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3 Surgical Treatment of Complications of Acute Myocardial Infarction: Postinfarction Ventricular Septal Defect and Free Wall…
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subtended by the occluded coronary artery. Often, the ventriculotomy incision is made close to and parallel to either
the left anterior descending or the posterior descending
artery. Invariably these arteries are included in the ventriculotomy closure sutures.
Ventricular Septal Defect
The principles of repair of postinfarction ventricular septal
defect are as follows:
• Trans-infarct approach to ventricular septal defect with
the site of ventriculotomy determined by the location of
the transmural infarction.
• Inspection of the left ventricular papillary muscles and
concomitant replacement of the mitral valve only if there
is frank papillary muscular rupture.
• Closure of the septal defect without tension by which the
technique of endocardial patch repair with infarct exclusion is most reliable (see below).
• Closure of the ventriculotomy without tension with generous use of prosthetic material as indicated, and/or epicardial placement of the patch (double velour Dacron) to
the free wall as indicated, to avoid strain on the friable
endocardial tissue.
• Buttressing of the suture lines with pledgets or strips of
Teon felt to prevent sutures from cutting through friable
muscle and supporting the suture line with application of
haemostatic adhesive such as BioGlue.
The technique of infarct exclusion is attractive as instead
of closing the septal defect, it is simply excluded from the
high-pressure zone of the left ventricle. It does not require
resection of myocardium; excessive resection results in
depression of ventricular function and insufcient resection
predisposes to recurrence of septal rupture. In addition, it
maintains ventricular geometry, which enhances ventricular
function. Lastly it avoids tension on friable muscle, which
may diminish postoperative bleeding.
In patients with anterior septal rupture, the interventricu-
lar septum is exposed via a left ventriculotomy, which is
made through the infarcted anterolateral wall starting at the
apex and extending proximally parallel to, but 1–2cm away
from, the anterior descending artery (Fig.3.1). Stay sutures
(2-0 Prolene) are passed through the margins of the ventriculotomy to aid in the exposure of the infarcted septum.
Alternatively, a self-retaining retractor can be used.
The septal defect is located, and the margins of the
infarcted muscle identied. A glutaraldehyde-xed bovine
pericardial patch is tailored to the shape of the left ventricular infarction as seen from the endocardium but 1–2 cm
larger. The patch is usually oval and measures approximately
Fig. 3.1 Repair of postinfarction anterior ventricular septal defect
using infarct exclusion. Ventriculotomy made parallel to left anterior
descending artery through infarcted heart myocardium with exposure of
ventriculotomy using stay sutures
4–6cm in most patients. The pericardial patch is then sutured
to healthy endocardium all around the infarct. Suturing
begins in the lowest and most proximal part of the noninfarcted endocardium of the septum with a continuous 3-0
Prolene suture (Fig. 3.1). Interrupted mattress sutures (4-0
Prolene) with felt pledgets should be used to reinforce the
repair.
The patch is also sutured to the non-infarcted endocardium of the anterolateral ventricular wall. The stitches should
be inserted 5mm deep in the muscle and 5mm apart. The
stitches in the patch should be at least 5mm from its free
margin to allow the patch to cover the area between the
entrance and exit of the suture in the myocardium. This technique minimises the risk of tearing muscle as the suture is
pulled taut. If the infarct involves the base of the anterior
papillary muscle, the suture is brought outside of the heart
and buttressed on a strip of Teon felt applied to the epicardial surface of the left ventricle. Once the patch is completely
secured to the endocardium of the left ventricle, the left ventricular cavity becomes largely excluded from the infarcted
myocardium.
The ventriculotomy is closed in two layers with two strips
of Teon felt on either side of the ventriculotomy using 2-0
VSD
15
Patc
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ventriculostomy
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C. Ng
Patch
Direct closure of
Fig. 3.2 Repair of postinfarction anterior ventricular septal defect using infarct exclusion. Left gure demonstrate direct closure of ventriculotomy. Right gure is a cross-sectional view demonstrating location of patch suture line
or 3-0 Prolene sutures. The rst layer is an interrupted horizontal mattress going through the full thickness of the
ventricular wall and the felt strip (Fig.3.2). It is important
when tying the individual suture of this rst layer, there
should be just enough tension to gently opposed both muscle
edge. The second layer is a running stitch with 3-0 Prolene.
Alternatively, a separate bovine pericardial patch can be used
to cover the whole suture line with the edges sutured onto the
Teon felt strip. No infarctectomy is performed unless the
necrotic muscle along the ventriculotomy is sloughing at the
time of its closure.
If the edges of the ventriculotomy are very friable and
some degree of resection of infarcted myocardium need to be
performed, direct closure described above may not be possible. In this situation, 2-0 or 3-0 Prolene sutures can be
passed through the ventricular free wall and through a tailored (to t over the defect) patch of double velour Dacron in
an interrupted horizontal mattress fashion to form a new ventricular free wall (Fig.3.3).
In patients with posterior septal defect, an incision is
made in the inferior wall of the left ventricle 1 or 2mm from
the posterior descending artery. This incision is started at the
midportion of the inferior wall and extended proximally
toward the mitral annulus and distally toward the apex of the
ventricle. Care is taken to avoid damage to the posterolateral
papillary muscle. Stay sutures are passed through the fat pad
of the apex of the ventricle and margins of the ventriculotomy to facilitate exposure of the ventricular cavity.
In most cases, the rupture is found in the proximal half of
the posterior septum and the posteromedial papillary muscle
is involved by the infarction. A bovine pericardial patch is
tailored in a triangular shape of approximately 4–7 cm in
most patients. The base of the triangular-shaped patch is
sutured to the brous annulus of the mitral valve with a continuous 3-0 polypropylene suture starting at a point corresponding to the level of the posteromedial papillary muscle
and moving medially toward the septum until the noninfarcted endocardium is reached. At that level, the suture is
interrupted, and any excess patch material trimmed (Fig.3.4).
The medial margin of the triangular-shaped patch is sewn
to healthy septal endocardium with a continuous 3-0 or 4-0
Prolene suture taking bites the same size as those described for
anterior defects. In this area of the septum, reinforcing pledgeted sutures (4-0 Prolene) may be required. The lateral side
icardial
Pe
3 Surgical Treatment of Complications of Acute Myocardial Infarction: Postinfarction Ventricular Septal Defect and Free Wall…
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Fig. 3.3 Repair of
postinfarction anterior
ventricular septal defect using
infarct exclusion with external
patching of ventricular free
wall
VSD
17
Per
patch
Patch
ricardial
patch
Papillary
muscle
Fig. 3.4 Repair of postinfarction posterior ventricular septal defect using infarct exclusion with infarct exclusion
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C. Ng
of the patch is sutured to the posterior wall of the left ventricle
along a line corresponding to the medial margin of the base of
the posteromedial papillary muscle. Because the posterior
wall of the left ventricle is infarcted, it is usually necessary to
use full-thickness bites and anchor the sutures on a strip of
Teon felt applied on the epicardial surface of the posterior
wall of the left ventricle right at the level of the posteromedial
papillary muscle insertion. Once the patch is completely
sutured to the mitral valve annulus, the endocardium of the
interventricular septum, and the full thickness of the posterior
wall, the ventriculotomy is closed as described above.
Ventricular Free Wall Rupture
In patients with signicant cardiac tamponade, cardiac arrest
may result during the induction of anaesthesia. This should
be anticipated, and measures such as completing the sterile
preparation, draping of the patient, and even access to the
femoral artery before inducing anaesthesia should be considered. A median sternotomy is quickly performed but the pericardium should be decompressed gradually as the systemic
blood pressure can otherwise rebound to the other extreme
and may even increase the size of the ventricular free wall
defect. In most cases, however, the ventricular tear is sealed
off by clot, and there is no active bleeding.
Repair should be undertaken with cardiopulmonary
bypass and aortic cross clamping as cardiac standstill and
left ventricular decompression make the procedure much
easier and controlled. There are generally two techniques
used and it depends on the size of the defect and the degree
of myocardial necrotic tissue present.
The easiest techniques is the application of BioGlue to a
wide area around the defect and placing an appropriately
sized patch of Bovine pericardium over it. This is best done
in cardiac standstill, and one must allow sufcient time for
the BioGlue to x. This time can be utilised to tack down the
patch with a running 4-0 Prolene suture to the epicardial
surface.
The more substantive repair involves a limited infarctectomy back to myocardium that will hold a ventriculotomy
suture line and using the techniques of ventriculotomy closure described above. Concurrent coronary artery bypass
graft surgery may be considered.
Suggested Reading
Giblett JP, Matetic A, Jenkins D, Ng CY, Venuraju S, MacCarthy T,
et al. Post-infarction ventricular septal defect: percutaneous or
surgical management in the UK national registry. Eur Heart J.
2022;43(48):5020–32. https://doi.org/10.1093/eurheartj/ehac511.
Ronco D, Matteucci M, Kowalewski M, De Bonis M, Formica F,
Jiritano F, etal. Surgical treatment of postinfarction ventricular sep-
tal rupture. JAMA Netw Open. 2021;4(10):e2128309. https://doi.
org/10.1001/jamanetworkopen.2021.28309.
Complications ofMyocardial Infarction:
Anterior /
Mural /
y cord
P
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Papillary Muscle Rupture
FrancisC.Wells
The mitral valve leaets are supported through the papillary
muscle projections from the left ventricular wall and their
tendinous cords which extend to the leaet margins and the
belly of the leaets (Fig.4.1). There are usually two primary
papillary muscle complexes, supero-lateral (antero-lateral/
anterior) and infero-septal (postero-septal/posterior). The
true anatomical descriptive name is used rst but the papillary muscles are frequently simply referred to as anterior or
posterior in the surgical forum (Fig.4.2). They have a relatively discreet and still relatively poorly understood blood
supply with little or no collateralisation. The posterior
(infero-septal) papillary muscle derives its blood supply
from either branches of the right coronary artery or the circumex branch of the left in a left dominant system. Work
done by Voci et al. [1] demonstrated that the situation was
sometimes not even that straight forwards and that in a right
dominant coronary situation the inferior wall may be perfused by the right coronary artery, whereas the inferior papillary muscle was not. A combination of right coronary
occlusion and signicant circumex artery disease in the setting of a dominant right coronary artery is the usual presentation. The incidence is low, less than 5% of myocardial
infarctions. More commonly found is inferior wall dyskinesia with acute functional mitral regurgitation.
In hearts where the inferior papillary muscle blood supply
is abruptly interrupted, muscle necrosis followed by rupture
of the papillary muscle can occur, precipitating sudden
severe mitral regurgitation, a life-threatening complication
of myocardial infarction (Fig.4.3). Under the force of ventricular systole, the high closing pressure can cause acute,
severe mitral regurgitation rapidly followed by pulmonary
oedema. Rupture commonly occurs on days 2–7. The mortality is high. Emergency hospital admission is necessary
Aortic leaflet
Tendinous
cord
apillary
muscles
Fig. 4.1 The mitral valve and papillary muscle complex
posterior leaflet
Primar
Secondary
cord
with positive pressure ventilation and medical treatment to
decompress the lungs and to clear the pulmonary oedema.
Emergency surgery is indicated. Whilst valve repair/
reconstruction is accepted as the gold standard treatment for
mitral regurgitation, reconstruction in this setting carries
poor results with early disruption of the reconstituted muscle
as a result of the extent of ischaemia in the surrounding muscle. Therefore, the only reliable solution is the insertion of a
prosthetic valve with preservation of as much subvalvar connections as possible.
Appropriate coronary artery bypass grafting should also
be undertaken. The results depend upon the amount of surrounding myocardial death as a result of the vascular
occlusion.
4
F. C. Wells (*)
Royal Papworth Hospital, Cambridge University Group of
Hospitals, Cambridge, UK
e-mail: francis.wells@nhs.net
© 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_4
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papillar
y muscle
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Fig. 4.2 The arrangement of
the papillary muscles within
the left ventricle
F. C. Wells
Fig. 4.3 Following the acute
event of coronary obstruction,
the affected muscle will
necrose and, as a result, the
muscle will rupture
Supero-medial
y muscle
Ruptured papillary
muscle head
Infarcted
muscle
Infero-lateral
papillar
Papillary muscle rupture
Reference
1. Voci P, Biltta F, Caretta Q, Mercanti C, Marino B.Papillary muscle
perfusion pattern. A hypothesis for Ischaemic papillary muscle dysfunction. Circulation. 1995;91:1714–8.
Part II
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Valve Surgery: Aortic Valve Surgery
Timing ofHeart Valve Surgery
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MadalinaGarbi
5
In the presence of symptoms, heart valve surgery is offered
to patients with severe heart valve disease, based on currently accepted severity thresholds on imaging at rest.
Outcomes data dening severe heart valve disease exist only
for echocardiography; consequently, recommendations and
guidelines refer mainly to severity thresholds derived from
echocardiography. However, in case of non-diagnostic echocardiography, cardiac magnetic resonance imaging and cardiac computed tomography can be used reliably for timing of
heart valve surgery, when they diagnose the heart valve disease as severe.
The reporting of symptoms is subjective and the develop-
ment of symptoms depends on physical activities performed,
being less likely in sedentary patients and highly trained
individuals. Consequently, the absence of symptoms must be
conrmed with exercise testing. Exercise echocardiography
provides objective assessment of exercise tolerance and
symptoms, as well as detection of exertion-induced changes
that predict decompensation. Furthermore, exercise echocardiography can be used in symptomatic patients with nonsevere heart valve disease based on imaging at rest, to
reclassify the severity based on exercise-induced changes.
Symptoms represent a strong (class I) indication for
mitral valve surgery in all guidelines. In the absence of
symptoms, heart valve surgery is offered to patients with
severe heart valve disease and haemodynamic consequences
typical for the type of valve disease.
Mitral Regurgitation
Primary Mitral Regurgitation
1. Degenerative mitral valve disease is the most common
cause of mitral regurgitation. Timing of surgery in asymptomatic patients with severe mitral regurgitation depends
rstly on the patient’s surgical risk and on the likelihood
of successful durable mitral valve repair. Young patients,
with low surgical risk and highly repairable valve can be
offered early surgery. Drop in left ventricular ejection
fraction below 60% signals decompensation and represents a strong indication for mitral valve surgery (class I
in all guidelines) without waiting for symptoms.
Pulmonary hypertension with estimated systolic pulmonary artery pressure (SPAP) at rest on echocardiography
of 50mmHg, rise in estimated SPAP during exercise to
over 60mmHg, an enlarged left atrium with an indexed
volume>60mL/m2 BSA and development of atrial brillation represent softer indications for mitral valve surgery, depending on the patient’s life expectancy and
surgical risk.
2. Mitral regurgitation due to calcic mitral valve degeneration with mitral annular calcication invading or retracting the mitral valve leaets is a form of primary mitral
regurgitation usually affecting older individuals with a
higher surgical risk, further increased by the typical
mitral valve morphology. Consequently, taking into consideration risk and benet, surgery is most likely offered
in symptomatic patients. However, radiation-induced
mitral valve calcication can affect younger individuals
and, in this case, risk and benet considerations differ.
Timing of surgery for mitral regurgitation varies, depending
on the primary or secondary nature of the regurgitation and
specic considerations for each category.
M. Garbi (*)
Department of Cardiology, Royal Papworth Hospital,
Cambridge, UK
e-mail: madalina.garbi@nhs.net
© 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_5
Secondary Mitral Regurgitation
1. Ventricular-secondary mitral regurgitation of ischaemic
or non-ischaemic cause responds to heart failure medical
treatment, revascularization, and/or cardiac resynchronisation therapy. Mitral valve surgery should be offered
only if the regurgitation remains severe and the patient
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M. Garbi
remains symptomatic or requires surgical revascularisation of coronary disease.
2. Atrial-secondary mitral regurgitation responds to ofoading and rate or rhythm control of atrial brillation. Mitral
valve surgery should be offered only if the regurgitation
remains severe and the patient remains symptomatic.
Mitral Stenosis
1. Rheumatic mitral stenosis is treated mainly with transcatheter balloon commissurotomy and mitral valve surgery is offered only in case of unfavourable morphology.
In the asymptomatic patient, depending on surgical risk,
surgery can be offered in case of pulmonary hypertension
with estimated systolic pulmonary pressure>50mmHg
on echocardiography at rest, or in case of high thromboembolic risk (history of systemic embolization, dense
spontaneous contrast in the left atrium, recent onset paroxysmal atrial brillation).
2. Calcic mitral stenosis implies similar considerations of
risk and benet with calcic mitral regurgitation. The
rst treatment should comprise rate control and diuresis,
and care should be taken to avoid overestimation of mitral
stenosis severity.
threshold of 50% for a strong (class I) indication. Surgery
should be also offered in case of increase in mean gradient
during exercise by more than 20mmHg, in case of rise in
BNP and in case of very high transvalvular velocities
(>5m/s) and gradients.
Tricuspid Regurgitation
Timing of surgery for tricuspid regurgitation varies, depending on the primary or secondary nature of the regurgitation
and coexistent pathology.
Primary Tricuspid Regurgitation
Primary tricuspid regurgitation of degenerative aetiology can
coexist with mitral valve prolapse. Primary tricuspid regurgitation due to a ail leaet, usually of traumatic cause can
manifest in isolation. Surgery should be offered to symptomatic patients without severe right ventricular systolic dysfunction, better assessed by cardiac magnetic resonance
imaging. Surgery can be offered to asymptomatic patients
with dilatation of the right ventricle and low surgical risk.
Aortic Regurgitation
In asymptomatic patients, aortic valve surgery is offered
when the systolic function of the left ventricle drops, as
assessed by an increase in the end-systolic diameter of the
left ventricle or by a decrease in left ventricular ejection fraction. A drop in left ventricular ejection fraction to <50% represents a strong (class I) indication in the European Society
of Cardiology (ESC) guidelines [1], with a drop to <55%
representing a softer indication. The NICE guidelines [2]
recommend surgery when the ejection fraction drops to
<55%.
Aortic Stenosis
In asymptomatic patients with severe aortic stenosis, aortic
valve surgery is offered when the left ventricular ejection
fraction drops. The NICE guidelines recommend a left ventricular ejection fraction threshold of 55%; this threshold
represents a soft indication in the ESC guidelines, with a
Secondary Tricuspid Regurgitation
For secondary tricuspid regurgitation, a strong (class I) indication exists only in patients undergoing left heart valve surgery. Surgery can be also offered for severe isolated
secondary tricuspid regurgitation in case of symptoms or
dilatation of the right ventricle without severe right ventricular systolic dysfunction or pulmonary hypertension, however
this represents a softer indication (class IIa). A similarly soft
indication exists for mild or moderate tricuspid regurgitation
with a dilated annulus (>40 mm on echocardiography)
undergoing left heart valve surgery.
References
1. Heart valve disease presenting in adults: investigation and management. NICE guideline [NG208]. 2021. https://www.nice.org.uk/
guidance/ng208
2. Vahanian A, Beyersdorf F, Praz F, Milojevic M, Baldus S,
Bauersachs J, etal. 2021 ESC/EACTS guidelines for the management of valvular heart disease. Eur Heart J. 2022;43(7):561–632.
https://doi.org/10.1093/eurheartj/ehab395. Erratum in: Eur Heart J.
2022 Feb 18.
Surgery forAortic Valve Replacement
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IsmailVokshi andStevenTsui
6
In Western countries, aortic valve replacement surgery is
increasingly performed in the elderly for senile calcic aortic
stenosis. The other common indication for aortic valve
replacement is bicuspid aortic valve disease with severe stenosis and/or regurgitation. In developing countries, rheumatic aortic valve disease remains the predominate indication
for surgical intervention. Pure aortic valve regurgitation is a
less common indication that patients require aortic valve
replacement. This could be secondary to aortopathies, such
as an aneurysmal aortic root or ascending aorta with effacement of the sinotubular junction or due to infective bacterial
endocarditis leading to the destruction of the aortic valve
apparatus.
Degeneration of the aortic valve is frequently accompanied by brosis and calcication of the valve leaets. The
calcication often extends into the aortic annulus and may
involve the aortic root as well as the anterior mitral valve
leaet.
The timing and indications for surgery, especially in the
asymptomatic patient, are evolving and updated at intervals
according to the latest evidence. These are covered in depth
in international guidelines and will not be discussed here
[1, 2].
I. Vokshi
Department of Cardiothoracic Surgery and Transplantation,
Royal Papworth Hospital NHS Foundation Trust, Cambridge, UK
e-mail: ismail.vokshi@nhs.net
S. Tsui (*)
Department of Cardiothoracic Surgery and Transplantation, Royal
Papworth Hospital, Cambridge, UK
e-mail: steven.tsui@nhs.net
Surgical Techniques
Cardiopulmonary Bypass andVenting
Following sternal incision and systemic heparinisation, cardiopulmonary bypass is established via a high ascending
aortic and a two-stage right atrial cannulation. Moderate systemic hypothermia of 32°C is preferred to reduce warming
of the heart during cardioplegic arrest.
Venting is deployed to avoid distension of the left ventricle especially in cases of aortic regurgitation and to provide
a clear operating eld during surgery. This is achieved by
inserting a vent in the right superior pulmonary vein and
using a trocar to direct it across the left atrium, the mitral
valve and into the left ventricle. For cardioplegia delivery
and subsequent de-airing of the heart at the end of surgery, an
8F cannula is secured to the most anterior aspect of the mid
ascending aorta.
Once fully set up, an aortic cross-clamp is applied and
1–1.5L of cold blood cardioplegia is delivered into the isolated aortic root. Finger palpation is performed to ensure that
an adequate aortic root pressure is generated by the cardioplegia infusion, the left ventricle did not distend due to regurgitant ow across the aortic valve and that prompt
electromechanical arrest of the heart is achieved. Inadequate
aortic root pressure without obvious left ventricular distension suggests a modest leakage of the infused cardioplegia
across the aortic valve. This could effectively be managed by
increasing the infusion rate and total volume of the cardioplegia with simultaneous increased cardiotomy suction on
the pulmonary vein vent.
In cases of left ventricular distension during cardioplegia
infusion into the aortic root, the 8F aortic cannula is detached
from the cardioplegia line and connected to a cardiotomy
sucker to decompress the left heart. An aortotomy is then
performed, and an appropriately sized coronary ostial cannula is used to deliver the required amount of cardioplegia
directly into the left coronary artery (600mL) and right coronary artery (400mL) in turn. In cases of known severe aortic
© 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_6
25
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