Congestive heart failure (CHF) is a major medical problem facing Western society today. It is the leading cause of death in the United States, representing over one-quarter of all deaths and is expected to become even more significant in the years ahead.¹ The incidence of new CHF cases are on the rise as more than 400,000 new cases per year continue to add to the over 5 million people living with CHF in the United States.¹ Ischemic cardiomyopathy (ICM) is the leading cause of CHF, affecting some 75 percent of patients with this condition.^2,3 Medical and surgical therapies have been shown to be effective in improving survival and quality of life in CHF patients.⁴ Coronary artery bypass grafting (CABG) has been shown to be effective in some patients with ICM, but heart transplantation and left ventricular assist devices are more effective in patients with advanced heart failure.⁵ Surgical ventricular remodeling (SVR) is a surgical procedure whose roots arise from the surgical treatment of left ventricular aneurysms. Also known as surgical ventricular restoration, endoventricular circular patch plasty, and the Dor procedure, SVR has been shown to be an effective treatment for select patients with ICM. In this chapter we will review the pathophysiological basis and the clinical experience with SVR.

The pathophysiology of ICM is related to the changes that occur following full-thickness myocardial infarction (MI). Following infarction, the left ventricle (LV) undergoes a well-described process of ventricular remodeling.⁶ Left unchecked, this process can lead to a progressive dilation of the ventricle, resulting in an increase in the end-diastolic diameter and volume, an increase in LV wall stress and oxygen demand, a loss of the ventricle’s natural elliptical shape with the development of a more rounded contour, the development of mitral insufficiency and, ultimately a worsening of global systolic function.^6,7 The development of mitral regurgitation is due to factors specific to ventricular remodeling as well as unrelated leaflet issues. They include annular dilation due to global ventricular enlargement, restricted leaflet motion and reduced coaptation due to leaflet tethering, or involvement of the papillary muscles with the infarction. These factors combine to prevent or limit leaflet coaptation in the proper plane, resulting in central regurgitation. Superimposed leaflet pathology can worsen the functional regurgitation.

Postinfarction dysfunction is further affected by both the electrical and mechanical dyssynchrony that develops following infarction.⁸ The concept of electrical dyssynchrony suggests that abnormalities in the conduction system following infarction result in differential timing of left and right ventricular contraction. This dyssynchronous contraction results in diminished overall LV function, a condition treated, in appropriate circumstances, with biventricular pacing. Mechanical dyssynchrony is a phenomenon of impaired LV function caused by nonuniform contraction, relaxation, and filling of the ventricle due to juxtaposed areas of akinesis, dyskinesis, and hypokinesis alongside normal areas. This has been associated with reduced survival.^8,9

The prognosis of patients with ICM is related to the size of the LV and the impact that remodeling has had on the function of the remote noninfarcted zones.^7,10,11 Infarction results in a disruption of the normal spiral arrangement of myocardial fibers.¹² The normal spiral architecture helps to resist deformation, direct blood flow toward the aortic valve, and optimize contractile efficiency. Loss of this architecture leads to a more spherical ventricle. Loss of an elliptical shape leads to a progressive reduction in contractile force, ultimately leading to death.^8,9 Since the seminal work of White, studies ranging from GUSTO to STICH have all shown that LV size is a surrogate marker of mortality in CHF.^10,12

Coronary artery revascularization, details of which are presented elsewhere in this book, has been shown to improve survival in both normal and abnormal ventricles.⁵ Improved blood flow, however, cannot improve the function of the scarred, noncontractile areas of the heart, reduce dyssynchrony, or reverse the morphological changes of infarction. Surgical techniques have been developed to arrest the progression and reverse the morphologic changes induced by the pathologic process of postinfarction ventricular remodeling. Such techniques are commonly referred to as SVR. SVR is not one techniquebut several, all of which have the same surgical goals: to reduce the size of the LV and restore a more normal elliptical shape to these enlarged spherical hearts to improve cardiac function. SVR is often performed in conjunction with coronary artery revascularization and mitral valve repair/replacement. In this chapter, these techniques are presented and the clinical outcomes discussed.

The history of the surgical approach to postinfarction remodeling begins with the approach to postinfarction LV aneurysms. Denton Cooley was the first to attempt to change the shape of the ventricle when he performed the first linear LV aneurysmectomy on cardiopulmonary bypass (CPB) to treat a calcified LV aneurysm in 1958.¹³

Many other techniques and approaches were developed over the years to treat postinfarction ventricular aneurysms.¹⁴ Fontan originally described the use of endoventricular purse-string sutures to reduce the size and reapproximate the wall of the LV.¹⁵ Jatene developed a technique of septoplasty and modified linear closure in the early 1980s.¹⁶ At the same time, Vincent Dor and colleagues introduced the technique of endoventricular circular patch plasty, which later, in 1985, came to bear his name.¹⁷ His approach was unique in that it approached akinetic areas and dyskinetic aneurysms equally. He later began to apply this technique to treat CHF and altered the way in which changes in ventricular morphology are approached. Cooley and colleagues later utilized a similar technique for aneurysmal resection by patching the anterior wall from within the ventricle but without the encircling purse-string suture to reduce the volume of the anterior wall of the LV.¹⁸

The concept of reconstructing the ventricle to a prescribed size based on the patient’s body size was introduced by Dor and popularized by Menicanti.¹⁹ The best methodology to determine the appropriate size of the reconstructed ventricle has yet to be determined. Some surgeons base it on the enlarged end-diastolic dimensions and others by indexed body surface area.¹⁹ Additional technical approaches that merit mention include a linear closure and septoplasty approach described by Mickleborough, a modified linear closure technique popularized by Guilmet in which there is direct endoventricular apposition of the lateral wall to the septum to create a new anterior wall, and a concentric purse-string or “cerclage” technique followed by linear closure utilized by McCarthy.^20,21 The end result of two decades of surgical innovation are four techniques used for ventricular remodeling procedures today.

Classically, patients are candidates for SVR if they have had an anterior MI, have a large area of akinesis or dyskinesis, and have clinical evidence of CHF. Specific characteristics of patients who have successfully undergone SVR are shown in Table 52-1. Ideal candidates have akinesis/dyskinesis in the anteroseptal area, have retained function of the basilar and lateral portions of the heart, and have good right ventricular function. They should also be candidates for revascularization and mitral valve repair if needed. Included in many clinical series of SVR are patients who have had anterior infarctions with areas of akinesis or dyskinesis with lesser degrees of ventricular enlargement and CHF. The indication for surgery in these patients is angina in other territories with the need for coronary artery revascularization. In such patients, the goal of therapy is to prevent dilation and the clinical development of CHF, which is an inevitable part of postinfarction remodeling. Relative contraindications are shown in Table 52-2. Many patients have additional cardiac conditions that will necessitate repair or replacement, and they should be candidates for surgical repair of any lesion that exists. Success has also been demonstrated in groups of patients with more complex pathologies such as multiterritory infarctions, truly advanced end-stage CHF, and the need for multiple concomitant procedures.^22,23

The surgical goals of SVR include complete revascularization of all viable territories, exclusion of akinetic and dyskinetic segments with a concomitant reduction in the size of the nonfunctioning anteroseptal portion of the heart, recreation of the elliptical shape of the heart, and repair of any valvular incompetence by valve repair or replacement.

Several different surgical approaches are used to achieve the goals stated above. Common among each of the approaches is the median sternotomy incision, which is standard in cardiac surgery. The surgical procedure begins with standard arterial and venous cannulation for CPB. If mitral valve repair or replacement is a strong possibility, cannulation of both the inferior and superior venae cavae is recommended. The LV can be vented directly through its apex, through the left atrium via the right superior pulmonary vein, or through the aortic root. Prior to systemic heparinization, femoral arterial access is obtained to make the later placement of an intra-aortic balloon pump easier if necessary. Since concomitant CABG is usually performed, a standard approach for CABG is utilized, including myocardial protection.

Once the patient is on CPB, the sequence of procedures performed is a matter of personal preference. Most commonly, CABG is performed first. Once this is accomplished, the SVR or mitral valve replacement (MVR) can be performed next.

The mitral repair can be done utilizing any technique preferred. An intraventricular repair as described by Menicanti is done through the ventriculotomy prior to performing the SVR.¹⁹ Our standard approach is to perform a reduction posterior annuloplasty through a standard interatrial groove incision prior to performing the SVR to avoid the remote possibility of disrupting our ventricular closure.

In the arrested heart with the LV vented, the LV will often collapse, demonstrating the area of thinned-out scar. If this does not happen, it may be due to a partial-thickness infarction. The absence of collapse does not contraindicate SVR and simply means that revascularization occurred early enough to prevent full-thickness infarction.

The technique employed at Hopkins is a variation of the endoventricular circular patch plasty popularized by Vincent Dor. It is depicted in Figures 52-1 to 52-7. An incision is made into the anterior wall of the LV through the area of scar. In a typical anterior infarction, the incision is extended distally to the apex and proximally parallel to the course of the left anterior descending coronary artery until normal muscle is encountered. Retention sutures are placed into scar to aid in achieving and maintaining exposure.

The ventricle is inspected and any thrombus is removed. During inspection of the ventricle, the extent as well as the transmurality of the scar is noted. A transition zone between infarcted and noninfarcted muscle is often palpable. This is particularly evident with full-thickness infarctions but is notably absent in some patients who have received thrombolytics or percutaneous revascularization prior to widespread cell death. These patients may demonstrate a mosaic pattern of ventricular scarring. Such ventricles often show akinesis rather than dyskinesis. The presence or absence of a clear transition zone is not known to be of clinical significance. The differences in the various operations are apparent from this point forward in the operation.

At this point in the procedure with many techniques, an encircling purse string of 2-0 polypropylene suture is placed along the anterior border of the sizing device. Placement of the purse-string, often called the “Fontan stitch,” is one of the key steps in the operation. It chooses the new apex of the heart and defines the outline of the new anterior wall. Selecting the location of the purse strings is usually done by personal preference. It can be done in a measured fashion, using one of several commercially available sizing devices, by selecting a site based on experience or proximity to a landmark such as the papillary muscles, or at the border of infarcted and noninfarcted tissue. Use of the “border zone” was most commonly recommended before the development of commercially available devices. If a sizing device is used, a variety of methods of determining the size of the device to be used have been recommended (Fig. 52-4). Our device is selected based on a volume of 50 to 60 mL/m² body surface area. Obese patients will have the volume titrated down slightly and cachectic patients will have it titrated up.

Once the anterior wall is encircled with the purse-string suture, it is reconstructed utilizing a variety of techniques. It is important to place the purse-string in such a fashion as to create an elliptical ventricle (Fig. 52-5). A patch of Dacron is used if the remaining defect is greater than 2 to 3 cm long. An oval patch is cut to the appropriate size and sutured in place, closing the defect. Care is taken to place the patch sutures around the anterior purse string. The patch may be sutured using a continuous or interrupted technique. Prior to completing the patch, the left ventricular vent is shut off, allowing the ventricle to fill with blood and forcing air to escape the ventricle through the partially completed closure (Fig. 52-6). After the patch is sutured into place, a linear closure is performed superficial to the patch or purse-string. Horizontal mattress sutures, buttressed with bovine pericardium, are used as a first layer of closure. The second layer is a continuous running stitch of 2-0 polypropylene (Fig. 52-7). If the defect is moderate in size but not large enough for patching, the ventricle can be reapproximated superficial to the purse-string using a linear closure, usually reinforced.

An alternative technique advocated by Linda Mickleborough employs a modified linear closure and patch septoplastyto accomplish the same SVR surgical goals. This technique uses the same anterior ventriculotomy approach to expose the septum and anterior wall. This technique employs a more traditional linear closure to exclude the akinetic or dyskinetic areas of the anterior wall. In addition, the dilated, fibrotic areas of the infarcted septum are addressed by either including the septum in the linear closure of the anterior wall or patching the septum and including the patch in the linear closure.²⁴

A technique of multiple purse strings is employed by Pat McCarthy. Also called the cerclage technique, it begins as the previous two techniques. Once the anterior wall purse string is placed and tied, additional purse strings are placed a few millimeters superficial to the previous purse string. This continues anteriorly until the final remaining defect is small and is closed with a standard linear closure.²⁵

A modified septoplasty technique, employed by Jatene, aimed to reduce the volume of the infarcted septum in conjunction with a patch or primary closure. This technique also begins in the same way as other SVR procedures. An anterior encircling purse-string is placed to define the borders of the anterior wall, as is done in some of the other SVR techniques. The distinguishing characteristic of this technique is the placement of mattress sutures in the septum to reduce the horizontal length of the septum. Once the septal reduction is performed, the anterior encircling purse-string is tied and the anterior wall closed primarily or with a patch.¹⁶

A final technique utilizes an internal linear closure described by Guilmet.²⁶ With this technique, the deep scar of the septum is directly sewn to the deep scar of the lateral wall internally. This excludes the more superficial scar and aligns the remaining septal and lateral scar tissue for a linear closure (Fig. 52-8).