Keywords : postinfarct ventricular septal defect, Operations for Coronary Artery Disease
Postinfarction Ventricular Septal
Defect Repair
Step 1. Surgical Anatomy
·
Postinfarction ventricular septal
defects (VSDs) are classified as occurring in three locations apical, anterior,
and posteroinferior (Fig. 8.1). Most common is an anterior or apical defect
caused by anterior septal myocardial infarction after occlusion of the left
anterior descending coronary artery. In about one-third of patients, the
rupture occurs in the posterior septum after an inferior septal infarction. The
inferior septal infarction is usually due to occlusion of a dominant right
coronary or, less frequently, of a dominant circumflex artery. An apical septal
defect can be considered a variant of an anterior defect, but it presents the
opportunity for a modified, and less involved, surgical technique.1,2
·
Associated with the septal defect
is a variable amount of adjacent myocardial damage, both septal and free wall.
In addition, the posterior papillary muscle is often involved in a posterior
postinfarction septal defect. When the free wall infarction involves the
papillary muscle, special techniques must be used to anchor the repair, or a mitral
valve replacement should be undertaken.1,2
Step 2. Preoperative Considerations
· Without surgery, 50% of patients
with a postinfarction VSD will die within 24 hours, and 80% will die within 4
weeks. Therefore, the presence of this defect is considered an urgent
indication for operation. The goal of preoperative management is to reduce the
left-to-right shunt by reducing both the systemic vascular resistance and left
ventricular pressure.
·
In addition, efforts are made to
maintain cardiac output and arterial pressure to aid in end- organ perfusion.
Placement of an intraaortic balloon pump is greatly beneficial and should be
done as soon as the diagnosis is made. Patients in severe failure who are
deemed hopeless candidates for immediate operation can be managed with an
intraaortic balloon pump or with mechanical circulatory support in an attempt
to delay surgery.
·
The use of a ventricular assist
devices and extracorporeal membrane oxygenation (ECMO) with staged repair of
the postinfarct VSD has been described. Left ventricular assist devices may
result in a greater degree of right-to-left shunting; therefore, biventricular
assist devices are preferred. ECMO may allow for support and resuscitation of
critically ill patients in cardiogenic shock. ECMO can be instituted using
central or peripheral cannulation. The type of cannulation should be determined
on a case by case basis. Mechanical circulatory support for a short amount of
time can be used to reverse end-organ damage. In addition, it can provide some
time for infarct maturation, allowing for firmer tissue at the time of surgical
repair.3,4
· In select patients, percutaneous
closure is possible. The primary limitation is the friable condition of the
surrounding septal muscle and proximity to the mitral valve or papillary
muscles. Given reports of frequent early failure, this approach may best be
used as an interim measure before surgery. The approach is more likely to be
successful in delayed presentations or as treatment for recurrent defects that may
occur between a repair patch and adjacent noninfarcted myocardium.5 The advent
of the Amplatzer Muscular VSD Occluder (St. Jude Medical, St. Paul, MN) has
shown potential for being an effective percutaneous treatment for extremely
high-risk patients with postinfarct VSD.6
· Controversy exists over the role
of preoperative coronary angiography and concomitant bypass surgery. Those who
argue against preoperative catheterization have noted that there is no survival
benefit and that it is a time-consuming procedure. In addition, because all
patients present with a completed full-thickness infarction, revascularization
of the infarcted territory is of limited value. A selective approach is
appropriate, with catheterization performed in the subset of patients who are
not in shock or severe failure before surgery,7 because some
patients may benefit from revascularization to noninfarcted territories in
which flow-limiting coronary lesions exist.
Step 3. Operative Steps
1. General Principles
· A standard median sternotomy is
performed. Cardiopulmonary bypass is accomplished through the distal ascending
aorta, with bicaval venous drainage. A variety of myocardial protection
strategies are available. Satisfactory protection has been demonstrated with
moderate hypothermia and frequent administration (every 15 to 20 minutes) of
cold oxygenated blood cardioplegia with a combination of antegrade and
retrograde perfusion through the coronary sinus. Other strategies, including
continuous warm cardioplegia, have been used. A flexible left ventricular vent
is placed through the right superior pulmonary vein. To prevent postbypass
coagulopathy, an antifibrinolytic is administered before commencing
cardiopulmonary bypass and is continued as an infusion. The use of surgical
sealants on the epicardial surface of the heart at the location of felt
buttresses may be recommended.
· Areas of full-thickness myocardial
infarction will not hold sutures against pressure. Regardless of the operative
technique or location of the defect, it is critical to anchor suture lines to
noninfarcted tissue. In the endocardium, this is done by taking stitches at
least 5 mm from the zone of necrosis. When this is not possible, stitches are
taken through the full thickness of the free wall, and a buttress of Teflon
felt is used. In this way, strength is afforded by the epicardial portion of
the ventricular wall, and the stress is distributed.7
· There are two general approaches
to the treatment of the necrotic muscle. The first approach emphasizes
débridement of necrotic tissue and tension-free repair, and it usually involves
a prosthetic patch to replace excised tissue. The second approach is to leave
the necrotic tissue in place, but to exclude it by placing a bovine pericardial
patch that circumscribes the infarction. Both techniques are described.
2. Standard Technique: Débridement of Necrotic Tissue
Anterior Apical Defects
◆ The VSD is approached through an incision through the anterior apical
left ventricle (LV), passing through the area of necrosis. After débridement of
necrotic tissue, smaller defects, particularly at the apex, can be closed by
approximating the free walls of the right ventricle (RV) and LV with the septum
using interrupted size 0 polypropylene sutures over Teflon felt strips (Fig.
8.2). It is critical that the stitches pass through healthy muscle.7
◆ Usually, the size of the necrotic tissue prevents a primary
tension-free repair, requiring the use of prosthetic patch material.
Low-porosity Dacron is generally used, although glutaraldehydetreated bovine
pericardium is an alternative. The patch is fashioned to be larger than the
defect. Pledgeted sutures of 1-0 Tevdek are passed from the RV through the
intraventricular septum and then through the patch material (Fig. 8.3A). In the
apical portion, pledgeted sutures are taken through the free wall of the RV
(see Fig. 8.3B). The ventriculotomy is then closed with Teflon felt strips and
no. 1 Tevdek, first using interrupted mattress sutures and then a running
suture as a second layer7
(see Fig. 8.3C).
Posteroinferior Defects
·
Closure of posteroinferior septal
defects poses a greater technical challenge. Simple plication of these defects
is rarely possible. With large defects, this results in unacceptable tension
and reopening or catastrophic disruption. Depending on the size and location of
the defect, one or two patches may be required. In addition, rupture of the
posterior papillary muscle occasionally requires replacement of the mitral
valve.
· A transinfarct posterior incision
is made just to the left ventricular side of the posterior descending coronary
artery (Fig. 8.4A). This incision is started at the midportion of the posterior
wall and extended toward the mitral annulus and apically. Most commonly,
rupture is found in the proximal half of the posterior septum (see Fig. 8.4B)
and involves the pos- teromedial papillary muscle. The necrotic portion of the
ventricular septum is excised, along with the involved portion of the posterior
ventricular free wall (Fig. 8.5A). The free edge of the RV is shaved back to
expose the margins of the defect clearly.
· Rarely, repair of a small septal
rupture can be undertaken primarily. An appropriate lesion would appear as an
unhinging of the posterior attachment to the septum, with little adjacent
myocardial necrosis. The repair is accomplished by approximating the posterior
septum to the free wall of the RV with felt-buttressed mattress sutures of 1-0
Tevdek. The LV can then be closed with a separate suture line, again with
interrupted mattress sutures of no. 1 Tevdek buttressed with felt. A second
running suture line is then taken to reinforce the ventriculotomy closure.
·
More commonly, patches are
required. A single patch can be added to aid in a tension-free closure of the
LV after primary closure of the septum (see Fig. 8.5B). When the defect in the
septum is larger, a two-patch technique is used. Interrupted mattress sutures
of buttressed 2-0 Tevdek are placed circumferentially around the defect. The
sutures are placed on the right ventricular side of the septum and then
transitioned to the epicardial surface of the diaphragmatic right ventricular
free wall. An appropriately shaped Dacron patch is parachuted down after
passage of the stitches. Use of additional felt on the exterior of the patch
cushions the sutures and aids in the even distribution of forces (Fig. 8.6A). A
second patch is now required for closure of the remaining defect into the LV.
·
Mattress sutures of buttressed 2-0
Tevdek are placed circumferentially around the margins of the posterior left
ventricular free wall. The stitches are taken from the endocardial surface
through the ventricular wall so that the patch will lie on the epicardial
surface when the repair is complete (Fig. 8.7; see Fig. 8.6B). Again, use of
additional felt on the outside of the patch may be advantageous (Fig. 8.8).
·
Involvement of the posterior
medial papillary muscle may preclude the placement of stitches through
infarcted tissue. In these cases, as in the case of papillary muscle rupture, a
mitral valve replacement is performed after patch placement. The mitral valve
is exposed through a left atriotomy. On occasion, a transseptal approach via
the dome of the left atrium may be required. The valve is excised and replaced
with a low-profile prosthesis. Interrupted, felted 2-0 Tevdek sutures are used,
with the needle passing from the left atrium through the annulus.
3. Modification of Technique: Infarct Exclusion
Anterior Apical Defects
· The apical portion of the
ventricle is opened through the infarction, with extension onto the anterior
LV. A glutaraldehyde-preserved bovine pericardial patch is secured to
noninfarcted areas of the left ventricular septum using running 3-0
polypropylene sutures. The stitches should be inserted 5 to 7 mm deep in the
muscle and 4 to 5 mm apart. The stitches in the patch should be 5 mm from its
free margin to allow the patch to cover the area between the entrance and exit
of the sutures (Fig. 8.9A).
· The suture line is begun at the
most proximal part of the septum, and suturing begins traveling toward the
apex. The suture line continues from the septum onto the left ventricular free
wall. If the infarct involves the anterior papillary muscle at its base, the
suture is brought outside the heart at this point and continued as full-thickness
interrupted 2-0 polypropylene sutures buttressed on the epicardial surface with
a strip of bovine pericardium or Teflon felt. The LV is then closed with
interrupted mattress sutures of 2-0 polypropylene buttressed by Teflon felt
strips, followed by a running 2-0 polypropylene stitch (see Fig. 8.9B).8
Posteroinferior Defects
◆ A transinfarct incision is made in the inferior wall of the LV, just
lateral to the posterior descending coronary artery, to expose the defect and
is extended toward both the mitral valve and apex. Care is taken to avoid
damage to the posterior lateral papillary muscle. A bovine pericardial patch is
tailored in a triangular shape. Its size will be approximately 4 × 7 cm in most
patients. The base of the triangle is sutured to the mitral valve annulus with
continuous 3-0 polypropylene sutures. The medial suture line then transitions
from the mitral annulus to the endocardium of the ventricular septum and is
continued along that structure apically. Laterally, the suture line transitions
to the endocardium of the posterior LV.
◆ After several stitches, the posterior papillary muscle is encountered.
If the area of necrosis is small, and if healthy tissue allows for
continuation, the running sutures are continued toward the apex. Usually, on
reaching the posterior papillary muscle, it is necessary to bring the running
stitch through the muscle to the outside of the LV. The suture line is then
continued with interrupted, full-thickness, 2-0 polypropylene sutures and
buttressed with felt on the outside (Fig. 8.10A). The suture line continues
until the patch is completely secured, and then the ventriculotomy is closed in
two layers of full-thickness sutures buttressed on strips of Teflon felt. The
infarcted right ventricular wall is left undisturbed8 (Fig. 8.10B).
Right Ventricular Approach
Hosoba et al.9 have described repairing postinfarct VSDs
using a right ventricular approach and two Dacron patches. For anterior septal
defects, an incision is made in the RV wall parallel to the distal left
anterior descending artery. Sutures are placed transseptally from the LV cavity
via the VSD and into the octagonally shaped patch. The patch is placed through
the VSD, into the LV, and secured into place. A second Dacron patch is secured
over the defect in the RV. For posterior VSDs, a similar two-patch technique is
used, with an incision in the RV parallel to the midportion of the posterior
descending artery.
Step 4. Postoperative Care
· If an intraaortic balloon pump was
not inserted before surgery, one should be placed. Inotropic support is
instituted with milrinone (phosphodiesterase inhibitor). This drug is preferred
because, in addition to its inotropic properties, it has vasodilatory
properties in the pulmonary vascular bed.
· Posterior defects are associated
with a right ventricular infarction and more often result in right heart
failure on separation from bypass. In such a case, inhaled nitric oxide (20
ppm) is instituted before attempted separation. Additional maneuvers may
include right-sided infusion of prostaglandin E1 (0.5 µg/kg/min) and left-sided
norepinephrine infusion through a left atrial line.7,10
· For patients who are still in
cardiogenic shock despite these maneuvers, mechanical circulatory support may
be warranted.11 ECMO may allow for support and resuscitation of
these patients in the postoperative stage. Central cannulation may be preferred
postcardiotomy but the cannula location should be individualized based on the
clinical picture.
· Extubation usually requires
aggressive early postoperative diuresis. After fully rewarming, intravenous
infusion of furosemide at doses of 5 to 20 mg/hr is used to maintain urine
output greater than 100 mL/hr. Continuous venovenous hemofiltration is used for
nonresponders.
Step 5. Pearls and Pitfalls
· The common problems during
separation from bypass are low cardiac output, with or without right
ventricular failure and bleeding.
· Recurrent or severe ventricular
ectopy is common. Before attempted separation from cardiopulmonary bypass,
amiodarone is begun with a bolus of 150 mg, followed by ongoing infusion at 1
mg/min. The bolus may be repeated up to six times for malignant ectopy.
· Inadequate hemodynamics on
separation from cardiopulmonary bypass may require placement of a ventricular
assist device or ECMO. Left ventricular assist devices may result in increased
right-to-left shunting, and biventricular devices may be preferable.
References
1. Cooley DA.
Postinfarction ventricular septal rupture. Semin Thorac Cardiovasc Surg.
1998;10:100–104.
2. Daggett
WM. Postinfarction ventricular septal defect repair: Retrospective thoughts and
historical perspectives. Ann Thorac Surg. 1990;50:1006–1009.
3.
Pitsis A,
Kelpis T, Visouli A, et al. Left ventricular assist device as a bridge to
surgery in postinfarction septal defect. J Thorac Cardiovasc Surg.
2008;135:951–952.
4. Conradi L,
Treede H, Brickwedel J, et al. Use of initial biventricular mechanical support
in a case of postinfarction ventricular septal rupture as a bridge to surgery. Ann
Thorac Surg. 2009;87:e37–e39.
5. Michel-Behnke
I, Trong-Phi L, Waldecker B, et al. Percutaneous closure of congenital and
acquired ventricular septal defects: Considerations on selection of the
occlusion device. J Interv Cardiol. 2005;18:89–99.
6. Calvert
PA, Cockburn JC, Wynne D, et al. Percutaneous closure of post-infarction
ventricular septal defect: in-hospital outcomes and long-term follow-up of UK
Experience. Circulation. 2014;129:2395–2401.
7. Agnihotri
AK, Madsen JC, Daggett WM Jr. Surgical treatment of complications of acute
myocardial infarction: postinfarction ventricular septal defect and free wall
rupture. In: Cohn LH, ed. Cardiac Surgery in the Adult. 3rd ed. New
York: McGraw-Hill; 2008:753–784.
8. David TE,
Armstrong S. Surgical repair of postinfarction ventricular septal defect by
infarct exclusion. Semin Thorac Cardiovasc Surg. 1998;10:105–110.
9. Hosoba S,
Asai T, Suzuki T, Nota H, et al. Mid-term results for the use of the textended
sandwich patch technique through right ventriculotomy for postinfarction
ventricular septal defects. Eur J Cardiothorac Surg. 2013;e116-e120.
10.
Taghavi S,
Mangi AA. Postinfarction ventricular septal defect and ventricular rupture. In:
Selke F, del Nido SJ, Swanson SJ, eds.
11.
Sabiston
and Spencer Surgery of the Chest.
9th ed. Philadelphia: Elsevier; 2016:1653–1662.
12.
Firstenberg
MS, Blais D, Crestanello J, et al. Long-term mechanical support for complex
left ventricular postinfarct pseudoaneurysms.
13.
Heart
Surg Forum. 2009;12:E291–E293.
