CARDIOVASCULAR
Cardiac “Fitness” Training: An Experimental
Comparative Study of Three Methods of Pulmonary
Artery Banding for Ventricular Training
Emmanuel Le Bret, MD, PhD, Jean Marc Lupoglazoff, MD, PhD,
Nicolas Borenstein, DVM, Gaelle Fromont, MD, François Laborde, MD,
Jean Bachet, MD, and Pascal Vouhé, MD
Departments of Cardiac Diseases and Pathology, Institut Mutualiste Montsouris, and Pediatric Cardiac Surgery, Hôpital Necker
Enfants Malades, Paris, France
Background. When the left ventricle is unable to sus-
tain a systemic pressure in transposition of the great
arteries (TGA), left ventricular retraining is mandatory
before the morphologic left ventricle under the aorta is
switched. This is currently achieved by creating a ven-
tricular overload through pulmonary artery banding,
usually associated with an aortopulmonary shunt in case
of a TGA with an intact ventricular septum. Our experi-
mental study compared three different modes of in-
creased ventricular afterload to obtain ventricular
hypertrophy.
Methods. Fifteen lambs (mean weight 48 kg) under-
went pulmonary artery banding. Five animals (group I)
received a classic band; 5 (group II) received a classic
band which was adjusted at week 1 and 3; and 4 (group
III) received a band which was tightened for 1 hour,
twice a day (early morning and late afternoon). After 5
T he arterial switch operation (ASO) is the currently
preferred mode of treatment for transposition of the
great arteries (TGA) with an intact ventricular septum
(IVS) [1, 2]. After birth, progressive regression of the left
ventricular mass in TGA-IVS [3, 4] restricts the adequate
period for primary ASO to within the first [5] or second
months [6] of life. First described by Yacoub and col-
leagues in 1977 [7], left ventricular preparation has been
reported for a two-stage arterial switch in infants with
simple TGA [8 –10], but also when atrial baffles are
converted into ASO [11–12] or when a double switch
intervention for corrected transposition of the great ar-
teries is to be performed [12, 13].
Preoperative left ventricular retraining consists of pul-
monary artery banding (PAB), usually associated with an
aortopulmonary shunt in case of TGA with IVS. One of
the main limitations of this method is proper adjustment
of the PAB to obtain an adequate level of ventricular
constraint. For many authors, a minimum of two proce-
Accepted for publication June 25, 2004.
Address reprint requests to Dr Le Bret, Department of Cardiac Diseases,
Institut Mutualiste Montsouris, 42 Bd Jourdan, 75014 Paris, France;
e-mail: emmanuel.lebret@imm.fr.
© 2005 by The Society of Thoracic Surgeons
Published by Elsevier Inc
weeks, the lambs were evaluated hemodynamically be-
fore they were sacrificed and their hearts harvested for
histologic examination.
Results. No difference was noted in the hemodynamic
data between groups 1 and II. Group III showed a greater
ability to increase ventricular pressure in this model. No
significant difference was noted between the three
groups in terms of macroscopic alterations, but all ani-
mals demonstrated an increase in right ventricular wall
thickness compared with control animals. Several fibro-
sis areas were evident in group I and II but none in group
III.
Conclusions. Intermittent pulmonary artery banding is
able to induce hemodynamically sufficient ventricular
hypertrophy without fibrosis.
(Ann Thorac Surg 2005;79:198 –203)
© 2005 by The Society of Thoracic Surgeons
dures is necessary to adjust the pulmonary constriction
for good ventricular preparation [12].
To avoid those reinterventions, many authors have
developed various techniques of adjustable PAB [14 –19].
We have developed our own adjustable device, which
was used in the present experimental study [20]. How-
ever, the best technique to create an adequate ventricular
hypertrophy with an adjustable band that results in good
hemodynamic efficacy is not yet well defined yet. There-
fore, this study compared three protocols of PAB: perma-
nent, progressive, or intermittent (“fitness” banding) to
evaluate the differences in hemodynamic efficacy and
histologic alterations between the three methods.
Material and Methods
Animal Model and Anesthesia Protocol
Fifteen lambs (Ile de France), weighing from 35 to 61 kg
and 4 to 10 months old, were operated for PAB.
Anesthesia was induced with sodium thiopental (10
mg/kg intravenously) and maintained with a mixture
of isoflurane (Forene; Abbot, Rungis, France) (1% to
2%) and oxygen. Animals were ventilated through a
single lumen tube at 10 mI/kg with a volume-cycled
0003-4975/05/$30.00
doi:10.1016/j.athoracsur.2004.06.088
Ann Thorac Surg LE BRET ET AL 199

CARDIOVASCULAR
2005;79:198 –203 CARDIAC FITNESS

Table 1. Evolution of the Maximal Right Ventricular Pressure/Aortic Pressure Ratio During the Five Weeks of Training in
Each Group
Initial Data Max RVP/AoP Five Weeks Data Max RVP
Ratio /AoP Ratio
Student’s
Group Mean SD Mean SD t Test

I Fixed 0.58 0.1 0.86 0.35 NS

II Progressive 0.59 0.025 0.73 0.03 NS
III Fitness 0.73 0.06 0.81 0.08 NS

AoP ⫽ aortic pressure; Max RVP ⫽ maximal right ventricular pressure; SD ⫽ standard deviation.

ventilator at 20 breaths per minute and Fio2 60%.
Monitoring included continuous electrocardiographic
tracing, invasive blood pressure through the auricular
artery, and central venous pressure through the jugu-
lar vein. Anesthetized animals were reclining on the
right side for left lateral thoracotomy.
Pulmonary Artery Banding
After opening the chest through the fourth left intercostal
space, the pericardium was opened anterior and parallel
to the left phrenic nerve, and the pulmonary trunk was
dissected at its mid portion. The right ventricular pres-
sure was monitored by direct catheterization. Baseline
right ventricular pressure, pulmonary pressure, and
maximal right ventricular pressure were recorded.
In group I, (5 lambs) the PAB was achieved by using a
4 mm wide Dacron (DuPont, Wilmington, DE) band. The
degree of constriction was adjusted according to the
method described by Mee [21]. After tightening the band
acutely for 4 to 5 seconds and recording the maximal
right ventricular pressure, the band was loosened until
hemodynamic stability returned. The band was then
gradually tightened to achieve a right ventricular pres-
sure of about 70% to 80% of the previously observed
maximal pressure. The band was then fixed to the pul-
monary artery wall and hemodynamic stability was as-
sessed for 20 to 30 minutes before the chest was closed.
The lambs were left with the pulmonary artery banding
for 5 weeks.
In group II, (5 lambs) the first PAB was achieved
exactly in the same way as in group I, but all animals
were reoperated at week 1 and 3 to readjust the PAB. The
maximal right ventricular pressure was reassessed, and
whenever necessary, the band was retightened to achieve
a right ventricular pressure of about 70% to 80% of the
maximal right ventricular pressure. The total duration of
PAB was also 5 weeks.
In group III, (5 lambs), our adjustable pulmonary
artery band was used to perform the PAB [20]. The
balloon was snared around the pulmonary artery trunk,
the maximal right ventricular pressure was measured,
and sterile water was injected to inflate the balloon. The
volume of sterile water required to obtain a ventricular
pressure of about 70% to 80% of the maximal ventricular
pressure was noted for each animal. The balloon was
connected to the subcutaneous chamber placed on the
lateral face of the chest. In this group of lambs, ventric-
ular training was achieved by inflating the balloon for 1
hour twice a day (early morning and late afternoon) at
the level noted during implantation. Duration of training
was also 5 weeks. No statistical difference was noted
concerning weight and age of the animals in the three
groups.
Animal Care
After surgery and the following day, if needed, the
animals were left to recover with the required analgesic
regimen (morphine, 0.5 mg/kg; flunixin, 1 mg/kg).
The study was approved by the institutional ethics
committee for animal research, and all animals received
humane care in compliance with the Guide for the Care
and Use of Laboratory Animals prepared by the Institute of
Laboratory Animal Resources, National Research Coun-
cil, and published by the National Academy Press, re-
vised 1996.
Hemodynamic Exploration
After 5 weeks of training, the lambs were reanesthetized
and reoperated to remove the band and to record the
hemodynamic data. Under control of central venous and

Table 2. Evolution of the Maximal Right Ventricular Pressure/Initial Right Ventricular Pressure Ratio During the Five Weeks
of Training in Each Group
Initial Data Five Weeks Data
MaxRVP/iRVP ratio MaxRVP/iRVP
Student’s
Group Mean SD Mean SD t Test

I Fixed 1.89 0.52 2.32 0.55 NS

II Progressive 1.97 0.26 2.19 0.31 NS
III Fitness 2.23 0.35 3.23 0.66 p ⫽ 0.007

iRVP ⫽ initial right ventricular pressure; MRVP ⫽ maximal right ventricular pressure; SD ⫽ standard deviation.
 200 LE BRET ET AL Ann Thorac Surg
CARDIOVASCULAR

CARDIAC FITNESS 2005;79:198 –203

Table 3. Analysis of Variance (Bonferonni Test)

Max RVP /AoP Ratio Max RVP/iRVP
Bonferroni
Test Initial Data Five Weeks Data Initial Data Five Weeks Data

Gr I / Gr II NS NS NS NS
Gr III / Gr I NS NS NS p ⫽ 0.03
Gr III / Gr II NS NS NS p ⫽ 0.013

AoP ⫽ aortic pressure; iRVP ⫽ initial right ventricular pressure; Max RVP ⫽ Maximal right ventricular pressure; NS ⫽ not significant.

systemic arterial pressures, the right ventricular pressure Results

was measured and the maximal right ventricular pres-
sure was estimated by acute clamping of the pulmonary
trunk for a few seconds. Two ratios were calculated: the
maximal right ventricular pressure/systemic arterial
pressure ratio and the maximal right ventricular pres-
sure/initial right ventricular pressure ratio. These ratios
were compared with the equivalent ratios obtained dur-
ing the implantation of the band.
Histologic Studies
After recording the hemodynamic data, the animals were
sacrificed and the hearts were harvested for histologic
examination. They were compared to a control group of
nonoperated animals. Macroscopic data included the
weight, the size, and the right and left ventricular wall
thickness in fresh and fixed heart. Microscopic examina-
tion was particularly focused on evidencing fibrotic reac-
tions on the right ventricular free wall or on the inter-
ventricular septum. Histologic examination was carried
out in a blind fashion regarding the mode of training.
Statistical Analysis
Hemodynamic variables are expressed as mean ⫾ stan-
dard deviation. They were compared in each group by
means of the Student’s t test. As the Levene test for equal
variances was not significant when the results of the
different ratios were studied, we have compared the
three groups by an analysis of variance with the Bonfer-
roni test. Macroscopic data were compared by means of
the Student’s t test, and the existence of myocardial
fibrosis in each group was compared by means of the ␹2
test with the Yates adjustment for little subgroup (Fisher
test). Results were considered as significant if p was less
than 0.05.
Hemodynamic Results
The hemodynamic data are summarized in Tables 1 and
2. No differences were noted among the 3 groups in terms
of preoperative hemodynamic data. After 5 weeks of
training, the maximal right ventricular pressure/systemic
pressure ratio had significantly increased in the three
groups compared with the calculated baseline ratio. The
mean increment was 28%, 15%, and 18% in group I, II,
and III, respectively, without any significative difference
between the groups. The maximal right ventricular pres-
sure/basic right ventricular pressure ratio increased after
5 weeks of training. Student’s t test revealed that this
increase was not significant for groups I (p ⫽ 0.14) and II
(p ⫽ 0.32) but was significant for group III (p ⫽ 0.007).
Analysis of variance (Bonferroni) showed that the incre-
ment in group III was significant when compared with
group II (p ⫽ 0.013) and group I (p ⫽ 0.037). There was no
significant difference between group I and II (Table 3).
No hemodynamically adverse effect was noted con-
cerning the right ventricular function.
Histologic Results
MACROSCOPIC EXAMINATION. The results of the macroscopic
examination are reported in Table 4. To avoid variations
caused by the differences in the weight of the animals, all
data were indexed to the weight. Weights were compa-
rable in the three PAB groups and in the control group.
All three PAB groups demonstrated an increase in the
ventricular wall thickness compared with the control
group (p ⬍ 0.05), but no significant differences were
noted among the three groups. The left ventricular wall
thickness was similar in the three PAB groups.

Table 4. Histologic Results (Indexed Data)

RV Wall LV Wall
Heart Weight Thicknessa Thicknessa
Group (g/kg) (mm/kg) (mm/kg) Fibrosis

I: Fixe 4.9 (3.5–6) 0.18 (0.1–0.26) 0.29 (0.2–0.5) 2/5

II: Progressive 5.52 (4.41–6.9) 0.180 (0.12–0.22) 0.3 (0.26–0.4) 3/5
III: Fitness 5.62 (4.5–6.65) 0.175 (0.123–0.22) 0.3 (0.24–0.37) 0
Control 5.3 (4.9–6.1) 0.11 (0.09–0.14) 0.28 (0.24–0.4) 0
a
Expressed as mean and extremes values.
LV ⫽ left ventricle; RV ⫽ right ventricle.
Ann Thorac Surg
2005;79:198 –203
Fig 1. Trichrome-Masson staining shows the myocardial fibrosis in
blue. (A) Focal myocardial fibrosis is present in group I and II
(⫻20). (B) No fibrotic reaction in group III (⫻20).
MICROSCOPIC EXAMINATION. Fibrosis was noted in 2 patients
out of 5 in group I and in 3 patients out of 5 in group II.
Fibrosis was present on the septal portion of the right
ventricle in 1 patient and on the right ventricular wall in
4 patients (Fig 1). In each sample, no more than one
limited area of fibrosis (less than 2 mm in diameter) was
observed. No quantitative measurement was performed.
No area of fibrosis was noted in group III or in the control
group. No other morphologic differences were noted
among the groups.
Comment
When the concept of a two-stage arterial switch was
introduced in 1977, Yacoub and colleagues suggested
that this should allow anatomic correction of TGA to be
performed after the neonatal period (at a mean of 12 to 24
months). Others have reported successful left ventricular
“slow” retraining in patients until teenage or early adult-
hood [22]. However, a two-stage arterial switch has been
associated with a certain drawbacks:
LE BRET ET AL 201
CARDIOVASCULAR
CARDIAC FITNESS
● The incidence of aortic regurgitation (anatomic
pulmonary valve) is consistently higher in case of
PAB for left ventricular retraining than with a
primary repair [23].
● Sievers and colleagues have demonstrated that a
certain degree of dilatation of the pulmonary root
may occur in response to pulmonary banding [24].
● Several authors have reported the need for a tube
to reconstruct the pulmonary outflow tract after
the two-stage correction.
● The Lecompte maneuver can be performed for a
direct anastomosis after a short interval period of
preparation, but it seems to be very difficult in the
presence of adhesions after PAB.
● Most authors report the necessity of several inter-
ventions to adjust the pulmonary artery band.
All these shortcomings of left ventricular retraining had
led most authors to favor an early, rapid, two-stage
arterial switch whenever possible. It has also been re-
ported that, despite the reduced duration of pulmonary
artery banding, left ventricular retraining in an early
two-stage procedure may adversely affect myocardial
function in some patients.
Myocardial hypertrophy because of chronic pressure
overload is known to be associated with depressed ventric-
ular function in animals and adult humans, [25] although
the mechanism is unclear. The myocardial response to
hemodynamic constraint by myocyte hypertrophy results
in an increase in oxygen uptake and requires a proportional
growth of the mitochondria responsible for supplying en-
ergy. Although myocardial angiogenesis and coronary per-
fusion were reported to be preserved in young lambs with
pressure overload hypertrophy, limitations in coronary vas-
cular reserve have been observed in adult animal and
human models of pressure-overload hypertrophy.
In addition, the increment of the ventricular wall stress
contributes to the reduction in myocardial perfusion
especially in the subendocardial area. Ventricular hyper-
trophy secondary to acute pressure overload may be
associated with focal areas of necrosis and collagen
fibrosis [26, 27]. In the present study, this type of fibrosis
was observed in group I and II but not in group III. It
seems that the ventricular hypertrophy observed in this
“fitness” group remained adaptive, with no pathologic
consequences, mimicking the results observed in trained
athletes.
This experimental study has demonstrated that inter-
mittent PAB can produce almost the same results as
permanent or progressive pulmonary artery banding.
The hemodynamic results show that acute maximal right
ventricular pressure after 5 weeks of the “fitness” pro-
gram is higher than in the groups with regular PAB. The
results of the cardiac fitness group can be explained by
several observations made on athletes in training.
De Maria and colleagues in 1977 [28] reported a study
of 26 healthy subjects, 20 to 34 years old, who participated
in an 11-week program of endurance physical condition-
ing. The training sessions consisted of a walk-jog-run
program, designed to maintain the heart rate at 70% of
 202 LE BRET ET AL
CARDIOVASCULAR
CARDIAC FITNESS
exercise-determined maximum, for a 1-hour period, 4
days a week. Echocardiography was performed before,
during, and after the training program. The results of the
echocardiographic study indicated that physical condi-
tioning induced significant alterations in cardiac anat-
omy. The left ventricular end diastolic dimension was
increased, the left ventricular end systolic dimension was
decreased, and stroke volume and shortening fraction
were increased. The mean fiber shortening velocity and
left ventricular mass were also increased. Cardiac output
and peripheral vascular resistance were identical. This
study suggested that the mature human myocardium
also responds within days to an acute increase in work-
load. Similarly, Ehsani and colleagues [29] demonstrated
in 8 swimmers (17 to 19 years old), who were followed up
with weekly echocardiograms during a 9-week training
program, that the left ventricular mass increased from
84.1 to 103 g/m2 within only 1 week and then plateaued
for the remainder of the training period.
Interestingly, the reverse was observed with decondi-
tionning. The fact that the maximal result in terms of left
ventricular mass increment appears after only 1 week of
training has been also reported in left ventricular training
for two-staged arterial switch. For Boutin and colleagues
[9], the compensatory hypertrophy after pulmonary ar-
tery banding was almost complete after 7 to 10 days.
That intermittent cardiac fitness can train a ventricle
can be explained by molecular biology studies [30 –35].
As soon as 1968, Nair and colleagues [30] demonstrated
that banding of the adult rat aorta resulted in a rapid
increase in heart weight within 2 to 3 days. Within 48
hours, cardiac weight increased by a mean of 30% and
RNA content increased by 65%. The heart weight and
RNA content reached a plateau by the second or third
day. More precisely, gene expression of c-myc, c-fos
proto-oncogene, which regulates the growth of cardio-
myocytes, occurs in rat cardiac cells within 1 hour of an
acute pressure load. Similarly, hsp70, the gene of a major
heat shock protein that protects the cell under various
conditions, is also induced within 1 hour. Transcription of
c-myc, c-fos and hsp70 messenger ribonucleic acids
ceases within 24 to 48 hours, but the presence of the
related proteins in the nucleus may play a permissive
role in facilitating the hypertrophic response. Thus an
acute right ventricular pressure overload elicits a rapid
change in the gene expression and can initiate the
processus of cardiac hypertrophy.
After the 2-hour training done in group III, the stress
condition of the myocardium was released, and this rest
condition may have facilitated tissue oxygenation and
protein synthesis when compared with groups I and II.
Study Limitations
This study suffers from certain limitations: no molecular
biology study was done to measure the molecular re-
sponse, but such a study will be implemented in the near
future. In addition, no cellular count was done to evalu-
ate hyperplasia and angiogenesis. We think that such a
count would have been meaningless because the animals
Ann Thorac Surg
2005;79:198 –203
in this study were to old to show evidence myocardial
hyperplasia in response to ventricular training.
In conclusion, adequate training of a ventricle can be
obtained by an intermittent increase of afterload, similar
to fitness training. The probable mechanism is that the
hypertropic process initiates a molecular cascade that can
develop in good conditions during periods of rest and
optimal oxygen transfer and, therefore, without the de-
velopment of fibrosis related to ischemia. This mode of
training could represent a safe and effective method for
retraining the left ventricle in view of late arterial switch
for TGA.
This work was supported by a grant from the Fondation de
l’Avenir pour la Recherche Médicale Appliquée. The authors
wish to thank the members of the Centre d’Experimentation et
de Recherche Appliquée for technical assistance and collabora-
tion, and Fabrice Larrazet for statistical support.
References
1. Okuda H, Nakazawa M, Imai Y, et al. Comparison of
ventricular function after Senning and Jatene procedure for
complete transposition of the great arteries. Am J Cardiol
1985;55:530 – 4.
2. Prêtre R, Tamisier D, Bonhoeffer P, et al. Results of the
arterial switch operation in neonates with transposition of
the great arteries. Lancet 2001;9;357(9271):1826 –30
3. Bano-Rodrigo A, Quero-Jimenez M, Moreno-Granado F,
Gamallo-Amat C. Wall thickness of ventricular chambers in
transposition of the great arteries. J Thorac Cardiovasc Surg
1980;79:592–7.
4. Huhta JC, Edwards WD, Feldt RH, Puga FJ. Left ventricular
wall thickness in complete transposition of the great arteries.
J Thorac Cardiovasc Surg 1982;84:97–101.
5. Castaneda AR, Norwood WI, Jonas RA, Colan SD, Sanders
SP, Lang P. Transposition of the great arteries and intact
ventricular septum: anatomical repair in the neonate. Ann
Thorac Surg 1984;38:438 – 43.
6. Foran JP, Sullivan ID, Elliot MJ, de Leval MR. Primary
arterial switch operation for transposition of the great arter-
ies with intact ventricular septum in infants older than 21
days. J Am Coll Cardiol 1998;31:883–9.
7. Yacoub MH, Radley-Smith R, MacLaurin R. Two stage
operation for anatomical correction of transposition of the
great arteries with intact interventricular septum. Lancet
1977;1:1275– 8.
8. Jonas RA, Giglia TM, Sanders SP, et al. Rapid, two stage
arterial switch for transposition of the great arteries and
intact ventricular septum beyond the neonatal period. Cir-
culation 1989;80(suppl I):I203–I208.
9. Boutin CH, Jonas RA, Sanders SP, Wernovsky G, Mone SM,
Colan SD. Rapid two-stage arterial switch operation. Acqui-
sition of left ventricular mass after pulmonary artery band-
ing in infants with TGA. Circulation 1994;90:1304 –9.
10. Lacour-Gayet F, Piot D, Zoghbi J, et al. Surgical management
and indication of left ventricular retraining in arterial switch
for transposition of the great arteries with intact ventricular
septum. Eur J Cardio Thorac Surg 2001;20:824 –9.
11. Mavroudis C, Backer CL. Arterial switch after failed atrial
baffle procedures for transposition of the great arteries. Ann
Thorac Surg 2000;69:851–7.
12. Helvind MH, McCarthy JF, Imamura M, et al. Ventriculo-
arterial discordance: switching the morphologically left ven-
tricle into the systemic circulation after 3 months of age. Eur
J Cardiothorac Surg 1998;14:173– 8.
13. Devaney EJ, Charpie JR, Ohye RB, Bove EL. Combined arterial
switch and Senning operation for corrected transposition of the
Ann Thorac Surg
2005;79:198 –203
great arteries. Patient selection and intermediate results.
J Thorac Cardiovasc Surg 2003;125(3):500 –7.
14. Muraoka R, Yokota M, Aoshima M et Al. Extrathoracically
adjustable pulmonary artery banding. J Thorac Cardiovasc
Surg 1983;86:582– 6.
15. Solis E, Heck C, Seward J, Kaye M. Percutaneously adjustable
pulmonary artery banding. Ann Thorac Surg 1986;41:65–9.
16. Higashidate M, Beppu T, Imai Y, Kurosawa H. Percutane-
ously adjustable pulmonary artery band. J Thorac Cardio-
vasc Surg 1989;97:864 –9.
17. Ahmadi A, Rein J, Hellberg K, Bastanier C. Percutaneously
adjustable pulmonary artery band. Ann Thorac Surg 1995;
60:(6 Suppl):S520 –S522.
18. Leewenburgh BPJ, Schoof PH, Steendijk P, Baan J, Mooi WJ,
Helbing WA. Chronic and adjustable pulmonary artery
banding. J Thorac Cardiovasc Surg 2003;125(2):231–7.
19. Corno AF, Sekarski ??, Bernath MA, Payot M, Tozzi P, von
Segesser LK. Pulmonary artery banding: long term telemet-
ric adjustment. Eur J Cardiovasc Surg 2003;23(3):317–22.
20. Le Bret E, Bonhoeffer P, Folliguet T, et al. A new percutane-
ously adjustable, thoracoscopically implantable, pulmonary
artery banding: an experimental study. Ann Thorac Surg
2001;72:1358 – 61.
21. Mee RBB. Arterial switch for right ventricular failure follow-
ing Mustard or Senning operations. In: Stark J, Pacifico A,
eds. Reoperations in Cardiac Surgery. Heidelberg: Springer,
1989;217–32.
22. Padalino MA, Stellin G, Brawn WJ, et al. Arterial switch
operation after left ventricular retraining in the adult. Ann
Thorac Surg 2000;70:1753–7.
23. Gibbs JL, Qureshi SA, Wilson N, Radley-Smith R, Yacoub
MH. Doppler echocardiographic comparison of haemody-
namic results of one and two stage anatomic correction of
complete transposition. Int J Cardiol 1987;18:85–92.
24. Sievers HH, Lange PE, Arensman FW, et al. Influence of
two-stage anatomic correction on size and distensibility of
the anatomic pulmonary / functional aortic root in patients
LE BRET ET AL 203
CARDIOVASCULAR
CARDIAC FITNESS
with simple transposition of the great arteries. Circulation
1984;70:202– 8.
25. Panidis IP, Kotler MN, Ren JF, Mintz GS, Ross J, Kalman P.
Development and regression of left ventricular hypertrophy.
J Am Coll Cardiol 1984;3:1309 –20.
26. Bishop SP, Melsen LR. Myocardial necrosis, fibrosis, and DNA
synthesis in experimental cardiac hypertrophy induced by
sudden pressure overload. Circ Res 1976;39:238 – 45.
27. Weber KT, Janicki JS, Pick R, et al. Collagen in the hyper-
trophied, pressure-overloaded myocardium. Circulation
1987;75(suppl I):I-40 –I-47.
28. DeMaria AN, Neumann A, Lee G, Fowler W, Mason DT.
Alterations in ventricular mass and performance induced by
exercise training in man evaluated by echocardiography.
Circulation 1978;57:237– 44.
29. Ehsani AA, Hagberg JM, Hickson RC. Rapid changes in left
ventricular dimensions and mass in response to physical
conditioning and deconditioning. Am J Cardiol 1978;42:52– 6.
30. Nair KG, Cutilletta AF, Zak R, Koide T, Rabinowitz M.
Biochemical correlates of cardiac hypertrophy. Circ Res
1968;23:451– 62.
31. Izumo S, Lompre AM, Matsuoka R, et al. Myosin heavy
chain messenger RNA and protein isoform transitions dur-
ing cardiac hypertrophy. J Clin Invest 1987;79:970 –7.
32. Bauer EP, Kuki S, Zimmermann R, Schaper W. Upregulated
and downregulated transcription of myocardial genes after
pulmonary artery banding in pigs. Ann Thorac Surg 1998;
66:527–31.
33. Bauer EP, Kuki S, Arras M, Zimmerman R, Schaper W.
Increased growth factor transcription after pulmonary artery
banding. Eur J Cardiothorac Surg 1997;11:818 –23.
34. Di Donato R, Fujii AM, Jonas RA, Castaneda AR. Age-
dependent ventricular response to pressure overload. J Tho-
rac Cardiovasc Surg 1992;104:713–22.
35. Simpson PC. Role of proto-oncogenes in myocardial hyper-
trophy. Am J Cardiol 1988;62:13G.