**6. Natural History**

with low ejection fractions, cardiomyopathies, or suspicion for unusual cardiac anatomy, might have cardiac MRI performed to assess for myocardial viability, fibrosis, or valvular pathology. In these patients, a PI-VSD may be an unsuspected finding (Figure 3). Although there is little experience describing the role of cardiac MRI in PI-VSDs, using concepts de‐ rived from the literature on congenital shunts and defects, cardiac MRI might be of value in assisting in defining the extent of the defect, the shunt fraction, right ventricular function, and other associated pathophysiology [17]. Cardiac MRI might be of additional value in sit‐ uations of questionable catheterization or echocardiographic results or in the assessment of the post-operative patient when a residual shunt is suspected. Nevertheless, MRI is, in gen‐

**Figure 3.** Cardiac MRI demonstrating an apical defect. Gated cine images indicated a left to right shunt in which

The pathophysiology reflects two different types of defects. The first, a simple rupture, is a direct through-and-through defect that is typically located anteriorly when associated with a LAD territory infarct. Alternatively, complex defects are believed to result from tracking of blood as it dissects thru the septum with left ventricular entry sites remote from right ven‐ tricular exit sites – these tracks then enlarge over time due to the pressure gradient between the left and right ventricle. Obviously, with unpredictable injury to the septum, there can be a combination of the 2 different pathologies. Multiple defects are found in 5-11% of cases and emphasized the need for a complex pre-operative and intra-operative assessment of all

quantitative assessment can be used to calculate the shunt fraction and size of the defect.

**5. Pathophysiology**

eral, not considered a first-line diagnostic imaging tool.

298 Principles and Practice of Cardiothoracic Surgery

The natural history of untreated PI-VSD is also poorly understood. As advances in the acute and chronic management of coronary artery disease continues to evolve, so does complica‐ tions of CAD such as AMI. In general, 25% of patients with PI-VSDs die within the first 24 hours [6]. Death is most commonly related to pre-existing comorbidities and the potentially irreversible and severe heart failure that comes from not only the acute pump failure from the inciting infarct but also the significant acute left to right heart shunting that only com‐ promises systemic perfusion further. The sudden increase in pulmonary overcirculation also contributes to the development of significant right heart failure. For those patients who sur‐ vive the acute event, 1, 2, and 4-week survival is 50%, 35%, and 20% respectively [31]. It is easy to appreciate that those patients who survive the first month may have inherently fa‐ vorable variables that might further self-select for a good post-operative outcome. Pro‐ longed untreated survival has been reported with up to 7% of patient surviving to 1 year – obviously the physiologic insult and over-circulation is minimal in these rare cases.

#### **7. Timing/Indications for surgery**

The mere presence of a PI-VSD is considered an indication for surgery with the majority of patients undergoing urgent or emergent operative intervention [38]. The primary goal of VSD closure is to reduce the end-organ damage from the combined insults of acute right ventricular overload/failure and systemic cardiogenic shock.

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‐ ative assessment.

restart a P2Y12 inhibitor, if indicated (i.e. for recent coronary stents), clearly needs to be a balance between the risk of bleeding and the risk of a stent thrombosis or recurrent ische‐ mia. Hopefully, newer agents, such as cangrelor, which is an IV, short-acting, reversible, an‐ ti-platelet agent might lead to protocols that can assist in bridging patients to such high-risk

Management And Controversies of Post Myocardial Infarction Ventricular Septal Defects

http://dx.doi.org/10.5772/53396

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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]

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‐

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,

tered. In cases of antibiotic allergies, appropriate alternatives should be chosen.

surgical interventions – such as an acute PI-VSD [2].

**8. Operative Management**

**8.1. Basic Principles and Considerations**

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 restart a P2Y12 inhibitor, if indicated (i.e. for recent coronary stents), clearly needs to be a balance between the risk of bleeding and the risk of a stent thrombosis or recurrent ische‐ mia. Hopefully, newer agents, such as cangrelor, which is an IV, short-acting, reversible, an‐ ti-platelet agent might lead to protocols that can assist in bridging patients to such high-risk surgical interventions – such as an acute PI-VSD [2].
