**8. Operative Management**

As soon as the diagnosis is made an intra-aortic balloon pump (IABP) should be placed. Coronary augmentation will assist the ischemic and injured myocardium. More important‐ ly, an IABP will unload the left ventricle and improve cardiac output, and end-organ perfu‐ sion. By decreasing afterload, there will also be an improvement in pulmonary shunting and over-circulation. However, the physiologic improvements with IABP and other inotropic or vasoactive medications should only be viewed as transient and allow finishing the pre-oper‐

While some advocate a strategy of delayed repair, this approach is rarely successful. The hy‐ pothesis of this management plan is to give the friable necrotic myocardium time (3-6 weeks) to fibrosis thereby allowing for an easier and more secure repair. The scarred tissue will better hold suture and less likely to tear apart and result in an early post-operative fail‐ ure. This approach appears reasonable, in theory, but it is rare that patients remain stable or can be supported during this time period. While guidelines for delayed surgical manage‐ ment are lacking, this might be an option in those who are hemodynamically or physiologi‐ cally stable with a delayed presentation, have no or minimal signs of pulmonary hypertension or over-circulation, and have a stable fluid balance with good renal function. Unfortunately, such patients are rare and less than 5-10% of all PI-VSD patients will survive to allow for delayed repair. Such an approach may represent a "survival of the fittest" ap‐ proach in those with minimal shunting and with strict attention to medical comorbidities and nutrition a period of close careful waiting may be clinically successful. This approach may also be used to justify waiting in patients who have other severe comorbidities preclud‐ ing intervention and would, in theory, require optimization prior to surgery. Nevertheless, it is hard to argue that any other comorbidities would improve enough to the point of mak‐ ing surgery safer in the setting of worsening right ventricular heart failure – a problem that by itself is very difficult to treat both pre and post-operatively. Although, one can also sug‐ gest that in these patients, unless early surgical repair is clearly contraindicated, that their physiologic reserve combined with a minimal pathophysiologic insult might predispose

them to a good outcome regardless of whether an early or late repair is performed.

Of growing concern regarding the timing of surgery and the implications of peri-operative management is the use of potent, and often irreversible, anti-platelet inhibitors and/or anticoagulants. The data and experience on operating on patients with some of these newer agents, the impact on the ability – or lack thereof – to achieve surgical hemostasis with such drugs is both limited and evolving. As many of these patients might have already been pre‐ treated with P2Y12 inhibitors such as clopidogrel, or the more potent agents such as prasu‐ grel or ticagrelor, the impact on bleeding and the timing of surgery can be worrisome. Furthermore, other agents used to facilitate coronary interventions, such as Gp IIb/IIIa in‐ hibitors such as eptifibatide, or direct thrombin inhibitors such as bivalirudin might require an appropriate 'wash-out' period. The risk for a massive transfusion (particularly with pla‐ telets) at the time of surgery with these agents still active cannot be understated. In fact, at patient who already might be considered physiologically high-risk might be considered in‐ operable in the setting of recent Dabigatran (Pradaxa) exposure due to the risk of cata‐ strophic, irreversible, surgical hemorrhage. In the post-operative period, the decision to

ative assessment.

300 Principles and Practice of Cardiothoracic Surgery

The initial surgical techniques for PI-VSDs followed a surgical approach similar to that for congenital ventricular septal defects. The approach was through a ventriculotomy in the right ventricular outflow track (RVOT) [12]. It was quickly realized that this approach had significant drawbacks. Firstly, in an already dysfunctional and acutely injured right ventri‐ cle, the outflow tract incision only further reduced residual, crucial RV function. As impor‐ tantly, while suited for many common types congenital septal defects near the aortic valve, the RVOT incisions offered poor exposure of defects that tended to be much further down the septum towards the apex. Most importantly, since the patch and suture line was on the RV side, the defect was still exposed to LV pressures and consequently was at increased risk for patch dehiscence, early recurrence, extension of the defect, and clinical failure. Pioneer‐ ing animal studies by [22] advocated an approach to the VSD thru the left ventricle in the region of the culprit vessel through infracted myocardium – specifically, anterior defects ap‐ proached through the anterior wall while posterior defects through the inferior wall. These techniques addressed many of the deficiencies of a RVOT approach [22]. The benefits of these animal studies were subsequently validated clinically within several years [26][8]

#### **8.1. Basic Principles and Considerations**

After the patient arrives in the operative room, routine anesthesia is induced. If not already in place, all patients should have arterial monitoring lines and a pulmonary artery (Swan-Ganz) catheter inserted. Pressures and oxygen saturations should be obtained to determine shunt fractions and to assist in determining the completeness of repair. Since these patients have left-to-right shunting, it is of critical importance to avoid pharmacologic agents that cause pulmonary vasodilation. Such agents would worsen the shunt, increase pulmonary over-circulation, and potentially worsening right heart dysfunction. Preoperative antibiotics including a first generation cephalosporin, such as cefazolin, and vancomycin are adminis‐ tered. In cases of antibiotic allergies, appropriate alternatives should be chosen.

Median sternotomy is performed and the patient is prepared for cardiopulmonary bypass. Minimally invasive techniques are typically not advocated for this type of extensive and complex procedure in which complete exposure of heart is helpful. However, in situations of re-operative surgery, depending on surgeon preferences, consideration should be given to peripheral cannulation (i.e. femoral or axillary) prior to sternotomy as a re-entry injury to an already compromised and dilated RV can be fatal. The patient is heparinized prior to standard aortic – right atrial cannulation. Some advocate routine bicaval venous drainage, but typically, as procedures on the tricuspid or mitral valves are not performed unless clear‐ ly indicated by pre-operative studies, this is not necessary. Cold-blood antegrade and retro‐ grade cardioplegia is delivered via conventional root and coronary sinus catheters. Topically cooling to further reduce the metabolic demands of the already compromised heart is also liberally used. This author routinely uses ice-slush wrapped in gauze to further cool the right ventricle to assist in reducing the temperature and assists further in myocardial protec‐ tion – a key component in minimizing post-operative biventricular dysfunction. Active or passive systemic cooling is performed with an ideal temperature of 25º-28ºC to further assist end-organ protection. Regardless, the key concept is an appropriate and well thought out approach to myocardial protection.

infracted tissue of the cardiac apex. The necrotic myocardium is then excised until healthy muscle is exposed and deemed adequate for repair. The healthy tissues of the right and left ventricle are then approximated to the septum using interrupted, felt pledgeted, heavy Ty‐ cron suture in a mattress fashion (Figure 4). Felt strips are placed along the right and left septal walls during this process to create a 'felt sandwich'. The apical repair can be rein‐ forced with a second layer of suture. While meticulous hemostasis is critical, too much ten‐ sion on the suture repair can tear through the muscle and result in uncontrolled post-

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**Figure 4.** Apical repair involves excising the apical defect and bringing together the residual edges of the left and

**Figure 5.** Left: Intra-operative view of the extensive apical infarction that has resulted in the echocardiographic find‐ ings demonstrated in Figure 2. The left anterior descending artery (LAD) is shown. Right: The same patient after open‐ ing and debridement of the infracted apex. The necrotic septum is visualized with a probe in the left ventricle (LV) and

The anterior septal defect involves the anterior septum as well as the anterior left ventricular free wall. This, as discussed earlier, is typically a result of acute infarct of the LAD territory. The initial approach is via an incision in the left ventricular myocardium parallel to the LAD and through the non-viable or ischemic tissue. The infracted area is then excised and debrid‐ ed back to healthy, viable myocardium. The septum is then inspected and necrotic tissue is excised in the same fashion. This is can be straightforward in a single, obvious defect. How‐

right ventricular walls using a primary repair reinforced with pledgets.

the bypass "pump sucker" is in the right ventricle (RV).

**8.3. Anterior Defects**

operative hemorrhage.

In general, once the defect is identified, a piece of either glutaraldehyde-fixed bovine peri‐ cardium or Dacron is cut to not only cover the defect but a generous rim of surrounding, and potentially non-viable, myocardium. Continuous suture or interrupted pledgeted su‐ tures are used to suture the patch to the residual septum. Tension on the repair must be avoided to minimize the risk of the sutures tearing through once the ventricle is pressurized and begins to contract. The "Sandwich Technique" approach has been described to mini‐ mize the tension and risk for leakage of the final repair. In this technique, a patch is posi‐ tioned on the RV side and re-enforced with pledgets. The defect, much like a "pot-hole" in the road, is then filled a gelatin-resorcin-formalin (GRF) glue and then covered on the left ventricular side with a similar patch and pledgets. The proposed advantage of this techni‐ que is that the glue serves as a cement to re-enforce the repair, minimize tension on the su‐ tures lines, attempts to preserve ventricular geometry, and most importantly, reduces the risk of leaking. Early [24] and midterm results [25], although in limited studies, support this adjuvant to traditional patch repair techniques as described below. Although the "sandwich technique" advocated a repair via a right ventricular incision, such an approach, for reasons already outlined, may not be desirable – nevertheless, experience with this technique is growing and this might be a reasonable approach in selected patients [4]. For posterior de‐ fects the patch might require anchoring to the annulus of the mitral valve. For cases in which the annulus of the mitral valve and/or peri-valvular tissues is involved, mitral valve replacement may be required. The choice of prosthesis is up to the surgeon, but given the 5 year limited survival of these patients in general and the post-operative challenges that might come from the need for anticoagulation with a mechanical valve, a tissue valve in these cases is a reasonable option regardless of the patient's age and co-morbidities.

The intra-operative approach and management of the defect is based upon the location of the VSD and the need for concomitant procedures. The pre-operative assessment of the loca‐ tion of the defect is critical in determining the optimal approach to closing it.

#### **8.2. Apical Defects**

Apical septal defects involve the apical portion of the right ventricle, septum, and the left ventricle. As mentioned, such defects are typically the result of acute occlusion of the distal left anterior descending artery. Daggett and colleagues first described the technique of api‐ cal amputation and repair of the PI-VSD in 1970. The initial incision is created through the infracted tissue of the cardiac apex. The necrotic myocardium is then excised until healthy muscle is exposed and deemed adequate for repair. The healthy tissues of the right and left ventricle are then approximated to the septum using interrupted, felt pledgeted, heavy Ty‐ cron suture in a mattress fashion (Figure 4). Felt strips are placed along the right and left septal walls during this process to create a 'felt sandwich'. The apical repair can be rein‐ forced with a second layer of suture. While meticulous hemostasis is critical, too much ten‐ sion on the suture repair can tear through the muscle and result in uncontrolled postoperative hemorrhage.

**Figure 4.** Apical repair involves excising the apical defect and bringing together the residual edges of the left and right ventricular walls using a primary repair reinforced with pledgets.

**Figure 5.** Left: Intra-operative view of the extensive apical infarction that has resulted in the echocardiographic find‐ ings demonstrated in Figure 2. The left anterior descending artery (LAD) is shown. Right: The same patient after open‐ ing and debridement of the infracted apex. The necrotic septum is visualized with a probe in the left ventricle (LV) and the bypass "pump sucker" is in the right ventricle (RV).

#### **8.3. Anterior Defects**

but typically, as procedures on the tricuspid or mitral valves are not performed unless clear‐ ly indicated by pre-operative studies, this is not necessary. Cold-blood antegrade and retro‐ grade cardioplegia is delivered via conventional root and coronary sinus catheters. Topically cooling to further reduce the metabolic demands of the already compromised heart is also liberally used. This author routinely uses ice-slush wrapped in gauze to further cool the right ventricle to assist in reducing the temperature and assists further in myocardial protec‐ tion – a key component in minimizing post-operative biventricular dysfunction. Active or passive systemic cooling is performed with an ideal temperature of 25º-28ºC to further assist end-organ protection. Regardless, the key concept is an appropriate and well thought out

In general, once the defect is identified, a piece of either glutaraldehyde-fixed bovine peri‐ cardium or Dacron is cut to not only cover the defect but a generous rim of surrounding, and potentially non-viable, myocardium. Continuous suture or interrupted pledgeted su‐ tures are used to suture the patch to the residual septum. Tension on the repair must be avoided to minimize the risk of the sutures tearing through once the ventricle is pressurized and begins to contract. The "Sandwich Technique" approach has been described to mini‐ mize the tension and risk for leakage of the final repair. In this technique, a patch is posi‐ tioned on the RV side and re-enforced with pledgets. The defect, much like a "pot-hole" in the road, is then filled a gelatin-resorcin-formalin (GRF) glue and then covered on the left ventricular side with a similar patch and pledgets. The proposed advantage of this techni‐ que is that the glue serves as a cement to re-enforce the repair, minimize tension on the su‐ tures lines, attempts to preserve ventricular geometry, and most importantly, reduces the risk of leaking. Early [24] and midterm results [25], although in limited studies, support this adjuvant to traditional patch repair techniques as described below. Although the "sandwich technique" advocated a repair via a right ventricular incision, such an approach, for reasons already outlined, may not be desirable – nevertheless, experience with this technique is growing and this might be a reasonable approach in selected patients [4]. For posterior de‐ fects the patch might require anchoring to the annulus of the mitral valve. For cases in which the annulus of the mitral valve and/or peri-valvular tissues is involved, mitral valve replacement may be required. The choice of prosthesis is up to the surgeon, but given the 5 year limited survival of these patients in general and the post-operative challenges that might come from the need for anticoagulation with a mechanical valve, a tissue valve in

these cases is a reasonable option regardless of the patient's age and co-morbidities.

tion of the defect is critical in determining the optimal approach to closing it.

The intra-operative approach and management of the defect is based upon the location of the VSD and the need for concomitant procedures. The pre-operative assessment of the loca‐

Apical septal defects involve the apical portion of the right ventricle, septum, and the left ventricle. As mentioned, such defects are typically the result of acute occlusion of the distal left anterior descending artery. Daggett and colleagues first described the technique of api‐ cal amputation and repair of the PI-VSD in 1970. The initial incision is created through the

approach to myocardial protection.

302 Principles and Practice of Cardiothoracic Surgery

**8.2. Apical Defects**

The anterior septal defect involves the anterior septum as well as the anterior left ventricular free wall. This, as discussed earlier, is typically a result of acute infarct of the LAD territory. The initial approach is via an incision in the left ventricular myocardium parallel to the LAD and through the non-viable or ischemic tissue. The infracted area is then excised and debrid‐ ed back to healthy, viable myocardium. The septum is then inspected and necrotic tissue is excised in the same fashion. This is can be straightforward in a single, obvious defect. How‐ ever, great care must be taken if the defect is noted to be tracking through the myocardium – a finding that might not be obvious. In general, the larger the patch the better - as a too small of a patch is more likely to pull through and dehisce.

ventricular free wall and tagged with hemostats (Figure 7). All sutures are placed prior to placing them through the patch. They can now be placed through the designated anterior region of the prosthetic patch and then through a second pledget if desired prior to tying the suture knots. The left ventricular free wall is then re-approximated using interrupted, mat‐ tress suture similar to apical repairs. A second layer of running suture, often with a strip of

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The posterior or inferior septal defect involves a transmural infarction of the myocardium in the posterior descending artery distribution. The inferior wall is often thin and after infarc‐ tion, is quite friable. For this reason, primary repair is not a durable option and is rarely suc‐ cessful. Attempt at primary repair, in which the myocardium is placed under tension, can have disastrous immediate, and potentially fatal, consequences. Hence, posterior/inferior

After the heart is arrested, the inferior wall is lifted out of the pericardial well and exposed. The transmural infarct may involve both ventricles, or the septum and left ventricle alone. The transinfarct incision is created in a longitudinal fashion in the left ventricle. The nonvia‐ ble myocardium is excised, which will create adequate exposure of the septal defect which is critical for a durable repair. The papillary muscles are inspected. If the base is involved in the infarct resulting in ruptured papillary muscle, then mitral valve replacement is indicat‐ ed. If a small posterior defect (<1.0 cm) is identified, primary repair to the ventricular free wall using pledgetted suture as described earlier is satisfactory – but this situation is very rare and placement of a small patch may result in a more durable outcome than risking a

**Figure 8.** Similar to anterior repairs, the high pressure left ventricular cavity is isolated from the necrotic septum with a patch repair. The incision is along the distal right coronary along and parallel to the posterior descending artery

As with anterior defects, most posterior defects will require a tension free repair by utilizing a patch closure. This technique often necessitates the use of two separate patches, one dedi‐ cated to the septal repair and the other to the wall of the ventricle. Principles as described previously apply. The pledgetted mattress sutures are placed from the right ventricle to the left along the circumference of the defect. The sutures are passed through the contoured patch and tied down. Great care should be taken to avoid lacerating the myocardium. Some authors suggest placing a second pledget on the patch side of the repair to minimize this

felt to distribute the tension of the closure, is placed for reinforcement.

septal defects are the most technically demanding of the PI-VSDs.

primary repair involving ischemic myocardial tissue.

through the infracted basal muscle.

**8.4. Posterior Defects**

**Figure 6.** Picture representation of the various steps used to repair an anterior defect with the patch excluding the necrotic septum from the higher pressure left ventricular cavity. The incision is through the infracted muscle on the anterior wall, parallel to the left anterior descending artery.

Small defects can be plicated with a primary repair to the right ventricular free wall using interrupted, pledgeted suture as first suggested by Shumacker [42]. For anything other than very small (<1.0 cm) defects, most anterior septal infarcts will require repair with a patch. This is fashioned in a manner that will allow for a tension-free repair. Excess tension in the repair can lead to devastating consequences either with acutely life threatening bleeding or a delayed dehiscence and residual shunt.

**Figure 7.** Intra-operative picture with the apex of the heart elevated (head and aortic cannula to the right). The inci‐ sion is through the infarcted anterior wall. The septal defect is shown in the middle of the cavity with circumferential sutures around a wide margin. The sutured will then be placed through a pericardial patch to exclude the infracted septal muscle and defect from the left ventricular cavity.

Larger defects require the use of a prosthetic patch that is anchored to the posterior wall of the septum using interrupted, pledgeted Tycron or Proline suture to distribute the tension. The suture is passed from the RV through the LV so that the patch-septum interface lies in the left ventricle, as opposed to the RV. The anterior sutures are placed through the right ventricular free wall and tagged with hemostats (Figure 7). All sutures are placed prior to placing them through the patch. They can now be placed through the designated anterior region of the prosthetic patch and then through a second pledget if desired prior to tying the suture knots. The left ventricular free wall is then re-approximated using interrupted, mat‐ tress suture similar to apical repairs. A second layer of running suture, often with a strip of felt to distribute the tension of the closure, is placed for reinforcement.

#### **8.4. Posterior Defects**

ever, great care must be taken if the defect is noted to be tracking through the myocardium – a finding that might not be obvious. In general, the larger the patch the better - as a too small

**Figure 6.** Picture representation of the various steps used to repair an anterior defect with the patch excluding the necrotic septum from the higher pressure left ventricular cavity. The incision is through the infracted muscle on the

Small defects can be plicated with a primary repair to the right ventricular free wall using interrupted, pledgeted suture as first suggested by Shumacker [42]. For anything other than very small (<1.0 cm) defects, most anterior septal infarcts will require repair with a patch. This is fashioned in a manner that will allow for a tension-free repair. Excess tension in the repair can lead to devastating consequences either with acutely life threatening bleeding or

**Figure 7.** Intra-operative picture with the apex of the heart elevated (head and aortic cannula to the right). The inci‐ sion is through the infarcted anterior wall. The septal defect is shown in the middle of the cavity with circumferential sutures around a wide margin. The sutured will then be placed through a pericardial patch to exclude the infracted

Larger defects require the use of a prosthetic patch that is anchored to the posterior wall of the septum using interrupted, pledgeted Tycron or Proline suture to distribute the tension. The suture is passed from the RV through the LV so that the patch-septum interface lies in the left ventricle, as opposed to the RV. The anterior sutures are placed through the right

of a patch is more likely to pull through and dehisce.

304 Principles and Practice of Cardiothoracic Surgery

anterior wall, parallel to the left anterior descending artery.

a delayed dehiscence and residual shunt.

septal muscle and defect from the left ventricular cavity.

The posterior or inferior septal defect involves a transmural infarction of the myocardium in the posterior descending artery distribution. The inferior wall is often thin and after infarc‐ tion, is quite friable. For this reason, primary repair is not a durable option and is rarely suc‐ cessful. Attempt at primary repair, in which the myocardium is placed under tension, can have disastrous immediate, and potentially fatal, consequences. Hence, posterior/inferior septal defects are the most technically demanding of the PI-VSDs.

After the heart is arrested, the inferior wall is lifted out of the pericardial well and exposed. The transmural infarct may involve both ventricles, or the septum and left ventricle alone. The transinfarct incision is created in a longitudinal fashion in the left ventricle. The nonvia‐ ble myocardium is excised, which will create adequate exposure of the septal defect which is critical for a durable repair. The papillary muscles are inspected. If the base is involved in the infarct resulting in ruptured papillary muscle, then mitral valve replacement is indicat‐ ed. If a small posterior defect (<1.0 cm) is identified, primary repair to the ventricular free wall using pledgetted suture as described earlier is satisfactory – but this situation is very rare and placement of a small patch may result in a more durable outcome than risking a primary repair involving ischemic myocardial tissue.

**Figure 8.** Similar to anterior repairs, the high pressure left ventricular cavity is isolated from the necrotic septum with a patch repair. The incision is along the distal right coronary along and parallel to the posterior descending artery through the infracted basal muscle.

As with anterior defects, most posterior defects will require a tension free repair by utilizing a patch closure. This technique often necessitates the use of two separate patches, one dedi‐ cated to the septal repair and the other to the wall of the ventricle. Principles as described previously apply. The pledgetted mattress sutures are placed from the right ventricle to the left along the circumference of the defect. The sutures are passed through the contoured patch and tied down. Great care should be taken to avoid lacerating the myocardium. Some authors suggest placing a second pledget on the patch side of the repair to minimize this risk. The posterior ventricular wall is repaired with the second patch using mattress sutures. Occasionally, depending on the size and quality of free wall myocardium, the free-edges can be approximated and closed primarily (and re-enforced with a pericardial or felt strip) rath‐ er than using a second patch.

associated with worse outcomes, the relationship to a poor outcome is the need for its use and the potential delay in initiating therapy rather than the therapy itself that influences the adverse outcome. Right heart failure is common and often these patients require con‐ siderable therapies directed specifically at assisting in right heart management. Convention‐ al intravenous agents such as epinephrine, milrinone, and dobutamine are often required – and sometimes at high doses. Inhaled agents that selectively reduce pulmonary vascu‐ lar resistance and assist in reducing RV afterload such as inhaled nitric oxide (20-80 ppm) or epoprostenol (2,500 – 20,000 ng/min) may be required [37]. Ventricular arrhythmias are also common from the residual ischemic/necrotic myocardium (as well as secondary to the ventriculotomy) and anti-arrhythmic medications, such as amiodarone, should be used lib‐ erally. In addition, as the repaired septal defect and free wall are often quite friable, strict attention to avoid hypertension is important as even transient elevations in blood pres‐ sure can result in disruptions in either the patch repair or the ventriculotomy closure su‐ ture line that might precipitate uncontrolled and fatal cardiac bleeding. Any acute increase in chest tube drainage should raise the concern for ventricular suture line dehiscence and there should be a low threshold for returning the patient to the operating room for reexploration – however, excess manipulation of the heart in the search for bleeding should be avoided at the risk of catastrophic suture-line tearing in a beating and pressurized ven‐ tricle. Any post-operative coagulopathy must be aggressively corrected. Although recov‐ ery in these patients is unpredictable, it may be prolonged. A slow wean of inotropes may be required and there should be a low threshold for repeat and/or frequent echocardiograph‐ ic evaluations in a patient who is not improving as anticipated. Repeat echocardiography might show a residual shunt or valvular dysfunction, more importantly may identify easy

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The increasing rarity of PI-VSD implies that few centers are able to report an extensive ser‐ ies. Even though several large single center experiences and outcomes have been reported, most summarize years of experience and may not take into consideration the improvements in peri-operative management, surgical skills, and – probably most importantly – the clinical

In the GUSTO trial in which 41,021 patients were randomized to different strategies of re‐ perfusion during AMI, 84 developed a PI-VSD. 34 of these were managed surgically, with 31 (90%) undergoing early treatment and 3 (10%) undergoing delayed surgery. Survival in the surgical group was 53% at 30 days and 47% at 1 year. Conversely, for those treated medical‐ ly, as an indicator of the lethality of this problem, survival at 30 days and 1 year was 6% and

Deja and colleagues reported their experience with 117 patients from the Glenfield General Hospital in England. In their series, there were 76 anterior defects and 34 posterior defects. The mean age was 65 ± 8 years and 43 of the 117 were females. One third of patients were in

3%, respectively [13]. All patients who presented in Class III or IV heart failure died.

judgment necessary for the management of these critically ill patients.

to correct problems, such as tamponade.

**10. Outcomes: Predictors of Survival**

#### **8.5. General Principles**

Closure of the ventriculotomy is performed by folding the free edge of the patch to the edge of the ventricle to exclude it from the circulation. The ventriculotomy repair is then closed with a primary closure re-enforced with strips of either Teflon felt or pericardium. Exclusion of the necrotic myocardium from the left ventricular is also important in minimizing the risk of small debris breaking off at any point and causing a systemic embolism. Biologic glues can be liberally used for small suture leaks, but it should be avoided in more significant bleeding as this might suggest a less than stable closure.

Regardless of the location of the ventriculotomy, it cannot be emphasized enough the im‐ portance of a tension free closure. Any unnecessary tension through injured or friable myo‐ cardium may predispose to catastrophic and potentially fatal post-operative bleeding once the ventricle becomes pressurized. In extreme cases involving extensive myocardial (free wall and septal) damage, temporary mechanical support with either extra-corporeal mem‐ brane oxygenation (ECMO) or a left ventricular assist device may help unload the ventricle to assist in recovery. The hypothesis behind this approach is by reducing the LV pressure, it will encourage recovery, reduce the pressure on the repair, and allow for further decision making in patients in whom there is extensive ventricular destruction and residual ventricu‐ lar function may not be adequate to support physiologic needs [19].

Although the benefits of concomitant revascularization on long-term outcomes are debata‐ ble, complete coronary revascularization, if possible, is typically advocated [23]. As with other risk models for outcomes after surgery (e.g. EuroScore and STS models), it is the need for revascularization and the extent of underlying CAD that defines the long-term outcome rather than the actual performing of the procedure. Overall, the paradigm of complete and/or optimal revascularization should apply in cases of PI-VSD management. It is hard to refute the benefits of revascularization in the setting of an already acutely and chronically ischemic myocardium.
