INTRODUCTION

Despite tremendous advances in the medical management of HF, the gold standard for the treatment of end-stage HF remains cardiac transplantation. Several surgical alternatives for the treatment of HF are currently being investigated. Some approaches involve an extension of current conventional cardiac operations like mitral valve repair while others seek to induce changes in the geometry of the left ventricle to render it a more efficient pump. This chapter outlines surgical approaches to congestive HF in the most common clinical situations.

CORONARY REVASCULARIZATION IN THE PATIENT WITH SEVERE LEFT VENTRICULAR DYSFUNCTION

Numerous studies over the last decade have demonstrated that left ventricular dysfunction secondary to myocardial stunning and hibernation can be a reversible phenomenon following coronary revascularization.1,2 Therefore, it is believed that selection of patients who have coronary artery disease and left ventricular dysfunction for surgical revascularization be based on the presence of viable myocardium.3–5 The implications of distinguishing viable from nonviable myocardium are important in determining which patients may benefit from coronary revascularization. A recent meta-analysis, which pooled 24 studies and some 3000 patients, suggested that viable myocardium may represent an unstable substrate leading to improvement in survival with revascularization.

The Coronary Artery Surgery Study (CASS) trial was the first clinical trial that assessed the impact of surgical coronary revascularization in patients with left ventricular dysfunction.6 In comparing 420 medically treated and 231 surgically treated patients with left ventricular ejection fraction (LVEF) ≤35% in the nonrandomized registry cohort, Alderman et al. reported that coronary artery bypass graft (CABG) improved survival. The benefit was most apparent for patients with angina and LVEF ≤25%; medically treated patients in this cohort had a 43% 5-year survival while CABG recipients benefited from a 63% 5-year survival. Operative mortality in the CASS series was 6.9%. Clearly, much has changed in the medical and surgical treatment of advanced coronary disease since that time. The CASS trial was conducted prior to the routine use of angiotensin-converting enzyme (ACE) inhibitors, b-blockers, and statins. Advances in surgical management including routine use of internal mammary and other arterial conduits, improved cardioplegic solutions, and off-pump techniques, among others, have resulted in marked reductions in operative morbidity and mortality in increasingly ill patients. These radical changes have lessened, if not obviated, the applicability of the results of the CASS and other early trials to current practice.

In an attempt to identify differential indications for CABG versus cardiac transplantation, Hausmann studied patients with end-stage ischemic cardiomyopathy and LVEF between 10% and 30% who underwent CABG. The 225 study patients had been referred as possible cardiac transplant candidates.7 The major candidacy criterion for bypass grafting was ischemia diagnosed by myocardial thallium scintigraphy and echocardiography. The operative mortality was 7.1%, with an actuarial survival of 90.8% at 2 years, 87.6% at 4 years, and 78.9% at 6 years. During the same time period, 231 patients with end-stage coronary artery disease and a mean LVEF of 21% underwent orthotopic heart transplantation at the same institution. The operative mortality in the transplant group was 18.2%, and the actuarial survival at 6 years was 68.9%. Significant causes of early death in the transplant group were infection (40.5%) and early rejection (26.2%). Among their observations, the authors noted that an area of 20% or more of the total heart mass defined as viable by preoperative testing portends promising results after CABG. A summary of several reports depicting the results of conventional CABG in patients with severe left ventricular dysfunction is depicted in Table 15-1.

Off-pump revascularization has emerged as another option for the treatment of severe ischemic left ventricular dysfunction. Recent evidence indicates that some of the associated morbidities encountered with conventional arrested heart technique may be reduced with beating heart surgery.8 Off-pump beating heart CABG is typically performed by total avoidance of cardiopulmonary bypass and minimization of aortic manipulation. Arom et al. compared 45 patients with LVEF <30% who underwent off-pump revascularization with 132 similarly impaired patients who underwent conventional grafting during the same time period.9 The former benefited from reduced perioperative blood loss and perioperative myocardial injury. Operative mortality was lower in the off-pump group, but it did not reach statistical significance. Goldstein et al. reported on 100 consecutive patients with a mean ejection fraction (EF) of 26 ± 4% who underwent beating heart revascularization.10 Patients received a mean of 3.5 grafts with 83% internal mammary artery use. Observed mortality was 3% with a predicted mortality of 5.3%. Observed-toexpected ratio was 0.56. Incidence of adverse events compared favorably with both that reported in the Society of Thoracic Surgeons Database for all CABG patients regardless of left ventricular function, and also to a concurrent CABG cohort. One-year survival was 85%. Freedom from cardiac readmission was 88% and freedom from angina was 83%. No patient required repeat percutaneous or surgical intervention. Further studies are necessary to define the indications for off-pump revascularization in this high-risk cohort of patients.

In the absence of confirmatory randomized data, it is generally accepted that in the presence of documented contractile reserve (myocardial viability) and graftable targets with good runoff, and in the absence of significant right ventricular dysfunction, pulmonary hypertension, and marked left ventricular dilation, patients with coronary artery disease and left ventricular dysfunction should be strongly considered for coronary revascularization rather than cardiac transplantation. As mentioned later (page 205 of this chapter), the comparative safety and efficacy of coronary revascularization plus optimal medical therapy versus optimal medical therapy alone is under evaluation in a large randomized controlled trial in patients with ischemic HF who are not considered sick enough for cardiac transplantation.

AORTIC STENOSIS AND SEVERE LEFT VENTRICULAR DYSFUNCTION

The most common etiology of aortic stenosis (AS) is age-related degeneration of the aortic valve followed by a congenitally bicuspid valve and then rheumatic disease. Regardless of the etiology, the resulting left ventricular obstruction from chronic AS leads to chronic pressure overload of the left ventricle, leading to compensatory hypertrophy. Uncorrected AS eventually leads to systolic and diastolic dysfunction as the hypertrophied myocardium cannot compensate for the increased wall stress generated.

Aortic valve replacement (AVR) is possible in patients with severe AS and HF. In order to identify patients who may be better candidates for high-risk AVR, attempts have been made to stratify patients on the basis of presence or absence of reversible left ventricular dysfunction.11 A recent study documented the use of dobutamine echocardiography to differentiate between those patients with severe AS, left ventricular dysfunction, a low transvalvular gradient, and irreversible myocardial damage from those with reversible myocardial dysfunction.12 Dobutamine echocardiography is thus used to determine aortic valve area in two different flow states (baseline and stress), so that severe AS, which is fixed, can be distinguished from AS that is flow-dependent. Patients with flow-dependent AS will demonstrate a decrease in valve area with the increased flows caused by the enhanced inotropic-mediated contractile state. AVR is more likely to be beneficial in these patients, as the depressed contractility is due to increased afterload, also known as “afterload mismatch,” and is, therefore, recoverable.

Only a few published series have been undertaken to examine the outcomes of patients with severe AS (valve area <0.75 cm2) and LVEF<35% or New York Heart Association (NYHA) Class IV symptoms who undergo AVR.13 A report by Powell et al. described an operative mortality of 18%, with prior myocardial infarction being a risk factor for perioperative mortality. Based on the high operative mortality, the authors suggested avoiding AVR in these patients.14

Review of the published studies (Table 15-2) suggests high perioperative mortality (7–21%) but improved functional capacity in most survivors. Long-term survival was not recorded in most studies, but in those studies that did, 5-year survival was at least comparable to that achieved with cardiac transplantation. Based on these reports, the general consensus is that in patients with AS and severe left ventricular dysfunction in whom contractile reserve can be documented, AVR (1) can be performed with an acceptable operative mortality, (2) leads to symptomatic improvement in most survivors, and (3) confers a short- and long-term survival benefit in comparison to medical therapy.

AORTIC REGURGITATION AND SEVERE LEFT VENTRICULAR DYSFUNCTION

Aortic regurgitation (AR) results from improper coaptation of the aortic valve leaflets leading to regurgitant blood flow into the left ventricle during diastole. The pathophysiology of AR involves both volume and pressure overload of the left ventricle. AR has numerous etiologies, including hypertension, calcific, degenerative and rheumatic disease, endocarditis, and aortic annular dilatation as a result of connective tissue disorders (such as Marfan syndrome), or even trauma. Chronic AR leads to left ventricular eccentric hypertrophy to compensate for the volume and pressure overload. With continued uncorrected AR, myocardial fibrosis eventually occurs, resulting either from subclinical ischemia secondary to increased wall stress and diminished diastolic coronary flow, and/or from stress-triggered myocyte apoptosis. Progressive fibrosis leads to irreversible cardiac dysfunction and severe HF symptomatology.

The natural history of patients with chronic AR and low EF (<35%) and/or NYHA Class III–IV symptoms treated medically is extremely poor.15 Survival for medically treated severe AR at 5 years has been reported to be between 20% and 66%. Current guidelines for patients with AR recommend AVR best for symptomatic patients and for those asymptomatic patients who show signs of deteriorating left ventricular function or have an EF <35% or diastolic diameter approaching 75 mm or an end-systolic diameter approaching 55 mm. AVR is best tolerated and associated with acceptable morbidity and mortality in patients with preserved or slightly disturbed ventricular function. AVR is currently recommended in severe AR even when EF is depressed. Clearly defining the risks and benefits of AVR in this patient population would allow better allocation of treatment options, which include AVR, medical vasodilator therapy, and cardiac transplantation.16

MITRAL VALVE SURGERY IN SEVERE LEFT VENTRICULAR DYSFUNCTION

It is well established that secondary or functional mitral regurgitation worsens both symptoms and prognosis in patients with left ventricular dysfunction of ischemic and nonischemic etiology. Volume overload resulting from mitral valve regurgitation leads to ventricular dilatation and dysfunction, which subsequently leads to further regurgitation through annular dilatation. Thus, a vicious downhill cycle is perpetuated whereby ventricular dilatation potentiates mitral regurgitation and mitral regurgitation potentiates ventricular dilatation. Despite maximal medical therapy, these patients face an extremely poor probability of survival unless they undergo cardiac transplantation.

In the majority of patients, the functional regurgitation produces a central jet, which is easily treated with reduction ring annuloplasty. Zealous supporters of either rigid or flexible annuloplasty rings exist and no convincing data exist to support one type over the other. There appears to be a growing consensus, however, that a complete rather than a partial (or posterior) ring should be used as recent data suggest improved freedom from recurrent regurgitation. Some authors suggest that the intertrigonal distance does, in fact, increase in the setting of cardiomyopathy. In the presence of leaflet pathology, more sophisticated repairs like triangular and quadrangular resections, chordal shortening and transfers, and edge-to-edge (Alfieri) repairs have been successfully used to preserve the mitral apparatus and avoid the adverse effects of mitral prosthetic implantation.

Bolling et al., in 1995, were the first to report the early outcome of remodeling mitral annuloplasty with a flexible posterior ring in 16 patients with severe HF and mitral regurgitation.17 Twelve of their patients had a nonischemic cardiomyopathy and the other 4 an ischemic cardiomyopathy. Functional capacity was improved in all patients, and mean LVEF rose from 16% to 25%, with reduction in regurgitation volume and left ventricular volume. The most impressive result of this study was that patients with severe left ventricular systolic dysfunction in whom LVEF was probably overestimated by the presence of severe mitral regurgitation were able to tolerate a major surgical procedure for correction of mitral regurgitation. This observation was instrumental in reversing the widely held opinion that corrective surgery should not be performed in patients with severe mitral regurgitation and an EF <30%. A summary of reports evaluating the outcomes of mitral valve repair in dilated cardiomyopathy are outlined in Table 15-4.

Rothenburger et al. recently reported a series of 31 patients with mitral regurgitation and EF <30% who underwent isolated repair or replacement with complete preservation of the subvalvar apparatus.18 They reported comparable results between the two groups, with 1-, 2-, and 5-year survival rates of 91%, 84%, and 74%, respectively. Functional results were also equally good. Similarly, early available data from David et al. indicate that replacement of the mitral valve with preservation of the subvalvular structures can result in postoperative left ventricular systolic function that is comparable to that with valvular repair.19 In situations where the native valve leaflet(s) is (are) excised, preservation of the subvalvular structures can be achieved by incorporating the chordal leaflet attachments between the annular suture line and the prosthetic cloth rim. In other situations where one or both valve leaflets are kept intact, this can be achieved by incorporating the plicated leaflet structure with transannular sutures. In these latter instances, clinical and functional studies have suggested that preservation of the posterior leaflet is more important in maintaining left ventricular systolic function. Although preservation of the anterior leaflet is technically feasible, obstruction of the left ventricular outflow tract is possible if too much of the anterior leaflet structure is left intact. Such outcomes with chordaepreserving mitral valve replacement are certainly at odds with the previously reported superiority of repair over replacement in terms of left ventricular function and hemodynamics.

In conclusion, functional mitral regurgitation commonly occurs in patients with severe left ventricular dysfunction regardless of etiology. Presence of even mild regurgitation has been associated with poor long-term prognosis. Early and intermediate results with implantation of an undersized flexible ring in the mitral annulus suggest that correction of functional regurgitation results in partial reversal of left ventricular remodeling and in symptomatic improvement. Intermediate results are superior to medical treatment alone and comparable to cardiac transplantation. The long-term benefit of this procedure remains to be demonstrated, and only randomized trials comparing optimal medical management with mitral valve surgery will ascertain the potential benefits of surgically attained mitral competence on the long-term outcomes of patients with dilated cardiomyopathies.

VENTRICULAR REMODELING THERAPIES

Several studies have documented that left ventricular volume is a sensitive prognostic parameter for both early and late mortal and morbid events after a myocardial infarction.20–23 The paradigm of progressive left ventricular dilatation is grossly oversimplified but simply understood through Laplace’s Law. Left ventricular wall stress/tension (d ) is proportional to the radius (r) and pressure (P) within the left ventricular chamber and inversely proportional to left ventricular wall thickness (T), with average wall stress estimated by the following equation: d = rP/(2)T. Whether approaching the concept from the level of the individual myocyte (tension-length) or from the level of the left ventricular chamber (pressure-volume), increasing cardiac myocyte stress becomes an impediment to effective contraction. Therefore, a solution is to reduce left ventricular chamber radius/volume and thereby reduce myocardial wall stress.

Surgical ventricular reconstruction (SVR) is by far the most extensively studied and applied technique for reshaping the dilated left ventricle. Its goal is to reduce left ventricular volume and create a more geometrically optimal chamber by excluding scar in either akinetic or dyskinetic antero-apical and septal segments. Unlike partial posterior left ventriculectomy or the Batista24 procedure, SVR attempts to directly address specific diseased areas of the left ventricle, most commonly the anterior apex. SVR reshapes the endoventricular contour by placing a patch, often at the level of a purse string suture that encircles the transition zone of myocardial asynergy (Fig. 15-1). The operation is accompanied by complete revascularization including a graft to the left anterior descending artery (to perfuse septal perforators and viable myocardium), and mitral valve repair or replacement as necessary. By grafting the left anterior descending artery, the high intraventricular septum is preserved, thereby enhancing postoperative circumferential shortening. The trade-off comes in the extent to which the longitudinal axis of the left ventricle can be reduced and is ultimately determined by the position of the new apex. In an attempt to avoid catastrophic postoperative restrictive ventricular physiology, Vincent Dor (who began performing the procedure in the early 1985) has recommended that ventricular sizing be routinely performed using a balloon sizer/shaper. Furthermore, it has been suggested that the purse string suture and patch be sutured at an oblique angle toward the aortic outflow tract while still excluding septal akinetic segments in order to prevent the creation of a “box-like” ventricle.

The validity of the SVR procedure was documented by the RESTORE group, an 11-center multinational group that evaluated the efficacy and durability of this procedure. In the most recent update from the group’s registry, the outcome of 1198 postinfarction patients was reported.25 Concomitant procedures included bypass grafting in 95%, mitral valve repair in 22%, and mitral valve replacement in 1%. Overall 30-day mortality was 5.3% and the need for perioperative mechanical support was uncommon (<9%). Global systolic function improved with an increase in EF from 29% ± 11% to 39% ± 12% and a reduction in left ventricular end-systolic volume index from 80 ± 51 mL/m2 to 57% ± 34% mL/m2. Overall 5-year survival was 69% ± 3%. Predictors of death were EF ≤30%, advanced NYHA class, age ≥75 years, and left ventricular end-systolic volume index ≥80 mL/m2. Remarkably, 5-year freedom from rehospitalization for HF was 78% and 85% of patients who were in NYHA Class I or II.

While the RESTORE group’s data are compelling, randomized evaluation of this procedure is absent, especially in comparison to coronary bypass surgery alone. To this end, the National Heart, Lung, and Blood Institute’s (NHLBI) multicenter, international, randomized Surgical Treatment for Ischemic Heart Failure (STICH) trial began enrolling patients with HF and CAD in the spring of 2002.26 The goal of this trial is to determine whether a benefit over medical therapy can be found for coronary revascularization in patients with multivessel coronary artery disease, LVEF ≤35%, HF, and no indication for bypass surgery (left main or unstable angina). In addition, STICH will examine whether any benefit from coronary bypass surgery can be enhanced by ventricular reconstruction surgery in patients with dilated ventricles. One major focus of the STICH trial will be to determine the long-term outcome and durability of SVR.

There is some evidence demonstrating further remodeling and left ventricular redilatation after SVR. Franco-Cereceda and colleagues noted that a cohort of patients who underwent SVR had indirect physiological evidence of progressive reductions in diastolic compliance.27 This yet to be understood phenomenon may be attributed to (1) progression of left ventricular myocyte hypertrophy and fibrosis;

(2) further progression of coronary artery disease; and/or (3) iatrogenic factors, namely, too aggressive a reduction in left ventricular volume at SVR, thereby creating a restrictive ventricular physiology that precludes adequate diastolic function.

It is likely, given the chronicity of disease prior to surgical therapy and the preexistence of remodeled remote myocardium, that, despite decreased systolic wall stress, there is not an adequate augmentation of diastolic elastance in some patients to allow for complete reversal or attenuation of continued left ventricular remodeling. The surgeon, though able to reduce left ventricular chamber size dramatically, does not reduce chamber volume back to normal values (normal left ventricular end-systolic volume index = 24 mL/m2 vs. RESTORE group postprocedure = 69 mL/m2). It is not surprising that improved survival rates and less physiological derangements are seen in those patients with better preoperative function, less left ventricular dilatation, and shorter delay to surgical therapy. Therefore the intrinsic properties within the chronically remodeled myocardium limit the surgeon’s ability to completely return chamber size (wall stress) to normal without risking too small a ventricle and compromised diastolic function.

One solution to the problem of chronicity is earlier identification of patients at risk for progressive dilatation and compromised function post myocardial infarction. Left ventricular dilatation generally follows global decreases in left ventricular function by up to several months and exercise challenge may be a predictor of those that will eventually develop left ventricular dilatation. If the promise of earlier intervention holds true, it may be possible to surgically exclude areas of asynergy prior to crossing the yet to be defined threshold of wall stress that inevitably leads to progressive and possibly irreversible ventricular remodeling, dilatation, and global left ventricular systolic dysfunction.

VENTRICULAR ASSIST DEVICES

Ventricular assist devices (VADs) are blood pumps used to support the failing heart in critically ill patients with end-stage HF. Whether placed intracorporeally or paracorporeally, these pumps take over the function of the damaged left (or right) ventricle and restore more normal hemodynamics and end-organ perfusion.28 Left ventricular assist devices, or LVADs, have been used in three clinical situations: (1) as bridge to transplantation in patients who are listed for transplantation but decompensate before a suitable donor heart becomes available, (2) as bridge to recovery in patients who are expected to recover left ventricular function (e.g., fulminant myocarditis), or (3) as permanent alternatives to transplantation in patients who are not considered to be candidates for transplantation.

Bridge to Transplantation

“Bridge to transplantation” is the most common indication for use of LVADs. Typical patients supported are those with large myocardial infarctions, those with myocarditis, and, most commonly, patients with chronic progressive end-stage HF.

It has been shown that patients bridged with an LVAD have excellent survival to transplantation and post-transplant survival equal to that seen with unsupported patients.29 Furthermore, because most LVADs are wearable, patients can be discharged home to recover and rehabilitate and hence can undergo cardiac transplantation in a more stable condition.30

The usual clinical scenario is that of a patient listed for transplantation who deteriorates clinically requiring inotropic and/or balloon pump support. As results are markedly better when mechanical support is instituted early, HF physicians now alert their surgical colleagues of patients who are demonstrating more subtle signs of deterioration including worsening urine output, more marked hyponatremia, need for escalation of diuretics, and/or the need to institute inotropic support.

Several devices have received approval by the U.S. Food and Drug Administration (FDA) for use as a bridge to cardiac transplantation. These include the HeartMate VE (Thoratec Corporation), the Thoratec paracorporeal (PVAD) and intracorporeal (IVAD), and the Novacor LVAS (WorldHeart Corporation). Three second-generation axial flow pumps (DeBakey VAD, HeartMate II, and Jarvik Flowmaker) are undergoing clinical trials for bridging to transplantation in the United States. Characteristics of devices currently available or in clinical trials in the United States are outlined in Table 15-5. In experienced centers, successful bridging to transplantation occurs for 70–80% of VAD recipients.

Left Ventricular Assist Devices as a Destination Therapy (Alternative to Transplant, Lifetime Support)

The Randomized Evaluation of Mechanical Assistance for the Treatment of Congestive Heart failure (REMATCH) trial sought to compare maximum medical therapy to implantation of the Thoratec HeartMate device for a group of extremely ill patients with end-stage heart disease who, by any account, were the sickest patients ever enrolled in a randomized HF trial.31 In this landmark NHLBI-supported trial, patients randomized to receive an LVAD benefited from improved survival and quality of life compared to the medically treated cohort. The trial highlighted the limitations associated with these large, pulsatile pumps including the high incidence of septic complications and their limited long-term reliability, thereby establishing benchmarks for the development of newer pump technologies. The positive results of this trial opened the doors to FDA and CMS approval and reimbursement of the Thoratec HeartMate XVE device as alternative to transplantation. Two second-generation miniaturized axial flow pumps (DeBakey VAD and HeartMate II) are currently undergoing randomized trials in the United States for the destination therapy indication.32 Regardless of indication, institution of mechanical support with a VAD(s) is associated with significant morbidity and mortality. This should not be unexpected as patients undergoing these procedures suffer from end-stage heart disease, are often supported with inotropic and pressor medications as well as intra-aortic balloon pumps, and carry other comorbidities associated with low-flow states.

The most common early complications of left VAD support are perioperative bleeding and right HF.33 The former occurs in close to 60% of VAD recipients (regardless of type of device used) and is a result of a large operation often associated with prolonged extracorporeal circulation and hypothermia. In addition to the expected perioperative coagulopathy and platelet dysfunction induced by cardiopulmonary bypass, the propensity for bleeding is further increased by (1) routine use of anticoagulants, antiplatelet drugs, and broad-spectrum antibiotics among these patients with advanced cardiac disease; (2) the malnourished state of many of these patients; and  (3) hepatic dysfunction associated with low-flow state and congestive hepatopathy from right HF.

Right HF occurs in approximately 30% of patients and is defined as the need for inotropic support for more than 2 weeks postoperatively or the need for institution of right heart support. The exact etiology of right HF following institution of LVAD support remains controversial. Late complications of VAD support vary among the different devices but involve issues of device-related infection and limited reliability.

HEART TRANSPLANTATION

Orthotopic replacement of the failing heart with a donor allograft remains the gold standard therapy for the treatment of end-stage heart disease. Indeed, cardiac transplantation is associated with unrivaled late survival and quality of life resulting from improvements in immunosuppression and in the prevention and treatment suppress of infection.34 Unfortunately, the number of donors has reached a plateau over the past few years, at a time when the number

of potential recipients has continued to grow. This critical discrepancy mandates that patients be strictly evaluated for candidacy for transplantation. This typically occurs during a multidisciplinary session where all clinical, psychological, and sociological aspects of each patient are discussed. In most centers, the minimum requirements for consideration for transplantation include (1) a history of repeated hospitalization for congestive HF, (2) escalation in the intensity of medical therapy, and (3) a reproducible of <14 mL/Kg/min. Unfortunately, many

VO2max

patients who meet the above criteria are excluded from transplantation because of the presence of absolute exclusionary criteria. These include (1) irreversible pulmonary hypertension (increased risk of right ventricular failure and death), and (2) active infection and malignancy. Several other relative contraindications exist and are weighed in when the final decision is made. These include advanced age (usually >65 years), presence of end-organ complication of diabetes, advanced restrictive or obstructive lung disease, advanced liver disease, renal insufficiency unrelated to low-flow state, significant peripheral vascular disease, morbid obesity, unstable social/family environment, demonstrable lack of compliance with medical/dietary therapy, active substance (alcohol, tobacco, or drug) abuse, and presence of a psychiatric disorder that would compromise adherence to medical therapy.

Patients on the waiting list are classified into one of three classes based on their clinical status, defined as follows: UNOS status 1A patients are those who have either been on mechanical circulatory support for <30 days, or have an intraaortic balloon pump, or are on high-dose inotropic agents with continuous hemodynamic monitoring, or are expected to live <1 week. Status 1B is assigned to those patients who have been on mechanical circulatory support for >30 days or are on continuous low-dose inotropic support (without hemodynamic monitoring) on an inpatient or outpatient basis. UNOS status 2 includes all other active patients on the waiting list, namely those who are homebound and on no mechanical or inotropic support; and UNOS status 7 are patients who have been placed on the list because they satisfied the criteria for listing but who were inactivated because of some recent medical condition.

Once a suitable heart donor is identified and the organ is allocated, a timetable is set and organized to keep the transportation time and cold ischemia time of the procured organ to a minimum. Implantation occurs almost exclusively in the orthotopic position. In most centers, bicaval (as opposed to biatrial) technique is preferred as the latter is associated with a higher incidence of postoperative arrhythmias and tricuspid valve dysfunction.

Survival following transplantation has continued to improve. At present, 1-year survival approaches 85%, 5-year survival is approximately 75%, and 50% of adult recipients will be alive for 10 years.35 Survival is best for patients (1) with congenital and dilated cardiomyopathies, (2) who are younger recipients, (3) who underwent transplantation since 1999, (4) with lower pulmonary vascular resistance, (5) who did not receive a VAD as a bridge to transplantation.

The most important dichotomous factors associated with 1-year mortality include congenital heart disease etiology, presence of temporary circulatory support, ventilator dependency, presence of renal failure requiring dialysis, hospitalization at the time of transplantation, donor history of cancer, a female recipient-to-male donor pairing, and cerebrovascular disease as the cause of donor death. Continuous factors associated with 1-year mortality include recipient age, recipient weight, donor age, donor/recipient weight ratio, transplant center volume, ischemia time and preoperative pulmonary artery diastolic pressure, bilirubin, and serum creatinine.

Functional status of transplant recipients is excellent on short- and long-term follow-up. Indeed, 80–85% of recipients have no activity limitations for up to 7 years following transplantation, and <5% require total assistance at any time. Cardiac transplant recipients benefit from freedom from rehospitalization that exceeds 70% for 7-year survivors.

Immunosuppressive strategies have evolved since the advent of cyclosporine in 1983. Approximately 46% of patients receive induction immunosuppression consisting of polyclonal globulin, OKT3, or interleukin-2R antagonist. Maintenance immunosuppression consists of a triple drug therapy that most often includes a calcineurin inhibitor (cyclosporine or tacrolimus), an antimetabolite (mycophenolate mofetil or azathioprine), and prednisone. In most centers, efforts are directed towards a progressive reduction of steroid therapy to minimal levels. Novel immunosuppressive agents including molecularly engineered humanized monoclonal antibodies are being evaluated in an effort to reduce the complications associated with the use of the traditional triple drug therapy.

The most common complications of transplantation include hypertension, renal dysfunction, hyperlipidemia, diabetes, and coronary artery vasculopathy. Malignancy is a well-recognized complication of prolonged immunosuppression and it is documented in 3%, 16%, and 26% of transplant recipients at 1, 5, and 8 years following transplantation. Cutaneous malignancies and lymphoma are by far the most commonly encountered. The latter often regresses with a reduction in immunosuppression.

Causes of death vary according to time after transplantation. The most common early (within 30 days) cause of death is primary allograft failure. Acute rejection, infection, coronary vasculopathy, and graft failure are the most commonly cited causes of death from 30 days to 3 years after transplantation. Malignancy and coronary vasculopathy are the predominant causes of death in long-term survivors.

SUMMARY

Despite tremendous advances in the medical management of congestive HF, the gold standard for the treatment of end-stage congestive HF remains cardiac transplantation. The acknowledged critical limitation of sufficient suitable organ donors has resulted in the refinement and development of novel surgical alternatives for the treatment of congestive HF. These approaches include the extension of current conventional cardiac operations such as mitral valve repair to the failing ventricle, surgically reconstructing the size and shape of the failing left ventricle in order to render it a more efficient pump, and partial replacement of the ventricle with a mechanical device. One day the continued evolution of such therapies is likely to have a significant epidemiologic impact on patients suffering from end-stage HF.

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