Вспомогательное кровообращение с использованием скелетных мышц
Автор - один из наиболее известных в мире кардиохирургов, активно разрабатывающих теоретические и экспериментальные основы вспомогательного кровообращения с помощью
биологического скелетно-мышечного желудочка. В настоящей статье представлены результаты изучения в хроническом эксперименте на животных динамической кардиомиопластики,
аортомиопластики (контрпульсации) и скелетно-мышечного желудочка в целях органосохраняющего хирургического лечения кардиомиопатии. Также дан обзор современного клинического опыта и отдаленных результатов использования кардиомиопластики.
Ключевые слова:кардиомиопатии, сердечная недостаточность, динамическая кардиомиопластика, скелетно-мышечный желудочек
Клин. и эксперимент. хир. Журн. им. акад. Б.В. Петровского. 2017. № 3. С. 71-80.
Статья поступила в редакцию: 20.06.2017. Принята в печать: 07.07.2017.
Energy derived from the contraction of skeletal muscle has been used experimentally
and clinically to augment native heart function. Skeletal muscle is capable of efficient
transformation of chemical energy into mechanical
work. Investigators have shown that it is possible
to transform a fatigue-sensitive skeletal muscle
into a fatigue-resistant muscle capable of repeated
contractions over a sustained period of time.
Investigators have used this transformed muscle
in an attempt to assist the heart and circulation
in a number of novel ways.
Two methods of skeletal muscle cardiac assist -
cardiomyoplasty and aortomyoplasty have been used
clinically and will be discussed. Cardiomyoplasty
involves wrapping the latissimus dorsi muscle around
the cardiac ventricles and stimulating the muscle
during cardiac systole in an attempt to assist the
failing heart. Aortomyoplasty requires that skeletal
muscle be wrapped around the aorta and stimulated
during diastole to unload the failing ventricle.
A third approach to skeletal muscle cardiac
assistance uses skeletal muscle ventricles (SMVs),
which so far have only been used in laboratory animals. In contrast to the procedures already mentioned,
separate pumping chambers are constructed from
the muscle and then connected to the circulation in
various ways and used as auxiliary blood pumps.
Since Alain Carpentier and Juan Carlos
Chachques in Paris, France introduced clinical
dynamic cardiomyoplasty in 1985, an estimated
1000 patients have had these procedures worldwide
(Fig. 1) . Latissimus dorsi muscle is wrapped
around the heart and stimulated to contract in
synchrony with the cardiac ventricles. In the
phase II clinical trials conducted in the United
States under the auspices of FDA (Food and Drug
Administration), about 80-85% of hospital survivors
showed improvement in their signs and symptoms
for heart failure from several months up to a year
and sometimes much longer .
The phase III randomized clinical trial, again
under the auspices of the FDA, commenced in
June 1995 and ended in 1998. Slightly more than
100 patients entered this study which was designed
to determine similar improvement in the signs and
symptoms of heart failure as in the phase II trial
and also when compared with control (medically
treated) patients. There was no improvement,
however, in survival of the cardiomyoplasty patients
when compared to the medically randomized controls
followed for about two years. This fact and difficulty
in recruiting patients into the study resulted in
Medtronic, who was sponsoring the study, terminating
the phase III trial. This study was thought to
need outcomes from about 200 patients for valid
statistical comparisons. With Medtronic’s withdrawal
from the study and their decision to no longer
manufacture cardiomyostimulators, cardiomyoplasty,
from a clinical standpoint, was essentially abandoned
in the United States .
Some groups in other countries continue to
perform this procedure, using other available
cardiomyostimulators. As new clinical data and
laboratory research becomes available, it is possible
that there could be a resurgence of cardiomyoplasty.
In 2003, Benicio and colleagues reported on
long-term results with cardiomyoplasty. Their group
from Sao Paulo University in Brazil has been among
the leaders and has been one of the most reputable
groups in this field for many years. They presented
their results with cardiomyoplasty over a 10-year
period, and compared their results by patients who
were initially NYHA (New York Heart Association)
Functional Class III for heart failure versus those who
were Functional class IV. When cardiomyoplasty was
first performed, there was controversy as to whether
the latissimus dorsi muscle should be stimulated
with every heartbeat or every other heartbeat. Their
data clearly showed that over time the 1:2 mode of
stimulation was better. They concluded, based on the
marked improvement of the long term performance
of skeletal muscle obtained with a 1:2 stimulation
mode, that the use of cardiomyoplasty continues to
be justified as an alternative treatment for patients
with dilated cardiomyopathies .
In 2009 the French reported on a multicenter
experience (6 centers) with long term results of
cardiomyoplasty since the very first clinical case in
1985 to the last patient entered in the series in 2006.
This totaled 212 cardiomyoplasty procedures. Patient
all had preoperative symptoms of chronic heart failure
despite maximal medical management. The etiology was
ischemic (48%), idiopathic (45%), or other (7%). During
the follow up 88% of the hospital survivor’s patients
improved clinically. Hospital deaths occurred in 14%
of the patients and were related to the severity of the
preoperative heart failure symptoms. Late mortality
occurred in 99 patients due to heart failure (44%),
sudden death (37%), or non-cardiac causes (18%).
Cardiomyoplasty was combined with implantation of a
cardiac rhythm management system in 22 patients and
26 eventually underwent heart transplantation after
recurrent heart failure occurred. Long term functional
improvement was observed in most patients undergoing
cardiomyoplasty and the best outcome was achieved
in those with isolated right ventricular failure. The
authors concluded that dynamic cardiomyoplasty can
be considered a destination therapy or a mid to long
term bridge to heart transplantation .
Aortomyoplasty is a surgical procedure, where
the skeletal muscle is wrapped directly around the
aorta instead of the heart. This operation has been
performed in more than 29 humans worldwide and
shows some promise .
The muscle has been wrapped around the
ascending aorta just as it comes out of the heart or
wrapped around the descending aorta (Fig. 2). In the
animal laboratory sometimes the aorta is enlarged
with a patch to increase stroke volume as the muscle
contracts around it.
Because aortomyoplasty and cardiomyoplasty
work on different parts of the anatomy, the
muscle is trained to contract at different times.
In cardiomyoplasty, the muscle is stimulated to
contract at the same time as the heart ventricles. In
aortomyoplasty, the latissimus muscle is stimulated
to contract during diastole while the heart ventricles
are relaxing which is similar in principle to that of an
intraortic balloon pump.
One advantage this procedure has over
cardiomyoplasty is that the sick heart itself does not
need to be manipulated. In some cases, the heart is
so large that the latissimus muscle cannot even be
wrapped around it. In this case, cardiomyoplasty
would not be performed, but an aortomyoplasty could
be an option.
Skeletal Muscle Ventricle
Our laboratory has used the latissimus dorsi
muscle of dogs for construction of the SMV. Both the
right and left latissimi have been used, depending on
the type of assist to be performed. The operation is
begun by making an incision from the axilla to the tip
of the eleventh rib. The overlying platysma and soft
tissue are elevated from the muscle. The attachments
to the eleventh and twelfth rib are then incised. The
attachment along the posterior spinous processes is
then incised, taking care to include a wide margin of
the thoracodorsal fascia. The underlying collateral
blood vessels from the chest wall are then divided.
The muscle is fully mobilized up to its humeral
attachment, taking care to avoid injury to the
The thoracodorsal nerve is encircled with a
bipolar nerve lead, which is then connected to a nerve
stimulator and placed in a subcutaneous pocket over
the rectus abdominis muscle. Next, a thoracotomy
at the fifth intercostal space is performed to harvest
the pericardium, which will line the inner surface of
the SMV. The pericardium is then sutured to a Dacron
cuff that encircles a plastic mandrel, and the chest is
closed. The muscle is wrapped around the mandrel,
anchored by the Dacron cuff. Generally, one to two
wraps of the muscle are obtained. The thoracodorsal
fascia is oriented so that this firm tissue is sewn to
the Dacron cuff. Absorbable sutures are then used
to secure the layers of the muscle together and to
close the end of the muscle to form the apex of the
pumping chamber. The chamber is then sewn to the surrounding tissue. The SMV has thus been either
anchored in the subcutaneous tissue on the chest
wall or placed in an intrathoracic position after
excision of several ribs.
After mobilization of the muscle, there is relative
ischemia in the distal portion. This portion is not able
to increase its blood flow in response to the increased
demands of stimulation. Mannion and colleagues
showed that over the next 3 to 4 weeks, the muscle
gradually recovers its ability to increase its blood
flow in response to stimulation. We refer to this 3- to
4-week period as the period of vascular delay [5, 6].
The muscle is allowed to recover during this
vascular delay period and is then stimulated at 2 Hz
continuously over the next 5 to 7 weeks. Following
this period of electrical conditioning, the muscle
of the SMV has become fatigue resistant and can
be used to assist the native heart in a variety of
configurations. A second operative procedure is then
performed whereby the mandrel is extracted and the
SMV is connected to the circulation. A ventricular
sensing lead is placed on the myocardium, and the
SMV is stimulated to contract synchronously with the
heart, using an implantable cardiomyostimulator.
Skeletal Muscle Ventricles as Cardiac
Aortic Diastolic Counterpulsators
The following configuration represents the model
most studied in our laboratory. The SMV is connected
to the circulation using the bifurcated graft that is
anastomosed to the base of the SMV and then to two
locations on the descending thoracic aorta. The aorta
is ligated between the two limbs of the graft to obligate
blood flow through the circuit. A myocardial lead is
then used to sense the electrical activity of the native
ventricle, and an implantable cardiomyostimulator is
used to synchronize contraction to occur in cardiac
diastole (Fig. 3).
The contraction of the SMV during cardiac diastole has several useful purposes. First,
blood is pumped proximally and distally from the
descending aorta to the periphery. Second, because
the coronary arteries are perfused during diastole,
there is an increase in coronary artery flow. Finally,
relaxation of the SMV chamber at the end of diastole
provides a low-pressure system into which the native
heart is able to eject, decreasing the energy required
for the heart to pump blood, thereby decreasing the
heart’s oxygen consumption. These hemodynamic
improvements are similar to those produced with
an intra-aortic balloon pump. Representative figure
tracings are shown in Fig. 4.
Fig. 4. Pressure and
tracings recorded from the
longest surviving animal
at the time of connection
to the aorta (A), and after
1 year (B), 2 years (C),
and 4 years (D) in the
burst frequency is 33 Hz
at a 1:2 assist ratio.
Carotid P - pressure
measured at the carotid
artery. Fem P - blood
pressure measured at the
Early acute experiments showed that electrically
pre-conditioned SMVs were able to generate a power
output of 0.68×106 erg, which was approximately
half the power output of the native left ventricle and
roughly three times the power output of the right
ventricle . In 1987, Acker reported on experiments
involving five dogs that had SMVs constructed with a
modification of the SMV design . These chambers
had a cylindrical geometry with inflow and outflow
at opposite ends of the chamber. The SMVs were
then monitored over time while pumping blood
continuously in the circulation. These chambers
functioned as diastolic counterpulsators for up to
11 weeks. During periodic measurements of SMV
function, the burst frequency was increased from
chronic 25 Hz setting to 43 Hz and then to 85 Hz.
These pumps improved aortic flow by 29, 40, and
63% at 25, 43, and 85 Hz of thoracodorsal nerve
stimulation, respectively. Two-dimensional short-axis
echocardiograms of the SMB chambers were obtained;
they showed a 70, 90, and 100% decrease in the cross-
sectional area at the midpoint of the SMV as the
burst stimulation frequency increased. The decrease
in cross-sectional area was somewhat similar to the
ejection function of the SMV. These chambers, however,
were prone to thrombus formation, and although all
animals had a functional SMV at the time of death,
the two longest-surviving animals, 5 and 11 weeks,
demonstrated multiple splenic and renal infarctions at
the time of autopsy. Neither animal, however, showed
evidence of cerebral or coronary embolization.
Over the past decade, modification in the
diastolic counterpulsator model have allowed for
improvements in survival. In 1992, Mocek reported
on a series of four dogs that survived for more
than 6 months with an SMV pumping continuously
in circulation . One animal from this series
survived for 836 days but showed evidence of some
thrombus formation within the chamber at the time
The use of autologous pericardium as a blood-
SMV surface lining was then investigated as a
possible method of decreasing the incidence of
thrombosis. The animal’s pericardium was removed
at the time of the initial construction of the SMV
and wrapped around the mandrel before the muscle
wrap was applied. The tissue was oriented so that
the inner surface of the pericardium was in contact
with the plastic mandrel. When the mandrel was
removed several weeks later and the SMV connected
to the circulation at the second operation, the
blood came in contact with the inner surface of the
pericardium. Interestingly, there was no thrombosis
noted in either the group with autologous lining or
the control group (constructed with the inner layer
of the muscle serving as the contact surface for the
circulatory blood flow). However, the group with
the autologous lining demonstrated a significantly
reduced rate of rupture. Sixty-three percent of the
SMVs in the control group ruptured over time, as
compared to 0% in the group with autologous lining.
These investigators concluded that the autologous
pericardium improved the structural integrity of the
pumping chamber . One animal in the group was
electively sacrificed after continuously pumping
blood for more than 4 years. To our knowledge, this represents the longest reported survival - clinical or
experimental - with a functioning, indwelling cardiac
assist device of any type .
Thomas also demonstrated that it is possible to
line these chambers with autologous endothelial cells
and to retain the endothelial surface while the SMV
pumps blood in the arterial circulation. The animal’s
own jugular vein was used to obtain endothelial
cells. After the cells were harvested and grown in culture, the suspended cells were then delivered into
the space between the muscle itself and the plastic
mandrel at a separate surgical procedure . After
allowing several weeks for the endothelial cells to
grow and attach, a confluent monolayer of endothelial
cells was histologically shown to be present on the
inner surface of the pumping chambers. This group
also demonstrated that this same result could be
obtained by percutaneously injecting the suspended
endothelial cells into the space around the mandrel
. Finally, they showed that this endothelial cell
layer was retained after the SMV had pumped blood in
the arterial circulation for 3 h . We believe that
this was the first report of the endothelium remaining
intact on the surface of a heart assist device while
the device pumped blood in the circulation.
The aortic diastolic counterpulsator model has
been investigated in the setting of heart failure .
Because blood supply to the SMV muscle itself may
be impaired in the setting of low cardiac output, the
possibility of impaired SMV hemodynamic function
exists. Propranolol was used to induce heart failure,
and it was shown that the percentage improvement in
several hemodynamic parameters in this setting was
actually better than without propranolol with the SMV
functioning. Mean diastolic pressure increased 27.6%,
as compared to a 12.9% increase in the same group
of SMVs before the induction of heart failure. The
endocardial viability ratio, a ratio of myocardial oxygen
delivery to myocardial oxygen demand, also increased
28.7% in the setting of heart failure, versus an 11.2%
increase before heart failure induction. However, the studies were performed in an acute setting over 1 h,
and the animal’s cardiac output promptly returned to
normal upon discontinuation of the propranolol.
More recently, our laboratory used a stable
chronic heart failure model that allows evaluation
of the function of SMVs in the setting of chronic low
cardiac output. We used the rapid ventricular pacing
(RVP) technique in conjunction with the aortic
diastolic counterpulsator model. Patel examined
six dogs with pericardium-lined SMV’s created from
latissimus dorsi muscles. Each SMV was anastomosed
to the descending thoracic aorta with a two-limbed
bifurcated polytetrafluoroethylene (PTEE) graft after
the usual electrical conditioning period, and the
aorta was ligated between the limbs. The SMV was
stimulated to contract during diastole at a 1:2 to 1:3
ratio. Chronic heart failure was then induced over the
next 7 weeks with the initiation of rapid ventricular
pacing at 220 to 230 bpm. SMV contraction resulted
in augmentation of the diastolic pressure-time index
(DPTI) by 12.1% prior to initiation of RVP and by
33.6% after 7 weeks of RVP .
The rapid ventricular pacemaker was turned off
temporarily during measurement of the left ventricle
function, while the SMV was appropriately stimulated
with the cardiomyostimulator to again contract
synchronously with the heart in a 1:2 or 1:3 ratio.
In addition, significant afterload reduction was
demonstrated, with increases in peak left ventricular
ejection velocity of 22.7% and stroke volume of
6.2%. In three of the six animals coronary blood flow
was shown to be augmented by an average of 47.6%.
Guldner’s group in Germany has recently reported
success in chronic studies using an aortic diastolic
counterpulsation configuration somewhat similar to
ours but with a unique blood contacting chamber
device. They used the latissimus dorsi muscle of
the boer goat and reported pumping blood in the
circulation for up to 414 days .
Hooper and colleagues constructed SMVs and
connected the left atrium to the SMV and the SMV
to the aorta by using two valved conduits . In
this parallel circuit model, the left atrial pressure
served as the preload for the SMV. A portion of the
systemic cardiac output that would normally have
been pumped by the left ventricle (LV) was routed
through the parallel SMV circuit and pumped by
the contraction of the SMV. Thus, the work required
by the native heart was decreased even though
the net blood flow produced the LV and SMV were
similar to control. The SMVs in this configuration,
as in the aortic diastolic counterpulsator model,
are stimulated to contract during diastole because
contraction during systole would result in the SMV
attempting to eject against an afterload equal to
the systolic pressure generated by the LV. Acute
experiments over 3 h by Hooper showed that the
SMV was able to pump between 21 and 27% of the
cardiac output. Although these results showed
promise, we have not pursued this model in a
chronic setting because of our observation that
higher SMV preloads seem to be necessary for
optimal SMV performance.
Left Ventricular Apex-to-Aorta Model
In terms of hemodynamic augmentation, the left
ventricular apex-to-aorta model is a highly effective
experimental model for ventricular assistance, both in
vivo and via computer model . This model involves
construction of a SMV that is connected in circulation
by two valved conduits (Fig. 5) One conduit is placed
from the apex of the left ventricle to the SMV, and
the other joins the SMV to the descending thoracic
aorta. This model makes use of the higher pressure
generated by the left ventricle to serve as preload for
the SMV. In addition, when the SMV relaxes and the
left ventricle ejects into this low-pressure system,
the left ventricle is effectively “unloaded”. Figure 6
shows representative hemodynamic tracings of this
model after 1 year of functioning in circulation .
The blood flow to the muscle layers of the SMV
is also likely to be improved in the left ventricular
apex-to-aorta configuration when compared to that
of the aortic diastolic counterpulsator model. With
the left ventricular apex-to-aorta model, there is a substantial period of time during which the pressure
inside the SMV itself is much lower than the systemic
diastolic pressure. In contrast, with the aortic
diastolic counterpulsator model, the walls of the
pumping chamber are always exposed to a pressure
at least equal to the systemic arterial pressure, which
could potentially cause problems with impaired blood
flow to the SMV muscle layers.
Fig. 6. Hemodynamic
recording obtained after 1 year in circulation from
a canine with an SMV
positioned between the LV apex and the aorta. The
SMV is contracting at a 1:2
ratio with the native heart
and stimulated at a 33 Hz
burst frequency. Arrows
indicate effects of SMV
contraction in the pressure
and flow traces ECG - electrocardiogram;
LV - left ventricle; SMV - skeletal muscle
Initially, acute 3 h experiments were performed;
they showed significant improvement in the systolic
tension-time index, a measure of myocardial oxygen
demand, when the SMV was pumping . The
endocardial viability ratio was also significantly
improved. At the time of implant and at 1, 2, and 3
h in circulation, the ratio was increased by 68, 66,
62, and 63%, respectively. The SMV circuit in these
acute studies pumped 47% of the cardiac output.
Stevens and colleagues demonstrated a 31% increase
in cardiac output in chronic heart failure in dogs with
a left ventricular apex-to-aorta SMV of their own
design and constructed from the rectus abdominis
Fig. 7. SMV in LV apexto-
Pressure recordings were
made at the time
of connection of the SMV
to the systemic arterial
circulation. Transition from
the control state with the
SMV off to stimulation
at 33 Hz, 1:2 ratio, can be
seen, with corresponding
changes in the flow and
Subsequently, Thomas documented an SMV in
a left ventricular apex-to-aorta configuration that
was electively sacrificed after functioning well
for 1 year . In a chronic heart failure study,
skeletal muscle ventricles were constructed from the
latissimus dorsi muscle in 10 dogs. After conditioning,
the SMVs were connected to the left ventricle and
aorta with two valved conduits, and the SMV was
programmed to contract during diastole . At the
time of implantation, SMVs stimulated at 33 Hz and
in a 1:2 ratio, the power output of the SMVs was 59%
of left ventricular power output at 33 Hz and 93% at
50 Hz (Fig. 7). Animals survived 7, 11, 16, 17, 72, 99,
115, 214, and 248 days. Three deaths were directly
related to the SMV. In the animal that survived 248
days, SMV power output at 8 months with a 33 Hz
stimulation frequency and a 1:2 contraction ratio was
57% of left ventricular power output and 82% at 50
Hz. At a 1:1 contraction ratio, SMV power output was
97% and 173% of the left ventricle at 33 and 50 Hz,
respectively (Fig. 8).
Fig. 8. A. The SMV in the LV apex-
is contracting at 33 Hz at a 1:2 ratio (chronic
stimulation setting) with
the heart. The shaded
areas in the SMV flow trace
indicate SMV stroke volume
B. Pressure recoding made
after 248 days of pumping
blood continuously in the
circulation. The SMV is
at 50 Hz, 1:1 ratio
This study demonstrated that SMVs in a LV apex-to-aorta configuration are able to function effectively
in the circulation. Maintenance of significant power
output was confirmed in one animal at the one
year follow-up when the animal was then electively
sacrificed according to the studies protocol. Skeletal
muscle ventricles significantly unloaded the left
ventricle, resulting in decreases in the LV peak
pressure, LV end-diastolic pressure, the LV tension-
time index, and LV stroke and minute work. During
SMV contraction, flow was redirected from the LV
outflow tract and through the aortic valve instead of
through the SMV. Total systemic flow did not change
We have found that with the chronic model it
is desirable to narrow the aorta just above the
anastomoses of the efferent SMV conduit to the
aorta. By doing this, a slight pressure gradient in the
aorta occurs at this point, which allows some passive
flow of blood through the SMV system into the aorta
during every other cardiac cycle (ie, the unassisted beats) and thereby reduces the chances of blood
clot formation in the system. To determine whether
the redistribution of flow dynamics caused by this
50% constriction of the aorta would compromise
cerebral circulation during SMV contraction, a
flow probe was placed around the carotid artery
in one animal during a measure session. During SMV stimulation at 33 and 50 Hz, mean carotid
flow was 97.1 and 97.4% of control flow with
the SMV off.
The left ventricular apex-to-aorta configuration
is the most hemodynamically efficient model for left
ventricular assistance that we have tested.
Bridges showed that skeletal muscle ventricles
were effective in replacing the native right ventricle
. As with other series, the SMVs received 3 weeks
of vascular delay and 4 to 6 weeks of continuous
low-frequency electrical preconditioning at 2 Hz.
Larger mandrels (49 to 69 mL) were used in the
construction of these SMVs in an effort to improve
chamber compliance (ie, fewer muscle wraps
around the mandrel and, consequently, decreased
SMV wall thickness) so as to make it more suitable
to accommodate the low-pressure right-heart
circulation. At the second operation, valved conduit
grafts were used to route all systemic blood flow
from the superior and interior venae cavae to
these high-compliance chambers. Outflow from the
SMVs was returned to the pulmonary artery. Upon
stimulation of the SMV, the systolic blood pressure
increased to the 100 mm Hg range from a systolic
pressure of 50 to 60 mm Hg associated with passive
flow without SMV stimulation. The SMV stroke work
was 169 and 174% of the canine right ventricular
stroke work at 2 and 4 h of continuous pumping,
Despite the intriguing nature of these
experiments, our laboratory observed that the SMVs
seemed to function better at higher preload levels
than that achieved with the venous system alone.
Consequently, we developed a model where the
pressure generated by the native right ventricle was
used for the SMV pre-load . One valved conduit
connected the right ventricle to the SMV, and a
second valved conduit connected the SMV to the
pulmonary artery. The pulmonary artery was then
ligated proximal to the conduit to obligate right
ventricular flow through the SMV circuit. At 1 h, the
cardiac output of these animals increased by 27%
with the SMV stimulated, as compared to an increase
of 30% at 4 h with the stimulator off. Similarly, systemic arterial pressure increased by 12 and 13%
at 1 and 4 h, respectively. Further studies have
demonstrated that this model can continue to pump
effectively and augment the native circulation for up
to 16 weeks .
Dynamic Cardiomyoplasty (DCM)
Currently survival at 1 and 2 years stand around
72 and 60% respectively. Late postoperative
deaths were usually caused by progressive heart
failure and ventricular arrhythmia. Incorporation
of a cardioverter defibrillator into the device may
help to improve the outcome. Approximately 80%
of survivors report subjective benefits including
improvement in functional status (NYHA) and
quality of life. A survival advantage at 18 months
over medically treated controls had also been
demonstrated [2, 27]. However, such parameters
have not been matched by improvements in objective
measures such as haemodynamic and exercise
Although there are reports that patients with failing
hearts have benefited from aortomyoplasty, it should be
considered experimental, particularly until more clinical
cases are reported with long-term follow-up.
Skeletal Muscle Ventricles
Even though we have had our best long-term success
left ventricular apex-to-aorta configuration remains
the most hemodynamically efficient model. Although
several animals have survived for periods between 6
months and 1 year, the morbidity and mortality of this
model must be reduced significantly, and the model
must be tested during chronic heart failure prior to
attempting clinical studies.
The use of an autologous biologic pump would
obviate the need for patients to wear an external
power unit, and transformed skeletal muscle is an
efficient means of assisting the failing heart. With
continued study and refinement of technique, it is
hoped that SMVs will be available someday for clinical
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