12
0.770 0.01
0.866 0.01
111.20
7.00
y=
0.061x + 103.55
0.252
NS
y =
0.104x + 104.40
0.333
NS
145.60 12.40 y = 0.051x + 139.29
(mm Hg)
Aortic diastolic pressure
92.80
4.90 y = -0.005x + 93.44
(mm Hg)
248.80 63.20 y = 1.165x + 104.80
TPR (dyn-sec-cm5)
71.60 26.80 y = 0.316x + 32.49
APR (dyn-sec-cm-5)
1120.00 234.00 y = -5.538x + 1804
SVR (dyn-sec-cmi-5)
116.33 21.70 y = 0.539x + 49.67
LVSW (g-m/beat)
7.40 y = 0.065x + 44.62
52.74
LVSWI (g-m/beat/m2)
1.70 y = -0.044x + 9.22
3.68
LVSWI/LVEDP ratio
373.00 y = -7.218x + 2217
Max dP/dt (mm Hg/sec) 1325
0.92
0.36 y =-0.008x + 1.93
Vmax (ml/sec)
Abbreviations: See legend to table 1.
0.118
NS
y =
0.142x + 136.37
0.258
NS
-0.030
0.529
0.338
-0.678
0.712
0.253
-0.755
-0.554
-0.649
NS
NS
NS
0.05
0.05
NS
0.05
NS
0.05
-0.015x + 93.83
1.534x + 149.14
=
y
0.511x + 38.35
y = -6.440x + 1539
y = 0.765x + 66.58
y = 0.134x + 44.01
y = -0.055x + 7.31
-0.072
y=
0.150x + 2.96
y = 0.197x - 7.73
=
0.263x + 6.37
y =
y=
y =
y
=
-7.244x + 1795
-0.009x + 1.532
0.875 0.001
NS
0.546 NS
0.429 NS
-0.619 NS
0.792 0.01
0.407 NS
-0.739 0.05
-0.436 NS
-0.580 NS
-
CIRCULATION
480
VOL 64, No 3, SEPTEMBER 1981
1.8 -
y -0.008x+ 1.936
s
r
_
N
=-0.649
_
-
1.5
4
ov
E
U
Cotn
1.2 _
E 60
0
l
E 0.9 _
3:n
401
I0.6 W *
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201
0 5 10 15 20 25 30 35
LVEDP (mm Hg)
0.3
80
FIGURE 1. Left ventricular (L V) function curve. The
points of eight of 10 obese subjects lie below the range of
normal variability. '
right atrial and pulmonary wedge pressure curves,
which were related to increased weight, are signs of
volume overloading of the ventricles resulting from increased blood volume in the presence of reduced ventricular compliance.7' 16
The mean pulmonary artery pressure was increased
and correlated well with weight and overweight, while
mean aortic pressure was normal and did not correlate
10
I
I
160
120
WEIGHTS (kg)
FIGURE 3. The significant negative correlation between
Vmax and body weight shows that the reduction of left ventricular performance is related to the degree of obesity.
with the degree of obesity; however, hypertensive subjects were excluded from the study. The different
responses of pulmonary and systemic pressures must
be ascribed to the different responses of pulmonary
and systemic resistances to the increased CO. The inIr
1.v
t J
I
y =-0.055x + 7.31
r =-0.739
y=-OQ044x +9.22
cm
E
r =-0.755
8
~
a
Z-E6
E
E
8_
'4
E
A zE 6
4%*~~~~~~~~~~1*
200
Sm£
E E
4%
6-
**%
41
4
I\
4~~
3
tn 3 2 1
21
1
1
D 44.~~~~~~~~~~11
* 4%~~~~
"
L
I
0*~~~~~~~
_ l
0 N.1I- I
nW.
60
*
i1
) W
180
140
100
WEIGHTS (kg)
0
0
4%
1
1
A
I
*4%4
@4%\
\%,
21
0
,W
X
.
\
-1
@114%4%\
1
1~4
40
80
120
AMOUNT OVERWEIGHT (kg)
FIGURE 2. The significant negative correlation between the ratio ofthe stroke work index (SWI) to the left
ventricular end-diastolic pressure (L VEDP) and the weights and amounts of overweight shows that the
higher the degree of obesity, the greater the impairment of left ventricular function.
T-- -
OBESITY AND CARDIAC FUNCTION/de Divitiis et al.
1.8
y=3.878x+0.088
1.6
/
/
r = 0.821
I
1.4
In
-%
X
a
/
1.21
0,
1.01
/
/
1
0
/
0.8
/
Downloaded from http://circ.ahajournals.org/ by guest on July 12, 2017
II.
/0
0.61
n4L
0
'I
10
6
8
4
2
SWI (gm m /beat/m2
)
mm Hg
LVEDP I
FIGURE 4. Very good correlation between Vmax and ratio
of stroke work index (SWI) to left ventricular end-diastolic
pressure (LVEDP).
crease in CO induced an increase in pulmonary
pressure in the presence of normal total and arteriolar
pulmonary resistances. An augmented pressure
gradient was not present between pulmonary artery
and pulmonary capillaries, the values of which increased as a consequence of increased LVEDP. On the
other hand, systemic vascular resistance was normal
to low and correlated negatively with body weight; as
a consequence, the increased CO did not induce elevation of arterial pressure.
The left ventricular function curve shows that ventricular function was impaired in eight of the subjects
(fig. 1). To compare our data with those of Ross and
Braunwald,'3 we had to normalize the stroke work,
CO and SV for body surface area. We used the formula of Du Bois and Du Bois to obtain body surface
area, although we realize this method could cause
some error for subjects who weigh more than 150 kg.
In only one of our patients, who weighed 183 kg, was
the formula considered unsuitable, but we considered
this negligible in view of the advantage of having comparable hemodynamic data. Therefore, despite the increased ventricular filling pressure and volume, the
contractile response does not allow adequate systolic
work.
Although the increase of CO is related to the degree
of obesity, ventricular function remained inadequate.
The degree of impairment of ventricular function is in
481
turn related to the degree of obesity. In fact, the subjects whose ventricular function was normal are the
least heavy ones. Further, the LVSWI/LVEDP ratio
shows a significant negative correlation with weight
and excess weight. The impaired ventricular function
is confirmed by the behavior of the isovolumic indexes: dP/dt max, which is notoriously17' 18 affected by
factors not related to changes in myocardial contractility, was normal and did not correlate significantly
with weight. We believe the increased preload could
have masked the effect of reduced contractility.17
Instead, Vm.., which is less influenced by preload,'0' 19
tended to be reduced and negatively correlated to body
weight. Thus, a higher degree of reduction of cardiac
performance corresponds to a higher degree of obesity. On the other hand, Vmax and the LVSWI/
LVEDP ratio both suggested reduced LV performance and were negatively correlated with the degree
of obesity.
Our results that show impaired cardiac performance in obese subjects confirm the observations
of Alexander et al.,3 who showed, echocardiographically, increased LV wall stress and posterior
wall thickness in patients with morbid obesity and
reduced ventricular performance. Hypertrophy has
been documented by echocardiography and also by
postmortem examination20 in morbid obesity. Increased wall thickness and LV hypertrophy have been
shown to be associated with increased LV diastolic
stiffness,21 22 reduced diastolic compliance23 24 and
probably, normal end-diastolic muscle fiber length
and "stretch."2' 24 Such LV wall variations may account for the shift to the right of the ventricular function curve: The hypertrophic ventricle may underutilize Starling's law.2'
The reduced ventricular performance we found
could also be explained as a consequence of impaired
myocardial contractility. The variations of Vmax we
obtained could support this thesis, but this index has
been judged inadequate in the evaluation of myocardial inotropic state.23' 2 In addition, the concept that
myocardial hypertrophy is associated with decrease in
contractility is controversial.27-32
In conclusion, our results show that ventricular
function is impaired in asymptomatic obese subjects
who have no other clinically appreciable cause of heart
disease and that it is related to the degree of obesity.
References
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O de Divitiis, S Fazio, M Petitto, G Maddalena, F Contaldo and M Mancini
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Circulation. 1981;64:477-482
doi: 10.1161/01.CIR.64.3.477
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