New Approaches to the Surgical Treatment of End-Stage Heart Failure

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Chapter 21 New Approaches to the Surgical Treatment of End-Stage Heart Failure

According to the American Heart Association, there are approximately 6–7 million people in the United States with congestive heart failure (HF). Available statistics indicate that the incidence of HF in the population approaches 10 per 1000 after age 65, with 550,000 new cases each year. Heart failure (HF) is the leading cause of hospitalization in patients older than age 65, with a reported associated cost of $24 to $50 billion annually. On a global scale, HF reportedly affects 0.4% to 2.0% of the adult population.1

Despite great advances in the understanding of the pathophysiology of HF and the development of medications that can potentially attenuate the progression of that pathophysiology, morbidity and mortality from this disease remain very high. The incidence of hospitalization for HF rose by 70% during the 1990s, and patients with New York Heart Association (NYHA) class IV symptoms currently have a reported 1-year mortality rate of 30% to 50%. By comparison, the corresponding rates for NYHA class I-II patients and class II-III patients are 5% and 10% to 15%, respectively. Thus, one of the major goals in the management of HF is the prevention of progression to advanced stages.

While many patients successfully achieve temporary relief of HF symptoms with medical management, the underlying pathophysiology inevitably progresses and pharmacologic interventions alone will eventually become inadequate in the vast majority. A variety of surgical procedures can be performed to improve cardiac function and potentially arrest (or even reverse) the progression to severe dysfunction, but until very recently, surgical intervention (short of transplantation or placement of a ventricular assist device) was considered contraindicated in patients with advanced HF. Surprisingly good outcomes with “corrective” interventions, however, have now resulted in patients presenting for surgical treatment of their HF on a regular basis.2,3

SURGICAL OPTIONS FOR HEART FAILURE

A growing number of surgical procedures exist (or have been developed) to relieve HF symptoms and arrest the progression of the disease through correction of abnormal myocardial depolarization, enhancement of myocardial blood supply, improvement in ventricular loading conditions, and restoration of more normal ventricular geometry. Box 21-1 provides a list of current surgical interventions for HF.

Cumulative worldwide experience with such interventions thus far suggests that these procedures not only relieve symptoms but may also attenuate or possibly arrest the progressive myocardial remodeling that accompanies chronic HF. In some cases, partial reversal of the adverse myocardial remodeling has been demonstrated and combination therapy (surgical intervention with targeted pharmacologic treatment) intended to enhance reverse remodeling is actively being investigated.4

Thus, interventions previously considered contraindicated by low ejection fraction (EF) are now being used precisely for that indication. It remains to be determined, however, which procedures will ultimately benefit which subpopulations of HF patients. Despite the common final pathway that leads to dilated pathophysiology seen in the majority of these patients, an individual’s initial underlying etiology may again become an important consideration as these procedures are used earlier and earlier in the course of deterioration as a treatment intended to halt the progression of the disease.

REVASCULARIZATION

Coronary artery disease has become the most common etiology of HF. Of those patients currently listed for heart transplantation, 39% carry a primary diagnosis of ischemic heart disease.

Where viable myocardium and feasible targets exist, revascularization of chronically ischemic, hibernating myocardium can improve ventricular function, downgrade NYHA functional class, and improve prognosis. While the primary benefit of revascularization appears to be functional improvement of the LV, reducing ischemic substrate for arrhythmias and retarding adverse myocardial remodeling are important secondary benefits.

Despite an increased perioperative risk of morbidity and mortality in this population, the world’s literature reports current survival between 57% and 75% at 5 years with in-hospital mortality between 1.7% and 11%. A recent review reported an 83.5% survival at 2 years after revascularization compared with only 57.2% survival in patients with congestive heart failure (CHF) who were not revascularized.5 In general, morbidity and mortality tend to correlate inversely with EF and directly with NYHA functional class. Additional factors predisposing patients to higher morbidity and mortality include advanced age, female sex, hypertension, diabetes, and emergent operations. The decreases in morbidity and mortality after revascularization in this high-risk population in recent years are at least partially attributable to improvements in surgical technique and myocardial protection, but the concurrent performance of mitral valve repair and ventricular reshaping address the adverse ventricular loading conditions present and may also contribute to improved outcomes. The results of ongoing clinical trials evaluating combinations of surgical procedures (e.g., revascularization plus ventricular reshaping versus revascularization alone) are eagerly awaited.

The importance of determining the viability of myocardium in the area to be revascularized cannot be understated because the potential for recovery of function depends on residual contractile reserve, integrity of the sarcolemma, and metabolically preserved cellular function. Methods to detect viable myocardium include dobutamine echocardiography, single-photon emission computed tomography (SPECT), and positron-emission tomography (PET). While dobutamine stress echocardiography has often been shown to have the highest predictive accuracy, there are important limitations that need to be taken into account. Dobutamine stress echocardiography, for example, can have false-negative results if there is loss of contractile proteins in the presence of preserved function of the muscle fiber membrane.

CORRECTION OF MITRAL REGURGITATION

Mitral regurgitation (MR) may result from several different pathophysiologic states (e.g., leaflet prolapse, annular dilation, leaflet perforation), but the MR seen in patients with HF is most often functional, owing primarily to restriction of leaflet motion with subsequent limitation of leaflet coaptation because the papillary muscles are tethered by the dilated LV.

Historically, many physicians considered MR advantageous for the failing LV. It was believed that a low-pressure atrial “pop off” allowed the failing ventricle to protect itself from the high afterload of the systemic circulation and gave the illusion that the heart had a better overall contractile state than really existed. This misconception was “supported” by the fact that surgical replacement of the mitral valve was associated with a very high mortality rate in patients with depressed LV function. It is now known, however, that mitral valve replacement or repair can improve overall cardiac performance by eliminating the increased myocardial oxygen demand that accompanies the progressive pressure and volume overload due to MR.

Despite the slightly increased operative risk, the current literature supports mitral valve repair or replacement as beneficial to patients with severely depressed LV function, HF, and MR. In a recent series, Romano and Bolling reported operative mortality of 5% with 1- and 2-year survival rates of 80% and 70%, respectively.6 Not only was long-term mortality reduced, but the increase in LV systolic function (on average by 10%) enabled a downgrading of NYHA class and resulted in an improved quality of life. It has been shown that 1-, 2-, and 5-year survival rates of 91%, 84%, and 77%, respectively, can be obtained in patients with LVEF less than 30%. In addition, the rate of re-hospitalization for HF was decreased during the period of follow-up compared with a cohort that did not receive a mitral repair. Thus, both medical and economic benefits may result from mitral valve repair in this population.

While the majority of end-stage HF patients will exhibit functional MR, there may be additional concurrent valvular pathology present in a given patient. An intraoperative transesophageal echocardiography (TEE) evaluation of the valvular anatomy, the mechanism of the MR, and direct surgical inspection will determine the feasibility of repair. It is generally believed that valve repair is preferable to valve replacement, because there are demonstrated hemodynamic advantages associated with preservation of the subvalvular apparatus7 and long-term anticoagulation is not required.

LEFT VENTRICULAR RESHAPING

In 1996, Batista introduced the concept of surgically reshaping the dilated and failing LV of NYHA class IV patients to improve systolic performance. In the Batista procedure, resection of a wedge of normal myocardium from the LV apex to the base (laterally, between the papillary muscles) restored more normal ventricular geometry and decreased wall tension. Functional MR was also addressed during the Batista procedure by a valve replacement or repair. While many patients did benefit initially from this procedure (reduction of NYHA functional class to NYHA I in 57% and NYHA II in 33.3%), perioperative mortality was high (>20% in both Batista’s own series and in the large Cleveland Clinic experience). Additionally, the experience of several centers was that many patients required rescue mechanical circulatory assistance after the procedure and many patients experienced a re-dilation of their LV, resulting in a return to NYHA class IV status. Thus, despite a short-lived period of initial enthusiasm in the 1990s, the Batista procedure has essentially been abandoned. The concept of ventricular reshaping, however, remains of interest.

The modified Dor procedure (endoventricular circular patch plasty) is successfully used to reshape the dilated, spherical LV of patients who have had an anterior wall myocardial infarction with resulting aneurysm and akinesis/dyskinesis. Essentially, a Dacron patch is placed within the LV cavity so as to exclude the large akinetic/dyskinetic area of the anterior wall. This restores LV geometry to a more normal elliptical shape and improves systolic function. When performed concurrently with coronary artery bypass grafting (CABG), significant early and late improvements in both NYHA functional class and EF have been demonstrated with an in-hospital mortality rate of 12%. A trial of 439 patients undergoing this procedure found an improved in-hospital mortality of 6.6% and an 18-month survival of 89.2%. In this series, CABG was performed concurrently in 89%, mitral valve repair in 22%, and mitral valve replacement in 4%.8

PROCEDURES TO ARREST THE DILATION OF THE FAILING VENTRICLE

The intent of extrinsic constraint is to arrest the progressive dilation of the failing ventricle. Decreasing the radius of the LV will reduce wall tension (Laplace’s law), which will decrease myocardial oxygen demand. In addition, this may result in improved systolic and diastolic function, as well as subjective improvements in functional capacity. This type of ventricular reshaping can be accomplished with biological tissues and devices applied to the external surface of the heart.

Acorn CorCap Cardiac Support Device

The CorCap Cardiac Support Device (Acorn Cardiovascular, Inc., Minneapolis, MN) is an investigational mesh fabric that is surgically wrapped around the heart in an attempt to prevent further dilation. This device has been shown in animal models to reduce wall stress, myocyte hypertrophy, and myocardial fibrosis. A global multicenter study by Oz and coworkers9 showed promising results. There were significant reductions in LV end-diastolic dimensions, MR grade, and NYHA classification in patients 12 months after CorCap implantation. At the same time, a significant improvement was seen in LVEF and quality of life. Ongoing randomized clinical trials in Europe and the United States will further address the safety of implantation of the CorCap device and ultimate outcomes.

CARDIAC RESYNCHRONIZATION THERAPY AND IMPLANTABLE CARDIOVERTER-DEFIBRILLATORS

The progression of disease resulting in advanced cardiac failure is typically accompanied by conduction defects and arrhythmias, and pacemakers and implantable cardioverter-defibrillators (ICDs) are commonly used in this population. In addition to the well-known defects in sinus or atrioventricular node function, intraventricular conduction defects delay the onset of RV or LV systole in 30% to 50% of patients with advanced HF.10 This lack of coordination of LV and RV contractions further impairs CO and has been reported to increase the risk of death in this population.

Cardiac resynchronization therapy (CRT) entails biventricular pacing to optimize the timing of RV and LV contractions. The right atrium (RA) is paced by a lead in the RA, the RV by a lead in the RV, and the LV by a lead in a coronary vein (accessed via the coronary sinus). While CRT is more an interventional cardiology procedure than a surgical procedure per se, anesthesiologists are frequently asked to provide sedation (if not general anesthesia) for these sometimes lengthy implantation procedures.

Studies have shown that atrial-synchronized biventricular pacing (pacing the LV and RV in a carefully timed manner) can “resynchronize” RV and LV contraction, improving CO and overall hemodynamics. This enhances these patients’ ability to exercise (which improves their NYHA functional class) and decreases the length and frequency of their hospitalizations, which improves their quality of life.11

Sudden death from ventricular fibrillation (VF) accounts for approximately 300,000 deaths annually in the United States. Patients with advanced HF experience VF with a frequency 6 to 9 times that of the general population, and VF causes 40% of all deaths in this population even in the absence of apparent disease progression based on symptoms. Thus, ICDs are commonly indicated for patients with advanced cardiac failure. An ICD is a device capable of arrhythmia detection and automatic defibrillation. ICDs successfully terminate VF in greater than 98% of episodes, and studies have demonstrated that an ICD increases survival and decreases the risk of sudden death in patients with ischemic cardiomyopathy and decreased LV function.12

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