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European Journal of Preventive Cardiology
http://cpr.sagepub.com/content/early/2012/03/27/2047487312444372
The online version of this article can be found at:
DOI: 10.1177/2047487312444372
published online 28 March 2012European Journal of Preventive Cardiology
Werner Budts
Alexander Van De Bruaene, Pieter De Meester, Roselien Buys, Luc Vanhees, Marion Delcroix, Jens-Uwe Voigt and
type secundum
Right ventricular load and function during exercise in patients with open and closed atrial septal defect
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Original scientific paper
Right ventricular load and function during
exercise in patients with open and closed
atrial septal defect type secundum
Alexander Van De Bruaene, Pieter De Meester, Roselien Buys,
Luc Vanhees, Marion Delcroix, Jens-Uwe Voigt and
Werner Budts
Abstract
Purpose: This study aimed at evaluating (1) right ventricular (RV) mean power during exercise, (2) the contribution
of flow and pressure to RV mean power, and (3) the impact of pulmonary artery pressure on RV function during exercise.
Methods: Fifty patients with atrial septal defect (ASD) type secundum (20 open, 30 closed) were enrolled. All under-
went standard echocardiography, a bicycle stress echocardiography, and symptom-limited cardiopulmonary exercise
testing. RV mean power was calculated as the product of RV cardiac output and mean pulmonary artery pressure
(mPAP). RV function was assessed using RV fractional area change (FAC) at rest and at peak exercise.
Results: RV mean power was linearly related with oxygen uptake (VO
2
) in patients with open (R
2
¼0.88; p<0.0001)
and closed ASD (R
2
¼0.90; p<0.0001). The increase in RV mean power was steeper in open than in closed ASD patients
(p<0.0001). The change in RV cardiac output (7.13.4 vs. 5.7 2.4 l/min; p¼0.132) was not statistically different, but
the change in mPAP (21.7 9.6 vs. 12.8 4.6 mmHg; p<0.0001) and RV mean power (0.97 0.56 vs. 0.53 0.22 W;
p¼0.009) were higher in patients with an open ASD. The change in RV FAC from rest to peak exercise was related to
peak mPAP in open (R¼0.589; p¼0.010) and closed (R¼0.450; p¼0.021) ASD patients.
Conclusion: RV mean power during exercise is higher in patients with an open than in patients with a closed ASD. The
workload of the RV in patients with an open ASD is higher at rest due to a left-to-right shunt, at peak exercise due to an
additional increase in mPAP. A higher increase in afterload may affect RV function during exercise.
Keywords
Atrial septal defect, exercise, pulmonary circulation, right ventricular function
Received 19 January 2012; accepted 15 March 2012
Introduction
Atrial septal defect (ASD) type secundum is a common
congenital heart defect with an estimated birth preva-
lence of 1.43 per 1000 births and an expected probabil-
ity of survival into adulthood of 97%.
1,2
Because of a
higher compliance and therefore lower end-diastolic
pressure in the right ventricle (RV), these patients ini-
tially present with a left-to-right shunt causing what is
considered to be a pure volume overload of the RV and
pulmonary circulation.
3
This volume overload causes a
dilatation of the RV and will eventually lead to RV
systolic dysfunction.
4
The energy used by the RV to pump blood in the
pulmonary circulation is called the extrinsic hydraulic
power and consists of oscillatory power and mean
power. Although oscillatory power in the pulmonary
circulation is considerable and proportional to
mean power, it does not contribute to blood flow.
5
University Hospitals Leuven, Leuven, Belgium
Corresponding author:
Werner Budts, Congenital and Structural Cardiology, University
Hospitals Leuven, Herestraat 49, B-3000 Leuven, Belgium
Email: werner.budts@uz.kuleuven.be
European Journal of Preventive
Cardiology
0(00) 1–8
!The European Society of
Cardiology 2012
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DOI: 10.1177/2047487312444372
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Mean power is the energy per time expended to
produce a steady flow and is the product of mean
pulmonary artery pressure (mPAP) and mean flow
6,7
Little is known about mean power of the RV in patients
with open ASD at rest and during exercise.
The RV is able to sustain a volume load for a long
period of time, but poorly tolerates increases in after-
load. Patients with an open ASD or an ASD closed
later in life present with a steeper increase in PAP
during exercise,
8
which may translate into increases in
wall stress, coronary perfusion, and oxygen extraction
in the RV.
9
Although a few studies have evaluated RV
function during exercise,
10–13
they failed to address
whether this is influenced by different changes in
afterload.
This study aimed at evaluating (1) right ventricular
(RV) mean power during exercise, (2) the contribution
of flow and pressure to RV mean power, and (3) the
impact of pulmonary artery pressure on RV function
during exercise.
Materials and methods
Study population
In total, 20 patients with open ASD, all scheduled
for repair (10 males and 10 females, mean age
39.3 17.5 years) and 30 with closed (seven males
and 23 females, mean age 42.4 16.8 years, mean
age at repair 35.6 20.0 years) ASD type secundum
gave informed consent to participate in the study.
Patients were consecutively enrolled in the outpatient
clinic of congenital heart disease of the University
Hospitals of Leuven. Patients younger than 17
years and patients with known coronary artery
disease, significant valvular diseases other than mild
tricuspid or mitral regurgitation, pulmonary disease,
a history of pulmonary embolism, or concomitant
congenital heart disease were excluded from the
study. Patients with a history or current arrhythmias
were also excluded. The University Hospitals
Leuven Institutional Review Board approved the
study and informed consent was obtained from all
patients.
Transthoracic echocardiography
Echocardiography was performed with a Vivid 7 or 9
ultrasound system (General Electric Vingmed
Ultrasound, Horten, Norway) equipped with a 3-MHz
transducer and tissue Doppler imaging technology.
Before exercise, a complete resting echocardiography
study was performed in the supine position in all stand-
ard views. Two-dimensional, Doppler, and tissue
Doppler images were digitized for off-line analysis
using dedicated software (EchoPac BT08; General
Electric Vingmed Ultrasound).
Bicycle stress echocardiography
Exercise echocardiography was performed on a semi-
supine ergometer (Easystress, Ecogito Medical, Lie
`ge,
Belgium). The exercise table was tilted laterally by
20 30to the left. The protocol started at 25 W with
an increment of 25 W at every 2-min stage, until the
maximum tolerated load. Blood pressure and 12-lead
electrocardiogram were recorded at rest and at every
2 min during exercise. A single observer performed
the on-line and the off-line analyses. All measurements
were made in triplicate and results are presented as
means.
Hemodynamic calculations
Right ventricular (RV) and left ventricular (LV) stroke
volume and cardiac output were calculated from the
outflow tract diameter and flow velocity time integral
in the outflow tract of both ventricles respectively. The
diameter of the outflow tract was assumed to remain
constant throughout exercise. Systolic pulmonary
artery pressure (sPAP) was calculated from tricuspid
regurgitant velocities using the simplified Bernoulli
equation (4 velocity squared) without addition of
right atrial pressure estimates. During exercise echocar-
diography, RV cardiac output was recorded at each
stage. sPAP was measured with contrast enhancement
using agitated geloplasma as previously validated at
rest and during exercise.
14–16
RV mean power was
calculated as the product of mean RV cardiac output
and mPAP. For the purpose of calculating RV mean
power, mPAP was calculated as 0.6 systolic
PAP þ2.
17
Power was expressed in Watts, with
1W¼7.5 10
3
mmHg.ml/s. RV fractional area
change (FAC) was obtained by tracing the RV end-
diastolic area (DA) and end-systolic area (SA) in the
apical 4-chamber view using the formula (DA–SA)/
DA 100.
18
Cardiopulmonary exercise test
Supine exercise testing was performed on a bicycle erg-
ometer (Ergometrics 800S; Ergometrics, Bitz,
Germany) with the room temperature stabilized at
18–22C. The initial workload of 20 W was increased
by 20 W every minute until exhaustion. A 12-lead elec-
trocardiogram (Max Personal Exercise Testing,
Marquette, Wisconsin, USA) and respiratory data
through breath-by-breath analysis (Oxygen AlphaR;
Jaeger, Mijnhardt, Bunnik, The Netherlands) were con-
tinuously registered. Cuff blood pressure measurements
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were obtained at 2-min intervals during exercise, at
peak exercise and at 2 and 4 min after exercise.
Oxygen saturation was monitored by pulse oximetry
throughout the study. Prior to each test, spirometric
measurements were obtained. The exercise testing was
calibrated before each test. Oxygen uptake (VO
2
) was
determined from continuous measurement of oxygen in
the inspired and expired air. Peak oxygen consumption
(peak VO
2
) was obtained and expressed as percentage
of the predicted value according to age, gender, and
size.
19
Statistical analysis
We analysed the data using SPSS for Windows version
16 (SPSS, Chicago). Descriptive data for continuous
variables are presented as means SD or as medians
with ranges, when appropriate. Descriptive data for
discrete variables are presented as frequencies or per-
centages. Continuous variables were evaluated between
subgroups using independent Student’s t-test.
Proportions were evaluated between subgroups using
chi-squared analysis.
For linearity assessment between VO
2
, RV cardiac
output, and RV mean power, a Poon-adjusted mean
slope for each subgroup was calculated, allowing for
similar linear or mildly non-linear data from different
subjects to be grouped together while effectively mini-
mizing intersubject variabilities.
20
For each measure,
there were at least three values from which to derive a
linear regression. Slope values were then used for
between group comparisons (independent t-test) and
the mean values are quoted for each relationship.
Open and closed ASD patients were stratified into
two groups according to the median change in RV FAC
from rest to peak exercise. All tests were two-sided and
p<0.05 was considered statistically significant.
Results
Patient characteristics
Patient characteristics are summarized in Table 1. Four
patients with open ASD and eight patients with closed
ASD were taking beta-blockers. There tended to be less
female patients in the control group when compared to
patients with a closed ASD. Invasive haemodynamic
measurements showed no evidence of pulmonary
hypertension at rest.
Relation between oxygen uptake (VO
2
) and haemo-
dynamic parameters during exercise
There was a strong linear relation between RV cardiac
output and VO
2
in patients with an open ASD
(R
2
¼0.88; p<0.0001) and a closed ASD (R
2
¼0.90;
p<0.0001). However, the slope of the relation was sig-
nificantly different in patients with a open ASD
(p¼0.001) when compared to patients with a closed
ASD, indicating that RV cardiac output increases
more rapidly with increasing VO
2
in patients with an
open ASD (Figure 1). A linear relationship between
mPAP and VO
2
was present in patients with an open
(R
2
¼0.86; p<0.0001) and a closed (R
2
¼0.88;
p<0.0001) ASD. Patients with an open ASD had a
significantly steeper slope when compared to patients
with a closed ASD (p¼0.002). There was a highly
linear relationship between RV mean power and VO
2
in patients with an open ASD (R
2
¼0.88; p<0.0001)
and a closed ASD (R
2
¼0.90; p<0.0001). However,
RV mean power increased more rapidly in patients
with an open ASD than in patients with a closed
ASD (p<0.0001). Figure 2 indicates that in order to
increase oxygen uptake to 1 l/min, the RV had to
develop 0.53 W in patients with a closed ASD and
0.86 W in patients with an open ASD.
Table 1. Clinical and standard echocardiographic parameters
Open ASD
(n¼20)
Closed ASD
(n¼30) p-value
Age (years) 39.3 17.5 42.4 16.8 0.527
Male gender (%) 50 23 0.051
Defect size (mm) 18.2 7.1 16.8 4.9 0.447
Qp:Qs invasive 1.8 1.0 1.8 0.8
a
0.999
Qp:Qs echo 1.6 0.7 – –
BMI (kg/m
2
) 25.1 4.7 26.0 5.0 0.503
SBP (mmHg) 117 16 120 16 0.573
DBP (mmHg) 76 10 72 11 0.176
HR (bpm) 76 12 71 12 0.217
sPAP (mmHg) 23.8 6.0 22.5 6.2 0.492
Mean PAP (mmHg) 19.3 3.6 18.5 3.7 0.492
TAPSE (mm) 29.0 5.9 23.6 5.0 0.001
RV end-diastolic
area index (cm
2
/m
2
)
16.4 5.0 12.7 2.3 0.005
RV end-systolic area
index (cm
2
/m
2
)
10.7 2.5 8.5 1.4 0.002
RV FAC (%) 53.0 19.0 48.8 12.5 0.348
RV SV index (ml/m
2
) 49.8 13.9 39.2 10.0 0.003
RV CI (l/min/m
2
) 3.4 1.0 2.4 0.5 <0.0001
LV EF (%) 60 5626 0.226
Peak VO
2
(%pred) 78 18 88 17 0.072
Values are mean SD.
a
Shunt ratio before ASD repair. BMI, body mass
index; CI, cardiac index; DBP, diastolic blood pressure; FAC, fractional
area change; HR, heart rate; LVEF, left ventricular ejection fraction;
(s)PAP: (systolic) pulmonary artery pressure; Qp:Qs, shunt ratio; RV,
right ventricular; RVSP, right ventricular systolic pressure; SBP, systolic
blood pressure; SV, stroke volume; TAPSE, tricuspid annular systolic
excursion; VO
2
, oxygen uptake.
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26
RV cardiac output (L/min)
24
22
20
18
16
14
12
10
8
6
0.0 0.5 1.0 1.5 2.0
VO2 (L/min)
Open ASD
Y = 4.7x + 3.5
Closed ASD
Y = 6.4x + 4.7
2.5 3.0 3.5 4.0 4.5
4
2
0
Figure 1. Relationship between right ventricular (RV) cardiac output and VO
2
in patients with an open or closed atrial septal defect
(ASD). Blue, open ASD; Red, closed ASD. The full line represents the mean value of the regression lines of each individual patient. The
mean slope in open ASD patients is significantly higher than in closed ASD patients (p¼0.001).
2.7
2.4
2.1
RV mean power (Watt)
1.8
1.5
1.2
0.9
0.6
0.3
0.0
0.0 0.5 1.0 1.5 2.0
VO2 (L/min)
Open ASD
Y = 0.83x + 0.03
Closed ASD
Y = 0.47x + 0.06
2.5 3.0 3.5 4.0 4.5
Figure 2. Relation between right ventricular (RV) mean power and VO
2
in patients with an open or closed atrial septal defect (ASD).
Blue, open ASD; Red, closed ASD. The full line represents the mean value of the regression lines of each individual patient. The mean
slope in open ASD patients is significantly higher than in closed ASD patients (p¼0.001).
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Contribution of RV cardiac output and mPAP to the
mean power
At rest, patients with an open ASD had a higher RV
cardiac output (6.8 2.3 vs. 4.4 1.0 l/min; p<0.0001),
a similar mPAP (19.7 3.9 vs. 18.4 3.7 mmHg;
p¼0.237), resulting in a significantly higher mean
power (0.30 0.14 vs. 0.18 0.05 W; p¼0.001) when
compared to patients with a closed ASD. At peak exer-
cise, patients with an open ASD had a higher RV car-
diac output (14.2 4.3 vs. 10.1 2.8 l/min; p¼0.002)
and a higher mPAP (41.3 10.2 vs. 31.4 5.4 mmHg;
Peak VO2 (mL/min)
Delta RVFAC (%)
4500
4000
3500
3500
2500
2000
1500
1000
500
–12.5–10.0 –7.5 –5.0 –2.5 0.0 2.5 5.0 7.0 10.0 12.5 15.0 17.5 20.5 22.5
Closed ASD
R=0.635; P<0.0001
Open ASD
R=0.517; P=0.033
Figure 3. Delta right ventricular RVFAC is related with peak VO
2
in patients with open and closed atrial septal defect (ASD).
60
50
40
30
20
10
0
60
50
40
30
20
10
0
*
*
Rest
*P<0.05 versus DRV FAC >5%
Closed ASD - RVFAC and mPAP rest and peak exercise
ΔRV FAC ≤5%
ΔRV FAC >5%
mPAP (mmHg)
RVFAC (%)
Peak Rest Peak Rest Peak Rest Peak
Figure 4. If right ventricular RVFAC increases 5% from rest to peak exercise, open and closed atrial septal defect (ASD) patients
present with a significantly higher mean pulmonary artery pressure (mPAP) at peak exercise.
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p<0.0001), resulting in a higher mean power
(1.276 0.58 vs. 0.71 0.25 W; p¼0.002) when com-
pared to patients with an closed ASD. Whereas the
change in RV cardiac output (7.1 3.4 vs. 5.7 2.4 l/
min; p¼0.132) was not statistically different, the
change in mPAP (21.7 9.6 vs. 12.8 4.6 mmHg;
p<0.0001) and RV mean power (0.99 0.58 vs.
0.54 0.22 W; p¼0.009) were significantly higher in
patients with an open ASD when compared to patients
with a closed ASD.
RV function during exercise and peak mPAP
In open ASD patients, RV FAC increased from rest to
peak exercise (43.8 6.2 to 48.4 9.7%; p¼0.020).
The change in RV FAC was related to mPAP at peak
exercise (R¼0.589; p¼0.010) and peak VO
2
(R¼0.517; p¼0.033), but not with RV mean power
at peak exercise (R¼0.027; p¼0.926). In closed
ASD patients, RV FAC increased from rest to peak
exercise (42.6 7.1 to 48.7 8.4%; p<0.0001). The
change in RV FAC was related to mPAP at peak exer-
cise (R¼0.450; p¼0.021) and peak VO
2
(R¼0.635;
p<0.0001), but not with RV mean power at peak exer-
cise (R¼0.076; p¼0.724) (Figure 3). Open and closed
ASD patients who increase RV FAC with 5% present
with a significantly higher mPAP at peak exercise when
compared to patients with an increase in RV FAC
>5% (Figure 4).
Discussion
This study showed that (1) RV mean power increased
more rapidly with increasing oxygen uptake in patients
with an open ASD than in patients with a closed ASD,
(2) the increase in RV mean power during exercise in
patients with an open ASD was higher than in patients
with a closed ASD, mainly caused by a higher increase
in mPAP during exercise in patients with an open ASD,
and (3) change in RV FAC is inversely related with
peak mPAP.
Relation between oxygen uptake and haemodynamic
variables during exercise
The strong linear relation between cardiac output and
VO
2
has been shown before.
21,22
The slope of the rela-
tion is lower in patients with an open ASD because of
the presence of a left-to-right shunt. Moreover, the
linear relation between RV cardiac output and VO
2
in
patients with an open ASD as shown in Figure 1 indi-
cates that the size of the shunt decreases during exercise
which is consistent with earlier published reports,
23
but
in contrast with other studies.
24
The ratio of both
slopes (1.34) is lower than the mean value of the
invasively measured shunt ratio (1.8), although differ-
ences may be present because the shunt ratios were
measured under general anaesthesia before ASD clos-
ure.
25
There was a weaker linear relationship between
VO
2
and mPAP in patients with an open and closed
ASD. Exercise-induced pulmonary hypertension has
been recognized as a clinical entity,
26
but is not
included in the current pulmonary hypertension prac-
tice guidelines.
27
Indeed, whether the increase in mPAP
in some patients with an open ASD is due to the inabil-
ity to further decrease pulmonary vascular resistance at
high RV cardiac output or due to the development of
pulmonary vascular lesions is hard to determine.
8
The VO
2
-work relation describes how much work is
performed by the RV in relation to how much oxygen is
utilized by the exercising subject. Compared with
patients with a closed ASD, the increase in oxygen
uptake is considerably lower in patients with an open
ASD than the increase in oxygen uptake in patients
with a closed ASD. Figure 2 indicates that in order to
increase oxygen uptake to 1 l/min, the RV had to
develop 0.49 W in patients with a closed ASD in con-
trast to 0.86 W in patients with an open ASD.
Contribution of RV cardiac output and mPAP to RV
mean power
The higher RV mean power at rest in patients with an
open ASD is mainly determined by a higher RV cardiac
output due to left-to-right shunting. However, there is a
larger increase in RV mean power from rest to peak
exercise in patients with an open ASD than in patients
with a closed ASD. As the increase in RV cardiac
output is almost similar, the larger increase in RV
mean power in patients with open ASD is also deter-
mined by the larger increase in mPAP. Using the slopes
of the regression lines, it can be estimated that cardiac
output and mPAP are responsible for 77% and 23%
respectively of the additional workload on the RV in
patients with and open ASD. Therefore, there is not
only a volume load of the RV in patients with an
open ASD, but also a pressure overload during
exercise.
Change in RV function and peak mPAP during
exercise
Our study indicated that the change in RV FAC was
related to peak mPAP and exercise capacity. The
behaviour of, and interaction between, the right ven-
tricle and pulmonary circulation during exercise has
gained interest.
28
It has been shown that the impact
of exercise is greatest on the RV, with structural
changes being related to haemodynamic stressors
during exercise.
9,29,30
We previously showed that
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patients with an open ASD or an ASD closed later in
life present with a steeper increase in PAP during exer-
cise.
8
A steeper and higher increase in PAP during exer-
cise may be clinically relevant as the RV poorly
tolerates increases in afterload. Indeed, Holverda
et al.
31
showed RV stroke volume response to exercise
is related to PAP increase during exercise. Moreover, in
heart failure patients, Lewis et al.
32
showed that a steep
increment in PAP was related with reduced exercise
capacity and reduced survival. However, failure to aug-
ment PAP (after a steep initial PAP increase; suggestive
of RV dysfunction) was related with the worst progno-
sis. So, although the work requirement of the RV of
open ASD patients is higher mainly due to a left-
to-right shunt (volume load), the additional increase
in PAP (pressure load) may be the main cause of a
decreased RV contractile reserve (and exercise capacity)
in some patients, which should be taken into account
when advising on physical activity.
33
The supplementary files (available online only) give
more information on a male aged 64 years with closed
ASD and a female aged 40 years with open ASD. The
patient with the open ASD develops a higher PAP
during exercise. However, in contrast to the patient
with the closed ASD, there is no increase in RV func-
tion as measured by TAPSE and RV FAC.
Limitations
It is important to underline a few limitations of the
study. First, we used non-invasive echocardiographic
parameters that have been validated against invasive
measurements at rest and during exercise.
14,34
In
order to enhance tricuspid regurgitation Doppler sig-
nals, we used agitated geloplasma. Pulmonary artery
pressure was measured without assessment of right
atrial pressures. Second, RV FAC is an imperfect meas-
ure of RV function and dependent on the image quality
obtained. Third, RV outflow tract diameter was con-
sidered constant during exercise.
Conclusion
RV mean power during exercise is higher in patients
with an open than in patients with a closed ASD. The
workload of the RV in patients with an open ASD is
higher at rest due to a left to right shunt, at peak exer-
cise due to an additional increase in mPAP. A higher
increase in afterload may affect RV function during
exercise.
Acknowledgements
We would like to thank Dr DaHae Lee for her invaluable
contribution to the article. We would also like to express
our gratitude to Jan Meertens and Dirk Schepers for perform-
ing the cardiopulmonary exercise tests.
Funding
Alexander Van De Bruaene is supported by the Research
Foundation Flanders (FWO).
Conflict of interest
The authors confirm there is no conflict of interest.
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