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S. Large and J. O. Louca
tricle (or both) in patients who are moribund and not t
enough or have contraindications to a long-term
VAD.These devices aim to stabilise the haemodynamic
state until a more denitive decision for treatment can be
made and are usually used for no more than 7 days.
ECMO may also be used in patients who are haemodynamically compromised and is typically used for up to
30days.
• Medium-term MCS—usually pulsatile pumps, from
7 days to 3 months. These are used as a bridge to
transplantation.
• Long-term MCS are more exible and can be used for
bridge to transplantation or candidacy as well as destination therapy.
The second classication system used to describe LVADs
is based upon the type of pump they use. First-generation
pumps were typically pulsatile. Second-generation pumps
were either axial or pulsatile, which enabled them to be
shrunk and inserted more easily. Third-generation pumps use
a centrifugal pump which enables continuous blood ow and
further reductions in size, enabling them to be inserted into
the pericardium.
Indications
In the UK, there are two indications for LVAD insertion.
1. Low cardiac output, (a cardiac index <2.2 L/min/m2)
despite an adequate preload (central venous pressure of
>12 mmHg or pulmonary capillary wedge pressure>16mmHg) and further mechanical support required
either in the form of an intra-aortic balloon pump (IABP)
or inotropes for:- systolic blood pressure<90mmHg or
secondary organ dysfunction due to the inadequate cardiac output.
2. In patients who do not yet meet these criteria, but are
deteriorating at a rate which means they will be unlikely
to survive until transplantation.
ally inserted using a median sternotomy. After the median
sternotomy is performed, the pericardium is opened up as far
to the left as possible, which creates a pericardial ap that
can be placed over the right ventricle at the end of the procedure. The driveline (which connects the LVAD to the external power supply) exit site is prepared before heparinisation.
The driveline is tunnelled beneath the rectus muscle and
exits the body in the left upper quadrant, a few centimetres
below the costal margin. At this point, the patient is heparinised and placed onto bypass. The inow portion of the VAD
is inserted into the apex of the heart, should lie parallel to the
septum and point towards the mitral valve. In order to reliably insert the inow tract, the sewing ring is inserted into
the epicardial surface of the anterior LV wall two cm lateral
to the left anterior descending coronary artery. Twelve deep
sutures are then inserted into the sewing ring and myocardium. After which point, an X-shaped incision is made into
the LV wall and a LV punch is performed. After the inow
tract is established, the LV is inspected for damage to the
chordae tendinae and thrombi. The LVAD is then rotated so
that it points towards the right hemithorax. The outow tract
is sown as an end-side anastomosis to the greater curvature
of the ascending aorta.
More recently, the LATERAL trial demonstrated the benets of using a less invasive approach. It compared outcomes
of conventional median sternotomy VAD insertion to those
using either an upper hemisternotomy or a right anterior thoracotomy. The study found improved QoL and functional
capacity in patients who received their VAD using a more
minimally invasive technique (Figs.21.1, 21.2, 21.3, 21.4,
and 21.5).
Electrical
lead
Inflow
This will differ between countries. However, the indications are broadly similar given that VADs are used in patients
with reduced ejection heart failure with severe haemodynamic compromise.
Implantation oftheLVAD
Due to their size, rst-generation VADs were inserted into
either the peritoneal or preperitoneal cavity. However, as
VADs became smaller, they were able to be inserted into the
pericardium and anterior mediastinum. They are convention-
Pump
Outflow
Fig. 21.1 LVAD diagram
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ab
Fig. 21.2 (a) Artist’s illustration of placement of the sewing ring on the LV surface. (b) Left ventriculotomy within the sewing ring that allows
for inspection of the LV cavity
Complications
Whilst VADs are immensely effective in improving both survival and QoL, they are not without problems. Many of these
complications have since become less severe with the development of second- and third-generation VADs, however they
are still important clinical issues. These include thromboem-
bolic complications, infections, right ventricular insufciency in patients with LVADs, and signicant bleeding
which can necessitate blood transfusion. Blood transfusion,
infection, and the device itself can all contribute to the development of autoimmune antibodies which increase the risk of
rejection in the case of future transplants.
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S. Large and J. O. Louca
Fig. 21.3 Minimally invasive LVAD access in the lateral trial
DCDD heart transplantation
Pressure (mmHg)
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Fig. 21.4 DCD heart
transplantation
150
100
159
Vasopressor
vein cannulation
Fig. 21.5 A heart on the rig
Left internal jugular vein cannulation
Arch
vessels
clamped
Aortic arch
cannulation
Right femoral
Femoral
arteries
clamped
Reservoir
50
0
Anoxia
WLST
Onset
FWIT
Leukocyte
filter
Oxygenator
Roller pump
ECMO reperfusion start
Asystolic period
0:00 5:00 10:0015:00 20:00 25:00
Time (mins)
Onset
death
+5min = confirmed
death
Reperfusion
Reanimation
taNRP DCDD
heart workin
Cardiac
Total Articial Heart andBiventricular
Assisted Devices
Up until this point, we have only focused on LVADs. This is
due to the fact that they are much more commonly used and
present fewer challenges. However, a problem that has persisted across all generations in LCADs is right ventricular
insufciency. In fact, as LVADs have become more efcient,
the challenges facing the right ventricle have increased further. Therefore, one may be tempted to think that biventricular assist devices (BiVADs) and the total articial heart
(TAH*) would make attractive options in place of LVADs.
However, patients on BiVADs and TAH have a higher morbidity and mortality. This is in part because these patients are
often more unwell, but also because replacing the function of
both ventricles proves to be more challenging than simply
replacing the function of one. Both of these techniques are
associated with higher rates of stroke. However, given the
challenges of RV dysfunction with LVADs, this remains an
important, but challenging area of research.
*The total articial heart offers biventricular support via
an implantable pneumatic pump.
reanimation
g
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S. Large and J. O. Louca
DCD Transplantation
DCD differs from conventional donation after brain death in
that the circulation has arrested. In heart transplantation, this
is usually known as controlled DCD (as opposed to uncontrolled which is typically in patients who have had a cardiac
arrest—these patients are not usually suitable heart donors
but other organs such as kidneys can be used). It is estimated
that DCD heart transplantation can increase the number of
transplants performed by 50%. Therefore, DCD offers an
immensely attractive method to increase the number of
transplants performed.
Whilst DCD is still in its infancy globally, the results have
been massively encouraging. DCD is as effective as DBD
transplantation in terms of patient survival and graft
function.
1
A quick note on nomenclature. It is worth noting that
DCD transplantation was formerly referred to as DCD which
stood for either donation after circulatory death or worse
donation after cardiac death. The issue with the former is that
it implies that there are multiple forms of death (death is only
a neurological event). The issue with the latter is that it
implies that the heart is dead and therefore not t for transplantation. We have therefore insisted on using the proper
term DCD, even if readers are not familiar with it.
Dierent Types ofDCD
The major downside of DCD is the functional warm ischaemic time (FWIT). This occurs in the time between the
withdrawal of treatment and restarting the circulation of the
heart.2 A common misconception is that ischaemia ends once
the heart has received cold cardioplegia. This marks the end
of FWIT but also the beginning of functional cold ischaemic
time (FCIT). FWIT and FCIT together are known as the
functional total ischaemic time (FTIT).
Given that ischaemia is the main enemy of the DCD heart,
it is simply logical that there have been various strategies to
perfuse the heart. The heart can be perfused either in situ (i.e.
in the donor)—otherwise known as thoraco-abdominal normothermic regional perfusion (taNRP) or ex situ—otherwise
known as Direct Procurement & Preservation (DPP) with
1
It is worth noting that some centres in the US have reported higher
rates of ventricular dysfunction—we believe this to be an injury due to
distension of the RV caused by tying off the pulmonary artery during
procurement and preservation of the heart. However, centres in the UK
have not shown any difference in heart function—because they do not
tie off the pulmonary trunk.
2
Note that FWIT commences when the systolic blood pressure drops
below 50mmHg.
Ex-Site Machine Perfusion (ESMP). These are both explored
further in the next section.
The Technique
General Points oftheDonor
In the cDCD donor, life supporting treatment is withdrawn.
The patient then becomes asystolic. Once the patient
becomes asystolic, a waiting time of 5min is observed. This
is because there has never been a report of a patient spontaneously recovering their circulation after 5min of asystole
after the withdrawal of life supporting treatment (WSLT). At
this point, the thoracic cavity is opened up and the procurement of the heart begins.
Heart function is assessed in the donor pre-withdrawal by
transthoracic echocardiogram (never by transoesophageal
echocardiogram as this is invasive and not appropriate for the
donor whilst they are still alive).
Thoraco-abdominal Normothermic Regional
Perfusion (taNRP)
In taNRP, the heart is not procured immediately. Instead, the
great arch vessels are clamped (in order to prevent cerebral
blood ow) and the right atrium and aorta are cannulated. (It
is worth noting that some centres—particularly across
Europe use peripheral circulation, however this seems to be
of little consequence on the outcomes of the operation).
Once the thoraco-abdominal circulation has been restarted,
heart function can be assessed in the same manner as DBD
hearts and procured in the same manner. Whilst there is very
little data in the literature on hearts that have used both
taNRP and ESMP (circa 20 hearts), there seems to be little
difference in outcomes between taNRP hearts preserved by
ESMP and cold storage (CS). This is in fact the same nding
as DBD hearts. Therefore, we can think of taNRP as the conversion of a non-heart beating donor to a heart beating donor.
This is benecial for two reasons. First, it reduces ischaemic
time (usually below the 30-min critical time period of ischaemia—after which permanent damage occurs. Second, it
allows for more thorough assessment of the heart in situ—as
in DBD transplantation via transoesophageal echocardiogram (TOE). However, taNRP has the added benet of
avoiding a Cushing’s reex with the subsequent stressinduced cardiomyopathy often seen in DBD hearts. Whilst
taNRP is still in its infancy, it seems massively promising
and could potentially be superior to conventional DBD heart
transplantation.
Direct Procurement andPreservation (DPP)
In Direct Procurement and Preservation, once the 5-min
period post-asystole has been observed, a thoracotomy is
performed and the heart is procured. The aortic arch vessels
are clamped, the aorta is cannulated, and the heart is cooled
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with cold cardioplegia. The heart is then excised in the standard method for DBD heart retrieval.
After the heart is excised, it is placed in a basin of ice-cold
storage solution which enables the surgeons to dissect the
aorta away from the pulmonary aorta and cannulate the aorta
with the correct size perfusion connector. The heart is placed
onto the OCS and drained of free air. The LV vent is inserted
via the left atrium to drain the left ventricle. At this point,
certain centres insert a cannula into the pulmonary artery
which prevents free drainage of the right ventricle, whilst
other centres do not insert a cannula and enables free
drainage.
There is currently no marker of transplantability for DCD
hearts. This issue is discussed further under the heading
‘Ex-Situ Machine Perfusion’.
The DCD Donor andRecipient
The Donor
Donor Inclusion Criteria
• ∙ Controlled DCD (Maastricht Category 3 and 4)
• ∙ Age≤50years
• ∙ Weight≥50kg
• ∙ Weight≥30kg—if suitable paediatric recipient at spe-
cialist paediatric centre discuss
• ∙ Consent/authorisation obtained from next of kin/organ
donor register.
Maastricht criteria 3 is dened as a donor who has had a
cardiac arrest in ITU after withdrawal of life supporting
treatment. Maastricht criteria 4 is dened as a donor who has
had a cardiac arrest after the declaration after brain neurological death.
Donor Exclusion Criteria
• ∙ Previous cardiac surgery
• ∙ Previous midline sternotomy
• ∙ Valvular heart disease
• ∙ Congenital heart disease
• ∙ Signicant coronary artery disease
• ∙ Chronic atrial brillation
• ∙ Insulin dependent diabetes
• ∙ Virology: HIV+
• ∙ Current IV drug abuse
• ∙ Tumour with high risk of transmission according to
SABTO guidelines.
The Recipient
The DCD recipient is similar to the DBD recipient in that
they also have refractory ESHF not amenable to medical
therapy. Some DCD recipients may be eligible for DBD
hearts, others may not have been eligible for DBD hearts but
may consent for a DCD heart instead of receiving no organ
at all. However, as the eld of DCD transplantation develops,
it will most likely be the case that DCD organs will be more
widely used and all patients will be consented for both DBD
and DCD hearts.
The current criteria for a recipient—either DBD or DCD
was put together by Brenner and colleagues in 2011. They
are split into absolute contraindications and relative
contraindications.
Absolute Contraindications
Fixed Pulmonary Hypertension.
Active malignancy and for individuals with a prognosis
that is non-cardiac that limits their survival to 3years.
Age > 65 (few patients above the age of 65 have been
transplanted before).
BMI > 35.
Diabetes with microvascular complications not including
non-proliferative retinopathy.
Sepsis and active infections.
Relative Contraindications
Poorly controlled diabetes—with a glycosylated haemoglobin >7.5%.
Chronic infections—usually of the brain, liver, or lungs.
History of non-adherence.
Recent pulmonary embolism.
Pharmacological immunosuppression.
Peripheral or cerebrovascular disease.
Skeletal myopathies.
Psychosocial issues.
Substance abuse.
Ex Situ Machine Perfusion
ESMP is an attractive method for heart preservation in DCD
transplantation. Ischaemia is the main challenge faced by
DCD transplantation. Therefore, perfusing the heart with an
oxygenated, energy rich solution is not only desirable, but
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S. Large and J. O. Louca
one would argue almost essential to ensure that the graft
quality is preserved.
Whilst ESMP shows a great deal of promise, it is still in
its infancy in cardiac transplantation and there are several
issues that it must overcome to ensure that it is effectively
utilised by centres worldwide. The rst would be the exorbitant cost. At the moment, each donor run costs in excess of
$50,000 and therefore is not nancially feasible for many
centres. In addition to the high cost, hearts preserved with
ESMP fall victim to oedema that even the high levels of
mannitol in the preservation solution cannot prevent. The
longest that a heart has been preserved with clinically is…
and it is unlikely that hearts will be preserved for longer until
the problem of oedema has been overcome.
The second issue that ESMP faces is the lack of a suitable
marker of transplantability. In earlier years, lactate was
used—based off limited work done in DBD heart transplants.
The logic for using lactate was that a metabolically competent, healthy heart should be able to utilise lactate. Therefore,
one would expect the lactate to trend downwards, or for there
to be a signicant arterio-venous difference in lactate levels.
However, clinically it has been shown that there is absolutely
no correlate between lactate levels and clinical outcomes.
Therefore, there is an urgent need for a suitable marker of
transplantability to ensure that appropriate hearts are transplanted and equally important to ensure that suitable hearts
are not mistakenly rejected.
Future Directions
that this method of transplantation becomes more widely utilised and can further reduce the ever-growing waiting lists of
recipients awaiting heart transplants.
Suggested Reading
Ali AA, White P, Xiang B, Lin HY, Tsui SS, Ashley E, etal. Hearts
from DCD donors display acceptable biventricular function after
heart transplantation in pigs. Am J Transplant. 2011;11(8):1621–32.
Cernic S, Page A, Messer S, Bhagra S, Pettit S, Dawson SN, et al.
Lactate during ex-situ heart perfusion does not predict the requirement for mechanical circulatory support following donation after
circulatory death (DCD) heart transplants. J Heart Lung Transplant.
2022;41(9):1294–302.
Dhital KK, Iyer A, Connellan M, Chew HC, Gao L, Doyle A, etal.
Adult heart transplantation with distant procurement and ex-vivo
preservation of donor hearts after circulatory death: a case series.
Lancet. 2015;385(9987):2585–91.
Louca J, Shah A, Messer S, Patel N, Sanghera R, Manara A, et al.
Clinical outcome following heat transplantation of 59 Tanrp donor
hearts. An international experience. J Heart Lung Transplantation.
2017;36(12):1311–8
Mehra MR, Uriel N, Naka Y, Cleveland JC Jr, Yuzefpolskaya M,
Salerno CT, etal. A fully magnetically levitated left ventricular
assist device. N Engl J Med. 2019;380(17):1618–27.
Messer S, Cernic S, Page A, Berman M, Kaul P, Colah S, etal. A
5-year single-center early experience of heart transplantation from
donation after circulatory-determined death donors. J Heart Lung
Transplant. 2020;39(12):1463–75.
Rose EA, Gelijns AC, Moskowitz AJ, Heitjan DF, Stevenson LW,
Dembitsky W, etal. Long-term use of a left ventricular assist device
for end-stage heart failure. N Engl J Med. 2001;345(20):1435–43.
Starling RC, Moazami N, Silvestry SC, Ewald G, Rogers JG, Milano
CA, et al. Unexpected abrupt increase in left ventricular assist
device thrombosis. N Engl J Med. 2014;370(1):33–40.
DCD is still in its infancy in many centres. Results so far
have demonstrated that DCD transplantation is a safe and
effective method of transplantation. There is a need to ensure
Part VII
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Pulmonary Thromboendarterectomy
Pulmonary Endarterectomy Surgery
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DavidP.Jenkins
22
The most common indication for pulmonary endarterectomy
(PTE) is chronic thromboembolic pulmonary hypertension
(CTEPH). Rarer indications include debulking of pulmonary
artery sarcoma and disobliterating stenosis caused by pulmonary artery vasculitis.
CTEPH occurs in up to 3% of people following a pulmonary embolism. The actual cause is uncertain, but pathologically there is failure of clot lysis, with organisation into
brotic obstruction within the pulmonary arteries. This manifests as laminated thrombus within the main pulmonary
artery branches, or lobar occlusion, or web-like stenoses at
the segmental branches and smaller subsegmental webs and
occlusions. These macroscopic obstructions increase pulmonary vascular resistance resulting in pulmonary hypertension
and ultimately right heart failure. As pulmonary hypertension develops, the microcirculation maladapts to increasing
pressure with wall thickening at arteriolar level that increases
the PVR further, the two-compartment model. More recent
pathological analysis has suggested further abnormalities in
the microcirculation with involvement of the bronchial artery
connections and abnormalities in pulmonary venules.
CTEPH can be difcult to diagnose as the symptoms are
non-specic, usually exertional breathlessness, and some
patients have no history of the acute event. There are no early
signs until progressive right heart failure develops. However,
awareness and diagnosis are increasingly important as
CTEPH is the most treatable form of precapillary pulmonary
hypertension. Enlarged pulmonary arteries and dilatation of
the right heart can be seen on a chest X-ray. An echocardiogram will show a dilated right heart with evidence of right
ventricular hypertrophy, impaired right ventricular function,
tricuspid regurgitation, and a small compressed underlled
left heart. A ventilation/perfusion scan will show wedge
shaped segmental perfusion defects without corresponding
D. P. Jenkins (*)
Department Cardiothoracic Surgery, Royal Papworth Hospital,
Cambridge, UK
e-mail: david.jenkins1@nhs.net
ventilation defects, so-called mismatched. Conrmation of
PH requires a right heart catheter to measure pulmonary
artery pressure and calculate cardiac output and pulmonary
vascular resistance. Imaging of the pulmonary circulation is
required to assess operability. CTPA, MRI, and conventional
pulmonary angiograms are used.
Surgical Technique
Set Up
The approach is via a median sternotomy incision with the
patient in a supine position as for usual cardiac surgery. The
key difference between pulmonary endarterectomy and standard cardiac surgery is the requirement for deep hypothermic
arrest (DHCA). There are therefore some additional anaesthetic, monitoring and perfusion requirements. All patients
have a PA catheter to monitor pre- and post-cardiopulmonary
bypass (CPB) PA pressures. Peripheral (nasopharyngeal)
and central (bladder) temperature probes are required to
monitor cooling and warming rates on CPB as patients are
cooled to 20°C and slowly rewarmed to 36°C.A centrifugal
pump is used on the CPB machine and a leukocyte lter
incorporated in the circuit. A cooling/warming mattress is
placed beneath the patient and a cooling cap wrapped around
the head (rather than ice). Near infrared spectrometry (NIRS)
is used to monitor brain oxygen saturation.
Cardiopulmonary Bypass
The institution and management of CPB are essential parts
of the PTE operation. Good venous drainage is essential. The
aorta is cannulated in the usual position anteriorly just proximal to the pericardial reection. I use a standard 2-stage
venous cannula positioned in the body of the right atrium and
inferior vena cava via a purse string in the appendage. An
additional straight venous cannula is inserted in the right
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
F. C. Wells (ed.), Atlas of Cardiac Surgery, Springer Surgery Atlas Series, https://doi.org/10.1007/978-3-031-43195-1_22
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atrium and directed into the superior vena cava (SVC). CPB
and cooling can then be commenced, and vents are placed.
The tissue between the aorta and main pulmonary artery is
divided using low power diathermy. Tapes are placed around
the aorta and pulmonary artery utilising the transverse sinus.
Vents are placed in the main PA and via the right superior
pulmonary vein to the left ventricle so that both sides are the
heart are well drained to avoid distension when ventricular
brillation occurs during cooling. A cardiplegia cannula is
placed in the aorta for delivery of antegrade cold blood cardioplegia. Mobilisation of the SVC is important to gain adequate access to the right PA. I choose to do this from the
patient’s left side prior to starting the right PA dissection. I
separate the fascia between the right PA and SVC with low
power diathermy and then blunt dissection to create a tunnel
under the SVC just wider than the diameter of the right
PA. The pericardium is then incised with diathermy vertically upwards, allowing the SVC to be retracted further laterally. A small self-retaining retractor can then be inserted
between the SVC and aorta to expose the right PA (Fig.22.1).
The pulmonary artery is opened and endarterectomy dissection is commenced prior to cardioplegic arrest and
DHCA. Progress is continued until the operating eld is
obscured by blood in the pulmonary artery. Most patients
with CTEPH have a well-developed compensatory bronchial
collateral circulation and it is for this reason that the DHCA
is required to see enough to perform a safe distal endarterectomy dissection. In most cases dissection on the one side can
be completed in a single 20-min DHCA session; clinical
practice and cognitive function studies have demonstrated
that this period is well tolerated at 20°C.If further time is
required for more difcult distal dissection, then a further
arrest can be made following a 10-min period of reperfusion
(Fig.22.1).
Endarterectomy
The right pulmonary artery is opened with a longitudinal
incision taking care to avoid the upper lobe branch and curve
the incision distally towards the lower lobe. The incision can
be extended laterally up to the origin of the middle lobe
Fig. 22.1 Exposure of the right pulmonary artery and arteriotomy
D. P. Jenkins
Fig. 22.2 Development of the dissection plane
branch orice to give better exposure to the lower lobe
branches. Stay sutures are placed on the artery edges.
Development of the dissection plane is fundamental to the
success of the endarterectomy. If there is thickening and
laminated thrombus proximally, this can sometimes be
developed at the arteriotomy from the cut edge of the artery.
More usually the endarterectomy plane is created with a beaver blade in the posterior wall of the artery by making a small
ap that can be extended by blunt dissection (Fig.22.2).
The plane may start very thin proximally but usually
thickens distally. The correct plane is usually the one that
extends most easily, leaving a pearly white smooth residual
vessel wall. Usually any atherosclerotic yellow plaques are
lifted clear with the dissected specimen. If the residual wall
becomes more brous or pink/purple-tinged, then the plane
is too deep.
Once the correct plane is achieved and extended circumferentially around the artery, it can be extended distally into
lobar, segmental, and subsegmental branches. Any proximal
laminated old thrombus should be cleared to allow room to
visualise and dissect the remainder of the artery. By mechanical traction on the endarterectomised specimen, the residual
vessel wall is pushed away using a blunt ended ne metal
sucker (Fig.22.3).
The dissection is advanced cm by cm following every
branch. The brous occlusive ‘tails’ are then pulled clear as
they taper distally into a ne strand. It is important to visualise every segmental branch and retrieve any broken tails. The
pattern of disease can be quite diverse from proximal laminated bulky thrombus to occlusive tails and to very ne distal
webs. The latter small distal webs can be targeted directly by
grasping the centre with a forceps and teasing free (Fig.22.4).
Once all disease is removed, the circulation is restarted, and
the arteriotomy closed with 5/0 prolene.
The procedure is then repeated on the left side. For the left
dissection, the main pulmonary artery is opened from just
distal to the pulmonary valve up to the pericardial reection.
To improve visualisation of the left lower lobe branches,
some surgeons elevate the heart, but I usually rely on manual
retraction with a handheld eyelid type retractor. Examples of
the different types of disease removed can be seen in
Figs.22.5, 22.6, and 22.7.
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