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Postinfarction ventricular septal defect (VSD) is an opening in the ventricular septum resulting from rupture of acutely infarcted myocardium.
In 1847, Latham first described a postinfarction VSD at autopsy, but it was not until 1923 that Brunn made the diagnosis clinically. In 1957, Cooley and colleagues first reported surgical repair of a postinfarction VSD 11 weeks after myocardial infarction (MI). The patient died 6 weeks later. The first long-term survivor of such repair was reported by the Mayo Clinic in 1963. Approach through the left ventricle (LV) was described in 1969 by Kay and Dubost and subsequently by Kitamura and colleagues, Javid and colleagues, and others. The double-patch method was described by Iben and colleagues and subsequently modified by Gonzalez-Lavin and Zajtchuk and by Daggett and colleagues. Repair of the ruptured septum through a right atrial approach was reported by Filgueira and colleagues in 1986. In 1987, David and colleagues introduced the concept of endocardial patch repair with infarct exclusion using autologous pericardium.
Postinfarction VSD is usually located in the anterior or apical portion of the ventricular septum (≈60% of cases) as a result of a transmural anterior MI. About 20% to 40% of patients have a VSD in the posterior portion of the ventricular septum as a result of an inferior MI. Ventricular septal rupture usually occurs as a complication of a first acute MI. Also, a well-developed collateral coronary circulation is uncommon in hearts with a postinfarction VSD. The defect is generally associated with complete occlusion (rather than severe stenosis) of a coronary artery, usually the left anterior descending coronary artery. Important stenoses often coexist in the right coronary artery system. VSDs may be multiple, and rather than occurring simultaneously, they may develop separately several days apart. The importance of concomitant right ventricular (RV) infarction in patients with postinfarction VSD is now evident. For many years, evidence of RV dysfunction was thought simply to represent poor “adaptation” of the RV to the sudden increase in pulmonary blood flow imposed by the postinfarction VSD. Accumulated information indicates that actual infarction of the inferior RV wall, or at least severe ischemia of that area, is responsible for the dysfunction. A posterior VSD, in particular, may be accompanied by mitral valve regurgitation secondary to papillary muscle infarction or ischemia (see Chapter 10 ). In about 40% of patients who survive the early period after ventricular septal rupture, the remainder of the infarcted septum and adjacent ventricular wall may become aneurysmal.
The first sign of ventricular septal rupture in a patient who has recently sustained an MI is development of a pansystolic murmur, usually at the left lower sternal border, with or without radiation to the axilla, and of varying intensity. If the murmur is overlooked or its importance ignored, most patients with ventricular septal rupture die undiagnosed. The chest radiograph provides evidence of pulmonary venous hypertension and increased pulmonary blood flow. A systolic murmur can result from acute mitral regurgitation secondary to MI as well as from postinfarction VSD, and the two conditions may coexist. Thus, after detection of the murmur, an examination with two-dimensional echocardiography (either transthoracic or transesophageal) with Doppler color flow imaging is performed to define the site of the VSD, quantify the magnitude of left-to-right shunt, and ascertain presence or absence of mitral regurgitation. Echocardiography is highly sensitive and specific and provides safe and rapid diagnosis. It also permits preoperative analysis of wall motion abnormalities in a high percentage of patients.
Magnitude of left-to-right shunt can also be quantified by the Fick principle (see “Whole Body Oxygen Consumption” under Cardiovascular Subsystem in Chapter 5 ). A pulmonary artery (Swan-Ganz) catheter is introduced at the bedside. Blood samples are obtained from the right atrium, the pulmonary artery, and a peripheral artery. The left-to-right shunt is usually large, with a pulmonary-to-systemic blood flow ratio ( ) of 2.0 or greater. Both pulmonary artery wedge pressure, reflecting left atrial and LV end-diastolic pressures, and pulmonary artery pressure are usually elevated. Once the presence of a left-to-right shunt is demonstrated and initial management implemented (see “Preoperative Preparation” under Technique of Operation), coronary angiography should be performed if the patient is hemodynamically stable.
Although some patients with postinfarction VSD will do well without addition of invasive studies, there is accumulating evidence that bypass grafting of stenotic coronary arteries supplying the noninfarcted areas of myocardium is associated with improved early and late survival. Multiple-system coronary artery disease is present in more than 50% of patients. If echocardiographic studies have adequately identified the VSD, presence or absence of mitral regurgitation and LV wall motion abnormalities, intracardiac pressure measurements, and left ventriculography are unnecessary.
Before the advent of thrombolytic therapy and acute percutaneous coronary artery interventions, postinfarction VSD developed in approximately 1% to 3% of patients. Following introduction of these therapeutic interventions, the frequency has been substantially reduced to less than 0.5% of patients. Ventricular septal rupture generally occurs during the first week after acute MI. There is a high incidence in the first day (94% in the GUSTO-I trial) ; median time for presentation in the SHOCK trial was 16 hours. Without surgical treatment, early death is common; less than 30% of patients survive 2 weeks, and only 10% to 20% survive more than 4 weeks ( Fig. 9-1 ). Risk of death is greatest immediately after myocardial rupture and then gradually declines. Women and the elderly may be more susceptible.
Because most patients with postinfarction VSD are seriously ill and require operation early after septal rupture, their management before operation is of critical importance. Once the diagnosis of acute postinfarction VSD has been confirmed by echocardiography and a pulmonary artery catheter has been inserted, additional diagnostic studies must be considered before proceeding with operation. (The only exception to this is the occasional patient with essentially no systemic hemodynamic disturbance, as described in “Indications for Operation.”) An intraaortic balloon catheter (IABP) should be inserted urgently, because these patients can deteriorate rapidly. If the patient remains hemodynamically unstable, cardiopulmonary bypass (CPB) can be established by peripheral cannulation (see “Cardiopulmonary Bypass Established by Peripheral Cannulation” under Special Situations and Controversies in Section III of Chapter 2 ). If indicated, the patient is taken immediately to the cardiac catheterization laboratory for special studies (see “Clinical Features and Diagnostic Criteria” earlier in this chapter), with the IABP or CPB in place and functioning. When the studies have been completed, or if they are not performed, operation is undertaken immediately, because permanent improvement is generally not achieved with support devices alone.
After the usual initial preparations in the operating room (see “General Comments and Strategy” in Section III of Chapter 2 ), a median sternotomy incision is made. The heart is disturbed as little as possible before CPB is established. While performing the median sternotomy, removal and preparation of saphenous vein is accomplished in the usual manner (see Chapter 7 ). Because of the length and complexity of the operation, the surgical plan must be efficient so that aortic-clamp and CPB times are kept to a minimum. CPB is promptly established using two venous cannulae and caval tapes. If CPB is established percutaneously before or immediately after the patient is brought to the operating room, central cannulation should be performed and CPB established using a pump-oxygenator designed for operating room use. The femoral lines are clamped and removed, and the femoral artery and vein are repaired at the end of the procedure. The aorta is clamped. Myocardial management may include warm induction of cardioplegia and controlled aortic root reperfusion (see “Cold Cardioplegia, Controlled Aortic Root Perfusion, and [When Needed] Warm Cardioplegic Induction” in Chapter 3 ). Because an acute coronary occlusion is typically present, the coronary sinus route of administration should be employed for at least part of the cardioplegic infusion (see “Technique of Retrograde Infusion” under Cold Cardioplegia [Multidose] in Chapter 3 ). The caval tapes are secured. A left atrial venting catheter may be inserted, but usually is not necessary.
The VSD is usually approached through the LV. When located anteriorly, it is approached through the anterolateral infarction (or aneurysm) that is generally present ( Fig. 9-2, A ). The defect in the septum is typically found immediately beneath this area ( Fig. 9-2, B ). It is repaired using a collagen- or gelatin-impregnated polyester patch or a patch of autologous or bovine pericardium. The patch is made sufficiently large to cover the adjacent intact but infarcted portion of the septum as well as the VSD. No part of the ventricular septum is resected. The patch is sewn into place on the LV side of the septum, with pledgeted mattress sutures placed away from the edge of the defect into noninfarcted myocardium. The sutures are placed close together and the pledgets placed on the RV side of the defect ( Fig. 9-2, C ). Alternatively, the patch can be sutured into place with a continuous No. 3-0 or 4-0 polypropylene suture, securing the patch to noninfarcted myocardium on the ventricular septum ( Fig. 9-2, D ). Infarcted or aneurysmal myocardium on the anterolateral wall of the LV is excised, avoiding the anterolateral papillary muscle. If more than a small amount of tissue is removed from the anterolateral wall, it may be necessary to close the defect in the LV wall with a polyester or pericardial patch. If this is not necessary, the incision in the LV is closed with interrupted heavy (No. 0 or 2-0) silk or polyester sutures placed through strips of polytetrafluoroethylene (PTFE) felt and through the patch that has closed the VSD ( Fig. 9-2, E ). This suture line is reinforced with a continuous suture of No. 0 or 2-0 polypropylene, which is passed through both strips of PTFE felt, both edges of the myocardium, and the ventricular septal patch ( Fig. 9-2, F ).
An alternative technique involves suturing a pericardial patch to the LV endocardium adjacent to the area of the infarction. The LV is opened through an incision in the infarcted anterolateral wall. An oval patch (approximately 4 × 6 cm) of bovine pericardium is sutured to the endocardium of the inferior portion of the noninfarcted endocardium of the ventricular septum with a continuous No. 3-0 polypropylene suture ( Fig. 9-3, A ). The suture line is continued into the noninfarcted endocardium of the anterolateral ventricular wall ( Fig. 9-3, B ). When placing the continuous suture through the transition zones (superiorly and inferiorly) between the septum and the free wall of the LV, care must be taken to anchor the patch securely to the myocardium to prevent residual communications between the LV and RV. Separate interrupted sutures may be required. Once the patch is completely secured to the LV endocardium, the LV cavity is essentially excluded from the infarcted myocardium ( Fig. 9-3, C ). The ventriculotomy is closed using two strips of bovine pericardium or PTFE felt ( Fig. 9-3, D ).
When the VSD is in the apical portion of the septum and is associated with an apical MI, the operation consists of amputating the apex of the ventricle, including the involved portion of the ventricular septum ( Fig. 9-4, A ). The LV is opened through the infarcted myocardium and the septum examined. If the VSD is immediately adjacent to the area of apical infarction, the apex of the heart is excised, including the involved portion of the septum and adjacent RV ( Fig. 9-4, B ). Using strips of PTFE felt on each side of the septum and on the edges of the right and left ventricular myocardium, heavy mattress sutures of silk or polyester are placed through these four layers of felt as well as through the right and left ventricular myocardium and the ventricular septum ( Fig. 9-4, C ). These sutures are tied, thus excluding the interventricular communication and the openings into both ventricles. The resulting suture line is reinforced with a continuous No. 0 or 2-0 polypropylene suture ( Fig. 9-4, D ).
VSDs located in the posterior septum are more difficult to expose and repair. The heart is lifted out of the pericardium with traction on the LV apex. The defect is approached through a vertical incision in the infarcted LV myocardium ( Fig. 9-5, A ). If the VSD is relatively small, the necrotic tissue can be excised, including the infarcted free wall of both the RV and LV, often with the overlying occluded posterior descending coronary artery ( Fig. 9-5, B ). The VSD patch (collagen- or gelatin-impregnated polyester or bovine or autologous pericardium) is placed on the LV side of the septum and secured using mattress sutures of No. 2-0 polyester, with pledgets placed on the RV side of the septum ( Fig. 9-5, C ). If little or no free wall myocardium has been excised, LV and RV edges are approximated, incorporating the septal patch and two strips of PTFE felt. A large defect in the free wall requires a second patch. The free edge of the septal patch is sutured to the free wall of the LV with interrupted mattress sutures of No. 2-0 polyester using pledgets on the patch and a strip of PTFE on the ventricular wall ( Fig. 9-5, D ). The patch for closure of the RV is attached to the septal patch already in position and to the free wall of the RV. Pledgets of felt are placed on the inner surface of the RV, and a strip of felt is placed on the outer surface (see Fig. 9-5, D ).
Muehrcke and colleagues describe an alternative technique for closure of the free wall when there is extensive infarction. No infarcted muscle on the RV or LV free walls is excised. The septal patch is sutured to the RV edge of the incision that was made to expose the septum. This suture line incorporates the infarcted free wall and a patch of polyester placed over the entire infarcted muscle of the free wall ( Fig. 9-5, E ). Pledgeted sutures are placed circumferentially around the area of infarcted muscle and through the polyester patch, then tied over a strip of PTFE felt ( Fig. 9-5, F ).
The technique developed by David and colleagues involves an incision in the inferior wall of the LV parallel to the posterior descending coronary artery. Traction sutures are placed on the edges of the ventriculotomy to facilitate exposure ( Fig. 9-6, A ). The VSD is identified, and a triangular patch of bovine pericardium approximately 4 × 7 cm is sutured first to the fibrous anulus of the mitral valve using a continuous No. 3-0 polypropylene suture. The medial margin of the patch is sutured to noninfarcted muscle of the septum adjacent to the defect ( Fig. 9-6, B ). The lateral edge of the patch is then sutured to the endocardium of the LV free wall adjacent to the posterior papillary muscle ( Fig. 9-6, C ). This excludes all infarcted muscle from the LV cavity ( Fig. 9-6, D ). The ventriculotomy is closed with two layers of sutures buttressed with strips of bovine pericardium or PTFE felt ( Fig. 9-6, E ).
Occasionally, mitral regurgitation may be associated with acute septal rupture, particularly when the infarction is posterior. The mitral valve is replaced (or occasionally repaired) under such circumstances. Replacement is usually best performed through the left ventriculotomy, using interrupted pledgeted mattress sutures with the pledgets on the atrial side of the anulus. It can also be replaced (or repaired) through a left atrial or biatrial incision (see Chapter 10 ).
When an LV aneurysm coexists with a postinfarction VSD, it is excised as the initial step in the operation. Then after repair of the VSD, the aneurysm is generally repaired as usual (see Chapter 8 ). However, improvisation in the repair may be necessary. Rarely, patients with postinfarction VSD are also found to have free wall rupture of the infarct. In surgical patients the rupture is usually small and can be repaired by excising the infarct. The possibility of such an associated lesion lends urgency to such situations.
In the case of important documented coronary artery stenosis, CABG should be performed. When feasible, the internal thoracic artery should be grafted to the left anterior descending coronary artery.
An essential part of the operation is controlled aortic root reperfusion (see “Cold Cardioplegia, Controlled Aortic Root Reperfusion, and [When Needed] Warm Cardioplegic Induction” in Chapter 3 ). During this maneuver, all suture lines are examined. Additional measures are used, if necessary, to establish hemostasis. The remainder of the operation is completed in the usual manner (see “Completing Operation” in Section III of Chapter 2 ). Particular care is taken to achieve hemostasis. Two right atrial and two RV temporary pacing wires are placed so that atrioventricular sequential pacing can be established, if needed. IABP is resumed during the rewarming phase of CPB and usually is continued into the postoperative period. If CPB cannot be discontinued after about 30 minutes of normothermic partial CPB, temporary ventricular assistance may be required (see “Temporary Ventricular Assistance” in Chapter 5 ).
Postoperative care is conducted as described in Chapter 5 . IABP is continued in a one-to-one mode until cardiac output is adequate; it is then gradually discontinued and the balloon catheter removed. If ventricular assist devices are in place, flow through them is gradually decreased as ventricular function and cardiac output improve (see “Temporary Ventricular Assistance” in Chapter 5 ). Because patients are often critically ill during the early postoperative period, with low cardiac output and often with complicating arrhythmias, a full therapeutic regimen is usually required. This includes optimizing preload with infusion (or removal) of volume, enhancing contractility with inotropic agents, and reducing afterload, if indicated. Attaining a heart rate that results in optimal cardiac output by pacing or pharmacologic agents is also important. Using the technique described earlier under “Clinical Features and Diagnostic Criteria,” measurements are made to detect residual shunt, which can be present because of friability of the septum and relative insecurity of the repair. Transesophageal echocardiography is also useful for this purpose. If the is 1.5 to 2.0 or greater and the hemodynamic state is poor, prompt reoperation should be considered. Care required late postoperatively by patients undergoing isolated CABG should be applied to those who have undergone repair of a postinfarction VSD (see “Special Features of Postoperative Care” in Chapter 7 ).
Hospital mortality after VSD repair is approximately 30% to 40%. Death may be difficult to prevent because of the extent of myocardial necrosis associated with rupture of the ventricular septum. However, mortality might be reduced by prompt surgical repair, better methods of myocardial management, and more aggressive use of ventricular assistance in the postoperative period.
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