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eMedicine Specialties > Thoracic Surgery > Cardiac

Congestive Heart Failure, Surgical Options

Craig H Selzman, MD, FACS, Associate Professor of Surgery, Division of Cardiothoracic Surgery, University of Utah

Updated: Oct 6, 2009

Introduction

Cardiovascular disease remains the leading cause of death in the United States. Ischemic heart disease accounts for a large portion of deaths due to cardiovascular disease. While the percentage of patients who acutely die from myocardial infarction has decreased nearly 30% in the last 2 decades, the number of patients dying from heart failure (HF) has doubled. Despite improvements in medical therapy, many patients continue to have functional decline and ultimately die. As a result, the management of heart failure has evolved into a steadily growing discipline.

Despite noteworthy improvements in medical therapy, overall death rates for patients with heart failure have not declined appreciably. Moreover, because heart failure is diagnosed in nearly 10% of the population older than 75 years, a group of patients with complicated disease is emerging and growing. In general, patients older than 65 years are not candidates for heart transplantation. Older patients can successfully be treated with traditional heart surgery,1 but resource allocation and increased morbidity and mortality raise important societal issues.2

A number of innovative surgical approaches have evolved to help treat these patients with diverse and refractory medical conditions. The aim of these approaches is to enhance ventricular function, quality of life, and, ultimately, survival.

Frequency

In its latest update, the American Heart Association (AHA) estimated that nearly 5,000,000 Americans have heart failure. More than 500,000 cases are newly diagnosed each year.3

Heart failure does not discriminate by sex, race, or age. It is increasingly prevalent among males and females, all races, and both young and old. At the age of 40 years, the lifetime risk of developing heart failure is 20%.4 Of importance, because the population is aging and because of advancements in medical therapy, patients with advanced heart failure are now much older than previous patients were, and they develop the attendant comorbidities.

Heart failure is associated with staggering costs to society. The financial burden is estimated to be more than $30 billion per year.3 These expenses are related to repeated hospitalizations, potential loss of work, and the cost of prescription medicines.

Although medical therapy has greatly increased the quality and length of life for patients with heart failure, the diagnosis of heart failure traditionally has carried mortality rates of 20% within 1 year and 50% within 2 years.5

Etiology

Heart failure is the clinical endpoint for a number of diseases resulting in myocardial dysfunction. Ischemic cardiomyopathies due to coronary artery disease and dilated cardiomyopathies, either idiopathic or familial, make up most cases. Many other diseases can also lead to end-stage heart failure. These include valvular, congenital, metabolic, and inflammatory disorders.

In terms of the pathology, cardiac remodeling is characterized by myocytic hypertrophy, chamber dilatation, and changes in the composition of the matrix. The fibrotic heart ultimately becomes somewhat spherical, and, subsequently, it loses efficiency as a pump. Therefore, an important goal is to identify and favorably intervene before terminal myocardial remodeling begins.

Clinical

Of historical note, patients with heart failure were described as early as 1600 BC in the Ebers papyrus. Hippocrates referred to dropsy (an accumulation of lymph fluid) and cardiac cachexia.

Patients with heart failure present with a variety of symptoms related to both systolic dysfunction (poor antegrade pump function) and diastolic dysfunction (poor ventricular relaxation and compliance).

Typical symptoms of heart failure include the following:

  • Dyspnea on exertion
  • Orthopnea
  • Paroxysmal nocturnal dyspnea
  • Fatigue
  • Abdominal symptoms related to right heart congestion

The aforementioned symptoms are often associated with several physical findings, such as the following:

  • Elevated jugular venous pressure
  • Third heart sound
  • Pulmonary congestion
  • Peripheral edema

Diagnostic Procedures

A host of diagnostic studies are available to examine patients with heart failure.

  • Transthoracic echocardiography with or without pharmacologic stress is inexpensive and provides functional and anatomic information.
  • Radionucleotide scanning can be performed to evaluate ejection fractions (EFs), especially of the right ventricle (RV).
  • MRI has recently proven to be a valuable resource in the assessment of myocardial function and viability.
  • Right and left heart catheterization can be performed to assess for the presence of coronary artery disease and pulmonary vascular disease.
  • Finally, measurement of peak oxygen consumption with exercise can help in stratifying the functional limitation of patients with heart failure.

Staging

The New York Heart Association (NYHA) classification has traditionally been used to define the functional limitations of patients with heart failure. Recent guidelines from the American College of Cardiology (ACC) and the AHA have suggested a new classification system that emphasizes the evolution, progression, and structural deterioration of heart failure.6 See the Table below.

This ACC/AHA staging system encourages clinicians to provide the same level of care for heart failure that they apply for cancer. That is, they should identify and treat the following groups of patients5 :

  • Patients at risk for heart failure (eg, because of hypertension)
  • Patients with early disease (eg, diastolic dysfunction)
  • Patients with established disease (eg, medically managed heart failure)
  • Patients with advanced disease (eg, medically refractory heart failure)

Classifications of Heart Failure6

NYHAACC/AHA
ClassDescriptionClassDescription
INo symptomsANo structural damage,
high risk for developing heart failure
IISymptoms with significant activityBStructural abnormality,
no symptoms
IIISymptoms with minimal activityCStructural abnormality,
previous or current symptoms
IVSymptoms at restDRefractory symptoms

Medical Therapy

Medical therapy, including preventive measures, is the first-line strategy for treating patients with heart failure.

In 1997, the Systolic Hypertension in the Elderly Program (SHEP) Cooperative Research Group observed nearly 5000 patients with isolated systolic hypertension.7 Heart failure occurred more than twice as often in a group given placebo than in a group treated with antihypertensive agents. In addition, the risk of heart failure was reduced by 80% among patients with a previous myocardial infarction who were treated compared with those who were not treated. Control of other risk factors, including diabetes, coronary artery disease, and structural valve disease, similarly prevents pathologic ventricular remodeling and the development of heart failure.

Once the diagnosis of heart failure is established, a number of pharmacologic strategies are available to limit and reverse the manifestations of congestive heart failure (CHF). In particular, blocking the renin-angiotensin system and the beta-adrenergic system improves mortality rates among patients with heart failure. Use of angiotensin-converting enzyme (ACE) inhibitors, as well as angiotensin receptor blockers, increase survival and decrease repeat hospitalizations.8 These benefits are also observed with several beta-blockers, including metoprolol and carvedilol.9

Patients often have difficulty tolerating either ACE inhibitors or beta-blockers. A number of additional drug regimens can be used in these cases. These drugs include loop and thiazide diuretics, as well as aldosterone antagonists. Diuretic therapy decreases ventricular diastolic pressure, reducing ventricular wall stress and maximizing subendocardial perfusion.

Digoxin, a cardiac glycoside, is used to improve symptoms associated with congestive heart failure by enhancing cardiac contractility. Although digoxin does not confer a survival benefit, it has reduced the number of hospitalizations because of worsening heart failure.

Enthusiasm for vasodilator therapy with a combination of hydralazine and isosorbide dinitrate has recently been renewed.10

Finally, when patients' conditions are refractory to standard therapy, they often require hospitalization to receive intravenous diuretics, vasodilators, and inotropes.

Surgical Therapy

Heart transplantation

When progressive end-stage heart failure occurs despite maximal medical therapy, the criterion standard for therapy has been heart transplantation. Since Christiaan Barnard performed the first orthotopic heart transplantation in 1967, the world has seen tremendous advancement in the field of cardiac transplantation.

Compared with patients who receive only medical therapy, transplant recipients have fewer rehospitalizations, marked functional improvements, enhanced quality of life, more gainful employment, and longer lives with 50% surviving to 10 years.11 Heart transplantation is associated with a 1-year survival rate of 83%, which decreases in a linear manner by approximately 3.4% per year. Careful selection of donors and recipients, as well as efforts to minimize potential perioperative dangers (ischemic times, pulmonary hypertension, mechanical support, cardiogenic shock), are critical to ensure good outcomes.

The single greatest advancement in ensuring long-term function of the allograft is the development of immunologic modulators. Pioneered by Dr Norman Shumway at Stanford University, steroids and antipurine metabolites including azathioprine and mycophenolate mofetil (MMF) have been widely used.

Central to the current immunosuppression regimens are calcineurin inhibitors, cyclosporine, and tacrolimus. These drugs inhibit cellular pathways responsible for the production of interleukin (IL)-2 and subsequent T-cell activation. They inhibit the nuclear translocation of cytoplasmic factors needed to bind to the IL-2 gene promoter. Immunosuppressive regimens have evolved from cyclosporin to a predominant use of tacrolimus.

Triple drug therapy consisting of steroids, calcineurin inhibitors, and MMF has become standard initial immunotherapy after heart transplantation.12 Additional agents, such as antithymocyte globulin, rapamycin, and IL-2 receptor antagonists, also have important roles in modern immunosuppression protocols.

The Achilles heel in the long-term success of heart transplantation is the development of coronary graft atherosclerosis, the cardiac version of chronic rejection. Coronary graft atherosclerosis is uniquely different from typical coronary artery disease in that it is diffuse and usually not amenable to revascularization. Furthermore, although heart transplantation is a feasible solution for patients with end-stage heart disease, its use is limited by an inadequate donor supply.

In the United States, fewer than 2500 heart transplantation procedures are performed each year.13 Each year, an estimated 10-20% of patients die while awaiting a heart transplant. Of the 5 million people with heart failure, approximately 30,000-100,000 have such advanced disease that they would benefit from transplantation or mechanical circulatory support.14 This disparity between the number of patients needing transplants and the availability of heart donors has refocused efforts to find other ways to support the severely failing heart.

Coronary artery bypass grafting

Studies of medical versus surgical therapy for coronary artery disease have historically focused on patients with normal left ventricular (LV) function. However, the Veterans Affairs Cooperative Study of Surgery demonstrated a significantly increased survival rate in a subset of patients with left ventricular ejection fractions (LVEFs) of <50% after coronary bypass surgery compared with patients who were randomly selected to receive medical therapy. This survival benefit was particularly evident at the 11-year follow-up point (50% vs 38%).

The Coronary Artery Surgery Study (CASS) of patients with left main equivalent disease showed that surgical revascularization, compared with medical therapy, prolonged survival in most clinical and angiographic subgroups.15 Of importance, this study demonstrated that surgical therapy markedly improved the 5-year cumulative survival rate in patients with an ejection fraction (EF) of <50% (80% vs 47%).16

These early randomized trials were limited by their inclusion of patients who had what is currently considered a good EF. That is, many patients referred for coronary revascularization live with EFs of <35%.

Investigators from Yale and the University of Virginia, among many others, have published their results of coronary artery bypass grafting (CABG) in patients with extremely poor LV function who were on the transplant waiting list. Elefteriades et al demonstrated that CABG in patients with EFs of <30% had a survival rate of 80% at 4.5 years, which remarkably approaches that of cardiac transplantation.17 Kron et al reported a similar 3-year survival rate of 83% in patients who underwent coronary bypass with an EF of <20%.18

With regard to the pathophysiology, patients who may gain the greatest benefit from surgical revascularization are those who have a hibernating myocardium. This term is used to describe regions of the heart that are dysfunctional under ischemic conditions but that can regain normal function after blood flow is restored.19

A number of studies have demonstrated that surgical revascularization can reduce mortality rates, improve NYHA classes, favorably alter LV geometry, and increase LVEFs in patients with ischemic heart failure and substantial areas of viable myocardium. For instance, surgical revascularization confers a dramatic survival benefit in patients with a substantial amount of hibernating myocardium.20 For patients with at least 5 of 12 segments showing myocardial viability, revascularization resulted in a cardiac mortality rate of 3% versus 31% for medically treated patients with viable myocardium.

MRI has become particularly useful for evaluating both abnormalities in wall motion and viable myocardium, and MRI results aid in predicting the success of revascularization in patients with low EFs.21

Many surgeons have evolved their practices to meet the demands of high-risk patients and to adopt measures to improve graft patency. The adoption of techniques both on and off cardiopulmonary bypass, as well as beating-heart techniques for revascularization, highlight the aim of treating high-risk patients.22 Regarding the latter aim, preventive strategies include the increased use of bilateral mammary and arterial grafting.23

Although results of randomized, controlled medical versus surgical trials from the 1970s established many standards for the treatment of coronary artery disease, no large studies have addressed similar issues in the modern medical era, especially those important to patients with ischemic cardiomyopathies.

The Surgical Treatment of Congestive Heart Failure (STICH) study is a prospective, randomized trial that has recently finished enrollment.24,25 Its purpose is to determine the role of CABG in patients with heart failure. The first hypothesis tests whether CABG with intensive medial therapy, as compared with medical therapy alone, confers an additional survival benefit in patients with an EF of <35%. End points of interest are morbidity and mortality rates, quality of life, and economic effects of the treatment strategies. Enrollment for this arm of the study was expected to reach its goal of 1000 patients by the end of 2006.

Aortic valve replacement

Diseases of the aortic valve can frequently lead to the onset and progression of congestive heart failure. Although the natural histories of both aortic stenosis and aortic regurgitation are well known, patients are often followed up conservatively after they present with clinically significant heart failure. Congestive heart failure is a common indication for aortic valve replacement (AVR), but one must be cautious in patients with low EFs and possible aortic stenosis. If no inducible gradient is present (a finding that suggests some ventricular reserve), the outcome with standard AVR is poor. In this situation, transplantation might be the only option, although the use of percutaneous valves, an apical aortic conduit, or a left ventricular assist device (LVAD) might offer an intermediate solution.

Of the 3 classic symptoms of aortic stenosis—syncope, angina, and dyspnea—the last is the most robust risk factor for death. Only 50% of patients with dyspnea in this setting are still alive within 2 years.26 Angina is associated with a mortality risk of 50% within 5 years, whereas syncope confers a 50% mortality risk in 3 years.

In the converse, the age-corrected survival rate of patients undergoing aortic valve replacement (AVR) for aortic stenosis is similar to that of the normal population.27 Once patients develop severe LV dysfunction, the results of AVR are somewhat guarded.28 Because of poor LV function, these patients are unable to develop significant transvalvular gradients (ie, low-output, low-gradient aortic stenosis). Critical in the preoperative decision process is determining if the ventricular dysfunction is truly valvular (which improves with replacement) or if it reflects other forms of cardiomyopathy, such as ischemia or restrictive processes (which does not improve with replacement).

Precise measurement of the area of the aortic valve is difficult because the calculated area is directly proportional to cardiac output. Also, the Gorlin constant varies at lower outputs. Therefore, in this situation, valvular areas might be considered critically small when, at surgery, the valve is found to be only moderately diseased. Preoperative evaluation with dobutamine testing to increase contractile reserve or with vasodilator-induced stress echocardiography by using the continuity equation rather than the Gorlin formula can be helpful in making this distinction. The results can guide the physician or surgeon in determining if the patient is a candidate for the relatively high-risk procedure.29 Nevertheless, because of the possibility of ventricular recovery and lengthened patient survival, most patients with heart failure and aortic stenosis are offered valve replacement.30

Timing of surgical intervention for aortic insufficiency is more challenging in patients just described than in patients with aortic stenosis. However, as before, once symptoms occur and once evidence of LV structural changes become apparent, morbidity and mortality due to aortic insufficiency increases.31

In a retrospective review from the Mayo Clinic, 450 patients receiving AVR for aortic insufficiency were compared according to ranges of EF (<35%, 35-50%, >50%).32 Although the group with severe dysfunction had an operative mortality rate of 14%, the EF improved, and the group's 10-year survival rate was 41%. As with aortic stenosis, early intervention before the onset of severe LV dysfunction is crucial to improving the survival of patients with aortic insufficiency.33

Mitral valve repair

Mitral valve regurgitation can both cause and result from chronic heart failure. Its presence is an independent risk factor for cardiovascular morbidity and mortality.34

In addition to frank rupture of the papillary muscle in association with acute myocardial infarction, chronic ischemic cardiomyopathies result in migration of the papillary muscle as the ventricle dilates. This dilation causes tenting of the mitral leaflets, restricting their coaptation. Dilated cardiomyopathies can have similar issues, as well as annular dilatation. In addition to mitral regurgitation, the alteration in LV geometry contributes to volume overload, increases LV wall tension, and leaves patients susceptible to exacerbations of heart failure.35

Mitral valve surgery in patients with heart failure has gained favor because it abolishes the regurgitant lesion and decreases symptoms. The pathophysiologic rationales for repair or replacement are to reverse the cycle of excessive ventricular volume, to allow for ventricular unloading, and to promote myocardial remodeling.

Among other researchers, a group from Michigan has advocated mitral repair in the population with heart failure. Bolling and colleagues demonstrated that mitral valve repair increased the EF, improved heart failure classes from 3.9 to 2.0, and decreased the number of hospitalizations.36

Additional effects with repair in these patients is the increase in coronary blood-flow reserve afforded by the reduction in LV volume.37

Despite the potential benefits of mitral reconstruction surgery, a retrospective review showed no decrease in long-term mortality among patients with severe mitral regurgitation and significant LV dysfunction who underwent mitral valve repair.38 Mitral valve annuloplasty was not predictive of clinical outcomes and did not improve mortality. Factors that did improve mortality were ACE inhibitor use, beta-blockade, mean arterial pressures, and serum sodium concentrations. The results of this analysis were not overly surprising. In most patients in this situation, heart failure is not due to flail leaflets, for example; instead, it is secondary to ventricular dysfunction.

Cardiomyopathy-associated mitral regurgitation most commonly involves the insertion of either a complete or a partial band attached to the annulus of the mitral valve. Thus, mitral repair deals with only 1 aspect of the patient's overall pathophysiologic condition. That is, annuloplasty rings may assist with tenting of the leaflet, but they do not address displacement of the papillary muscle with ventricular scarring.39 In many patients, the underlying problem (ie, primary myopathy) continues unabated.

In evaluating studies of heart failure with mitral regurgitation, it is important to separate the etiology (eg, ischemic vs dilated) as well as the surgical approaches. Future trials must be designed to distinguish differences among various surgical strategies, such as annuloplasty, resuspension of the papillary muscle, secondary chordal transection, ventricular reconstruction, passive restraints, and chordal-sparing valve replacement. Paramount in these procedures is to have little or no residual mitral regurgitation.40

If repair is deemed improbable, mitral replacement should be performed. Traditional mitral valve replacement includes complete resection of the leaflets and the chordal attachments. This destruction of the subvalvular apparatus results in ventricular dysfunction. Preservation of the chordal attachments to the ventricle with valve replacement might provide similar or even better results than those of annuloplasty in patients with mitral regurgitation and heart failure.41,42

Although the benefits in terms of quality of life (decreased heart failure) might not portend increased survival in these high-risk patients,43,44 they likely keep low–EF mitral valve interventions in the armamentarium of surgeons who manage heart failure.

In general, ischemic mitral regurgitation is a ventricular problem. Many operations allow for coaptation and no mitral regurgitation when the patient leaves the operating room. However, as the left ventricle continues to dilate, mitral regurgitation often recurs. Therefore, it is overambitious to say that annuloplasty cures this condition. As a result, many other approaches have been attempted (eg, chordal cutting, use of restraint devices, papillary relocation). However, results have been mixed.

Ventricular restoration

After a transmural myocardial infarction occurs, the ventricle pathologically remodels from its normal elliptical shape to a spherical shape. This change in geometry is in part responsible for the constellation of symptoms associated with congestive heart failure and decreased survival.45,46

Several ventricular restoration techniques exist. All aim to correct the pathologic alteration in geometry described above. Most approaches involve incising and excluding nonviable myocardium with either patch or primary reconstruction to decrease ventricular volume. Although the initial enthusiasm for ventricular resection to treat nonischemic dilated cardiomyopathies (the Batista procedure) has faded, a long-established finding is that resection of dyskinetic segments associated with LV aneurysms can increase patients' functional status and prolong life.47,48

The success of early lytic and percutaneous therapy for acute myocardial infarctions has decreased the incidence of true LV aneurysms. As such, ventricular restoration now focuses on excluding relatively subtle regions of akinetic myocardium.

In 2004, the International Reconstructive Endoventricular Surgery Returning Torsion Original Radius Elliptical Shape to the Left Ventricle (RESTORE) group reported the results of ventricular restoration by using the technique Dor described.49 EFs increased from 29.6% to 39.5%, the end-systolic volume index decreased, and a significant improvement in NYHA functional classes improved from 67% class III/IV before surgery to 85% class I/II after surgery.

Yamaguchi and colleagues similarly demonstrated significantly improved 5-year survival in patients with ischemic cardiomyopathy who underwent ventricular restoration and CABG versus those who underwent CABG alone.50 Survival rates were 90% versus 53.5%, respectively.

The current level of enthusiasm to perform ventricular remodeling surgery in patients with heart failure is high. Apart from the RESTORE trial, most studies have been single-institution, retrospective analyses. Although many believe that ventricular remodeling is warranted for dyskinetic and large akinetic segments of the myocardium, some are beginning to perform this procedure even on hypokinetic regions.

The major study of ventricular reconstruction was the aforementioned STICH trial funded by the National Institutes of Health. To test their second hypothesis, the STICH investigators are prospectively and randomly selecting patients with akinetic, low–EF ventricles to receive CABG versus CABG and ventricular reconstruction. After prolonged follow-up, the results should shed light on the importance of both revascularization and ventricular geometry in these very ill patients.24

Use of passive restraints

Fundamental principles in hemodynamics (ie, the Laplace law) hint at the progression of structural deterioration associated with heart failure. A cycle exists in which increasing ventricular volume raises wall tension. Thickening of the ventricle and its dilation compensates for the tension.

Dynamic cardiomyoplasty (ie, wrapping the latissimus dorsi muscle around the heart and entraining it to beat synchronously with the heart) was historically intended to augment systolic function. Although this technique was somewhat cumbersome and not overwhelmingly successful, investigators learned that this external fixation of the heart prevented cardiac dilation and improved heart failure. As such, recent work has focused on the use of devices that restrain the heart.

The most studied product is the CorCap device (Acorn Cardiovascular, St Paul, MN). When this device is used, a mesh-like support is sewn circumferentially around the ventricle. Animal studies demonstrated downregulation of stretch-response proteins, attenuation of myocytic hypertrophy, and improved calcium cycling involving the sarcoplasmic reticulum.51 Early reports in humans have demonstrated reduced dimensions of the ventricular chamber and improvement in EFs and NYHA class.52

In the Acorn Pivotal Trial, patients with NYHA class III/IV disease were randomly assigned to 1 of 4 treatment groups: optimal medical therapy, optimal medical therapy with use of a cardiac support device (CSD), mitral valve repair or replacement, or mitral valve repair or replacement with use of a CSD.53 Patients who received the CSD required fewer major cardiac procedures (eg, transplantation, application of a LVAD) than did control subjects after implantation. Use of the device was associated with an enhanced of reduction in LV end-diastolic and systolic volumes and with a significant improvement in quality of life.

Use of the CSD is not widespread because the US Food and Drug Administration (FDA) recently denied its approval. The FDA cite a need for further statistical evidence to demonstrate its efficacy.

Electrophysiology

Patients with heart failure and interventricular conduction abnormalities (roughly defined as those with a QRS interval >120-130 ms) are potential candidates for chronic resynchronization therapy (CRT) by means of an inserted biventricular pacemaker. CRT aims to improve cardiac performance by restoring interventricular septal electrical and mechanical synchrony of the heart. Thus, it reduces presystolic mitral regurgitation and optimizes diastolic function by reducing the mismatch between cardiac contractility and energy expenditure.54

Regarding technique, 3 cardiac leads are placed transvenously: an atrial lead, an RV lead, and an LV lead, which is threaded through the coronary sinus and out 1 of its lateral-wall tributaries. Surgeons have assisted difficult transvenous LV placements by epicardially inserting LV leads using a number of techniques. Examples include mini-thoracotomy, thoracoscopy, or robotically assisted methods.

Several prospective randomized trials have been performed to evaluate the effectiveness of CRT. The Multicenter InSync Randomized Clinical Evaluation (MIRACLE) study group demonstrated an improvement in NYHA functional class, quality of life, and EF.55

The potential benefit of cardiac-resynchronization therapy (CRT) with biventricular pacing for patients with mild cardiac symptoms, a reduced ejection fraction, and a wide QRS complex was studied in the Multicenter Automatic Defibrillator Implantation Trial with Cardiac Resynchronization Therapy (MADIT-CRT).56

In MADIT-CRT, 1820 patients with an ejection fraction of 30% or less, a QRS duration of 130 msec or more, and New York Heart Association class I or II symptoms were randomly assigned to receive CRT plus an implantable cardioverter-defibrillator (ICD) or an ICD alone. During an average follow-up of 2.4 years, death from any cause or a nonfatal heart-failure event occurred in 17.2% of patients in the CRT-ICD group versus 25.3% of patients in the ICD-only group (hazard ratio in the CRT-ICD group, 0.66; 95% confidence interval, 0.52-0.84; P = 0.001). In particular, a 41% reduction in the risk of heart-failure events occurred in patients in the CRT group, which was evident primarily in patients with a QRS duration of 150 msec or more. CRT was associated with a significant reduction in left ventricular volumes and improvement in the ejection fraction. No significant difference occurred between the two groups in the overall risk of death.56

In addition to augmenting functional capacity, CRT also appears to favorably affect mortality. The Comparison of Medical Therapy, Pacing, and Defibrillation in Heart Failure (COMPANION) trial demonstrated an increase in survival only when biventricular pacing was used with a defibrillator.57 However, the Cardiac Resynchronization-Heart Failure (CARE-HF) trial showed a 36% reduction in death with biventricular pacing alone.58 In both studies, mortality was largely due to sudden death.

Indeed, the role of the implantable cardioverter-defibrillator (ICD) has rapidly expanded over the last decade. Patients with heart failure are 5-10 times more likely to die of sudden death than the general population. Sudden death from both ischemic and nonischemic sustained ventricular tachyarrhythmias has been remarkably reduced such that current AHA guidelines recommend an ICD in virtually all patients with an EF of <35%.

Of interest, prophylactic use of an ICD at the time of low-EF CABG failed to improve survival compared with revascularization alone.59 This observation speaks to the importance of the independent influence of CABG on reducing mortality in ischemic cardiomyopathies. The present authors have currently adopted the approach of prophylactically placing LV epicardial leads on patients with conduction delays at the time of high-risk heart failure surgery. These leads are tunneled for future connection to a traditional transvenous atrial and RV biventricular pacer-defibrillator. The benefit of this strategy remains to be proven prospectively.

Atrial fibrillation, with or without heart failure, is an independent risk factor for cardiovascular morbidity and mortality. In a large retrospective study of patients with LV dysfunction, those with atrial fibrillation had elevated rates of all-cause mortality (34% vs 23%) and death attributed to pump-failure (16.7% vs 9.4%).60

Aggressive management of atrial fibrillation in patients with heart failure is receiving greater attention now than before. In 1 report, catheter ablation significantly improved LV function (EF increased by 21%); reduced LV dimensions; and improved exercise capacity, symptoms, and quality of life in patients with heart failure and concurrent atrial fibrillation compared with control subjects.61

The cardiac surgical community has increasingly adopted an aggressive approach to the treatment of atrial fibrillation during concurrent operations. The Cox-Maze procedure, developed in the early 1990s, involves the creation of multiple incisions to prevent atrial reentry and to allow normal sinus impulses to propagate. This technique proved successful in curing atrial fibrillation. However, the Cox-Maze procedure is technically challenging and time intensive; these disadvantages have lessened its widespread adoption.62

A number of variations of the original Cox-Maze technique have evolved in the last decade. Most involve the use of a host of adjunct ablation methods to replace many of the cut-and-sew lesions. Examples include cryothermy, radiofrequency ablation, microwave ablation, and high-intensity focused ultrasonography. The ease and efficacy of these technologies have allowed clinicians to adopt them in combination with other procedures performed to treat heart failure. Indeed, evidence suggests that LV function can be improved with concomitant ablation of atrial fibrillation during operations for structural (usually valvular) heart disease.63,64

Although restoring atrial function possesses conceptual advantages, no investigators have examined the effect of surgical atrial fibrillation ablation on the natural history of patients. To date, the application of surgical ablation for lone atrial fibrillation in patients with heart failure remains anecdotal.65

Mechanical Circulatory Support

Ventricular assist devices

In 1963, Dr Michael DeBakey reported the first clinical use of a ventricular assist device (VAD) in a patient who had cardiac arrest after aortic valve replacement (AVR). Unfortunately, the patient died. Three years later, Dr DeBakey successfully implanted a newer device in a patient who could not be weaned from cardiopulmonary bypass.66 This patient received mechanical support for 10 days, which allowed the myocardium to recover, and was successfully discharged from the hospital. Since this early era, the development of VADs has progressed rapidly, and these devices are now invaluable tools in the treatment of heart failure.

A number of devices are currently available to support both the acutely and the chronically decompensated heart. In some cases of extreme cardiopulmonary failure, the only recourse is complete support with extracorporeal membrane oxygenation (ECMO). Despite encouraging results with ECMO for the management of cardiogenic shock, most patients requiring circulatory assistance can be helped with ventricular support alone. Depending on the particular device used, both the RVs and the LVs can be assisted with an LVAD, a right ventricular assist device (RVAD), or a biventricular assist device (biVAD).

In concept, LVADs, RVADs, and biVADs are all similar. Blood is removed from the failing ventricle and diverted into a pump that delivers blood to either the aorta (in the case of an LVAD) or pulmonary artery (in the case of an RVAD). These devices can often be placed temporarily to allow the myocardium to recover, as in patients with acute viral myocarditis or those who have undergone cardiotomy.

VADs are most commonly used to bridge the acutely failing heart to eventual heart transplantation. This method allows patients to recover from end-organ damage, to obtain rehabilitation, and possibly to go home before definitive heart transplantation.

Patients with severe congestive heart failure who are not transplant candidates and who otherwise would die without treatment are candidates for lifetime use of VADs or destination therapy. In this situation, the devices can be placed and are intended for indefinite therapy. For example, patients with end-stage heart failure who are receiving inotrope therapy and who are not candidates for transplantation should be given an LVAD for lifetime use. The Randomized Evaluation of Mechanical Assistance for the Treatment of Congestive Heart Failure (REMATCH) trial and several later studies demonstrated that destination therapy with LVADs are superior to medical therapy in terms of both quantity and quality of life. How frequently this strategy is used might ultimately depend on healthcare economics.

At present, nearly 30 different mechanical circulatory devices are in use or are in the preclinical phase. These pumps conceptually differ in their modes of function. These devices include pneumatic, electric, pulsatile, and rotary pumps.

In the United States, several FDA-approved options are available for bridging the patient to recovery and transplantation. These options include the following:

  • Abiomed BVS 5000 circulatory support system (Abiomed, Inc, Danvers, Mass), which is typically used for short-term support
  • Abiomed AB5000 circulatory support system (Abiomed, Inc)
  • Centrimag or Levitronix system (Thoratec, Pleasanton, Calif)
  • Thoratec paracorporeal and intracorporeal LVAD and RVAD (Thoratec)
  • Novacor LVAD (World Heart Inc, Oakland, Calif)
  • HeartMate I LVAD (Thoratec)

In addition, several small, axial-flow devices, including the Heartmate II (Thoratec) and Jarvik 2000 Flowmaker (Jarvik Heart, Inc, New York, NY), are actively involved in clinical trials. Although the HeartMate LVAD (Thoratec) is the only device that is FDA approved for destination therapy, several other devices are actively being studied in the United States for use as destination therapy. These include the HeartMate II LVAD (Thoratec) and the DeBakey-Noon LVAD (MicroMed Cardiovascular, Inc, Houston, TX).

Each device used as a bridge to transplantation has its good and bad points. For example, the HeartMate device (Thoratec) does not require warfarin anticoagulation unlike the other well-known pulsatile pump (Novacor; World Heart). However, it is not as durable as the other pump. The newer axial-flow pumps are relatively small and easy to insert, and they reduce morbidity. However, the effect of long-term continuous flow has yet to be determined.

Despite the presumed weaknesses of the therapies just described, the survival rate through heart transplantation for patients receiving VADs is roughly 70%. This rate is impressive given this desperately sick cohort of patients. Furthermore, the evolving technology raises a host of clinical and physiologic questions that, when studied and answered, continue to advance the field.

Results of the REMATCH study have been widely discussed.67 They offer the only prospective, randomized data from a comparison of very sick, non–transplant-eligible patients with congestive heart failure receiving optimal medical therapy with patients receiving an early-generation HeartMate LVAD. In brief, respective survival rates of medically treated and LVAD-treated patients were 25% and 52% at 1 year, and 8% and 23% at 2 years. In addition to their survival advantage, LVAD patients had improvements in several measures of quality of life.

Recent modifications in technique and perioperative care have decreased the high rates of LVAD-related morbidity and mortality observed in the REMATCH trial.68 Although REMATCH was a single study in very-high-risk patients, the data serve as proof of concept for future development of VAD technologies.

Despite the need for an external energy source, most patients can use mechanical circulatory devices in the outpatient setting. Many patients have lived productive lives for longer than 4-6 years with their original device (depending on the device).

Total artificial heart

The creation of a suitable total artificial heart (TAH) for orthotopic implantation has been the subject of intense investigation for the past 40 years.69 In 1969, Dr Denton Cooley implanted the Liotta TAH (no longer made) into a high-risk patient after failing to wean the patient off cardiopulmonary bypass after LV aneurysm repair. He was sustained for 3 days until a donor heart became available. Unfortunately, the patient died from pneumonia and multiple organ failure.70

The historical development of the TAH is rich with technologic genius, device failure, and personal intrigue. Compared with LVADs, the TAH has several potential advantages, including the ability to assist patients with severe biventricular failure, a lack of device pocket and thus a lessened risk of infection, and the opportunity to treat patients with systemic diseases (eg, amyloidosis, malignancy) who are not otherwise candidates for transplantation.

At present, 2 TAHs are receiving the most attention.

  • CardioWest TAH (SynCardia Systems, Inc, Tucson, Ariz)
  • AbioCor TAH (Abiomed, Inc)

The CardioWest TAH is a structural cousin of the original Jarvik-7 TAH (Jarvik Heart, Inc) that was implanted into patient Barney Clark with great publicity in 1982. Investigators recently reported data allowing this device to become the only FDA-approved TAH for use as a bridge to transplantation. Nearly 80% of patients survived to transplantation versus only 46% in a control medical arm. Respective survival rates at 1 and 5 years with the device were 86% and 64% compared with 69% and 34% in the control group.71 The main limitation of this TAH is its external power source and large control console.

The AbioCor TAH involves a novel method of transcutaneous transmission of energy, freeing the patient from external drivelines. The patient exchanges the external battery packs, which can last as long as 4 hours. This TAH is unique in that it is the first TAH to use coils to transmit power across the skin; therefore, no transcutaneous conduits are needed. This feature allows for the advantages of a closed system, which potentially reduces sources of infection, a known complication of earlier devices.

The first clinical implantation of this TAH was performed in July 2001. To date, 14 patients have received this device as part of a trial of patients whose expected survival was <30 days.72 Although all subsequently died, 4 patients were ambulatory after surgery, and 2 were discharged from the hospital to a transitional-care setting. One of the discharged patients was discharged on postoperative day 209. A limitation of the AbioCor TAH is its large size, which permits its implantation in only 50% of men and 20% of women.

Both the CardioWest TAH and AbioCor TAH require recipient cardiectomy before implantation. They are similar in that they are sewn to atrial cuffs and to the great vessels after the native heart is explanted.

The next TAH to emerge clinically will be a second-generation TAH from Abiomed, Inc. The AbioCor II replacement heart is designed to be 35% smaller than older models and to function as a durable pump for longer than 5 years.

Despite more than 40 years of effort, the clinical application of artificial-heart technology is still immature. However, with the approval of the CardioWest device and with new efforts to create small pumps, TAHs will ultimately be routine components of heart failure surgery for very sick patients with heart failure and biventricular failure.

Future and Controversies

Although many therapies, such as CABG and AVR are time tested, others are maturing and awaiting further investigation with long-term follow-up and well-designed prospective studies. The future will be filled with advancements in mechanical devices as well as in translational strategies. Indeed, biologic approaches to heart failure are actively being pursued, both experimentally and clinically.

Hottest on the list of emerging therapies is the use of stem cells to augment cardiac function.73,74 Cellular transplantation is based on the theory that cardiac progenitor cells can become fully differentiated cardiac myocytes and subsequently replace damaged myocardium.75 Some conversely believe that these cells play more of a supportive role than a regenerative role by optimizing conditions for the heart to recover from ischemia.76,77 Many cell types are currently being studied both experimentally and clinically; these include bone marrow stem cells (mesenchymal and hematopoietic), dendritic cells, adipocytes, endothelial progenitor cells, and skeletal myoblasts.

Clinical trials have mostly been performed in single centers with limited numbers of patients. However, intriguing results have been reported. For example, intracoronary infusions of cardiac progenitor cells into patients with acute myocardial infarctions improved LVEF and end-systolic volumes.78 In a phase I clinical trial of autologous skeletal myoblasts given at the time of surgical revascularization, NYHA functional classes improved from 2.7 before surgery to 1.6 after surgery, and EFs increased from 24% to 32%.79 Furthermore, systolic thickening at the site of implantation (as evaluated with echocardiography) improved in 63% of patients. However, many of these patients developed ventricular arrhythmias.

Patel and colleagues80 randomly selected 20 patients with heart failure (EF <35%) to receive off–cardiopulmonary bypass revascularization with or without subepicardial injections of autologous bone marrow stem cells. Compared with the revascularization group, the group treated with stem cells had better EFs at 6 months (46% vs 37%).

Many variations on the stem-cell theme exist. These include the use of angiogenic therapy to increase vascularity at the site of infarct and the administration of growth factors to increase homing of native stem cells to injured myocardium.81,82

More questions than answers exist in this growing therapeutic field. Issues include optimal cell types and cell densities, identification of appropriate patients, the frequency of administration, and adjuncts for revascularization. Most clinical trials have varied tremendously in terms of many of these features and have not been randomized. Therefore, interpretation of their results is difficult. Although biologic therapy is in its infancy, early results show its potential promise.

Conclusion

The modern paradigm of treating patients with heart failure is truly multidisciplinary and involves cardiologists, cardiac surgeons, nurses, social workers, therapists, and basic scientists. Patients with heart failure uniformly have multiple comorbidities and are at high risk with any intervention. As such, their ultimate outcomes depend on the constellation consisting of preoperative evaluation, intraoperative conduct, and postoperative care. Meticulous attention to multiple organs is required to ensure success. A solid working relationship among caregivers is essential to an effective heart failure surgery program.83,84

The management of heart failure is truly multifaceted and constantly evolving. In both clinical and scientific aspects, surgeons are uniquely positioned to significantly affect treatment strategies for sick patients with heart failure. The number of options ranging from bypass and valvular surgery to transplantation and mechanical assist suggests that existing, developing, and creative solutions to the epidemic of heart failure are central to the longevity and quality of life for the increasingly aging population with this disease.

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Keywords

congestive heart failure, CHF, heart failure, congestive heart failure symptoms, congestive heart failure treatment, chronic heart failure, cardiac failure, inotropes, heart transplant, cardiac support device, ventricular assist device, total artificial heart, mechanical circulatory support, chronic resynchronization therapy, CRT, left ventricular assist device

Contributor Information and Disclosures

Author

Craig H Selzman, MD, FACS, Associate Professor of Surgery, Division of Cardiothoracic Surgery, University of Utah
Craig H Selzman, MD, FACS is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, American Physiological Society, Association for Academic Surgery, International Society for Heart and Lung Transplantation, Society of Thoracic Surgeons, and Southern Thoracic Surgical Association
Disclosure: Nothing to disclose.

Medical Editor

Joseph Cornelius Cleveland Jr, MD, Associate Professor, Division of Cardiothoracic Surgery, University of Colorado Health Sciences Center
Joseph Cornelius Cleveland Jr, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for the Advancement of Science, American College of Cardiology, American College of Chest Physicians, American College of Surgeons, American Geriatrics Society, American Physiological Society, American Society of Transplant Surgeons, Association for Academic Surgery, Heart Failure Society of America, International Society for Heart and Lung Transplantation, Phi Beta Kappa, Society of Critical Care Medicine, Society of Thoracic Surgeons, and Western Thoracic Surgical Association
Disclosure: Thoratec Heartmate II Pivotal Tria; Grant/research funds Principal Investigator - Colorado; E-Valve E-clip Grant/research funds Principal Investigator - Colorado; Paracor Peerless Trial Grant/research funds Principal Investigator

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Chief Editor

Brett C Sheridan, MD, FACS, Assistant Professor of Surgery, University of North Carolina at Chapel Hill School of Medicine
Disclosure: Nothing to disclose.

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