Abstract
Postinfarction ventricular septal defects (VSDs) classically occur in an apical, anterior, or posteroinferior location. These defects must be treated surgically, although select patients in severe cardiogenic shock may benefit with initial resuscitation with mechanical circulatory support, followed by later surgical repair. Operative intervention involves debridement of necrotic tissue followed by closure of the defect with a prosthesis, although small defects can rarely be closed primarily. Location of the defect will determine type of exposure. Postoperative care should involve liberal use of an intraaortic balloon pump and chemical inotropes.
Keywords
postinfarct ventricular septal defect
Step 1
Surgical Anatomy
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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.
Figure 8.1
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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.
Step 2
Preoperative Considerations
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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.
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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.
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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.
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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. 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.
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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, because some patients may benefit from revascularization to noninfarcted territories in which flow-limiting coronary lesions exist.
Step 3
Operative Steps
1
General Principles
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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.
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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.
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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
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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.
Figure 8.2
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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 glutaraldehyde-treated 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 layer (see Fig. 8.3C ).
