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10
Surgery for Mechanical Complications of Myocardial Infarction
The mechanical complications of acute myocardial infarction have serious clinical implications and are generally
associated with a poor prognosis. The onset of ischemia is usually heralded by pain that may be followed by
shock and ventricular failure owing to significant myocardial injury. The severity of symptoms and clinical
manifestations are intimately related to the magnitude of myocardial necrosis and loss of contractile strength.
Necrosis of the free ventricular wall may cause acute myocardial rupture. Necrosis of the ventricular septum may
result in an acute septal defect and sudden left-to-right shunt, leading to hemodynamic instability. Necrosis of
papillary muscles will result in papillary muscle dysfunction or rupture, causing severe mitral valve insufficiency.
Patients are initially stabilized with medical management and intraaortic balloon counterpulsation before
undergoing cardiac catheterization and coronary angiography. Most of them will require emergent surgery
because of intractable and progressive cardiogenic shock. Concomitant coronary artery bypass grafting should
always be contemplated, whenever possible, to achieve complete myocardial revascularization. A small
subgroup of these patients may compensate and present late with a pseudoaneurysm, left ventricular aneurysm,
ventricular septal defect, or ischemic mitral valve insufficiency.
EXPOSURE AND CANNULATION OF THE HEART
The heart is exposed through a median sternotomy. Venous drainage is accomplished through bicaval
cannulation, although a single large atrial cannula is adequate whenever the right heart remains a closed system
during the procedure. Arterial blood is returned by direct aortic cannulation.
Contained Bleeding within the Pericardium
When there is evidence of contained bleeding within the pericardium due to a pseudoaneurysm or rupture of the
heart, it is prudent to cannulate the aorta through a small enough opening in the pericardium overlying the aorta
to allow volume replacement during venous cannulation and initiation of cardiopulmonary bypass. Alternatively,
femoral cannulation should be contemplated.
Cardiogenic Shock
Most patients requiring surgical intervention for management of acute mechanical complications of myocardial
infarction are in cardiogenic shock. Many may be on intraaortic balloon pump support. Cardiopulmonary bypass
is initiated, and the heart is decompressed by a vent catheter introduced into the main pulmonary artery or
through the right superior pulmonary vein into the left ventricle. Core cooling to 30°C to 32°C is carried out, and
the aorta is clamped. Cold blood cardioplegic solution is then administered through the aortic root followed by
retrograde delivery into the coronary sinus (see Chapter 3).
ACUTE MYOCARDIAL RUPTURE
Cardiorrhexis is a dramatic and lethal event. It is virtually always associated with a transmural infarction. Through
a rent in the ventricular endocardium, blood gradually leaks into the area of infarction and distends the necrotic
tissue. This hematoma continues to expand and finally ruptures the myocardium. The incidence of myocardial
rupture after myocardial infarction has decreased with the introduction of modern management strategies for
acute coronary events.
The sudden onset of cardiogenic shock 3 to 4 days after acute myocardial infarction may herald the development
of cardiac tamponade due to myocardial rupture. Equalization of pressures in the right atrium, right ventricle in
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diastole, and pulmonary artery wedge, as measured with a Swan-Ganz catheter and aspiration of blood from the
pericardial cavity are significant clues to the accurate diagnosis.
Immediate surgical exploration through a standard median sternotomy should be undertaken. If the heart has
actually overtly ruptured, only a salvage operation may be successful. This entails prompt initiation of
cardiopulmonary bypass. The infarcted necrotic tissue is removed. An appropriate patch of Hemasheild or bovine
pericardium is sewn to the healthy normal myocardium with a continuous
suture of 3-0 Prolene buttressed with a strip of felt to cover the defect. The suture line may have to be reinforced
with additional sutures.
More commonly, the rupture consists of a small rent in the myocardium. The infarcted segment becomes spongy,
oozing with blood. At times there may be a small hole through which blood spurts out. This may be amenable to
suturing a large patch to the surrounding normal myocardium without resecting any muscle. Surgical
management of this type of myocardial injury has been simplified with the use of biocompatible glues, such as
cyanoacrylate or histoacryl. The technique entails applying the glue to the relatively dried surface of the infarcted
myocardium, and covering the area with an appropriately sized patch of Teflon felt or bovine pericardium. The
procedure does not require cardiopulmonary bypass support, and can be performed expeditiously with improved
patient survival.
The sutureless technique for left ventricular rupture is a lifesaving procedure. Coronary artery bypass grafts
are not performed, and generally these patients are taken directly to the operating room without undergoing
coronary angiography.
VENTRICULAR SEPTAL RUPTURE
The ventricular septum receives blood from perforating branches of the left anterior descending artery as well as
perforating branches of the posterior descending artery. Despite this dual blood supply, there is frequently no
septal collateral flow. Consequently, the interventricular septum remains quite vulnerable to ischemia and
occasionally ruptures after myocardial infarction. This is seen notably in patients whose infarction is the result of
single-vessel disease. As with ventricular aneurysm, the anteroapical area is the most common site; it is involved
in 65% of patients with ventricular septal rupture. The posterior segment of the septum is involved in 17% of the
cases, and the middle segment in 13% of the cases; only 4% of the ruptures involve the inferior segment of the
septum.
There is frequently a rapid progressive hemodynamic deterioration with myocardial failure following the rupture
of the ventricular septum. The initial diagnosis is confirmed by echocardiography and is later followed by cardiac
catheterization and coronary angiography. The goal of preoperative management is to decrease the left-to-right
shunt by reducing systemic vascular resistance but at the same time ensuring adequate systemic blood pressure
and cardiac output. Because these patients tend to die of end-organ failure rather than heart failure, prompt
temporary stabilization is achieved with the support of an intraaortic balloon pump, ionotropic agents, and
diuretics to maintain optimal tissue perfusion.
The operative mortality in this subgroup of patients is relatively high, but without urgent surgery, most of them
would not survive.
Technique for the Surgical Treatment of a Ventricular Septal Defect
The septal defect is approached through an incision parallel to the course of the left anterior descending
coronary artery in the center of the left ventricular infarct (Fig. 10.1). The septal defect and the extent of
surrounding friable necrotic tissue are identified. With a continuous 3-0 Prolene suture, a generous patch of
bovine pericardium is sewn to the left ventricular side of the septum, taking deep bites of normal, healthy
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muscular tissue as far away from the necrotic rim of the defect as possible. At times, this may necessitate sutures
being placed close to the mitral valve annulus. The septal necrosis often extends to the ventriculotomy. The
pericardial patch is then allowed to protrude outside the heart and be incorporated in the ventriculotomy closure
(Fig. 10.2).
This technique essentially excludes the infarcted area. The suture line on the septum is inspected and checked
for any residual defects. It is reinforced with multiple interrupted sutures buttressed with felt pledgets. The patch
is anchored to the anterior edge of the left ventricular wall with a felted suture. This technique is based on the
concept that the higher left ventricular pressure will force the pericardial patch against the entire septum, thereby
obliterating the septal defect. Because sutures are placed on the
normal healthy tissue, well away from the necrotic edges, the repair should be secure.
FIG. 10.1 Technique for surgical treatment of a ventricular septal defect.
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FIG. 10.2 A generous patch of bovine pericardium is sewn to the normal septal wall away from the defect.
The ventriculotomy is then closed with interrupted sutures of 3-0 Prolene with a layer of Teflon felt strip on each
side of the incision. This is reinforced with a continuous suture of 3-0 Prolene and Bioglue.
When the septal defect is a narrow, slit-like opening in close proximity to the anterior wall of the right ventricle,
the sutures are first passed through a strip of Teflon felt, then through the viable septal tissue along the posterior
edge of the defect, and again through another strip of Teflon felt on the right ventricular side of the septum (Fig.
10.3A). The sutures are brought out through the anterior wall of the right ventricle before they are passed
through another strip of Teflon felt. Finally, the sutures are tied down, and the ventriculotomy is closed as
described previously (Fig. 10.3B). Alternatively, the single pericardial patch technique could be used.
FIG. 10.3 A: The slit-like ventricular septal defect is closed with interrupted sutures incorporating strips of Teflon
felt on both sides of the septum and anterior wall of the right ventricle. B: The knots are then tied, and the
ventriculotomy is closed.
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If the apex of the heart has infarcted and is necrotic, it is amputated. The viable tissue is then reapproximated in
a sandwich manner by means of four strips of Teflon felt, one on each side of the septum and one each on the
right and left exterior ventricular walls, with a series of interrupted horizontal mattress sutures (Fig. 10.4).
The approach to a rupture of the posteroinferior aspect of the septum through the infarcted inferior left
ventricular wall is more challenging. Often the posteromedial papillary muscle is also involved in the necrotic
process, and concomitant mitral valve replacement may become necessary. Closure of the ventricular septal
defect is performed using the patch technique as described in preceding text. Most often, the inferior wall of the
ventricle is closed using an appropriately sized Hemashield patch so as not to interfere with the normal geometry
of the left ventricle. Coronary bypass grafting is performed judiciously on all bypassable vessels to ensure full
revascularization of the remaining myocardium.
The liberal application of biological glue (i.e., Bioglue Surgical Adhesive, Cryolife Inc., Kennesaw, GA) on all
suture lines has been a satisfactory hemostatic tool.
Percutaneous closure of postinfarction ventricular septal defects has become an alternative strategy in
many critically ill patients. This can be done in conjunction with coronary angiography and possible
percutaneous coronary revascularization.
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FIG. 10.4 A: Ventricular septal defect as the result of apical infarction. B: The necrotic apex of the left ventricle
is amputated. C: The septal defect and ventricular walls are reconstructed with interrupted sutures incorporating
strips of Teflon felt.
The very few patients who survive the acute phase may present in congestive heart failure at a later date.
By 3 to 4 weeks after acute myocardial infarction, some fibrosis occurs in the necrotic areas so that the tissues
are strong enough to hold sutures safely and surgical repair can be performed more easily.
PAPILLARY MUSCLE RUPTURE
The anterolateral papillary muscle has a rich blood supply from both the left anterior descending and left
circumflex coronary arteries. In 90% of hearts, the right coronary artery is dominant and supplies the
posteromedial papillary muscle. In the remaining 10%, its blood supply is provided by branches of the left
coronary artery system. Therefore, infarction of the posterior wall of the left ventricle frequently results in
necrosis of the posteromedial papillary muscle. A papillary muscle rupture usually occurs during the first week
after infarction or later with reinfarction. Because both leaflets of the mitral valve are attached to each papillary
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muscle by chordae tendineae, complete disruption of either one, usually the posteromedial papillary muscle,
results in gross mitral insufficiency, acute pulmonary edema, and death unless surgical intervention is
prompt. A tear of the apical head of a papillary muscle that supports a small segment of only one of the mitral
leaflets may result in a milder degree of mitral regurgitation (Fig. 10.5). Dysfunction of the papillary muscle is
probably more common. If myocardial infarction is not massive and left ventricular function is not severely
impaired, these patients can compensate long enough to undergo coronary angiography before semiurgent
surgical treatment.
FIG. 10.5 A: Spatial relationships of the anatomic components of the mitral valve apparatus. B: Rupture of
chordae tendineae. C: Partial rupture of the head of the papillary muscle. D: Complete tear of the papillary
muscle giving rise to gross valvular insufficiency (E).
Most commonly, conservative surgery will not be adequate because the infarcted papillary muscle is friable and
necrotic. Occasionally, a ruptured papillary muscle can be reimplanted, but it may be hazardous if the
reimplantation site is necrotic. Mitral valve replacement is the procedure of choice in most patients and can be
performed expeditiously with relative safety (see Chapter 6). Coronary artery bypass grafting to bypassable
vessels is highly desirable to revascularize the viable myocardium as completely as possible.
Significant mechanical complications occurring during the acute phase of myocardial infarction are quite rare.
Most patients following myocardial infarction will continue on a medical regimen and live a symptom-free
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productive life. There is, however, a subgroup of patients who develop symptoms reflecting the effects of chronic
changes secondary to an old myocardial infarction. Diagnostic evaluation of these patients with ischemic
cardiomyopathy
may reveal the presence of a large dyskinetic (aneurysmal) or akinetic segment of left ventricle, a
pseudoaneurysm, and/or ischemic mitral valve disease, all of which may require surgical intervention.
SURGICAL VENTRICULAR RESTORATION
Following myocardial infarction, a discrete scar develops, resulting in an akinetic or dyskinetic segment.
Traditionally, surgical ventricular restoration for ischemic cardiomyopathy has focused on recognizing the
borders of the scar tissue and excluding the scar by excision and primary closure or placement of a patch at the
junction between scar and normal muscle. More recently, the importance of ventricular chamber size and shape
has been appreciated. The goal of surgery to reconstruct the left ventricle is to achieve a normal-sized cavity and
to convert the more spherical shape to a more conical pattern.
Technique
Cardiopulmonary bypass is initiated in the standard manner. Usually, a single atriocaval cannula is adequate for
venous return. Cardioplegic arrest of the heart is accomplished by infusion of cold blood cardioplegic solution
through the aortic root after clamping the aorta. This is complemented by infusion of cold blood cardioplegia into
the coronary sinus by the retrograde technique (see Chapter 3). Venting of the left ventricle through the right
superior pulmonary vein helps to keep the field dry. When the heart is still and vented empty, the extent of the
old infarct is evaluated. The scar segment of the left ventricular wall, devoid of myocardium, tends to be sucked
in by the vent suction. The heart is carefully dissected free from the pericardium. Traction sutures are placed in
the scar tissue, and an incision is made through it (Fig. 10.6). The opening is then enlarged, and some excess
scar tissue may be excised to provide easy access for removal of blood clots from within the left ventricle and/or
aneurysm wall (Fig. 10.7).
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FIG. 10.6 Ventriculotomy through scar tissue.
Adherent Calcified Aneurysm Wall
Occasionally, there may be marked fibrous reaction or even calcification of the aneurysm wall, making its
mobilization tedious and time-consuming. The involved segment of the aneurysm can be amputated free from the
heart and left adherent to the pericardium and pleura (Fig. 10.8).
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FIG. 10.7 Excision of a scarred ventricular wall.
FIG. 10.8 Technique for leaving a scarred ventricular wall adherent to the pericardium.
Dislodgment of Blood Clots
Manipulation and dissection to free the left ventricular wall from the pericardium are performed after the aorta
has been cross-clamped to avoid dislodgment and systemic embolization of blood clots.
Loose Blood Clots
There are often loose blood clots in the ventricular cavity. A sponge should be placed in the outflow tract of the
left ventricle near the aortic valve before attempting to remove blood clots and debris from the ventricular cavity.
The sponge will prevent the escape of blood clots into the aortic root and possible embolization into the coronary
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