Chapter 68. Nontransplant Surgical Options for Heart Failure

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. More than 20 million people are affected worldwide. In the United States the estimated 2006 prevalence of heart failure in adults age 20 and older is 5.8 million yet less than 3000 are offered transplantation because of limitations of age, comorbid conditions, and donor availability. Despite the significant improvements with medical management hospital discharges for heart failure rose from 877,000 in 1996 to 1,106,000 in 2006 and mortality in the first year is one in five. CHF patients are repeatedly readmitted for inpatient care and the vast majority will die within 3 years of diagnosis.1

Orthotopic heart transplantation (OHT) offers successful and reproducible long-term results and is 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, down to only 3353 in 2008.3,4 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.

With significant technologic strides being made toward total implantability, the role for mechanical support is becoming more widely accepted as a bridge to recovery as well as a bridge to transplant. There have been a number of successful studies of ventricular assist devices (VADs) used as a bridge to recovery and the long-term efficacy for this purpose, and this use as a long-term therapy for chronic heart failure has become established by multicenter clinical trials.5–10 As a result continuous-flow left ventricular assist devices (LVADs) have emerged as the standard of care for advanced heart failure patients requiring long-term mechanical circulatory support. The long-term survival of circulatory support is increasing but does not yet equal survival after OHT, the gold standard treatment. Because many more people can benefit from this therapy, and with their improved durability, these devices are now an option in the management of patients with heart failure.

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 a possible 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 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.

We have known for nearly 25 years that revascularizing patients with left ventricular dysfunction can result in upward of a 25% improvement in long-term survival.11,12 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%.13,14

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 owing 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 a 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.16 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), 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.16–18

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. Because 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%.19–21

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 because of 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.

Myocardial revascularization and mitral valve repair reliably improve ventricular function. However, there remains a high mortality for those patients with dilated hearts. Techniques that attempt to augment LV function through a reduction in end-diastolic wall tension have been developed. From the principle of the law of LaPlace, ventricular wall tension is directly proportional to LV radius and pressure and inversely proportional to wall thickness. As heart failure progresses, the LV thins and dilates leading to increasing wall stress and regional LV dysfunction. Reducing wall stress through the surgical restoration of LV geometry is 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 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. These geometric ventricular changes may also result in loss of the zone of coaptation and MR following infarction. Moreover, when a dyskinetic region expands and becomes aneurysmal, cardiac work is further increased because of 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.22–25

Recently, many single-center reports revealed encouraging results with endoventricular repair of nondilated akinetic segments when combined with CABG. These findings spawned the multicenter Surgical Treatment of Ischemic Heart Failure (STICH) NIH trial to evaluate its long-term functional benefit. This study concluded that adding surgical ventricular reconstruction to CABG reduced the left ventricular volume, as compared to CABG alone.26 However, this anatomical change was not associated with a greater improvement in symptoms or exercise tolerance or with a reduction in the rate of death or hospitalization for cardiac causes. Although questions have been raised regarding the analysis of the STICH report including inaccurate conclusions after volume reduction and end points that do not relate to the SVR procedure, many feel that this should be considered a “negative study.”27 Unfortunately therefore, left ventricular reconstruction by endoventricular exclusion of nonfunctional segments has not been accepted as a standard treatment of heart failure and should not be placed alongside high-risk CABG and CHF-MR repair as a potential first-line surgical option for heart failure.

Batista furthered the concept of surgical ventricular remodeling with the contention that all mammalian hearts should share the same mass-diameter ratio regardless of size. He proposed 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.28,29 Batista performed over 150 procedures predominantly on patients with Chagas disease and dilated cardiomyopathy. Though this experience stimulated much interest, no meaningful follow-up data or statistical analyses are 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. They reported a 3.5% operative mortality with seven late deaths and a 1-year actuarial survival of 82%. 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.29 Moreover, a further 30% attrition rate at 2 years following PLV has been reported.30,31 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. 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 possible option for heart failure in this part of the world.32

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 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.

Currently, partial left ventriculectomy has not been widely accepted as a treatment option for dilated cardiomyopathy.

Functional mitral regurgitation (MR) is a significant complication of advanced systolic congestive heart failure (CHF) without organic mitral valve disease 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. Patel et al., from the Mayo clinic, looked at the prognostic implications of functional MR in patients with advanced systolic CHF evaluated in a heart failure clinic. Of 558 NYHA III-IV patients, those with moderate MR had a 5-year survival of only 27%.33 This is supported by several other studies that show that the severity of MR impacts survival as well.34–37

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. Consequently, patients with a low EF who underwent mitral valve replacement with removal of the subvalvular apparatus had prohibitively high mortality rates. 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 has been discouraged.

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 left ventricle (LV). These structures are aligned as if they form a cylinder with the papillary musculature directly aligned beneath the annulus. The maintenance of chordal, annular, and subvalvular continuity is essential for the preservation of mitral geometric relationships and overall ventricular function. MR in heart failure is not related to the valve but to ventricular pathology. The degree of LV distortion reflects the degree of MR.38 As the ventricle fails, progressive dilatation of the LV results in lateral papillary muscle migration, loss of cylinder closure, and thus loss of the zone of coaptation (Fig. 68-1). This gives rise to MR, which begets more MR and further ventricular dilatation (Fig. 68-2). We know that even a small amount of MR to be harmful in these patients. Grigioni et al. showed that when the regurgitant volume was greater than 30 mL, the 5-year survival was less than 35% compared with 44% for a regurgitant volume of 1 to 29 mL and 61% for no MR.39 With postinfarction remodeling and lateral wall dysfunction, similar processes combine to result in ischemic mitral regurgitation (Fig. 68-3). Left uncorrected, the end result of progressive MR and global ventricular remodeling is similar regardless of the etiology of cardiomyopathy. Reconstruction of this geometric abnormality serves to not only restore valvular competency but also improve ventricular function.

Surgical mitral annuloplasty improves symptoms in these patients with advanced CHF but has not been shown to improve survival. This is likely because surgery for CHF has not been “too little–too late” but “too much–too late.” We failed to correct mitral regurgitation early enough in the disease course because advanced heart failure patients were long felt to be nonoperative candidates. However, it has been shown that mitral repair is feasible with a low mortality, relief of MR, and better quality of life. Several authors have demonstrated 30-day mortality rates as low as 1 to 5 % for mitral repair for MR in CHF.40–48

The lack of a mortality benefit may also be explained by the absence of a durable repair. When McGee and associates showed no mortality benefit after mitral repair, they also noticed the rate of recurrent MR to be 30 to 40% in less than 1 year.49 This has led to an attempt to identify surgical predictors of recurrent MR and for improved surgical techniques that result in a more permanent repair. In order to observe a survival benefit in these patients after mitral repair, MR must be fixed permanently, because residual and recurrent MR will obscure or obliterate a survival benefit in any CHF-MVR trial.

Ischemic MR is not caused by organic or intrinsic disease of the valve, but by LV remodeling, dilation, and dysfunction leading to geometric reconfiguration of the mitroventricular apparatus, including papillary muscle displacement and annular dilation. Mitral valve (MV) leaflets become tethered, with failure of anterior-posterior leaflet coaptation, resulting in symmetric or asymmetric regurgitation. Surgical treatment options in ischemic MR include coronary artery bypass grafting (CABG) alone or with concomitant MV annuloplasty or replacement. Currently, the most common technique to restore valve competence is placing an undersized annuloplasty ring to reduce mitral annulus size. Mihaljevic et al. (Figs. 68-4 and 68-5).55 Unfortunatety, ischemic mitral regurgitation (IMR) often persists after restrictive mitral valve annuloplasty, in which case it is associated with worse clinical outcomes. In an attempt to determine whether persistence of MR and/or clinical outcome could be predicted from preoperative analysis of mitral valve configuration, in patients undergoing restrictive annuloplasty for ischemic MR, preoperative analysis of mitral valve configuration was shown to accurately predict persistence of MR and 3-year event-free survival. Patients with a posterior leaflet angle >45 degrees (ie, with high posterolateral restriction) should thus be considered poor candidates for this procedure, and concomitant or alternative procedures should be contemplated.

Important LV predictors of recurrent MR are coaptation depth greater than 1 cm as shown by Calafiore et al., and left ventricular end diastolic dimension (LVEDD) less than 65 mm as shown by Braun.43,50 At 4.3 years follow-up, intermediate-term cutoff values for left ventricular reverse remodeling proved to be predictors for late mortality. For patients with preoperative LVEDD of 65 mm or less, restrictive mitral annuloplasty with revascularization provides a mortality benefit for ischemic mitral regurgitation and heart failure; however, when LVEDD exceeded 65 mm, outcome is poor and a different approach to CHF should be considered.50

But perhaps, the strongest predictor of CHF MVR failure is anterior-posterior (AP) diameter greater than 3.7 cm.51 When the AP diameter after annuloplasty is greater than 3.7 cm the repair should be considered as a potential predictor of a failed repair.52 New and remodeling MV rings that significantly reduce the residual AP diameter have been shown to be a predictor of no recurrence of MR.53,54

When considering surgical techniques used in treating heart failure patients, the most significant determinant of leaflet coaptation and MR is the diameter of the mitral valve annulus. 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. 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 (Fig. 68-6).

Earlier use of flexible and incomplete annuloplasty rings was justified based on the belief that trigone distance was constant. However, Hueb et al., have demonstrated that trigone distance is not stable.56 This has led to the use of complete and rigid annuloplasty rings. Spoor et al. experienced a recurrent MR rate five times higher when using flexible rings.57 In addition, the Kaplan-Meier survival curve for the Acorn MV surgery stratum (rigid annuloplasty) showed a more enduring repair with less recurrence of MR with only 4.2% with 3+ or 4+ MR at 18 months. The overall survival for this group was 84%. In recent work, Bolling et al. have also shown a significant improvement in cumulative survival with undersizing the mitral valve annulus (Fig. 68-7).

The technique of undersizing in mitral reconstruction avoids SAM in these myopathic patients, likely because of widening of the aortomitral 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 (Fig. 68-8).

Many centers have reported similar consistent findings following MR. With outcomes equating to transplant while avoiding immunosuppression, this straightforward reparative operation performed in conjunction with medical management may be offered to carefully selected patients with MR and cardiomyopathy as a potential first-line therapy.

An alternative method to surgically optimize LaPlace's law is dynamic cardiomyoplasty (DCMP). The procedure uses the patient's own skeletal muscle to support the heart, helping to reduce wall stress and provide cardiac assistance. The latissimus dorsi muscle is wrapped around the failing heart and an implantable cardiomyostimulator is used to stimulate the muscle to contract in synchrony with cardiac systole. Long-term results show that this method was not considered to be satisfactory in terms of survival and antiarrhythmic effect because of fatigue of the skeletal muscle. DCMP is now only rarely performed in North America. Investigations into the mechanisms of DCMP have generated promising research in the fields of cellular cardiomyoplasty, myoblast transplantation, and remodeling surgery.58,59

The CorCap Cardiac Support Device (Acorn Cardiovascular, St. Paul, MN) is a mesh device that is implanted around the heart to reduce wall stress and the first therapy specifically designed to address left ventricular remodeling. The ACORN trial, a prospective, randomized, controlled, multicenter evaluation of the CorCap cardiac support device in patients with New York Heart Association (NYHA) class III or IV heart failure of ischemic or nonischemic etiology enrolled a total of 300 patients. Results of the trial were reported in 2007, and although LV geometry was favorably improved, it was found that there was no difference in survival between the treatment and control groups (25 deaths among 148 patients in the treatment group versus 25 deaths among 152 patients in the control group) and no significant with respect to the mode of death. Survival rates, serious adverse events, and hospitalizations between those patients who received a cardiac support device and those who did not were not significantly different. As a result there has been a decline in the application of the CorCap device in the heart failure population.60

The Coapsys device (Myocar Inc., Maple Grove, 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.61 However, the product manufacturer is developing a new device designed to achieve mitral valve repair along with ventricular volume reduction and the Myocor Myosplint has been set aside and further development is uncertain.

The Viacor percutaneous mitral annuloplasty system (PTMA) (Viacor, Wilmington, MA), Edwards Viking Endovascular coronary sinus ring (Edwards Lifesciences LLD, Irvine, CA), and Carillon mitral contour system (Cardiac Dimensions, Kirkwood, WA) all use an emerging technology approach to mitral annuloplasty using a catheter-based approach to the mitral valve. Using percutaneous catheters, a permanent nitinol strut is placed into the coronary sinus that wraps around the posterior annulus of the mitral valve and attempts to indirectly influence the action of the posterior mitral valve leaflet similar to a partial ring annuloplasty by reducing the anterior-posterior dimension of the mitral annulus. Initial results of mitral annular reduction to a more modest degree than after surgical correction have led to less improvement in MR.62 As these devices are under investigation and not currently approved for routine use, their clinical impact at this time is unknown.

The Milano endovascular edge-to-edge repair system (Edwards Lifesciences LLD, Irvine, CA) and MitraClip mitral repair system (Evalve, Menlo Park, CA) use a catheter-based approach to deliver a clip to both the anterior and posterior mitral valve leaflets using the principles of mitral repair pioneered by Dr Otavio Alfieri.63 Percutaneous catheters are introduced via the femoral vein and cross the atrial septum to enter the left atrium similar to a percutaneous mitral balloon annuloplasty approach. A catheter-based clip is then used to create a permanent coaptation point between the leading-free edges of the anterior and posterior mitral leaflets. The EVEREST II trial compared the MitraClip to surgery.64 A total of 279 patients enrolled completed 1-year follow-up. Early findings indicate that this technology is safe in the indicated patient population and not inferior in results compared with surgery. However, a clip was considered successful if MR was 2+ or less following application.64 This makes percutaneous repair attractive for high-risk surgical candidates, but may not be entirely impactful. Further investigation is ongoing comparing surgery to the MitraClip device.65

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. Rapidly evolving mechanical assist devices are playing a more prevalent role in myocardial recovery and destination therapy. With the growing disparity between donor availability and heart failure patients, experience with assist devices has shown them to be an effective nontransplant surgical solution.

The results of the more conventional techniques of CABG and mitral reconstruction when combined with the optimal medical management of heart failure may now be on a par with transplantation. These modalities now form the new first-line surgical therapy for heart failure. Patients with primary ischemic cardiomyopathy and favorable anatomy may be effectively managed with revascularization alone or in combination with mitral repair. Myopathic patients with MR, regardless of etiology, may be effectively managed with mitral reconstruction. The use of other techniques such as SVR, PLV, and DCMP is no longer 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 to be efficiently used for patients with 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.