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Badhwar V, Bolling SF. Nontransplant Surgical Options for Heart Failure.
In: Cohn LH, Edmunds LH Jr, eds. Cardiac Surgery in the Adult. New York: McGraw-Hill, 2003:15151526.

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Right arrow Congestive Heart Failure

Chapter 64

Nontransplant Surgical Options for Heart Failure

Vinay Badhwar/ Steven F. Bolling

CORONARY REVASCULARIZATION
GEOMETRIC MITRAL RECONSTRUCTION
GEOMETRIC VENTRICULAR RECONSTRUCTION
PARTIAL LEFT VENTRICULECTOMY
DYNAMIC CARDIOMYOPLASTY
EMERGING BIOMEDICAL DEVICES FOR HEART FAILURE
CONCLUSIONS
REFERENCES

?? INTRODUCTION
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Congestive heart failure (CHF) has become a major worldwide public health problem. In our ever-aging population, medical advances that have extended our average life expectancy have also left more people living with chronic cardiac disease than ever before. In the United States alone, there are nearly 4.9 million suffering with heart failure; yet of the 500,000 new patients diagnosed each year, less than 3000 are offered transplantation due to limitations of age, comorbid conditions, and donor availability. Despite the significant improvements with medical management, CHF patients are repeatedly readmitted for inpatient care and the vast majority will die within 3 years of diagnosis.1

The successful and reproducible long-term results with orthotopic heart transplantation (OHT) have made it the treatment of choice for patients with medically refractory end-stage heart failure.2 Unfortunately, the obvious limitations to OHT include the need for immunosuppression and the severe shortage of donor organs. This past decade has seen the annual number of transplants performed worldwide plateau at less than 4000.3 This lack of donor availability has thus necessitated a rigorous selection criteria be applied to potential recipients in order to optimize the utility of these precious organs, indicated only for patients with end-stage cardiomyopathy in whom all other modes of therapy have been exhausted. Access to OHT has thus been restricted to those without comorbid medical conditions and relatively restricted to those younger than age 65. This leaves the vast majority of CHF patients seeking other options.

Despite the technologic strides being made towards total implantability, the role for mechanical support presently remains primarily as a bridge to transplantation or for temporary support. Though there have been a number of clearly successful cases of ventricular assist device (VAD) use as a bridge to recovery, its long-term efficacy for this purpose or its use as a long-term therapy for chronic heart failure remains to be fully evaluated by multicenter clinical trials.49 Though assist device technology may be on the verge of being implemented as a destination therapy for CHF, its current primary indication as a bridge to transplantation results in the restriction of its use to patients fulfilling candidacy for OHT. These confines, and the high cost associated with these devices, have yet to make the VAD an unrestricted surgical solution for the management of most CHF patients.

This clinical dilemma has provided the impetus for surgeons to develop new alternatives for the treatment of heart failure. As OHT and VAD use is more stringently applied, techniques to restore myocardial perfusion, eliminate valvular regurgitation, and restore ventricular geometry have emerged as the first-line surgical approach to heart failure. In response to the growing need for the proficient application and critical appraisal of the expanding menu of surgical options, the new subspecialty of heart failure surgery has emerged. The following will briefly review established nontransplant surgical modalities for heart failure such as coronary revascularization, geometric mitral reconstruction, and geometric ventricular reconstruction. Alternative options such as partial left ventriculectomy and cardiomyoplasty as well as some innovative devices currently being evaluated for clinical application will also be discussed.


?? CORONARY REVASCULARIZATION
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We have known for nearly 20 years that revascularizing patients with left ventricular dysfunction can result in upwards of a 25% improvement in long-term survival.10,11 Early enthusiasm was tempered by reports of high operative mortality in patients with a low ejection fraction (EF). Since then, as success with the medical and surgical management of heart failure and transplantation grew, so did the interest in applying this experience to patients with ischemic cardiomyopathy. Successful revascularization can now be performed on patients with an EF less than 30% with hospital mortalities as low as 5%.1214

The premise behind the improvements in EF, long-term survival, and quality of life of these patients following coronary artery bypass grafting (CABG) is believed to be due to postoperative myocyte recruitment. Restoration of perfusion resuscitates dormant viable myocardium and serves to protect the previously functioning portions of the ventricle from further ischemic insults, arrhythmias, and infarction.

In order to minimize morbidity, a multidisciplinary approach to the preoperative management of heart failure is essential. Patients ideally suited for CABG are those who are medically optimized, with or without angina, who have good distal coronary targets, functional hibernating myocardium identified preoperatively, and no evidence of right ventricular dysfunction.15 As experience in managing these patients increases, many surgeons have operated on patients with ejection fractions less than 10%, those requiring reoperation, and those with moderate elevations in pulmonary artery pressure. Nevertheless, patients with clear documentation of poor right ventricular EF, clinical right-sided congestive symptoms, or fixed pulmonary hypertension above 60 mm Hg systolic should be approached cautiously, because these patients may in fact be better suited for transplantation.

The process of preoperative investigation should coincide with optimizing the patient's medical management. This should entail an aggressive regimen of diuretic and vasodilator therapy to minimize ventricular afterload and normalize the patient's circulating volume. For patients with severe heart failure, a brief period of inotropic therapy for ventricular resuscitation may be necessary to optimize their medical management. Inability to be weaned from this support is often indicative of severe myocardial injury and poor overall prognosis with any surgical therapy other than mechanical ventricular assistance or transplantation.

Preoperative investigations should begin with transthoracic echocardiography to grossly evaluate ventricular function and identify any underlying valvular pathology. Baseline screening physiological studies of oxygen consumption, pulmonary function, and cardiopulmonary endurance are recommended. Identification of reversible ischemia by means of a nuclear study can be helpful; however, for patients with angina, many centers will proceed directly to coronary angiography. Though angina may be indicative of living ventricular muscle, perhaps the most important correlate of successful surgical recovery is the quantification of myocardial viability. Not only is a determination of myocardial contractile reserve essential to ensure that the patient can be safely separated from cardiopulmonary bypass (CPB), but this information is predictive of ventricular recovery and long-term survival after operation. Though thallium-201 perfusion scans may distinguish myocytes with membrane integrity from scar, PET scanning and dobutamine stress echocardiography permit the preoperative identification of myocardial viability and the prediction of postoperative function.1618

The fundamental premise behind a successful operation is to attain an expeditiously performed and yet complete revascularization. As the failing myocardium is particularly intolerant to further episodes of ischemia, careful consideration should be given to the quality of the distal vessels and the ease with which good anastomoses can be achieved. Operative time expended grafting small or extensively diseased vessels, or performing additional techniques such as endarterectomy, may be counterproductive. Since the price to pay for incomplete revascularization or transient ischemia may be severe, off-pump techniques may not be ideally suited for these patients unless performed flawlessly.

Multiple groups have been uniformly successful in demonstrating improvements in survival, ventricular function, and functional status with coronary revascularization in patients with ischemic cardiomyopathy with ejection fractions less than 25%.1921 The 5-year survival with transplantation ranges from 62% to 82%, whereas with medical therapy alone, it is less than 20%. Most series report survival following CABG for ischemic cardiomyopathy ranging from 85% to 88% at 1 year, 75% to 82% at 2 years, 68% to 80% at 3 years, and 60% to 80% at 5 years. Operative mortality has been reported from 3% to 12%, with the main predictor of increased risk being urgency of operation. When compared to medical therapy, revascularized patients have significant improvements in quality of life. Most series consistently report considerable enhancements in patient mobility, peak oxygen consumption, and functional status. The average preoperative NYHA class of 3.5 reportedly drops to 1.5 after revascularization. Postoperatively, there are substantial reductions in readmissions for CHF and many patients return to work.

It is encouraging to note that the long-term survival of CHF patients following CABG is equivalent to transplantation in many series. The superior survival of CABG over transplant in the first 2 years postoperatively may be due to early attrition from rejection or infection in the latter group. Although there has been little reported on patients with ejection fractions under 10%, from the above data, one could infer that these patients would have a similarly better outcome than their nonrevascularized counterparts. As experience with heart failure surgery expands, refinements in preoperative and operative management of CABG patients will no doubt be reflected in the uniformity of future long-term results.


?? GEOMETRIC MITRAL RECONSTRUCTION
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Functional mitral regurgitation (MR) is a significant complication of end-stage cardiomyopathy and it may affect almost all heart failure patients as a preterminal or terminal event. Its presence in these patients is associated with progressive ventricular dilatation, an escalation of CHF symptomatology, and significant reductions in long-term survival estimated between only 6 and 24 months.22

A firm understanding of the functional anatomy of the mitral valve is fundamental to the management of MR in heart failure. The mitral valve apparatus consists of the annulus, leaflets, chordae tendineae, and papillary muscles as well as the entire LV. Thus the maintenance of chordal, annular, and subvalvular continuity is essential for the preservation of mitral geometric relationships and overall ventricular function. As the ventricle fails, the progressive dilatation of the LV gives rise to MR, which begets more MR and further ventricular dilatation (Fig. 64-1). With postinfarction remodeling and lateral wall dysfunction, similar processes combine to result in ischemic mitral regurgitation (Fig. 64-2). Left uncorrected, the end result of progressive MR and global ventricular remodeling is similar regardless of the etiology of cardiomyopathy. Incomplete leaflet coaptation, loss of the zone of coaptation, and regurgitation develop secondary to alterations in the annular-ventricular apparatus and ventricular geometry.23,24 Thus, reconstruction of this geometric abnormality serves to not only restore valvular competency but also improve ventricular function.2529



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FIGURE 64-1 Note the geometric changes that occur from the normal to the failing LV. With the ventricular and annular dilatation of heart failure, the mitral leaflets cannot adequately cover the enlarged mitral orifice. Geometric mitral regurgitation results from a combination of annular dilatation, papillary muscle displacement, increased leaflet tethering forces, and weakened leaflet closing forces.

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FIGURE 64-2 Note the structural changes that occur from the normal to the ischemic LV. With ischemic damage and thinning of the ventricular wall, there is lateral tethering and displacement of the papillary muscle resulting in an eccentric jet of mitral regurgitation. This illustrates the concept that ischemic mitral regurgitation results from "lateral wall dysfunction" that, if left untreated, will progress to global LV dysfunction and severe heart failure.

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Historically, the surgical approach to MR was mitral valve replacement, yet little was understood of the interdependence of ventricular function and annulus-papillary muscle continuity.30 Consequently, patients with low EF who underwent mitral valve replacement with removal of the subvalvular apparatus had prohibitively high mortality rates.31 In an attempt to explain these outcomes, the concept of a beneficial "pop-off" effect of mitral regurgitation was conceived. This idea erroneously proposed that mitral incompetence provided a low-pressure relief during systolic ejection from the failing ventricle, and that removal of this effect through mitral replacement was responsible for deterioration of ventricular function. Consequently, mitral valve replacement in patients with heart failure was discouraged. More recent studies documenting the importance of maintaining subvalvular integrity to preserve postoperative LV function have led to surgical techniques that have been applicable to patients with heart failure.32 Accordingly, preservation of the mitral valve apparatus in mitral surgery has been demonstrated to enhance ventricular geometry, decrease wall stress, and improve systolic and diastolic function.33 Therefore, maintenance of chordal, annular, and subvalvular continuity is essential for the preservation of optimal mitral geometry and overall ventricular function. Furthermore, preservation of both the leaflet integrity as well as the dynamic function of the mitral apparatus with mitral repair has unmistakable functional benefits.

In treating heart failure patients, the most significant determinant of leaflet coaptation and MR is the diameter of the mitral valve annulus. The left ventricular dimension is of less importance in functional MR, as the lengths of the chordae and papillary muscles are similar in myopathic hearts regardless of the presence of MR. Observations with medically managed patients with severe heart failure and MR reveal that decreasing filling pressure and systemic vascular resistance lead to reductions in the dynamic MR associated with their heart failure.34 This is attributed to a reduction in mitral orifice area relating to decreased LV volume and decreased annular distension. This complex relationship between mitral annular area and leaflet coaptation may thus explain why an undersized "valvular" repair may help a "ventricular" problem. This restoration of the mitral apparatus and ventricle forms the premise behind geometric mitral reconstruction (GMR) for the treatment of heart failure.

At the University of Michigan, over 150 patients with end-stage cardiomyopathy and refractory severe MR have undergone mitral valve repair with an undersized flexible annuloplasty ring (Fig. 64-3). All patients were in NYHA class III or IV heart failure despite receiving maximal medical therapy. Patients had severe preoperative LV dysfunction as defined by an EF under 25%, with a mean of 14%. On immediate postoperative echocardiograms, the mean transmitral gradient has been 3 ? 1 mm Hg (range 2-6 mm Hg). The overall operative mortality has been under 5%. There were 730-day mortalities: 1 from a cerebrovascular accident, 2 from CHF, 3 from multisystem organ failure, and only 1 intraoperative death, which resulted from right ventricular failure. Five patients have required intra-aortic balloon counterpulsation, yet mechanical LV assistance has not been necessary in any patient. The duration of follow-up of these patients has been between 2 and 83 months, with a mean of 45 months. There have been 27 late deaths: 12 from sudden ventricular arrhythmias, 9 from progression of CHF but without MR, 3 related to complications from other operative procedures, 2 that progressed to transplantation, and 1 suicide. The 1-, 2-, 3-, and 5-year actuarial survivals following GMR are 82%, 71%, 68%, and 57% respectively.



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FIGURE 64-3 Geometric mitral reconstruction for heart failure. Successful augmentation of the zone of coaptation and prevention of recurrent MR can be achieved with placement of an undersized circumferential annuloplasty ring performed with multiple annular sutures.

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At 24-month assessment, mean EF increased to 26% and all patients were in NYHA class I or II. NYHA symptom scores were reduced from 3.2 ? 0.2 preoperatively to $1.8 ? 0.4 postoperatively. These improvements paralleled subjective functional improvements reported by all patients. Echocardiographically, there were marked improvements in regurgitant fraction, end-diastolic volume, cardiac output, and sphericity index (Table 64-1). Although significant undersizing of the mitral annulus was employed to overcorrect for the zone of coaptation (Fig. 64-4), no systolic anterior motion (SAM) of the anterior leaflet or mitral stenosis was noted in these patients.


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TABLE 64-1 Matched preoperative and postoperative echocardiographic data at 24 months following mitral reconstruction for heart failure

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FIGURE 64-4 Technique of geometric mitral reconstruction. Bicaval cannulation, approaching the mitral valve through the interatrial groove, and the use of a self-retaining retractor greatly enhances exposure. Multiple circumferential annular sutures are placed followed by the implantation of an undersized flexible ring. Note the reduced size of the annulus after successful reconstruction.

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The technique of undersizing in mitral reconstruction avoids SAM in these myopathic patients likely due to widening of the aorto-mitral angle in these hearts with increased LV size. Furthermore, acute remodeling of the base of the heart with this reparative technique may also reestablish the somewhat normal geometry and ellipsoid shape the LV. As evidenced by the decreased sphericity index and LV volumes seen in these patients, the geometric restoration from mitral reconstruction not only effectively corrects MR but also achieves surgical unloading of the ventricle.

Recently, several centers have reported consistent findings following GMR.28,3538 With outcomes equating to transplant while avoiding immunosuppression, this straightforward reparative operation performed in conjunction with medical management may be offered to all patients with MR and cardiomyopathy as a first-line therapy.


?? GEOMETRIC VENTRICULAR RECONSTRUCTION
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Myocardial revascularization and GMR reliably improve ventricular function. However, further surgical techniques have been developed that attempt to augment LV function through a reduction of end-diastolic wall tension following the principles of the law of LaPlace. Since ventricular wall tension is directly proportional to LV radius and pressure and inversely proportional to wall thickness, any intervention to optimize this relationship would be beneficial. As heart failure progresses, so does the progressive thinning and dilatation of the LV thus leading to increasing wall stress and further dilatation. This remodeling process may result in regional LV dysfunction, as occurs following segmental myocardial infarction, or global LV dysfunction, which may arise from either ischemic or nonischemic etiologies. The concept of reducing wall stress through the surgical restoration of LV cavity size and geometry remains the guiding principle behind many innovative techniques including those developed for the isolation of LV aneurysms and nonfunctioning ventricular segments.

After an acute myocardial infarction, the noncontractile myocardium undergoes thinning and fibrous replacement often following the segmental distribution of the arterial occlusion. This nonfunctional LV segment may remain akinetic or transform into a dyskinetic aneurysm depending on factors such as age and regional collateral circulation. Though such postinfarct pathologic remodeling may occur in any area of the heart, the most common clinically relevant region that manifests is the anteroapical segment of the LV. The resulting loss of contractile function in the affected segment results in global increases in LV wall tension and myocardial oxygen consumption in turn leading to compensatory LV dilatation in accordance with the law of LaPlace. These geometric ventricular changes may also result in loss of the zone of coaptation and MR following infarction, as discussed earlier. Moreover, when a dyskinetic region expands and becomes aneurysmal, cardiac work is further increased due to the paradoxical systolic motion of the thinned segment. These pathological alterations often result in CHF. The principle of surgical restoration of LV geometry involves the isolation of these nonfunctional areas and a subsequent reduction in LV volumes. This concept has been clearly illustrated by Dor and others, who have revealed significant improvement in heart failure after endoventricular patch exclusion of dyskinetic or akinetic ventricular segments.3942

The preoperative selection and preparation for LV reconstruction should follow the identical medical optimization discussed earlier. In addition to viability assessment, echocardiography, and contrast ventriculography, cardiac MRI and LV-gated nuclear imaging have proved valuable tools for pre- and postoperative volume estimation and anatomic assessment of the LV wall and septum. The pre- and intraoperative decision on when to perform LV reconstruction should be based on the function, viability, and thinning of the segment as well as the location of viability-targeted concomitant coronary grafting. Benefits obtained from repairing dyskinetic thin aneurysmal defects are well established.40,43 More recently, however, preliminary reports have revealed encouraging results with endoventricular repair of nondilated akinetic segments when combined with CABG. These findings have spawned the multicenter Surgical Treatment of Ischemic Heart Failure (STICH) trial to evaluate its long-term functional benefit.

The operative principles of LV reconstruction involve optimal myocardial preservation, septal exclusion of the nonfunctioning segment with an endoventricular patch, and closure of the excluded ventricular myocardium. To improve the visual and tactile identification of the nonfunctioning segment, the ventricular repair is often performed on the perfused beating unvented heart decompressed with CPB. Entry should be at least 1 to 2 cm to the left of the anterior descending coronary artery to avoid the septum. The thinned segment often will pucker when the LV is decompressed, thus marking the initial access point. A point knife is used to gain entry to permit complete decompression and endocardial visualization under direct vision as the incision is further developed. This allows for the safe removal of any LV thrombus if present, as well as for the visual and tactile identification of the septum and demarcation zone between functioning and nonfunctioning myocardium (Fig. 64-5A). A circumferential monofilament suture or "Fontan stitch" is then placed within this zone and tied as advocated by Dor (Figure 64-5B). The resulting reduced size of the defect is then patched with bovine pericardium and the residual myocardial defect is buttressed closed with strips of bovine pericardium or felt. Though concomitant GMR and CABG can be performed before or after LV reconstruction, it is often advocated before so as to allow for improved myocardial recovery and reperfusion following removal of the aortic cross-clamp.



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FIGURE 64-5 (A) Left ventricular reconstruction on the beating heart decompressed on CPB. Palpation assists in identification of the demarcation zone between functioning and nonfunctioning myocardium. (B) Placement of a circumferential monofilament suture at the level of demarcation between functional and nonfunctional myocardium permits reduction of the ventricular opening in preparation for placement of a bovine pericardial patch. Patch closure is performed with either a running or interrupted technique and the covering myocardium is reapproximated with the aid of strips of bovine pericardium or felt.

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Results from LV reconstruction have been favorable and consistent between groups regardless if endoventricular circular patch plasty or a modified linear patch closure technique is utilized. Significant reductions in left ventricular end-systolic volume index and improvements in EF, NYHA class, and long-term survival have resulted. It is being regularly performed with hospital mortalities of under 8% and with a 12-month freedom from readmission for CHF of over 80%.4045 Therefore, geometric left ventricular reconstruction by endoventricular exclusion of nonfunctional segments should be placed alongside high-risk CABG and GMR as a first-line surgical option for heart failure.


?? PARTIAL LEFT VENTRICULECTOMY
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Batista has furthered the concept of surgical ventricular remodeling to optimize wall tension in dilated ventricles with the contention that all mammalian hearts should share the same mass-diameter ratio regardless of size. He proposes that all hearts not complying with this relationship should have a segment of the LV wall excised in order to diminish mural tension and improve myocardial oxygen consumption in accordance with the law of LaPlace.46,47 This interesting concept was initially presented as a case report of a 34-year-old patient who underwent a partial left ventriculectomy (PLV) that reportedly increased the EF from 17% to 44% at 2 months postoperatively. Batista performed over 150 such procedures predominantly on patients with Chagas disease and dilated cardiomyopathy. Though this experience stimulated much interest, unfortunately no meaningful follow-up data or statistical analyses has ever been made available from this series.

To further evaluate the potential benefits of PLV, the Cleveland Clinic performed 62 such cases on patients with idiopathic dilated cardiomyopathy awaiting transplant. The ventriculectomy involved resection of the lateral wall of the LV in the circumflex coronary artery distribution to the base of the papillary muscles with closure between two strips of felt or bovine pericardium. This was one of the largest North American series, reporting a 3.5% operative mortality with 7 late deaths and a 1-year actuarial survival of 82%. However, of the total 62 patients, 24 (39%) were considered short-term treatment failures: 11 required LVAD support, 6 were listed for transplantation again, and 7 non-LVAD patients died.48 Moreover, a further 30% attrition rate at 2 years following PLV has been reported.49,50 These results may be superior to no surgical treatment but they fall short of those obtained by other surgical options for heart failure. As a result, PLV has fallen into disfavor in North America. However, in the Asian-Pacific region, where transplantation is not widely available, efforts by Suma et al to improve selection criteria and introduce echo-guided surgical decision making have resulted in PLV persisting as a viable option for heart failure in this part of the world.51

In attempting to elucidate the mechanism behind the relative success of PLV, it is quite interesting to note that over 95% of the cases performed in the Cleveland Clinic experience also involved a mitral reconstruction. Therefore, it becomes difficult to discern the role mitral repair plays in the overall utility of PLV, since patients undergoing mitral reconstruction alone also attain normalization of the LV mass to volume ratio, but without the excision of viable myocardium.26 Furthermore, experimental models of heart failure have revealed that correction of the MR alone permits LV remodeling that may be rapid and complete with resulting regurgitant fractions of less than 30%.52

Though the concept of instantly remodeling the LV through PLV is mechanically appealing, discarding functioning myocardium is not. Patients with ischemic cardiomyopathy with a dyskinetic aneurysmal segment have undergone successful remodeling with an endoventricular patch repair. Patients with dilated cardiomyopathy and MR have undergone mitral reconstruction thereby altering the angulation of the base of the heart and promoting favorable LV geometry and remodeling. Thus at this time, when similar if not superior results can be obtained by methods that preserve myocardial integrity, the application of PLV to patients with end-stage heart failure should be approached with an element of caution.


?? DYNAMIC CARDIOMYOPLASTY
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Another alternative method to surgically optimize LaPlace's law is dynamic cardiomyoplasty (DCMP). This procedure is conceptually based upon imparting the contractile and supportive forces of the patient's own skeletal muscle for purposes of cardiac assistance and the reduction of myocardial wall stress. It is accomplished by wrapping the latissimus dorsi muscle (LDM) around the failing heart and, by means of an implantable cardiomyostimulator, stimulating the muscle to contract in synchrony with cardiac systole. DCMP has been proposed as an alternative to transplant or LVAD. It has the obvious advantages of total implantability; it avoids the power constraints and thromboembolic risks experienced with mechanical assist devices; and the LDM with its single neurovascular pedicle can be easily utilized with no loss of shoulder function.

Prior to using skeletal muscle as a power source, the concerns of fatigability and performance loss with altered geometry must be addressed. The biological principles governing the plausibility of biomechanical assistance center on three main concepts: transformation, conformation, and burst stimulation.

Skeletal muscle is comprised of variable amounts of oxidative slow-twitch type I fibers and glycolytic fast-twitch type II fibers. Early work with cross-innervation of muscle preparations noted that certain fiber types could be altered through neural stimulation.53 It was further noted that mixed type I and II fatigue-prone fibers could be morphologically converted into totally type II fatigue-resistant muscle with repeated low frequency electrical stimulation.54 This ability to phenotypically and histologically alter fiber composition and confer fatigue resistance to skeletal muscle is known as transformation.

All muscle, skeletal or myocardial, responds to strain following the principles of a Frank-Starling functional curve.55 In determining the ideal stretch or orientation of the muscle wrap for optimal performance, it has been observed that within weeks after DCMP the LDM adapts by altering its geometric shape to conform to the epicardial surface; this phenomenon persists even after the native heart is removed. This morphologic ability of skeletal muscle to delete or add sarcomeres to restore optimal resting tension and performance is known as conformation.56,57

Unlike the all-or-none contractile syncytium found in myocardium, skeletal muscle performance is a reflection of the recruitment of individual motor units. A single electrical impulse stimulates only a few motor units and results in only a twitch. By studying the application of a burst of stimuli in the form of a pulse train, it was deemed possible to induce a summation of twitches into a graded full contractile response.58 This technique of burst stimulation forms the basis of the design of the cardiomyostimulator used for DCMP.

For optimal results, indications for DCMP include patients with NYHA class III symptoms, EF greater than 20%, and maximal oxygen consumption (Vo2 higher than 15 mL/kg/min.59 Since adhesions may increase the technical difficulty and risk to these fragile patients, caution should be exercised when considering those with previous cardiac or thoracic procedures. Clinical experience has revealed a higher risk in patients with high pulmonary vascular resistance, Vo2 less than 10 mL/kg/min, poor EF, and NYHA class IV heart failure.60

As with other surgical approaches to heart failure, the preoperative preparation of the patient should be optimized. As the goal is to perform the operation off pump, anesthesia must be carefully induced with double-lumen endotracheal intubation and a primed CPB circuit; a perfusionist should be on standby. In the right lateral decubitus position, the left LDM is atraumatically dissected with preservation of its thoracodorsal pedicle. The graft is detached from its ligamentous humeral insertion, two intramuscular leads are placed along its proximal margin, and the graft is placed into the left chest through a window in the second interspace created by a segmental resection of the third rib. The ligamentous proximal portion of the LDM is fixed to the periosteum of the second rib and the wound is closed. The patient is repositioned, a median sternotomy is performed, and the left pleura is opened to retrieve the LDM. Two epicardial sensing electrodes are secured on the RV for LDM synchronization. Using minimal manipulation, the LDM is slid posteriorly where it is anchored to the posterior pericardial reflection. It is then folded from posterior to anterior as the edges are sutured together to form the completed cardiomyoplasty. The leads are then tunneled to a subcutaneously implanted cardiomyostimulator prior to sternal closure. Postoperatively, afterload reduction is reinstituted while avoiding high-dose vasoconstrictors due to the tenuous LDM blood supply, and care must be taken with intravenous infusions to avoid volume overload. The LDM is left unstimulated for a 14-day period of vascular delay, which is followed by a graded 8-week protocol of stimulation to induce LDM transformation and attain optimal burst capacity for cardiac assistance.61

Starting in 1985, Medtronic Inc. began coordinating a multicenter FDA trial to evaluate the cardiomyostimulator. In effect, the rigorous evaluation of this device uniquely subjected DCMP to the scientific analysis of a multiphase prospective trial. Phase I set out to assess the selection criteria for the procedure and safety of the stimulator. From July 1985 to April 1991, data from 118 patients revealed that patients with NYHA class IV failure and an EF less than 20% had a prohibitive mortality, but those with class III had an acceptable outcome and enjoyed a mean reduction of 1.6 functional classes at 3 months.59 With this refined selection criteria, the phase II trial set out to assess the efficacy of DCMP. From May 1991 to September 1993, data from 68 patients in refractory NYHA class III failure of mixed etiology revealed that DCMP could be performed with a mortality of 12% and result in an average EF increase of 15%. Over 85% of these patients had an improvement in their functional status and quality of life. This prompted a phase III randomized controlled trial to definitively assess the benefits of DCMP.62

Starting in 1994, the Cardiomyoplasty-Skeletal Muscle Assist Randomized Trial (C-SMART) was established to assess if DCMP has a benefit over conventional medical therapy for heart failure. The sample size calculation required to reach this conclusion was determined to be 400 patients. Unfortunately after 4 years, only slightly over 100 patients were enrolled in this North American trial. This illustrated the unique adversity C-SMART faced, as recruitment appeared impeded by slow physician referral that showed the "too well/too sick" phenomenon. Projecting that it would take over 9 years to complete the trial and surmising a lack of enthusiasm for DCMP, Medtronic decided to withdraw their device. At that time, over 54 patients had undergone DCMP with only a single mortality (1.9%).62 When attempting to ascertain its efficacy as a therapy for heart failure, pooled observations after DCMP reveal a paucity of positive quantitative hemodynamic data yet, paradoxically, patients report over 30% functional improvement when compared to medical therapy alone.63,64

Though DCMP is now only rarely performed in North America, the recently available LD Pace myostimulator out of Russia has allowed this procedure to continue to be an available in that country as well as throughout various centers in Europe, Asia, and the Caribbean.

Investigations into the mechanisms of DCMP, which continue today, have generated spin-offs in the fields of myoblast transplantation and remodeling surgery. As the initial vision of simple systolic assist did not sufficiently explain why unstimulated DCMP patients showed benefit, further studies revealed that the wrap actually contributes to significant reductions in myocardial wall stress.65,66 In effect, this conceptually protects myocytes from overt functional stresses and thereby prevents the adaptive progressive dilatation of heart failure. Working in favor of the law of LaPlace, this girdling effect of DCMP was seen with unstimulated adynamic cardiomyoplasty. Furthermore, original experiments comparing adynamic cardiomyoplasty to synthetic material revealed that this beneficial girdling effect even occurs when a passive constraint of prosthetic mesh fabric is applied to the ventricles.67 These findings of girdling and myocardial sparing provide a potential explanation for the reverse remodeling seen with DCMP, and they have spawned the development of novel biomedical devices currently under clinical investigation.


?? EMERGING BIOMEDICAL DEVICES FOR HEART FAILURE
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The Acorn Cardiac Support Device (ACSD; Acorn Medical, Minneapolis, MN) is a polyester mesh fabric that attempts to reduce ventricular wall stress by providing external support. Much like DCMP, the ACSD is placed around the ventricles from posterior to anterior, using stay sutures, as well as an anterior fabric seam for snug tailoring to the patient's heart (Fig. 64-6).



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FIGURE 64-6 The Acorn Cardiac Support Device.

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Taking advantage of the girdling effect, the purpose of this device is to passively support the failing ventricles and prevent further dilatation. Preclinical data have shown decreased LV volumes and improvements in regional wall motion, EF, and other functional parameters without any evidence of constrictive physiology.68,69 Histologic animal studies have also demonstrated decreased myocyte hypertrophy and interstitial fibrosis, as well as improvements in several biochemical markers of failure.70,71 A phase I-II clinical trial is underway to assess the safety and the early remodeling ability of the ACSD when used on heart failure patients with or without concomitant cardiac procedures. Preliminary experience reveals that the ACSD is easily applied, and may even be performed without the necessity of cardiopulmonary bypass.

The Myocor Myosplint (Myocor Medical, St. Paul, MN) is a second device developed to reduce ventricular wall stress by directly altering cardiac geometry. Working on the premise of optimizing the law of LaPlace, it involves the placement of transventricular tension bands through the RV and LV walls that have the unique ability to be individually tightened in order to achieve a 20% reduction in wall stress. Preclinical animal data have shown improvements in end-diastolic volume, end-systolic volume, and EF. These experiments reveal the Myocor device becomes readily incorporated within a fibrous capsule that has been free of thrombus formation. A phase I clinical trial is under way to assess device safety in patients prior to cardiectomy at the time of transplant. Preliminary data reveal that the device can be readily deployed without harm to other cardiac structures. Further chronic studies are required to address the efficacy of this unique device.


?? CONCLUSIONS
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As surgical therapies for heart failure rapidly evolve, the need for their critical appraisal is essential so that they may be offered to the growing population of CHF patients in a prompt yet effective manner. Transplantation continues to offer selected patients reliable long-term survival in a reproducible fashion, and it thus remains as a gold standard surgical therapy for heart failure. Though in time we may see mechanical assist devices play a more prevalent role in myocardial recovery or destination therapy, currently their main utility is as a bridge to transplantation. With the growing disparity between donor availability and heart failure patients, experience is mounting with effective nontransplant surgical solutions.

The results of the more conventional techniques of CABG, geometric mitral reconstruction, and ventricular reconstruction when combined with the optimal medical management of heart failure may now be on a par with transplantation. Therefore, these modalities now form the new first-line surgical therapy for heart failure when applicable. Patients with primary ischemic cardiomyopathy with favorable anatomy may be effectively managed with revascularization alone or in combination with LV reconstruction. Myopathic patients with MR, regardless of etiology, may be effectively managed with mitral reconstruction. With the superior results of these approaches, the use of other techniques such as PLV and DCMP should be reserved as viable alternative surgical options for heart failure. The prudent and effective application of the growing menu of surgical strategies for heart failure enables the scarcely available donor hearts be efficiently used for patients with truly no other surgical or medical alternatives. Along with the utility of emerging biomedical devices, each of these unique modalities has enhanced the clinically effective armamentarium of the modern surgeon treating patients with heart failure.


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