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(a) (b)
Fig.67.2 Left atrial isthmus lesion. (a)Radiofrequency; (b)Cryoablation.
excision/ exclusion in patients with persistent or long- standing
persistent AF.
Off- pump atrial fibrillationprocedure
An alternative surgical approach is based on o- pump bilateral pulmonary vein isolation with a bipolar RF clamp. is approach enables dissection around the pulmonary veins and introduction of
the bipolar clamp, creation of some connecting lesions, as well as
management of the LAA. However, the lesion set is not a Cox maze
IV and in the patient with symptomatic AF who requires CABG, we
recommend an on- pump procedure in order to facilitate a biatrial
Cox– maze IV procedure.
Perioperativemanagement
e maze procedure does not immediately cure AF in most patients.
us, both heart rhythm surveillance and heart rhythm management are necessary. Post- ablation AF occurs in 30– 60% of patients;
however, by 3months aer surgery, 65– 85% of these patients have
Fig.67.3 Right atrial lesions.
67 Coronary artery bypass grafting withthe maze procedure foratrialfibrillation 459
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returned to normal sinus rhythm. e precise cause of perioperative
AF is unknown, although changes in adrenergic tone and inammation may contribute.
Preoperative beta blockers should be continued in all patients
who do not have a contraindication. Additional antiarrhythmic
medication (most oen amiodarone, sotalol, or propafenone) is
recommended in patients with post- ablation AF for 4– 6 weeks. In
addition, a one- time in- hospital cardioversion attempt in the patient who fails chemical cardioversion should be performed. All
patients are discharged on warfarin for 6months with the target
international normalized ratio of 2.0. If a patient has no AF on a
long- term monitor performed at 3months, no le atrial smoke on
echocardiography, and a well- controlled LAA, and no other indication for anticoagulation, we believe that it is reasonable to discontinue warfarin. Electrical cardioversion is attempted at 3months
postoperatively for patients who remain in AF.
Post- CABG atrialfibrillation
New- onset postoperative AF aects one- third of patients undergoing cardiac surgery and it is associated with an increased immediate risk of stroke, morbidity, and 30- day mortality. Prophylactic
antiarrhythmic drug treatment may be initiated but will have to be
weighed against side eects. Furthermore, anticoagulation treatment with warfarin or non- vitamin K antagonist oral anticoagulants for stroke prevention in patients with postoperative AF should
also follow the guidelines for the antithrombotic treatment of AF
occurring outside the setting of CABG using the CHADS- VASc
(Cardiac failure, Hypertension, Age ≥75 (Doubled), Diabetes,
Stroke (Doubled)— Vascular disease, Age 65– 74, and Sex category
(Female)) score.
Conclusion
A substantial number of CABG patients are presenting with AF
and its association with decreased long- term survival and increased
risk of stroke and heart failure is well established. Avariety of new
low- risk procedures with new ablation technology can be applied
in patients undergoing concomitant CABG, and the addition of a
maze procedure does not increase operative mortality or morbidity.
Although these technologies have not been prospectively studied in
patients undergoing CABG, several clues have been identied so far:
1. Pulmonary vein isolation alone may be adequate for those with
paroxysmal AF but may not be the optimum strategy for patients
with persistent and long- standing persistent AF.
2. Ablation lines should be continuous and transmural.
3. Surgical ablation should include management of the le atrial
appendage.
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JC, etal. 2014 AHA/ ACC/ HRS guideline for the management of
patients with atrial brillation:a report of the American College of
Cardiology/ American Heart Association Task Force on Practice
Guidelines and the Heart Rhythm Society. J Am Coll Cardiol.
2014;64(21):e1– 76.
2. Hsu LF, Jaïs P, Sanders P, Garrigue S, Hocini M, Sacher F, etal.
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3. Nabauer M, Gerth A, Limbourg T, Schneider S, Oe M, Kirchhof
P, etal. e Registry of the German Competence Network on
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Europace. 2009;11(4):423– 34.
4. Williams L, Frenneaux M. Syncope in hypertrophic
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brillation:a Global Burden of Disease 2010 Study. Circulation.
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DM, Lytle BW, etal. Does preoperative atrial brillation reduce
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9. Ngaage DL, Scha HV, Mullany CJ, Sundt TM, 3rd, Dearani JA,
Barnes S, etal. Does preoperative atrial brillation inuence early
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Cardiovasc Surg. 2007;133(1):182– 9.
10. Lee R, McCarthy PM, Wang EC, Vaduganathan M, Kruse J,
Malaisrie SC, etal. Midterm survival in patients treated for
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without a history of atrial brillation. J orac Cardiovasc Surg.
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B etal. 2016 ESC Guidelines for the management of atrial
brillation developed in collaboration with EACTS. Eur Heart J.
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12. Cox JL. A brief overview of surgery for atrial brillation. Ann
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Svensson LG, Navia JL, etal. Surgery for permanent atrial
brillation:impact of patient factors and lesion set. Ann orac
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14. Gaita F, Riccardi R, Caponi D, Shah D, Garberoglio L, Vivalda L,
etal. Linear cryoablation of the le atrium versus pulmonary vein
cryoisolation in patients with permanent atrial brillation and
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and long- term clinical results. Circulation. 2005;111(2):136– 42.
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elimination of atrial brillation:a meta- analysis. J orac
Cardiovasc Surg. 2006;131(5):1029– 35.
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Ferguson TB, O’Brien SM, etal. Atrial brillation correction
surgery:lessons from the Society of oracic Surgeons National
Cardiac Database. Ann orac Surg. 2008;85(3):909– 14.
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https://t.me/medicina_free
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68
Coronary artery bypass graing with
postinfarction ventricular septal defect and
with ventricularpseudoaneurysm
Mitesh V. Badiwala
Introduction
Ventricular septal defect (VSD) and ventricular pseudoaneurysm
are potentially lethal complications following acute transmural myocardial infarction. Both require urgent treatment due to resultant
cardiogenic shock and/ or impending rupture resulting in sudden
death. Indeed, the most recent 2018 European Society of Cardiology/
European Association for Cardio- oracic Surgery Guidelines on
myocardial revascularization give a classI, level C recommendation that:‘In cases of haemodynamic instability, emergency surgical
or catheter- based repair of mechanical complications of ACS is indicated, as decided by the Heart Team’. Historically, patients suffering from these mechanical complications had a very high risk of
mortality without urgent surgical intervention. Unfortunately, early
experience with surgical repair also resulted in a high incidence of
early mortality, albeit still superior to medical management.
Cooley and colleagues were the rst to report surgical repair
of a postinfarction VSD; however, the patient died 6 weeks later.
ereaer, Daggett and colleagues introduced infarctectomy and
reconstructive techniques that reduced operative mortality. More
recently, improved surgical technique and particularly the infarct
exclusion technique for VSD repair, has resulted in improvement in
surgical outcomes and signicantly reduced mortality.
It is important to recognize, however, that both of these mechanical complications of acute myocardial infarction (AMI) have
become increasingly rare as prompt treatment of AMI with emergent percutaneous coronary intervention (PCI) has emerged as the
standard of care. As such, most surgeons do not gain signicant experience in their surgical treatment.
Epidemiology and naturalhistory
Early death from AMI is a result of cardiogenic shock and/ or cardiac
rupture. Two autopsy series reported the sites of cardiac rupture in
patients who had fatal AMI., e site of rupture in the majority
of these fatal cases was the le ventricular free wall (53– 62%). e
second most common site of cardiac rupture was the interventricular
septum (18– 25%). Arupture of both the free wall and septum was
observed in 3– 6% of cases.
Rupture of the interventricular septum resulting in a postinfarction
VSD, in the current era, is a rare complication in 0.25– 0.31% of patients presenting with AMI and although typically occurring between 2 and 4days aer transmural infarction can also occur earlier
or as late as 2 weeks following infarction. Postinfarction anterior
VSD is the most common location of septal rupture following
AMI, aer occlusion of the le anterior descending coronary artery and is most frequently located in the distal half of the anterior interventricular septum. is is in contrast to postinfarction
posterior VSDs which usually occur in the proximal half of the
interventricular septum as a result of occlusion of a dominant right
coronary artery, or rarely a dominant circumex artery and oen
accompanied by signicant right ventricular dysfunction. e incidence of single- , double- , and triple- vessel coronary artery disease
among patients with postinfarction VSD is evenly distributed.
e prognosis of postinfarction VSD is extremely poor. Moreyra
and colleagues reported the outcomes of 148,881 adult patients admitted to hospital with a diagnosis of acute ST- segment elevation
myocardial infarction. In- hospital death occurred in 50% of the
408 patients presenting with a postinfarction VSD compared to 18%
among those without a VSD. Moreover, the 1- year mortality rate
among those with postinfarction VSD was observed to be 65%.
Le ventricular pseudoaneurysm is a type of ‘contained’ free wall
rupture that occurs uncommonly. e majority of le ventricular
free wall ruptures result in acute hemopericardium, cardiac tamponade, and death within minutes. Rarely, a le ventricular free wall
rupture occurs with slow leakage of blood whereby the epicardium
may ‘control’ the bleeding while adhesions between the pericardium and epicardium provide reinforcement. When the adhesions
have sucient strength to ‘contain’ the rupture, a pseudoaneurysm
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develops. While this containment allows time for diagnosis and
intervention, le ventricular pseudoaneurysms have a high risk of
rupture.
Similar to postinfarction VSD, postinfarction pseudoaneurysm
is a rare complication of AMI. Csapo and colleagues examined
2600 consecutive patients undergoing coronary angiography following AMI and identied six pseudoaneurysms resulting in an
incidence of 0.26%. Importantly, the identication and diagnosis of a pseudoaneurysm occurred on average 37 days (range
3– 80 days) following infarction. Frances and colleagues further
characterized the presentation and natural history of le ventricular
pseudoaneurysms in 290 patients. ey found that posterior
pseudoaneurysms (43%) were more than twice as common as anterior pseudoaneurysms (18%), and that lateral (28%) and apical
(24%) locations were also common sites for pseudoaneurysm formation. Conservative treatment with only medical management occurred in 31 of the 290 patients, and 48% of these patients died at a
median of less than 1 week, presumably due to rupture. e 1- and
5- year survival of those treated medically was only 39% and 16%,
respectively. us, postinfarction le ventricular pseudoaneurysm
is a highly lethal diagnosis with a poor prognosis with conservative
medical management.
prompt surgery performed thereaer. In the haemodynamically unstable patient, medical management with inotropes and vasodilators
as well as mechanical support with an intra- aortic balloon pump are
generally used to stabilize the patient prior to coronary angiography
and immediate surgical therapy. Coronary angiography, if possible,
is necessary because revascularization of multivessel coronary artery disease at the time of surgical intervention improves operative
and long- term outcome.,–
With increasing surgical experience, mechanical circulatory
support (including venoarterial extracorporeal membrane oxygenation and total articial hearts) allows a dierent algorithm for
management for postinfarction VSD in haemodynamically unstable
patients. Cinq- Mars and colleagues have proposed alternative treatment strategies such as bridges to and/ or heart transplantation in
haemodynamically unstable patients. While these alternative
strategies may provide haemodynamic stability and time for necrotic muscle to be partially replaced by brous tissue to facilitate
repair techniques, they do not obviate the need for prompt denitive repair when the patient is stabilized from the acute phase of the
myocardial infarction. Conservative management of haemodynamically stable patients is not advised since most of these patients eventually develop congestive heart failure and/ or cardiogenic shock.
While the operative techniques for anterior versus posterior VSD
repair are unique, the operative planning and set- up are similar.
Clinical presentation anddiagnosis
Aer median sternotomy and aortic cannulation, both vena cavae
are cannulated and snared to ensure complete venous drainage and
e clinical presentation of postinfarction VSD, oen with congestive heart failure and/ or cardiogenic shock, is dependent on the
magnitude of the infarction and the resulting right and/ or le ventricular dysfunction as well as the degree of le- to- right shunting.
However, a VSD may be diagnosed prior to the development of heart
failure or cardiogenic shock with auscultation of a new heart murmur
or with routine transthoracic echocardiography. e diagnosis of a
postinfarction VSD can also occur in the cardiac catheterization laboratory on a contrast ventriculogram. In the haemodynamically
stable patient, coronary angiography should be performed in anticipation of prompt surgical intervention prior to further clinical
deterioration.
While the most common clinical presentation of patients with
postinfarction le ventricular pseudoaneurysm is congestive heart
failure, patients can also present with angina, syncope, ventricular
arrhythmias, and/ or thromboembolic complications. e diagnosis of ventricular pseudoaneurysm can be made with echocardiography, contrast ventriculography, computed tomography scan
with contrast, or magnetic resonance imaging. e diagnosis may be
incidental or conrmed by further imaging if prompted by suspicion
on echocardiography. If the patient is haemodynamically stable, coronary angiography should be considered, but in unstable patients,
emergent surgical intervention should take priority.
avoidance of air entrainment. Cardiopulmonary bypass with systemic hypothermia to 32°C is typically used with a combination of
antegrade and retrograde cold blood cardioplegia for myocardial
protection. Myocardial revascularization of signicant coronary
artery disease supplying non- infarcted myocardium is performed
prior to VSD repair. While most surgeons use an internal thoracic
artery in these patients, others use saphenous vein gra exclusively
to permit cardioplegia administration while performing the VSD repair. While a trans le ventricular approach is usual in most patients
presenting with an acute postinfarction VSD, others such as the
Mayo Clinic group, have reported successful results using a transatrial approach for basal ventricular septal defect.
Once revascularization and repair of the VSD are complete, the
patient is weaned from cardiopulmonary bypass oen with the support of an intra- aortic balloon pump and inotropic support, particularly if they were in cardiogenic shock and congestive heart failure
prior to surgery. In some cases, mechanical circulatory support may
be required as a bridge to recovery. Intraoperative transoesophageal
echocardiography is used to assess ventricular function, residual
shunts, and the presence of mitral regurgitation.
AnteriorVSD
An incision is made in the apex of the le ventricle 1– 2 cm parallel to the le anterior descending artery through the infarcted and
necrotic muscle. e margins of the ventriculotomy are secured
Operative timing andtechniques
Postinfarction ventricular septaldefect
As soon as the diagnosis of postinfarction VSD is made, urgent surgical treatment is mandatory. In the haemodynamically stable patient, coronary angiography should be performed immediately with
to the surgical drapes with a series of stay sutures to expose the
interventricular septum. e VSD is located and the margins of
the infarcted muscle are identied. Aglutaraldehyde- xed bovine
pericardial patch is tailored to the shape of the le ventricular infarction and is usually oval but 1– 2cm larger with an average size
of 4 × 6cm and is then sutured to the healthy non- infarcted endocardium all around the infarcted muscle using continuous 3- 0
68 Coronary artery bypass grafting with postinfarction ventricular septal defect and with ventricularpseudoaneurysm 463
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polypropylene suture starting at the lowest and most proximal part
of the intraventricular septum as depicted in Fig. 68.1. e patch is
sutured to the interventricular septum and then to the lateral ventricular wall, eectively excluding the infarcted muscle from the le
ventricular cavity. e stitches should be placed 5– 7mm deep within
the muscle and 4– 5mm apart. e stitches in the patch should be at
least 5– 7mm from the free margin so as to allow the patch to cover
the area between the entrance and exit of the sutures in the myocardium. is technique minimizes the risk of tearing the muscle as
the sutures are tightened. e sutures should be interrupted every
3 or 4cm and the knots le in the space between the patch and the
infarcted wall. e ventriculotomy is then simply closed over two
strips of bovine pericardium or Teon® felt in two layers using 2- 0 or
3- 0 polypropylene sutures as shown in Fig. 68.1. No infarctectomy
is performed unless the necrotic tissue along the ventriculotomy is
sloughing at the time of closure. is technique has been used exclusively at our institution since 1987 and has been called the ‘infarction exclusion technique’.
PosteriorVSD
In general, repair of the posterior VSD is a more technically challenging operation than repair of the anterior VSD due to dicult
exposure and more complex anatomy involving the mitral valve.
Similar to the technique described for anterior VSD repair, we have
Fig.68.1 Repair of anterior VSD by endocardial patch with infarct exclusion. Pericardial patch is sutured to septum first then to lateral wall.
Reproduced from David, TE., Dale, L., and Sun, Z.J Thorac Cardiovasc Surg. 1995;110:1315– 22 with permission from Elsevier.
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used the ‘infarction exclusion technique’ for VSD repair. An incision
is made in the inferior wall of the le ventricle 1 or 2cm from the
posterior descending artery. e incision is started at the midpoint
of the inferior wall and extended proximally towards the mitral annulus and distally towards the apex of the le ventricle. Exposure
of the le ventricular cavity is facilitated with stay sutures that are
passed through the apex of the le ventricle and margins of the
ventriculotomy as shown in Fig. 68.2. e VSD is located and frequently lies in the proximal half of the posterior septum. e extent
of the infarction is assessed and oen includes the lower third of
the interventricular septum, the posterior wall, and almost always
the posteromedial papillary muscle. Apatch of glutaraldehyde- xed
bovine pericardium is then tailored to the same shape as the infarct
in the le ventricle which is triangular in shape but 2cm wider
and longer and is usually 4 × 7cm in most patients. e base of the
triangular- shaped patch is then sutured to the brous annulus of the
mitral valve or to the adjacent ventricular muscle if it is not infarcted
with a continuous 3- 0 polypropylene suture starting at a point corresponding to the level of the posteromedial papillary muscle and
moving medially towards the septum until the non- infarcted endocardium is reached. At that level, the suture is interrupted and excess
patch material is trimmed. e medial margin of the triangularshaped patch is then sewn to the healthy septal endocardium with
a continuous suture. e lateral side of the patch is then sutured to
the posterior wall of the le ventricle along a line corresponding to
the medial margin of the base of the posteromedial papillary muscle.
Since the posterior wall of the le ventricle is infarcted, it is oen necessary to use full- thickness bites and to anchor the sutures on a strip
of pericardium or Teon® felt on the epicardial surface of the posterior wall of the le ventricle as shown in Fig. 68.2. Once the patch
is completely sutured to the mitral annulus, the endocardium of the
interventricular septum, and the full thickness of the posterior wall,
the ventriculotomy is closed in two layers of sutures buttressed on
strips of pericardium or Teon® felt. e infarcted right ventricular
wall is le undisturbed.
Alternative strategies to address a large posterior VSD have also
been utilized. e two- patch technique described by Madsen and
Daggett is one such technique that has been used frequently. In
brief, the posterior VSD is visualized by either a ventriculotomy
made through the inferior right or le ventricular wall parallel to
the posterior descending artery. e VSD is then closed with the
rst patch, usually placed from the le ventricular aspect of the
VSD. e defect in the right or le ventricle is then closed with a
second patch.
Postinfarction ventricularpseudoaneurysm
When the diagnosis of le ventricular pseudoaneurysm is made
soon (within a few months) aer myocardial infarction, urgent
surgery following coronary angiography is usually recommended
because of the unpredictability and high risk of rupture. If the diagnosis is made several months or years aer infarction, the timing of
an operation is generally determined by the symptoms and severity
of coronary artery disease instead of the risk of rupture which is generally considered much lower than in the acute phase.
Le ventricular pseudoaneurysms are repaired using techniques
that are similar to repair of true ventricular aneurysms. Most acute
ventricular pseudoaneurysms are optimally repaired with a circular
or endocardial patch of either glutaraldehyde- xed bovine pericardium or Dacron®. Chronic ventricular pseudoaneurysms can be repaired primarily with closure of the neck of the pseudoaneurysm
which is usually brotic aer it has healed. Importantly, posterior
pseudoaneurysms whether acute or chronic, are safer to reconstruct
and close with a patch so as to not distort the mitral valve apparatus
and cause worsening of mitral regurgitation.
Aer median sternotomy and aortic cannulation, a single two-
Fig.68.2 Repair of posterior VSD by endocardial patch with infarct
exclusion. Pericardial patch is sutured to mitral annulus, septum, and
posterior wall.
Reproduced from David, TE., Dale, L., and Sun, Z.J Thorac Cardiovasc
Surg. 1995;110:1315– 22 with permission from Elsevier.
stage cannula is placed in the right atrium with care taken to not
disturb the le ventricle as disruption of the pseudoaneurysm
may occur and there is a risk of embolization of intramural
thrombus. Cardiopulmonary bypass with systemic hypothermia
to 32°C is typically used. e ascending aorta is cross- clamped and
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antegrade cold blood cardioplegia is delivered through the aortic
root. Retrograde cardioplegia may also be used but the risk of disruption of the pseudoaneurysm with placement of the retrograde
cardioplegic cannula should also be considered and thus is usually avoided until the patient is placed on cardiopulmonary bypass. Ale ventricular vent is placed through the right superior
pulmonary vein. e location of the pseudoaneurysm with its adhesions to the pericardium are identied. Distal coronary targets
for bypass are also identied. e pseudoaneurysm is opened and
the neck of the aneurysm is identied between the le ventricle
and the pseudoaneurysm chamber. As mentioned previously,
generally a circular patch is used to close the defect which is usually small. Aglutaraldehyde- xed bovine pericardium or Dacron®
patch is trimmed to a circular shape larger (and much larger in
the setting of an acute infarct) in diameter than the neck of the
pseudoaneurysm. e patch is then sewn to either the brotic rim
at the neck of the pseudoaneurysm or in the acute infarct scenario,
to healthy viable myocardium using a running 3- 0 polypropylene
suture interrupted at three or four locations along the suture line
as shown in Fig. 68.3. e pseudoaneurysm wall is then closed
over the patch with a double layer of running 2- 0 or 3- 0 polypropylene sutures. Coronary artery bypass graing is then performed
in the usual manner. Once revascularization and repair of the
pseudoaneurysm are complete, the patient is weaned from cardiopulmonary bypass in the usual manner.
lethal complication of myocardial infarction continues to be a surgical challenge due to its rare occurrence.
e specic impact and long- term benet of concomitant coronary revascularization at the time of postinfarction VSD repair has
been reported by Muehrcke and colleagues in 75 patients undergoing
postinfarction VSD repair. Among patients who did not undergo
concomitant coronary bypass of angiographically demonstrated
stenotic coronary arteries at the time of VSD repair, 5- and 10- year
actuarial survival were 29% ± 11% and 0% compared to 72% ± 8%
and 48% ± 10% respectively in patients who underwent multivessel
bypass graing (P = 0.0015). Similarly, Cox and colleagues reported their experience with 109 consecutive patients undergoing
postinfarction VSD repair. In this cohort of patients, 41% underwent coronary artery bypass graing and the authors found incomplete revascularization was associated with a 12- fold increase in the
risk for late cardiac death (30days aer primary operation). us,
these results suggest that concomitant myocardial revascularization
at the time of postinfarction VSD repair signicantly improves late
survival and should be performed in all patients.
Repair of the postinfarction ventricular pseudoaneurysm continues to be a high- risk surgical procedure. In one of the rst series
of results of surgical treatment, 12 patients underwent repair of
ventricular pseudoaneurysm at our institution, with four patients
receiving mitral valve replacement, and nine receiving concomitant coronary artery bypass. e operative mortality was 25%,
and all deaths occurred in patients requiring mitral valve replace-
Outcomes
ment. Of the patients who survived the operation, all were alive
aer a mean follow- up of 62months. e largest experience with
postinfarction pseudoaneurysm repair was described by Frances
Surgical outcomes following repair of postinfarction VSD have
improved with advances in surgical technique. Daggett and colleagues reported an improved in- hospital mortality of 30% with
their strategy of prompt surgery, cold cardioplegia, and the liberal
use of infarctectomy and patch repair. e use of an infarction exclusion technique further improved the results of VSD repair in this
setting. Among 52 consecutive patients at our institute undergoing
postinfarction VSD repair using the infarction exclusion technique,
two- thirds of whom were in cardiogenic shock at the time of the
operation, a 19% operative mortality was observed. Furthermore,
the actual survival at 8years was 59% with only two patients having
a small residual VSD at a mean follow- up of 40 ± 34 months.
e largest report of the experience with postinfarction VSD repair has been described by Arnaoutakis and colleagues who performed a retrospective review of the Society of oracic Surgeons
National Database identifying 2876 adult patients who underwent
postinfarction VSD repair between 1999 and 2010. Of these patients, 65% were supported with an intra- aortic balloon pump pre-
and colleagues who reported an operative mortality of 23% among
107 patients undergoing surgical ventricular pseudoaneurysm repair. All 82 patients surviving the initial operation were alive at a
median of 46 weeks. Most recently, 30 patients undergoing repair
of postinfarction le ventricular pseudoaneurysm at the Cleveland
Clinic was reported by Atik and colleagues with a hospital mortality
of 20%. Among these patients, 57% received concomitant coronary artery bypass graing. Late survival in their cohort of patients
was 73%, 59%, and 45% at 1, 5, and 8years, respectively. us, repair of postinfarction le ventricular pseudoaneurysm continues to
have a high operative mortality, particularly in those requiring concomitant mitral valve surgery. e benet of concomitant coronary
bypass graing at the time of ventricular pseudoaneurysm repair
has not been specically evaluated; however, given the ischaemic nature underlying the postinfarction pseudoaneurysm, optimization
of coronary perfusion to viable myocardium would be anticipated
to confer long- term benet similar to that observed for concomitant
revascularization performed at the time of VSD repair.
operatively and concomitant coronary artery bypass graing was
performed in 64% of patients. e operative mortality was 54% if
a repair was performed within 7days of infarction and only 18%
Conclusion
if performed more than 7days aer infarction. e overall operative mortality was 43%. e most common cause of death (77%) was
cardiac in nature. Age, female sex, shock, preoperative intra- aortic
balloon pump use, moderate to severe mitral insuciency, redo operation, and emergency status were independently associated with
a greater odds of operative death. us, the general experience with
postinfarction VSD repair is relatively poor and this potentially
Postinfarction VSD and ventricular pseudoaneurysm continue to
be rare complications of AMI. Because they are rare, surgical experience with these conditions is generally limited. Advancements
in surgical technique and experience have, however, resulted in improved survival following these operations. e infarction exclusion
technique for repair of postinfarction VSD in particular has resulted
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Fig.68.3 Surgical treatment of a posterior left ventricle
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aneurysm walls. The black arrow shows the neck between the left
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pseudoaneurysm gateway (black arrow).
Reproduced from Garrido, J., Ferreiro, A., Rodríguez- Vázquez, J., Prada, P., Verdugo, S.,
Silva, J., López- Checa, S.and Sánchez- Montesinos, I.(2014) Left Ventricle Postinfarction
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