Breaking News

Postinfarction Ventricular Septal Defect Repair


Keywords : postinfarct ventricular septal defect, Operations for Coronary Artery Disease

Postinfarction Ventricular Septal Defect Repair
Step 1. Surgical Anatomy
·    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.1,2
·    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.1,2


Step 2. Preoperative Considerations
·  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.
·    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.
·    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.3,4
·  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.5 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.6
·  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,7 because some patients may benefit from revascularization to noninfarcted territories in which flow-limiting coronary lesions exist.

Step 3. Operative Steps
1. General Principles
·   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.
·  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.7
·   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
  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.7
  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 glutaraldehydetreated 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 layer7  (see Fig. 8.3C).

Posteroinferior Defects
·    Closure of posteroinferior septal defects poses a greater technical challenge. Simple plication of these defects is rarely possible. With large defects, this results in unacceptable tension and reopening or catastrophic disruption. Depending on the size and location of the defect, one or two patches may be required. In addition, rupture of the posterior papillary muscle occasionally requires replacement of the mitral valve.
·  A transinfarct posterior incision is made just to the left ventricular side of the posterior descending coronary artery (Fig. 8.4A). This incision is started at the midportion of the posterior wall and extended toward the mitral annulus and apically. Most commonly, rupture is found in the proximal half of the posterior septum (see Fig. 8.4B) and involves the pos- teromedial papillary muscle. The necrotic portion of the ventricular septum is excised, along with the involved portion of the posterior ventricular free wall (Fig. 8.5A). The free edge of the RV is shaved back to expose the margins of the defect clearly.
·   Rarely, repair of a small septal rupture can be undertaken primarily. An appropriate lesion would appear as an unhinging of the posterior attachment to the septum, with little adjacent myocardial necrosis. The repair is accomplished by approximating the posterior septum to the free wall of the RV with felt-buttressed mattress sutures of 1-0 Tevdek. The LV can then be closed with a separate suture line, again with interrupted mattress sutures of no. 1 Tevdek buttressed with felt. A second running suture line is then taken to reinforce the ventriculotomy closure.

·    More commonly, patches are required. A single patch can be added to aid in a tension-free closure of the LV after primary closure of the septum (see Fig. 8.5B). When the defect in the septum is larger, a two-patch technique is used. Interrupted mattress sutures of buttressed 2-0 Tevdek are placed circumferentially around the defect. The sutures are placed on the right ventricular side of the septum and then transitioned to the epicardial surface of the diaphragmatic right ventricular free wall. An appropriately shaped Dacron patch is parachuted down after passage of the stitches. Use of additional felt on the exterior of the patch cushions the sutures and aids in the even distribution of forces (Fig. 8.6A). A second patch is now required for closure of the remaining defect into the LV.
·    Mattress sutures of buttressed 2-0 Tevdek are placed circumferentially around the margins of the posterior left ventricular free wall. The stitches are taken from the endocardial surface through the ventricular wall so that the patch will lie on the epicardial surface when the repair is complete (Fig. 8.7; see Fig. 8.6B). Again, use of additional felt on the outside of the patch may be advantageous (Fig. 8.8).
·    Involvement of the posterior medial papillary muscle may preclude the placement of stitches through infarcted tissue. In these cases, as in the case of papillary muscle rupture, a mitral valve replacement is performed after patch placement. The mitral valve is exposed through a left atriotomy. On occasion, a transseptal approach via the dome of the left atrium may be required. The valve is excised and replaced with a low-profile prosthesis. Interrupted, felted 2-0 Tevdek sutures are used, with the needle passing from the left atrium through the annulus.


3. Modification of Technique: Infarct Exclusion
Anterior Apical Defects
·     The apical portion of the ventricle is opened through the infarction, with extension onto the anterior LV. A glutaraldehyde-preserved bovine pericardial patch is secured to noninfarcted areas of the left ventricular septum using running 3-0 polypropylene sutures. The stitches should be inserted 5 to 7 mm deep in the muscle and 4 to 5 mm apart. The stitches in the patch should be 5 mm from its free margin to allow the patch to cover the area between the entrance and exit of the sutures (Fig. 8.9A).
·   The suture line is begun at the most proximal part of the septum, and suturing begins traveling toward the apex. The suture line continues from the septum onto the left ventricular free wall. If the infarct involves the anterior papillary muscle at its base, the suture is brought outside the heart at this point and continued as full-thickness interrupted 2-0 polypropylene sutures buttressed on the epicardial surface with a strip of bovine pericardium or Teflon felt. The LV is then closed with interrupted mattress sutures of 2-0 polypropylene buttressed by Teflon felt strips, followed by a running 2-0 polypropylene stitch (see Fig. 8.9B).8
Posteroinferior Defects
   A transinfarct incision is made in the inferior wall of the LV, just lateral to the posterior descending coronary artery, to expose the defect and is extended toward both the mitral valve and apex. Care is taken to avoid damage to the posterior lateral papillary muscle. A bovine pericardial patch is tailored in a triangular shape. Its size will be approximately 4 × 7 cm in most patients. The base of the triangle is sutured to the mitral valve annulus with continuous 3-0 polypropylene sutures. The medial suture line then transitions from the mitral annulus to the endocardium of the ventricular septum and is continued along that structure apically. Laterally, the suture line transitions to the endocardium of the posterior LV.
     After several stitches, the posterior papillary muscle is encountered. If the area of necrosis is small, and if healthy tissue allows for continuation, the running sutures are continued toward the apex. Usually, on reaching the posterior papillary muscle, it is necessary to bring the running stitch through the muscle to the outside of the LV. The suture line is then continued with interrupted, full-thickness, 2-0 polypropylene sutures and buttressed with felt on the outside (Fig. 8.10A). The suture line continues until the patch is completely secured, and then the ventriculotomy is closed in two layers of full-thickness sutures buttressed on strips of Teflon felt. The infarcted right ventricular wall is left undisturbed8  (Fig. 8.10B).

Right Ventricular Approach
Hosoba et al.9 have described repairing postinfarct VSDs using a right ventricular approach and two Dacron patches. For anterior septal defects, an incision is made in the RV wall parallel to the distal left anterior descending artery. Sutures are placed transseptally from the LV cavity via the VSD and into the octagonally shaped patch. The patch is placed through the VSD, into the LV, and secured into place. A second Dacron patch is secured over the defect in the RV. For posterior VSDs, a similar two-patch technique is used, with an incision in the RV parallel to the midportion of the posterior descending artery.


Step 4. Postoperative Care
·  If an intraaortic balloon pump was not inserted before surgery, one should be placed. Inotropic support is instituted with milrinone (phosphodiesterase inhibitor). This drug is preferred because, in addition to its inotropic properties, it has vasodilatory properties in the pulmonary vascular bed.
·    Posterior defects are associated with a right ventricular infarction and more often result in right heart failure on separation from bypass. In such a case, inhaled nitric oxide (20 ppm) is instituted before attempted separation. Additional maneuvers may include right-sided infusion of prostaglandin E1 (0.5 µg/kg/min) and left-sided norepinephrine infusion through a left atrial line.7,10
·  For patients who are still in cardiogenic shock despite these maneuvers, mechanical circulatory support may be warranted.11 ECMO may allow for support and resuscitation of these patients in the postoperative stage. Central cannulation may be preferred postcardiotomy but the cannula location should be individualized based on the clinical picture.
·    Extubation usually requires aggressive early postoperative diuresis. After fully rewarming, intravenous infusion of furosemide at doses of 5 to 20 mg/hr is used to maintain urine output greater than 100 mL/hr. Continuous venovenous hemofiltration is used for nonresponders.

Step 5. Pearls and Pitfalls
·   The common problems during separation from bypass are low cardiac output, with or without right ventricular failure and bleeding.
·  Recurrent or severe ventricular ectopy is common. Before attempted separation from cardiopulmonary bypass, amiodarone is begun with a bolus of 150 mg, followed by ongoing infusion at 1 mg/min. The bolus may be repeated up to six times for malignant ectopy.
· Inadequate hemodynamics on separation from cardiopulmonary bypass may require placement of a ventricular assist device or ECMO. Left ventricular assist devices may result in increased right-to-left shunting, and biventricular devices may be preferable.

References
1.     Cooley DA. Postinfarction ventricular septal rupture. Semin Thorac Cardiovasc Surg. 1998;10:100–104.
2.  Daggett WM. Postinfarction ventricular septal defect repair: Retrospective thoughts and historical perspectives. Ann Thorac Surg. 1990;50:1006–1009.
3.      Pitsis A, Kelpis T, Visouli A, et al. Left ventricular assist device as a bridge to surgery in postinfarction septal defect. J Thorac Cardiovasc Surg. 2008;135:951–952.
4.   Conradi L, Treede H, Brickwedel J, et al. Use of initial biventricular mechanical support in a case of postinfarction ventricular septal rupture as a bridge to surgery. Ann Thorac Surg. 2009;87:e37–e39.
5.  Michel-Behnke I, Trong-Phi L, Waldecker B, et al. Percutaneous closure of congenital and acquired ventricular septal defects: Considerations on selection of the occlusion device. J Interv Cardiol. 2005;18:89–99.
6.     Calvert PA, Cockburn JC, Wynne D, et al. Percutaneous closure of post-infarction ventricular septal defect: in-hospital outcomes and long-term follow-up of UK Experience. Circulation. 2014;129:2395–2401.
7.    Agnihotri AK, Madsen JC, Daggett WM Jr. Surgical treatment of complications of acute myocardial infarction: postinfarction ventricular septal defect and free wall rupture. In: Cohn LH, ed. Cardiac Surgery in the Adult. 3rd ed. New York: McGraw-Hill; 2008:753–784.
8.    David TE, Armstrong S. Surgical repair of postinfarction ventricular septal defect by infarct exclusion. Semin Thorac Cardiovasc Surg. 1998;10:105–110.
9.   Hosoba S, Asai T, Suzuki T, Nota H, et al. Mid-term results for the use of the textended sandwich patch technique through right ventriculotomy for postinfarction ventricular septal defects. Eur J Cardiothorac Surg. 2013;e116-e120.
10.   Taghavi S, Mangi AA. Postinfarction ventricular septal defect and ventricular rupture. In: Selke F, del Nido SJ, Swanson SJ, eds.
11.   Sabiston and Spencer Surgery of the Chest. 9th ed. Philadelphia: Elsevier; 2016:1653–1662.
12.   Firstenberg MS, Blais D, Crestanello J, et al. Long-term mechanical support for complex left ventricular postinfarct pseudoaneurysms.
13.   Heart Surg Forum. 2009;12:E291–E293.

No comments