Repair of Postinfarction Ventricular Septa1 Defect
Tirone E. David
Postinfarction ventricular septa1 defect (VSD) is the
second most common form of cardiac rupture.1-2It has
been reported to complicate 1% to 2% of all acute
transmural myocardial infarction^."^ Although no re-
cent epidemiological data are available, we believe that
the incidence of this mechanical complication of myocar-
dial infarction is decreasing because of medical interven-
tions during the acute stages of the myocardial infarc-
tion.
Anterior postinfarction VSD is slightly more common
than posterior VSD."-s Most anterior ruptures occur in
the distal half of the septum and most posterior rup-
tures occur in the proximal half of the septum. The
myocardial infarction must be transmural and quite
extensive to cause a VSD.6 Quantitative analysis of
acute right and left ventricular infarction in autopsied
hearts with acute postinfarction VSD revealed that with
anterior VSD approximately 33% of the left ventricle
and 10% of the right ventricle was infarcted whereas
with posterior VSD approximately 20% of the left
ventricle and 33% of the right ventricle was infarcted.6
Right ventricular dysfunction appears to be a major
cause of heart failure and cardiogenic shock in patients
with posterior VSD.7-xIt appears that left ventricular
dysfunction caused by extensive loss of the leftventricu-
170 Operative Techniques in Cardiac Q Thoracic Surgery,Vol2, No 2 (May), 1997: pp 170-178
lar mass is the principal cause of cardiogenic shock in
patients with anterior VSD.'
The development of congestive heart failure and
cardiogenic shock are the most important determinants
of the outcome of patients with postinfarction VSD.''
These two factors are dependent on the magnitude of
the right and left ventricular infarctions. Almost 80% of
all patients with postinfarction VSD develop cardio-
genic shock or congestive heart failure leading to early
surgical treatment o r death."'-ll Cardiogenic shock has
been the single most important predictor of operative
mortality in these patients.8~'o-'sFor this reason conser-
vative treatment of hemodynamically stable patients is
not advisable because eventually most of then1 develop
congestive heart failure and/or cardiogenic shock. He-
modynamically stable patients should undergo coro-
nary arteriography as soon as the diagnosis of VSD is
made, and surgery should be performed on an urgent
basis. Patients in heart failure o r in cardiogenic shock
should be started on vasodilators and inotropes, have
an intra-aortic balloon pump inserted, and, if oxygen-
ation is a problem, they should have tracheal intubation
and be placed on assisted ventilation. Coronary arteri-
ography should be performed and followed by immedi-
ate surgery.
SEPTAL RlJPTURE 171

SURGICAL TECHNIQUE

The ascending aorta and both cavae are cannulated for
cardiopulmonary bypass. Because the majority of these
patients have suffered a recent myocardial infarction
and are in acute heart failure, attention to myocardial
protection is of utmost importance. Patients with mul-
tivessel disease should have coronary artery bypass
before the VSD is repaired. We d o not believe that the
artery that supplies the ruptured septum should be
bypassed, except in patients with apical VSD when the
occlusion of the left anterior descending is proximal to
the first septa1 perforator.

1 Repair of apical VSD. If the VSD is located in the apex of the left ventricle, simple excision of the apex and
reconstruction of the ventricles by reapproximating the right and left ventricular walls to the septum with large Teflon
buttressed sutures is all that is required to repair the ruptured septum. (Reproduced with permission from David TE:
Mechanical Complications of Myocardial Infarction. R.G. Landes, Austin, TX).
172 TIRONE E. DAVID

2 Hepair of anterior VSD. A ventriculotomy is performed in the apex of the left ventricle through the infarcted
anterolateral wall. This incision is started in the apex and extended into the anterior wall parallel to the left anterior
descending artery. Stay sutures are placed through the margins of the incision to expose the infarcted septum and the VSD. A
patch of glutaraldehyde fixed bovine pericardium is tailored in an oval shape of approximately 6 cm X 4 cm. This patch is
sutured to noninfarcted interventricular septum all around the rupture with a continuous 3-0 polypropylene suture. The bites
should be 5 mm from each other and at least 6-8 mm deep in the septal muscle. Care must be exercised not to tear the septal
muscle during this suturing. We find it safer to pass several separate bites through the patch and through the muscle before
gently pulling each loop of suture to approximate the patch to the septum. This suture is interrupted at the junction of the
septum and the anterior ventricular wall. Depending on the size of the infarct, the patch may have to be retailored to a smaller
size before it is sutured to the endocardium of the anterior wall of the left ventricle. The pericardial patch is sutured to
noninfarcted endocardium of the anterior wall with a continuous 3-0 polypropylene. If the infarct in the anterior wall extends
to the base of the anterior papillary muscle, the sutures should be brought outside of the heart just before the level of the base
of the anterior papillary muscle and anchored on a strip of pericardium or Teflon felt placed on the epicardial surface of the
anterior wall of the left ventricle. When the suturing is completed, the left ventricle will have been excluded from the infarcted
septum. (Reproduced with permission from David TE, et al: J Thorac Cardiovasc Surg 110:1315-1322, 1995.)
SEPTAL RUPTURE 173

3 The ventriculotomy is closed over the pericardial patch in two layers of sutures buttressed on a strip
of pericardium or Teflon felt on each side. The first layer is performed with interrupted horizontal
mattress sutures and the second layer with a continuous 2-0 polypropylene suture.
174 TIRONE E. DAVID

4 Repair of Posterior VSD. An incision is made in the inferior wall of the left ventricle 1or 2 mm from
the posterior dwcending artery. This incision is started at the midportion of the inferior wall and extended
proximally toward the base of the heart until the posterior mitral valve annulus is easily visualized. I t is
also extended toward the apex at least to the level of the base of the posterior papillary muscle which
invariably is infarcted in these patients. Stay sutures are applied to the margins of the ventriculotomy to
expose the septum and mitral valve. A bovine pericardial patch is tailored in a triangular shape of at least
4 rm X 7 cm. The base of this patch is sutured to the fibrous portion of the posterior mitral annulus with a
continuous 3-0 polypropylene suture starting 1 cm lateral to the midscallop of the posterior leaflet of the
mitral valve and moving medially until it reaches noninfarcted septum. This suture is interrupted at this
level, and a new one is used to sew the patch to noninfarcted septum. After the base and the septa1 side of
the patch are sutured, it is retailored as needed to fit inside the ventricular cavity. A new suture is started
in the junction of the base of the patch and the lateral aspect of the mitral annulus where the very first
suture was placed. These two sutures are tied together, and the new one is used to sew the patch of the
posterior wall of the left ventricle. These bites must be full-thickness because the posterior wall is
infarcted. The sutures are anchored on a strip of pericardium or Teflon felt placed on the epicardium. It is
safer to interrupt this suture after every two or three bites between the patch and posterior ventricular
wall. Care must be taken not to include chordae tendineae in this suture line. Once this suture line is
completed the patch will lie immediately medial to the posterior papillary muscle and the left ventricular
cavity will be excluded from the infarcted septum. (Reproduced with permission from David TE, et al:
J Thorac Cardiovasc Surg 110:1315-1322,1995.)
SEPTAL RUPTURE 175

5 The posterior ventriculotomy is closed in two layers of

sutures buttressed on strips of Teflon felt. (Reproduced with
permission from David TE, et al: J Thorac Cardiovasc Surg
110:1315-1322,1995.)
176 TIHONE E. DAVID

Case Illustration
The following photographs were t a k e n d u r i n g re-
pair of' a n acute posterior VSD i n a 78-year-old m a n
in cardiogenic shock. This patient required tempo-
r a r y dialysis for renal failure b u t remains alive f o u r
years postoperatively. (Reprinted with permission
from David T E : Mechanical Complications of Myo-
cardial Infarction. R.G. Landes Company, Austin,
TX, 1993.)

6 Surgeon's view with apex of heart retracted to upper left of

photo. A ventriculotomy is performed immediately lateral and
parallel to the posterior descending coronary artery.

7 The ventricrilotomy is extended from just 8 Bovine pericardium is sutured to the mitral
1)elow tht. apex (top of photo) to the base of the annulus with a continuous 3-0 polypropylene su-
heart. Stay sutures are placed on the margins to ture.
expose the septum and the mitral valve. Note the
extensive muscle necrosis and the ruptui sep-
tum.
SEPTAL RIIPIWRE 177

9 The medial aspc:ct of the patch is su tured to healthy

endocardium of the interveii tricular SISptum flrom the
mitral annulus to the apex.

10 The patch is re-tailored a n d its lateral 11 The ventriculotomy is closed with large
aspect is sutured to the infarcted posterior wall. I n sutures 1,uttresseci on strips of perirardium. N o
this suture line thv stitches must he brought outside infarctectomy was performed.
of the heart a n d buttressed on a strip of pericar-
ciium placed on the epicardial surface of the poste-
rior wall.
178
Discontinuation of Cardiopulmonary Bypass
Most patients with postinfarction VSD require inotro-
pes to he weaned from cardiopulmonary bypass. Intra-
operative Doppler echocardiography is a valuable tool
in these patients to assess ventricular function, dimen-
sions, residual shunt, and mitral regurgitation. Mitral
regurgitation in patients with posterior VSD is common
but seldom severe. Mitral valve replacement is neces-
sary when severe mitral regurgitation is present.
Patients with extensive infarction often remain in
c-ardiogenic shock after surgery and eventually die.
Experience with ventricular assist devices has been
limited in these patients. So is urgent heart trans-
plantation.8
Operative Mortality and Morbidity
The operative mortality for postinfarction VSD is high;
it ranges from 20% to 40%.8710,13-'6 The operative
mortality varies with the preoperative clinical status of
the patients, timing of operation in relation to the
myocardial infarction, location of the infarction and the
patients' age. Carcliogenic shock is the single most
important determinant of outcorne."-l6 Cardiogenic
shock in patients with anterior VSD is often an indica-
tion of extensive loss of left ventricular mass whereas
cardiogenic shock in posterior VSD is often caused by a
combination of factors but right ventricular dysfunc-
tion is probably the single most important ~ n e . The ~ - ~
highest operative mortality has been reported in pa-
tients with posterior VSD and cardiogenic shock.lS We
believe that this high mortality was because of operative
techniques that involved resection of the infarcted
septum and ventricular walls, particularly of the right
ventricle. Using the previously described technique of
infarct exclusion, the operative mortality in patients
with posterior VSD is the same as in anterior VSD.16 We
believe that the principal determinant of outcome is the
size of the infarct.
A residual or recurrent VSD has been reported to
occur in 10% to 25% of patients. 13,17-18 We have largely
eliminated this problem since we began to use the
'infarction exclusion technique. "yi12,16 Renal failure is
common in patients with preoperative cardiogenic shock;
one third of our patients in cardiogenic shock required
temporary renal dialysis postoperatively.
Low cardiac output syndrome and its complications
are the most common cause of death after repair of
postinfarction VSD.
Long-Term Survival
Patients who survive the operation have excellent
long-term survival.8~12-'3,1y The reported 5-year actu-
arial survival ranges from 44% to 83%, which is probably
TIRONE E. DAVID
attributed to the wide variation in operative mortal-
ity.8J2-13,1yConcomitant revascularization in patients
with multivessel disease enhances long-term survival. l9
REFERENCES
1. Reddy SG, Roberts WC: Frequency of rupture of the left ventricular
free wall and ventrirular septum among necropsy rases of fatal acute
myocartlial infarction cine introdurtion of coronary care units. Am J
Cartliol 63:906-911, 1989
2 , Vlodacer Z, Edwards JE: Rupture of ventricular septum or papillary
muscle complicating myocardial infarction. Circulation 55:815-822,
1977
3. Luntlbrrg S, Sudrrstrom J : Perforation of the interventric:ular septum
in myorardiai infarction: a study based on autopsy material. Acta Med
Scancl 172:413-418,1962
4. Frncley M, Chang VP, O'Rourke MF: Myorarilial r n p t u r r after acute
myocardial infarrtion: t r n year review. Br Heart J 49:550-556, 1983
5. Dellborg M, Held P, Sweclberg K, Bedin A: Rupture of the myocardium:
occurrenre and risk factors. Br Heart J 54:ll-16, 1985
6. Cummings RC, Reimer KA, Califf R, et al: Quantitative analysis (if right
and left ventricular infarction in the presence of postinfarction ventriru-
lar septal tlefert. Circulation 77:33-42, 1988
_I
Fanapazir L, Bray CL, Dark JF, et al: Right ventricular clyfifnnction a n d
snrgiral outcome in postinfarc-tion ventrirular septal defect. Eur Heart J
4:155-167, 1983
8 . Deville C, Fontan F, Chevalier JM. et al: Surgery of post-infarction
ventricular septal (1efei.t: risk factors for hospital death and long-term
results. E u r J Cardiuthorar Surg 5:167-175, 1991
9. David TE: Surgery for postinfarction ventrirular septa1 defert. In:
David T E , ed. Mechanical romplirations of myocartlial infarction.
Austin, TX, R.G. Lanties, 1993,p p 1 7 5 1 9 1
10. Radford MJ, Johnson RA, Daggett WM Jr, et al: Ventricular septal
rupture: a review of clinical and physiologir features and an analysis of
survival. Cirrulation 64:545-583, 1981
11. Lemery R, Smith HC, Giuliani ER, Gersh BJ: Prognosis in rupture of
the ventricular septum after acute myocardial infarction and role of
early surgical intervention. Am J Cardiol70:147-151, 1992
12. Koineda M, David T E , Fremes SE: Surgical repair of postinfarction
ventricular septal defect. Circulation 82:243-247, 1990
13. Skillington PD, Lamb RK, Monro JL, et al: Surgical treatment for
infarct related ventricular septal defects. Improved early results com-
bined with analysis of late functional status. J Thorar Cardiovasr Surg
99:798-808, 1990
14. Norell MS, Gershlick H, Pillai R, et al: Ventricular septal rupture
compliration myocardial infarction: Is early surgery justified? E u r
Heart J 8:1281-1286,1987
15. Moore CA, Nygaard TW, Kaiser DL, et al: Postinfarction ventricular
septal rupture: The importanre of location of infarction and right
ventricular funrtion in determining survival. Circulation 74:45-55, 1986
16. David T E , Dale L, Sun Z: Postinfarction ventricular septal rupture:
repair by enclocardial patch with infarct exclusion. J Thorac Cardiovasr
Surg 110:1315-1322,1995
17. Daggett WM, Burkley MJ, Akins CW, et al: Improved renults of surgical
management of postinfarction ventricular septal rupture. Ann Surg
89269-277, 1982
18. Sranlon PJ, Montoya A, Johnson SA, et al: Urgent surgery for
ventricular septal rupture complicating acute myocardial infarction.
Circulation 72(supplII):185-190, 1985
19. Heitmiller R, Jacobs ML, Dasgctt WM:Surgicalmanagementofpostinfarction
ventricular septal rupture. Ann Thorac Surg 41:683-691,1986
From the Division of Cardiovascular Surgery of the University of Toronto and
The Toronto Hospital, Toronto, Ontario, Canada.
Address reprint requests to Tirone E. David, MD, 200 Elizabeth Street,
13EN219, Tnronto, Ontario, Canada M5G 2C4.
Copyright 0 1997 by W.B. Saunders Company
1085-S637/97/0202-ooO7$5.~/0