From the Divisions of Circulatory Physiology (D.M., R.G., A.B.),
Cardiology (D.M., H.L., A.B.), and Cardiothoracic Surgery (E.R., K.C., M.F.,
M.O.), Columbia Presbyterian Medical Center, New York, NY.
Methods and Results—Exercise testing with
hemodynamic and respiratory gas measurements was
performed in 65 congestive heart failure (CHF) patients (age 53±10
years) and 20 LVAD patients (age 49±8 years). Peak
Conclusions—Hemodynamic measurements at rest and
during exercise are significantly improved in patients with devices
compared with those in ambulatory heart failure patients awaiting
cardiac transplantation. Similarly, the exercise capacity of device
patients is better than that of transplant candidates and in the
majority of patients is similar to that of patients with mild CHF.
The purpose of the present study was to compare upright exercise
hemodynamic and metabolic measurements in a
larger group of LVAD patients with those of ambulatory patients with
chronic severe heart failure.
Twenty LVAD patients (TCI HeartMate, Thermo Cardiosystems, Inc)
were studied. The mean age of the 18 men and 2 women was 50±9 years.
Ejection fraction averaged 18±4%. Seven patients had coronary
artery disease and 13 had cardiomyopathy. Eleven
patients had an electrical device and 9 a pneumatic device. Only 6
of these patients had a prior exercise test as evaluation for cardiac
transplantation. The LVAD patients were all moribund before device
implantation. Time since device implantation averaged 2.6 months, with
a range of 1 to 5 months.
The ages, left ventricular ejection fractions, and sexes of
the groups were comparable. All CHF patients were receiving treatment
with digoxin, diuretics, and vasodilators. In the LVAD group,
35% received digoxin and 45% received diuretic therapy. The
average dose of Lasix was 48 mg in the LVAD group versus 151 mg in the
CHF group. Only 40% of the device patients received vasodilators, with
15% receiving ACE inhibitors. Thus, the primary treatment
for the LVAD patients was the device, because medical therapy was
suboptimal.
The protocol was approved by the Committee on Studies Involving Human
Beings at Columbia University. Written informed consent was obtained
from all subjects.
Exercise Hemodynamic Study
The arteriovenous oxygen difference was calculated as
(arterial-venous O2
saturation)x(1.34 mL O2/g
hemoglobin)x(hemoglobin concentration). Arterial
O2 saturation was measured by oximetry (Ohmeda).
Hemoglobin concentration was measured by Coulter counter.
Pulmonary artery hemoglobin oxygen saturation was determined
with an Instrumentation Laboratories 282 Co-Oximeter. Cardiac output
was calculated from the Fick equation. Blood for lactate determination
was stored at 0°C and assayed with a spectrophotometric technique.
Normal values in our laboratory are <1.6 mmol/mL.
All tests for the LVAD patients were performed in the auto mode of the
device. Device output was recorded at rest and during exercise from
the measurement displayed on the power base unit. Fick cardiac outputs
were also obtained.
Statistical Analysis
The anaerobic threshold occurred at 67% of peak
Hemodynamic Measurements
Mean right atrial pressure tended to be lower in the LVAD patients at
rest and during exercise, but this did not reach statistical
significance. At peak exercise, mean right atrial pressure was 11
mm Hg in the CHF patients and 8 mm Hg in the LVAD patients.
In both the CHF and LVAD patient groups, pulmonary pressures
rose significantly with exercise (P<0.05 for all). However,
patients with severe CHF developed marked pulmonary
hypertension during exercise. In patients with CHF, mean
pulmonary artery pressure at rest averaged 28 mm Hg,
ranging from 11 to 51 mm Hg. At peak exercise, pulmonary
artery pressure averaged 48 mm Hg, ranging from 21 to 70
mm Hg. Mean pulmonary artery pressure was dramatically lower
at rest and throughout exercise in the LVAD patients (Figure 2
Cardiac output and cardiac index at rest and peak exercise were
significantly greater in the LVAD patients than the heart failure
patients. Cardiac index in the CHF patients rose from 2.1 to 3.8 L
· min-1 · m-2.
In the LVAD patients, in contrast, cardiac index rose from 2.6 to 5.8
L · min-1 ·
m-2. The cardiac output response to exercise for
the heart failure and LVAD patients is depicted in Figure 3
Echocardiography reveals that the aortic valve is
usually closed at rest during device support.4
With exercise, however, opening of this valve can be seen. Fick cardiac
output measures total cardiac output, whereas the LVAD sensor
measurement monitors flow through the device. Fick and LVAD sensor
measurements for each device patient at peak exercise are shown in
Figure 4
Ventilatory Measurements
The symptoms limiting exercise were comparable between the 2 groups of
patients (Table 3
Peak Exercise Performance
Before implantation of the device, all the device patients were
bedridden on multiple positive inotropic agents or temporary mechanical
support. The preimplant
The
The mechanism responsible for the delayed onset of the
anaerobic threshold may be improved skeletal muscle
perfusion and/or a training effect. With the improved cardiac output at
rest and throughout exercise, it is likely that skeletal muscle
perfusion was enhanced. Moreover, the vasodilatory capacity of the
patients on mechanical support has been shown to improve with the
duration of support. Unfortunately, no invasive or noninvasive measures
of limb perfusion were made during these exercise studies. Future
studies with measurement of skeletal muscle perfusion in these patients
are needed. All the device patients were enrolled in a cardiac
rehabilitation program after device
implantation.9 The timing of the
anaerobic threshold at >70% of peak
The measured peak
In the LVAD patients, the Fick cardiac output was significantly
greater than sensor measurements. Echocardiographic
studies demonstrate that the aortic valve is usually closed at
rest. With stress, there is an increased opening of the aortic valve
and thus a contribution from the native heart.4
The increase in Fick cardiac output over the device measurement may be
a useful parameter to evaluate myocardial recovery. The
increment in Fick cardiac output over device output ranged from none to
10.3 L/min. Two patients with dilated
cardiomyopathy in whom the Fick cardiac output
exceeded device output by 7.4 and 6.4 L/min, respectively, were
subsequently successfully explanted, ie, the device was removed without
transplantation. In 1 patient in whom Fick cardiac output was >10
L/min higher than that with the LVAD sensor, myocardial recovery at the
time of transplantation could not be evaluated because of surgical
difficulties. Conversely, a reduction in the Fick cardiac output versus
the LVAD sensor may also provide useful clinical information regarding
either device malfunction or native aortic insufficiency. In 2
patients, Fick cardiac output was less than that with the device. One
of these patients had moderate to severe aortic insufficiency that
necessitated reoperation.
Exercise Hemodynamic and Ventilatory
Measurements
During exercise, patients with heart failure have an excessive
ventilatory response, possibly due to early onset of lactic acidosis,
ventilation-perfusion mismatch from hypoperfusion leading to an
increase in dead space ventilation, or respiratory muscle
dysfunction.13 14 15 Surprisingly, the ventilatory
response to exercise was similar between the 2 groups. Relief of
pulmonary hypertension achieved with LVAD therapy had no impact
on the chronic ventilatory response to exercise. This finding is
consistent with prior reports that acute vasodilation does not
affect the ventilatory response in patients with chronic heart
failure.16
The improvement in cardiac output provided by the device could
alleviate dyspnea by mechanisms involving both the
peripheral skeletal muscle and lung
perfusion.17 Despite the improved
hemodynamics at rest and throughout exercise provided
by the LVAD, levels of perceived dyspnea during submaximal workloads
only tended to be less in LVAD patients. The absence of any significant
improvement in the level of dyspnea or ventilation in the LVAD patients
suggests that these abnormal responses may be due to chronic changes in
the lungs or the periphery.
Study Limitations
Conclusions
Received January 29, 1998;
revision received May 5, 1998;
accepted May 20, 1998.
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Comparison of Exercise Performance in Patients With Chronic Severe Heart Failure Versus Left Ventricular Assist Devices
Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
References
Background—Left
ventricular assist devices (LVADs) are frequently used as a
bridge to cardiac transplantation and may be useful as long-term
therapy. The purpose of this study was to compare the exercise
performance of LVAD patients with that of ambulatory heart
failure patients. 
O2 was significantly higher in the LVAD
than the CHF patients (CHF, 12±3; LVAD, 15.9±3.8 mL ·
kg-1 · min-1;
P<0.001), as was the O2
at the anaerobic threshold (CHF, 8.1±2.1; LVAD, 12.2±2.9
mL · kg-1 · min-1;
P<0.001). At rest, mean arterial blood
pressure (CHF, 87±11; LVAD, 94±9 mm Hg) and cardiac output
(CHF, 4±1; LVAD, 4.9±0.9 L/min) were increased, whereas mean
pulmonary artery pressure (CHF, 28±11; LVAD, 18±4
mm Hg) and pulmonary artery wedge pressure (CHF, 16±10; LVAD
5±3 mm Hg) were reduced (all P<0.01). At peak
exercise, heart rate (CHF,125±24; LVAD, 148±24 bpm), blood pressure
(CHF, 87±14; LVAD,96±12 mm Hg), and cardiac output (CHF,
7.6±2.2; LVAD, 11.2±2.6 L/min) were higher (all
P<0.01), whereas mean pulmonary artery pressure
(CHF, 48±12; LVAD, 30±5 mm Hg) and mean pulmonary
capillary wedge pressure (CHF, 31±11; LVAD, 14±6 mm Hg) were
lower in the LVAD group (both P<0.001). In the LVAD
patients, Fick cardiac output was higher than LVAD flow sensor value
measurements (Fick, 11.6±2.5; LVAD, 8.1±1.2 L/min;
P<0.001).
Key Words: exercise • heart failure • heart assist device
Introduction
Top
Abstract
Introduction
Methods
Results
Discussion
References
Left
ventricular assist devices (LVADs) are increasingly used as
a bridge to cardiac transplantation and may represent a
permanent alternative therapy for the management of end-stage heart
failure.1 If chronic mechanical support is to
become a therapeutic option, it is important to assess the functional
capacity of device patients. Prior reports have described peak exercise
performance with measurement of oxygen consumption in only
small numbers of patients.2 3 4 5 Murali et
al,4 in a preliminary report, described peak
O2 in 7 patients with the
Novacor System. Peak O2
averaged 16 mL · kg-1 ·
min-1. Jaskie et al2
reported on 2 patients with Thermo Cardiosystems (TCI) devices with an
average peak O2 of 15.5
mL · kg-1 ·
min-1. We previously examined the submaximal and
maximal exercise performance in 14 patients with TCI LVADs
compared with patients with mild, moderate, and severe congestive heart
failure (CHF).5 Peak
O2 averaged 17.0±4.5 mL
· kg-1 · min-1.
Six-minute walk and peak O2 in
device patients were comparable to those in patients with mild CHF.
Jaski et al reported on exercise hemodynamic
measurements in 10 TCI patients during supine bicycle exercise.
O2 during supine exercise was
8.2 mL · kg-1 ·
min-1, and during upright exercise, it averaged
14.1 mL · kg-1 ·
min-1.3
Methods
Top
Abstract
Introduction
Methods
Results
Discussion
References
Subjects
Sixty-five patients referred for cardiac transplantation
participated in the exercise study (Table 1
). Forty-seven patients were male and 19
female. The mean±SD age was 53±10 years. Twenty-nine percent of
patients had NYHA class II, 65% had class III, and 6% had class IV
heart failure symptomatology. The pathogenesis of heart failure was
coronary artery disease in 29% of patients, dilated
cardiomyopathy in 63%, and end-stage
valvular disease in the remaining 8%. Left
ventricular ejection fraction averaged 22±9%. Peak
exercise oxygen consumption averaged 12.1±3.0 mL ·
kg-1 · min-1. All
patients were receiving treatment with digoxin, diuretics, and
vasodilators. Patients who were limited by angina or claudication were
not eligible for study. All patients had had a prior exercise test as
part of their transplantation evaluation. Eighty-two percent of the CHF
patients were accepted as transplant candidates, with only 6% being
considered too well (n=4) for transplantation.
View this table:
[in a new window]
Table 1. Clinical Characteristics of Heart Failure and
LVAD Patients
Studies were performed at least 4 hours after meals with the
patients on their chronic medical regimen. Under local
anesthesia, a Swan-Ganz catheter was inserted through the
internal jugular vein and positioned in the pulmonary artery.
Sixty minutes after instrumentation, the patient arrived in the
exercise laboratory. The subject then sat on a Monark ergometer and was
connected to a Medical Graphics 2001 Metabolic Cart via a
disposable Pneumotach. Oxygen consumption
(O2), carbon dioxide
production (CO2), and
minute ventilation were measured at rest and throughout exercise. A
pulse oximeter was placed to monitor arterial saturation
(Ohmeda). Resting pulmonary artery, pulmonary wedge,
and right atrial pressures and respiratory gases were measured, and
blood samples were obtained from the pulmonary artery for
oxygen saturation measurements. The transducer was positioned at the
level of the fourth intercostal space in the midaxillary line.
Arterial blood pressure was assessed by cuff
sphygmomanometry. After 3 minutes of rest, the patient began unloaded
bicycle exercise. Workload was increased by 25 W every 3 minutes until
exhaustion. Respiratory gas and heart rate measurements were made
continuously. Blood sampling for pulmonary artery saturation
and lactate, arterial blood pressure, pulse oximetry, and
Borg scale recordings for dyspnea and fatigue were performed
during the last 30 seconds of each exercise
stage.6 After termination of exercise, the
catheter was removed and the patient was discharged. Peak
O2 was defined as the average
O2 during the last minute of
exercise. O2 at the
anaerobic threshold was identified using the nadir of the
respiratory equivalent for
O2.
Statistical analysis was performed with t
tests, ANOVA, or 
2 analysis for
continuous and noncontinuous variables as appropriate.
Results
Top
Abstract
Introduction
Methods
Results
Discussion
References
Oxygen Consumption Measurements
O2 at the
anaerobic threshold and peak
O2 were significantly greater
in the LVAD than in the CHF patients (Figure 1). In patients with CHF, peak
O2 averaged 12.1 mL ·
kg-1 · min-1,
ranging from 6 to 20 mL · kg-1 ·
min-1 versus a peak
O2 of 16 mL ·
kg-1 · min-1 in
the device patients, with a range of 9.6 to 29.7 mL ·
kg-1 · min-1. The
O2 at the
anaerobic threshold in the LVAD patients (12.2 mL ·
kg-1 · min-1) was
greater than the peak O2 of
the CHF group (12.1 mL · kg-1 ·
min-1). Thus, the heart failure patients were at
peak exercise when the device patients were just becoming
anaerobic. Respiratory quotient at peak exercise was
similar between the 2 groups, indicating similar efforts (CHF,
1.12±0.1; LVAD, 1.14±0.1).
View larger version (14K):
[in a new window]
Figure 1. Oxygen consumption (VO2) at rest,
anaerobic threshold (AT), and peak exercise in CHF and LVAD
patients. O2 in the CHF and 76% of peak
O2 in the LVAD patients.
Resting and peak lactate levels were similar between the 2 groups
(Table 2).
View this table:
[in a new window]
Table 2. Rest and Exercise Metabolic and Hemodynamic
Measurements in the CHF and LVAD
Patients
Resting heart rates were comparable for the 2 groups (Table 2
). At
peak exercise, maximum heart rate was significantly higher in the LVAD
group (CHF, 125 bpm; LVAD, 148 bpm; P<0.001). This may
reflect the greater amount of work performed by LVAD patients versus an
improvement in baroreceptor function during exercise. Resting and peak
mean arterial blood pressures were significantly higher in
the LVAD patients, averaging 94 and 96 mm Hg at rest and peak
exercise, respectively, versus 87 at rest and peak exercise in patients
with CHF. ). Indeed, the peak mean
pulmonary artery pressure of the LVAD patients at 30
mm Hg approximated the resting value in CHF patients. Similarly,
resting and peak pulmonary capillary wedge pressures were
significantly lower in the LVAD patients. In CHF, pulmonary
capillary wedge pressures rose from 16 to 31 mm Hg. In the LVAD
patients, in contrast, pulmonary capillary wedge pressures rose
from 5 to 14 mm Hg. Figure 2 shows the mean pulmonary
capillary wedge pressures at rest and throughout exercise for the heart
failure and device patients.
View larger version (17K):
[in a new window]
Figure 2. Mean pulmonary artery pressure and
pulmonary capillary wedge pressure at rest and throughout
exercise in CHF and LVAD patients. .
View larger version (13K):
[in a new window]
Figure 3. Cardiac output response at rest and throughout
exercise in CHF and LVAD patients. . In the LVAD patients, peak Fick
cardiac output averaged 11.6 L/min and was significantly greater than
the sensor measurement of 8.1 L/min. Moreover, the difference between
the Fick cardiac output and LVAD sensor output was incremental with
exercise workload. The differences were 1.8±1.3, 2.0±1.1, 2.5±1.5,
and 3.6±1.9 at 0, 25, 50, and 75 W, respectively
(P<0.002). These findings suggest some contribution from
the native heart.
View larger version (16K):
[in a new window]
Figure 4. Fick and LVAD sensor cardiac outputs at maximal
exercise in mechanical support patients.
Patients with CHF have an excessive ventilatory response to
exercise that may be due to increased physiological
dead space ventilation, early lactic acidosis, or reduced lung
perfusion. Despite the improved hemodynamic
measurements, minute ventilation (E) was the same at
rest and throughout exercise in the CHF and LVAD patients (Figure 5).
E/CO2, the
ventilatory equivalent for CO2 production
at the anaerobic threshold, can also be used to assess the
ventilatory response to exercise normalized for
CO2 production. The
E/CO2 was
the same for both groups, averaging 39 (normal, 
27).
View larger version (11K):
[in a new window]
Figure 5. Minute ventilation during exercise in CHF and LVAD
patients. ). Thirty-five percent
of patients with LVAD and 23% of patients with CHF were limited by
dyspnea; 55% of patients with LVAD and 71% of patients with CHF were
limited by fatigue. Ratings of perceived dyspnea and fatigue in the CHF
and LVAD patients are shown in Table 4.
At submaximal and peak workloads, ratings of fatigue were lower in the
LVAD patients. However, perceived dyspnea was similar between the two
groups at submaximal and peak exercise.
View this table:
[in a new window]
Table 3. Symptoms Limiting Exercise
Performance
View this table:
[in a new window]
Table 4. Ratings of Perceived Fatigue and Dyspnea During and
at Peak Exercise in the CHF and LVAD
Patients
Discussion
Top
Abstract
Introduction
Methods
Results
Discussion
References
This study demonstrates that the exercise capacity of ambulatory
device patients as measured by peak
O2 is significantly greater
than that of ambulatory patients with severe heart failure. Additional
findings included a higher O2
at anaerobic threshold in the device patients, improved
hemodynamic measurements at rest and throughout
exercise, and a similar ventilatory response to exercise in the two
groups.
The peak O2 of the device
patients was similar to that in previous reports of patients with the
TCI or Novacor systems.2 3 4 5 However, this is the
first large comparison study of maximal upright exercise in patients
with mechanical assist devices versus patients with severe heart
failure. Peak exercise performance of the LVAD patients was
significantly greater than that of the patients with severe CHF.
Medical treatment of the device patients was minimal, with only 15% of
patients receiving ACE inhibitors; therefore, their level
of exercise performance was achieved almost exclusively from
device therapy. Whether additional medical therapy could further
improve the exercise performance of the device patients is
unclear; however, it is likely, particularly in patients with
significant right ventricular dysfunction. O2 of
these patients is essentially a resting oxygen consumption (ie, 3.5
mL · kg-1 ·
min-1). The increment in peak
O2 afforded by the device is
>10 mL · kg-1 ·
min-1. An increase of
O2 
2 mL ·
kg-1 · min-1 is
considered clinically significant. Thus, the improvement in exercise
performance of these device patients is extremely dramatic and
is similar to that observed after cardiac
transplantation.7 8 O2 at the
anaerobic threshold is significantly higher in the device
patients than in the CHF patients. Indeed, the LVAD patients were just
becoming anaerobic when the CHF patients were at maximal
exercise. Perceived fatigue at submaximal and maximal exercise was
significantly reduced in the LVAD patients, concordant with the delay
in the onset of anaerobic metabolism. This
finding suggests an improvement in endurance in the LVAD patients.
Submaximal exercise capacity is a better marker of endurance.
Previously, we used the 6-minute walk test to quantify
submaximal exercise performance in patients with mild to severe
CHF and LVAD patients.5 The submaximal exercise
performance of the LVAD patients was substantially better than
that of the patients with severe heart failure and similar to patients
with mild CHF. The delay in onset of anaerobic
metabolism would help to explain the observed improved
performance of the LVAD patients. O2 suggests that a training
effect may be operative in these patients. An anaerobic
threshold occurring at >70% of peak performance generally
indicates a training effect or submaximal performance. Because
the respiratory quotient at peak exercise in the LVAD group was >1.1,
it is unlikely that the delay in onset of the anaerobic
threshold was due to submaximal effort. O2 in the
LVAD patients, although significantly better than that in the heart
failure patients, is lower than predicted on the basis of maximum
device output. For example, in a man weighing 70 kg, peak
O2 should approach 25 mL
· kg-1 · min-1,
given a maximum device output of 10 L/min. Inability to achieve maximal
performance may be the result of peripheral
abnormalities and/or right ventricular dysfunction, which
is not treated with LVAD support. Some of the abnormalities in the
vasculature and/or skeletal muscle described in patients with heart
failure may be irreversible. Katz et al10
demonstrated an improvement in the vasodilatory capacity of the LVAD
patients but not a total normalization of the peak hyperemic
response. Several studies have focused on acute right heart function
after LVAD insertion, but none have described the effect of extended
LVAD support on right ventricular function. Unfortunately,
we do not have measurement of right ventricular function in
our LVAD patients. Future studies on the contribution of right
ventricular function to peak exercise capacity in these
patients is also warranted.
During exercise, patients with heart failure develop substantial
pulmonary hypertension.11 12 The marked
pulmonary hypertension observed in heart failure patients
during exercise was not observed in the device patients. Indeed, the
pulmonary pressures of the device patients at peak exercise
were similar to those of the heart failure patients at rest.
This study is limited in that consecutive LVAD and transplant
candidates did not undergo study. Many LVAD patients refused Swan-Ganz
catheterization. Many LVAD patients received
transplants before the exercise study was scheduled. Patients with CHF
on inotropic support were not studied, and CHF patients who were
considered too well for transplantation on the basis of NYHA class,
exercise performance, ejection fraction, and/or suboptimal
medical regimens did not undergo right heart
catheterizations. The random sampling of both groups
may have skewed the results.
Exercise performance of ambulatory LVAD patients 3
months after device insertion is significantly better than that of
ambulatory transplant candidates. Exercise performance in the
majority of LVAD patients is comparable to that of patients with mild
CHF. The increase in O2 is
comparable to that afforded by cardiac transplantation and better than
any single medical therapy. LVAD therapy may provide not only an
effective temporary bridge to transplantation but also appropriate
chronic therapy.
Footnotes
Reprint requests to Donna M. Mancini, MD, Division of Circulatory Physiology, Department of Medicine, Columbia Presbyterian Medical Center, 622 W 168th St, New York, New York 10032.
References
Top
Abstract
Introduction
Methods
Results
Discussion
References
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