Arnaoutakis, George J.

Conte, John V.

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Repair of Postinfarct Ventricular Septal Defect: Anterior Apical Ventricular Septal Defect 

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mi.eduRepair of Postinfarct Ventricular Septal Defect:
Anterior Apical Ventricular Septal Defect
George J. Arnaoutakis, MD, and John V. Conte, MDA post–myocardial infarction (MI) ventricular septaldefect (VSD) is a rare but frequently fatal complication,
occurring in less than 1% of patients suffering MI in the era
of early reperfusion therapy.1 In patients with this
complication receiving medical therapy alone, mortality
rates exceed 90%, whereas in patients undergoing surgical
repair, mortality ranges between 19% and 60%. Cooley
performed the ﬁrst open repair of a VSD in 1957. Daggett
et al2 developed an infarctectomy and patch technique in
1977, which was the standard approach used by many
surgeons. The prognosis for these patients remained poor,
with mortality rates of approximately 50%. David and
Armstrong3 described an endocardial patch technique with
infarct exclusion in 1995, with documented reductions in
operative mortality to 19% in the Toronto series. Despite
advances in the perioperative management of these patients,
VSD repair still has the highest operative mortality among
operations reported to the Society of Thoracic Surgeons
adult cardiac surgery database.4
The diagnosis of a post-MI VSD should be suspected by
the history of a recent MI along with a new pansystolic
murmur. These patients often have signiﬁcant hemodynamic
compromise. Some patients may have small defects that limit
hemodynamic impairment, and may lead to a delayed
diagnosis. Other diagnoses that should be considered in the
setting of recent MI and new cardiac murmur include
ruptured papillary muscle with mitral regurgitation or
ischemic mitral regurgitation. A left-to-right shunt is usually
present, and the diagnosis can be conﬁrmed with either
transthoracic or transesophageal echocardiography. Ventri-
culography performed during coronary angiography can also
conﬁrm the diagnosis.
Anterior defects typically occur in the anterior septum in
patients who have left anterior descending artery occlusion.
Areas of left ventricular myocardium beyond the infarction
can be hyperdynamic owing to unloading of volume into the
lower-pressure right ventricle (RV). However, the acute
volume overload presented to the RV can lead to severe right
ventricular dysfunction and congestive heart failure. In a
minority of patients, VSDs are detected late after the original
MI because of investigations for an incidentally discoveredfront matter r 2014 Elsevier Inc. All rights reserved.
/10.1053/j.optechstcvs.2014.03.002
rgery, The Johns Hopkins Hospital, Baltimore, MD
ts to John V. Conte, MD, Division of Cardiac Surgery,
s Hospital, Baltimore, MD 21287. E-mail: jconte@jhpansystolic murmur. In these patients, the defects are usually
small and rarely cause hemodynamic compromise.Preoperative Considerations
Without surgical intervention, the prognosis for patients
with post-MI VSD is grave. Mortality ranges from 60%-70%
in the ﬁrst 2 weeks, with approximately 90% mortality at
3 months.4 However, patients who undergo surgical repair
in the setting of profound shock also have high operative
mortality. Therefore, it is important for the surgeon to
evaluate the patient carefully and optimize the cardiopulmo-
nary status before proceeding to the operating room.
Many patients with post-MI VSD will require preoperative
cardiovascular support with an intra-aortic balloon pump.
The intra-aortic balloon pump improves hemodynamics,
augments coronary perfusion, and may permit safer
coronary angiography. Vasodilators and inotropes should
be administered as necessary to preserve organ perfusion.
Inhaled nitric oxide or other pulmonary vasodilators are
important adjuncts in this setting to decrease pulmonary
resistance. However, a reduction in pulmonary vascular
resistance may increase shunting, so this must be considered
before administering these agents. Preoperative coronary
angiography must be performed to deﬁne coronary anatomy
and the need for concomitant revascularization.5 Extrac-
orporeal membrane oxygenation has been used with success
to stabilize patients and correct metabolic abnormalities
before surgery.
The timing of surgery is critical. Although high risk,
patients with continued hemodynamic decline should
undergo early surgical intervention, often within 24 hours
of diagnosis, to minimize the progressive organ dysfunction.
Though the data are retrospective, a Society of Thoracic
Surgeons (STS) report showed that patients with a longer
time interval between MI and surgical repair experience
improved outcomes. Therefore, patients who demonstrate
progressive hemodynamic improvement can await surgical
repair until the clinical condition has been optimized,
typically a period of 1-7 days.
When concomitant coronary revascularization is planned,
saphenous vein harvest should occur simultaneously
with the sternal incision. To avoid prolonged aortic cross-
clamp times, only severely stenotic coronary lesions should
be bypassed. Revascularization of the occluded artery
Repair of postinfarct VSD 97responsible for the VSD is of questionable beneﬁt, as this
territory generally represents nonviable myocardium. We
favor performing the anastomoses before VSD repair,
permitting infusion of cardioplegia through the conduit.
Because the infarcted myocardium is friable, manipulation
and retraction of the heart during coronary revascularization
should be done carefully to prevent dislodging necrotic
intracardiac muscle.Operative Considerations
There are many different techniques that have been used
successfully to repair post infarction VSD. Most techniques
break down into patch techniques, either single or double,
or infarct exclusion techniques. Primary repair techniques
and percutaneous or hybrid techniques using closure devices
are used less frequently.6
It is often difﬁcult to determine exactly where the actual
communication in the infarcted, hemorrhagic septum is
located, and the quality of the tissue often makes sutureplacement difﬁcult. Excessive debridement is generally
discouraged. Placing sutures a signiﬁcant distance away
from the infarcted septum and generous patches is a good
idea. Continuous or interrupted suture techniques may be
used. Reinforcing the patches or the ventriculotomy closure
with buttresses is sometimes helpful, and avoiding tension
on the suture lines is imperative.
Here we demonstrate the 2-patch technique and the
exclusion techniques. The quality of the superior septal
tissue affects how the sutures are placed to complete the
septal repair and how the 2 patches are related. The
2 patches can be completely separate or connected to
reconstruct the junction between the septum and the
anterior wall.
The exclusion technique is sometimes hard to visualize. A
patch of bovine pericardium, dacron, or other material is
used to separate the left ventricle from the infarcted septum.
Some ﬁnd it helpful to think of it conceptually as creating a
new left ventricle by constructing a new septum parallel to
the infarcted septum and leaving the old septum as part of
the RV cavity (Figs. 1-14).
Figure 1 Infarct in the region of the left anterior descending (LAD) coronary artery. Drawing by Timothy H. Phelps, MS FAMI, Associate
Professor, Department of Art as Applied to Medicine, Johns Hopkins University School of Medicine, Baltimore, MD.
Infarct Exclusion Technique
G.J. Arnaoutakis and J.V. Conte98
Figure 2 Anterior ventriculotomy through anterior wall infarct parallel to LAD vessel exposing infarcted septum with ventricular septal defect
(VSD). LAD ¼ left anterior descending. Drawing by Timothy H. Phelps, MS FAMI, Associate Professor, Department of Art as Applied to
Medicine, Johns Hopkins University School of Medicine, Baltimore, MD.
Repair of postinfarct VSD 99
Figure 3 Patch begun in inferior border of septum. The patch will be used to create a “neoseptum” between the LV and the old septum where
the VSD lies. Deep bites are taken through healthy tissue. Interrupted pledgeted sutures may be used primarily or to reinforce a continuous
suture line. Drawings by Timothy H. Phelps, MS FAMI, Associate Professor, Department of Art as Applied to Medicine, Johns Hopkins
University School of Medicine, Baltimore, MD.
G.J. Arnaoutakis and J.V. Conte100
Figure 4 Suture line continued cephalad creating “neoseptum.” Sutures must be passed through healthy tissue. The annulus of the mitral valve
can be used to secure patch to healthy tissue. Drawing by Timothy H. Phelps, MS FAMI, Associate Professor, Department of Art as Applied to
Medicine, Johns Hopkins University School of Medicine, Baltimore, MD.
Repair of postinfarct VSD 101
Figure 5 Continuation of suture line inferiorly and to completion. Drawing by Timothy H. Phelps, MS FAMI, Associate Professor, Department
of Art as Applied to Medicine, Johns Hopkins University School of Medicine, Baltimore, MD.
G.J. Arnaoutakis and J.V. Conte102
Figure 6 Cross-section of ventricle demonstrating “neoseptum” and separation of old infarcted septum from high pressure LV. VSD ¼
ventricular septal defect. Drawings by Timothy H. Phelps, MS FAMI, Associate Professor, Department of Art as Applied to Medicine, Johns
Hopkins University School of Medicine, Baltimore, MD.
Repair of postinfarct VSD 103
Figure 7 Completion of repair by linear closure reinforced with strips of felt or pericardium. Drawing by Timothy H. Phelps, MS FAMI,
Associate Professor, Department of Art as Applied to Medicine, Johns Hopkins University School of Medicine, Baltimore, MD.
G.J. Arnaoutakis and J.V. Conte104
Figure 8 Infarct in the region of the left anterior descending (LAD) coronary artery. Drawing by Timothy H. Phelps, MS FAMI, Associate
Professor, Department of Art as Applied to Medicine, Johns Hopkins University School of Medicine, Baltimore, MD.
Two Patch Technique
Repair of postinfarct VSD 105
Figure 9 Anterior ventriculotomy through anterior wall infarct parallel to LAD vessel exposing infarcted septum with ventricular septal defect
(VSD). Drawing by Timothy H. Phelps, MS FAMI, Associate Professor, Department of Art as Applied to Medicine, Johns Hopkins University
School of Medicine, Baltimore, MD.
G.J. Arnaoutakis and J.V. Conte106
Figure 10 Interrupted pledgeted sutures placed at base of septum through healthy tissue away from infarcted tissue and VSD. Sutures then
placed through “ﬁrst” patch, which is cut to size. Drawing by Timothy H. Phelps, MS FAMI, Associate Professor, Department of Art as Applied
to Medicine, Johns Hopkins University School of Medicine, Baltimore, MD.
Repair of postinfarct VSD 107
Figure 11 Completed septal patch repairing VSD. Drawing by Timothy H. Phelps, MS FAMI, Associate Professor, Department of Art as Applied
to Medicine, Johns Hopkins University School of Medicine, Baltimore, MD.
G.J. Arnaoutakis and J.V. Conte108
Figure 12 Drawing by Timothy H. Phelps, MS FAMI, Associate Professor, Department of Art as Applied to Medicine, Johns Hopkins University
School of Medicine, Baltimore, MD.
Repair of postinfarct VSD 109
Figure 13 (A) Cross-section of ventricle demonstrating patch repaired with sutures entirely within LV. VSD ¼ ventricular septal defect.
G.J. Arnaoutakis and J.V. Conte110
Figure 13 (Continued) (B) Cross-section of ventricle demonstrating patch repaired with sutures placed on anterior wall of right ventricle owing
to poor quality of superior septal tissue.
Repair of postinfarct VSD 111
Figure 13 (Continued) (C) Cross-section of ventricle demonstrating patch repaired with sutures from anterior surface of RV and through patch
to complete repair of septum and anterior LV wall with a patch-to-patch junction of septum and anterior wall. Drawing by Timothy H.
Phelps, MS FAMI, Associate Professor, Department of Art as Applied to Medicine, Johns Hopkins University School of Medicine,
Baltimore, MD.
G.J. Arnaoutakis and J.V. Conte112
Figure 14 Completed 2-patch repair with use of second patch to reconstruct anterior LV wall. Drawing by Timothy H. Phelps, MS FAMI,
Associate Professor, Department of Art as Applied to Medicine, Johns Hopkins University School of Medicine, Baltimore, MD.
Repair of postinfarct VSD 113
G.J. Arnaoutakis and J.V. Conte114Postoperative Management
Management in the intensive care unit is similar to any
patient with severely compromised ventricular function,
including ventilator and ﬂuid management. Early institution
of continuous hemodialysis is sometimes beneﬁcial. Ar-
rhythmias are common and striking a balance between
antiarrhythmic medications and inotropes is sometimes
difﬁcult. The intra-aortic balloon pump and inotropic
support often remain necessary for prolonged periods. We
customarily wean inhaled nitric oxide before discontinuation
of the intra-aortic balloon pump.Conclusions
Postinfarction VSD is a rare complication of MI, yet these
patients have high mortality. Both a national registry study
from Europe as well as data from the STS national database
documented 40% mortality after postinfarction VSD re-
pair.4,7 A single-institution series of 32 patients undergoing
postinfarction VSD repair reported a 31% operative mortal-
ity, but among patients who survived to hospital discharge,
the 5-year actuarial survival was 79%.8 Careful patient
selection and timing of repair before the onset of organ
dysfunction offers the best possible chance of survival with
surgical repair. We routinely employ 1 of the 2 techniques
described in this report to treat postinfarction VSD. There
are no good data favoring the use of either technique because
postinfarction VSD is such a rare condition. The decision on
which technique to use is patient dependent and often made
in the operating room, based on the extent of the defect as
well as the relative condition of the septal tissue surrounding
the defect. A recent report from the STS database suggests
that the use of percutaneous technology to treat VSDs does
not seem to have had an effect on the use of surgical
intervention, as annual numbers of procedures haveremained relatively constant.4 The keys to a successful
operation include the following: (1) optimal timing of
surgery with adequate preoperative resuscitation, (2) close
collaboration with anesthesia and perfusion colleagues
intraoperatively to maintain adequate organ perfusion,
(3) accurate and rapid assessment of the extent of the defect
size and devitalized tissue in the septum and anterior wall,
and (4) determination of the optimal surgical technique and
an efﬁcient intraoperative strategy to achieve a satisfactory
and durable repair.References
1. Crenshaw BS, Granger CB, Birnbaum Y, et al: Risk factors, angiographic
patterns, and outcomes in patients with ventricular septal defect
complicating acute myocardial infarction. GUSTO-I (Global utilization
of streptokinase and TPA for occluded coronary arteries) trial
investigators. Circulation 101:27–32, 2000
2. Daggett WM, Guyton RA, Mundth ED, et al: Surgery for post-myocardial
infarct ventricular septal defect. Ann Surg 186:260–271, 1977
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Repair of Postinfarct Ventricular Septal Defect: Anterior Apical Ventricular Septal Defect

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