Surgical Treatment of Heart Failure

Octavio E. Pajaro, M.D., PhD, Cardiothoracic Surgery,
Mayo Clinic, Jacksonville, FL

 

Introduction

The term "heart failure" is used to describe a constellation of clinical signs, symptoms and diagnostic findings that represent a spectrum ranging from early myocardial dysfunction to frank pulmonary edema. In its early stages, heart failure may represent only myocardial dysfunction detected clinically as impaired left ventricular diastolic relaxation in asymptomatic1-5 individuals. In the basic science laboratory this may be measurable as impaired myocyte or sarcomere relaxation6. In its later clinical stages, heart failure represents the impaired ability of the right or left heart to maintain forward flow and ultimately presents as either right-sided failure with liver congestion, ascites, and peripheral edema or as left-sided failure with hypotension, renal failure and the gradual shut down of the periphery as organ perfusion is severely compromised. In the laboratory, this can be measured as impaired sarcomere shortening and depressed myocyte tension development for a given length. Thus, heart failure ultimately becomes a multisystem disease that initially began as a molecular and cellular cardiac myocyte abnormality. Despite the myriad complex and initially compensatory neurohumoral mechanisms and the cascade of biochemical and molecular events leading to myocyte and ventricular death 7, it is felt that this spiraling downhill process can be reversed if end organ perfusion can be restored, either pharmacologically or surgically. Naturally, it is an obvious idea to attempt to find a way to replace a failing heart with a mechanical device. However, attempts at treating heart failure with surgical therapy raise a multitude of questions and are not limited to replacement with mechanical devices. This article reviews the indications and surgical methods that have been used or are currently being investigated to treat myocardial dysfunction leading to clinical right or left heart failure.

When Should Surgical Intervention be Considered?

This question cannot be answered without taking into account the actual clinical scenario leading to chronic heart failure. The three most common etiologies leading to severe cardiac failure are ischemic heart disease, dilated cardiomyopathies and hypertensive cardiomyopathies 8. These scenarios generally lead predominantly to left ventricular failure but can produce right-sided failure either because the disease itself affects both right and left sides or because the progression of left-sided failure leads to right ventricular failure with or without the development of pulmonary hypertension. Surgical therapy for cardiac failure (of which most are generally used for left ventricular failure) include coronary revascularization, ventricular remodeling, repair of mitral valvular regurgitation, the use of skeletal muscle pumps as assist devices and mechanical devices. In order to evaluate patients for surgical intervention, several parameters are used to assess the severity of myocardial dysfunction, to assess the optimal timing for surgical intervention and to evaluate the efficacy of any treatment. These commonly used parameters are summarized below.

The New York Heart Association functional classification (NYHA) 9-14 is a clinically useful stratification of patients in heart failure that has been shown to correlate well with treatment efficacy. Patients are classified as class I if they have no physical limitations, class II if they have mild limitations with symptoms of fatigue, shortness of breath or angina with moderate exertion, class III if minimal exertion elicits symptoms, and class IV if they have symptoms at rest. This classification has proven useful as a guide for recommending surgery in various settings and, in some studies, has been shown to reflect that pathophysiologic mechanisms in heart failure as functional class may correlate with levels of natriuretic peptides presumably secreted as part of the compensatory mechanisms 15-20. Thus, it has become an investigational tool when stratifying patients for experimental treatments 21;22. For the surgeon, this classification provides a useful means of evaluating treatment efficacy.

Noninvasive measurements (parameters primarily derived from echocardiography), while certainly inherently limited by loading conditions, are useful markers of left ventricular dysfunction. Left ventricular ejection fraction (the percentage of blood ejected by the ventricle with each contraction) is the most often measured parameter and, in the proper clinical scenario, is a rough estimate of how well a ventricle can contract. However, in certain situations this measurement can be misleading. In patients with significant mitral regurgitation the ventricle is able to eject against a decreased load toward the left atrium. Thus, the measured ejection fraction does not reflect the degree of myocardial dysfunction that is unveiled at the time of mitral valve repair or replacement. Measurement of left ventricular ejection fraction does not give any indication as to the ability of the ventricle to recover after removal of a given loading condition, but does appear to correlate with the degree of stimulation of compensatory neurohumoral mechanisms 21;22. Left ventricular ejection fraction is not helpful in deciding the need for, nor the timing of, cardiac replacement or mechanical support, but is used in the evaluation of treatments in which surgically produced ventricular remodeling is attempted.

Left ventricular dimensions at end-diastole and end-systole are useful indicators of the state of the ventricle. Serial measurements are useful in following the progression of cardiac failure, especially when associated with valvular abnormalities. Regional wall motion abnormalities are useful when assessing ventricular aneurysms and areas of ischemia or infarction. Left ventricular dimension measurements are an essential part of evaluating surgical procedures involving ventricular remodeling.

Invasive measurements as derived from right-heart catheterization data are useful in both the acute and chronic setting. Measurements of cardiac index, pulmonary artery pressures, left atrial and right atrial pressures, and systemic vascular resistance provide key information in deciding the proper timing and the method of intervention. In left ventricular failure, elevated left atrial pressures greater than 20mmHg, a cardiac index less than 2.0l/min/m2, and clinical signs of pulmonary edema and peripheral organ hypoperfusion despite aggressive medical therapy are indications for surgical intervention. Elevated right atrial pressures greater than 20mmHg and clinical evidence of liver congestion, ascites, and peripheral edema in the setting of aggressive support of left ventricular function may indicate the need for surgical intervention to support the right heart. Right-sided pressures and estimates of pulmonary vascular resistance may also determine the type of surgical intervention offered. Severely increased pulmonary vascular resistance, as measured by the difference between the mean pulmonary artery pressure and the pulmonary artery wedge pressure divided by the cardiac output (Wood units (mmHg/l/min)), will exclude heart transplantation or indicate the high-risk nature of the procedure. In general, a pulmonary vascular resistance greater than 4 Wood units increases the likelihood of right heart dysfunction or failure in a transplanted heart, and vascular resistance greater than 6-8 Wood units with pulmonary vasodilator therapy generally indicates that heart transplantation alone will be unsuccessful.

One of the most useful measurements in the evaluation of patients with cardiac failure has been the development of the concept of maximal exercise oxygen consumption (VO2 (ml/kg/min)). This measurement has allowed us to quantify the functional disability of patients in heart failure and currently provides the most helpful prognostic indicator 23. Patients who, despite poor left ventricular ejection fractions, have a VO2 maximum greater than 18ml/kg/min have a good prognosis and can generally postpone surgical interventions. A VO2 maximum of less than 12ml/kg/min carries a poor prognosis. The prognosis for the intermediate group is less clear.

Coronary Artery Bypass and its Role in Ischemic Heart Failure

Currently, the most common cause of clinical heart failure is left ventricular dysfunction resulting from ischemic heart disease 8;24. As such, the most common surgical intervention is coronary revascularization. In most cases in which patients present with ischemic dysfunction, revascularization of viable but ischemic myocardium leads to improvement in cardiac function. The most important preoperative question that needs to be answered in this scenario is "will revascularization lead to recovery of ventricular function?" *To determine the answer to this question, one must identify the extent of myocardial injury from previous infarctions and the amount of viable myocardium available. The amount of reversibly injured myocardium will determine the likelihood of improved ventricular function following revascularization. An estimate of the amount of viable myocardium can be obtained by various perfusion studies (single photon emission computed tomography studies (SPECT), positron emission tomography (PET) studies, dobutamine stress echocardiography, and dobutamine magnetic resonance imaging studies 24). In order for surgical revascularization to provide a potential benefit, the viability studies should indicate that at least 20% or more of the total left ventricular volume is ischemic but not irreversibly damaged 24. If not, the patient should be evaluated for medical or alternative surgical therapies.

Surgical Remodeling of the Left Ventricle

The concept of surgical intervention to reshape the left ventricle originates from various observations. First, patients suffering large transmural myocardial infarctions can go on to develop ventricular aneurysms. These areas of the ventricular wall are nonfunctional segments of scarred ventricular muscle and can become foci for the development of cardiac arrhythmias and intramural thrombi. Ventricular aneurysms can produce symptoms similar to angina and can cause obvious impairment of ventricular function by impeding mitral valve motion, resulting in mitral valve regurgitation. Repair of these aneurysms has been known for many years to lead to functional and symptomatic improvement 25,26. Second, previous studies of cardiac structure and function in the 1960s and 70s showed clearly that left ventricular dilatation, while appearing to be an initially compensatory mechanism, actually produces increased tension on each myocardial fiber and increases the energy demand of the ventricle, thus decreasing the efficiency of  the ventricle as a pump. These ideas were based somewhat on the view that the ventricle could be modeled as a sphere. The Law of Laplace dictates that the tension on the wall of a sphere is determined by the internal pressure, the radius of the sphere and the thickness of the wall. The tension (T) that each myofiber needs to generate is directly proportional to the intracavitary pressure (P) and the radius of the sphere (r) and is inversely proportional to the thickness of the sphere (th).

= P*r/ 2*th

Thus, by this simple model, decreasing the ventricular radius may decrease myocardial energy consumption and provide the ventricle with more mechanical advantage.

Some of the limitations of this model are immediately evident. One, the heart is not a sphere. The three-dimensional structure of the myocardial fiber lattice 27 indicates that the actual tension generated by each fiber is not appropriately modeled by assuming that all fibers are oriented in a circular fashion. Two, simply cutting the dysfunctional myocardium does not restore the ultrastructural design of the ventricle as described by Streeter many years ago 28;29. Third, evaluating the results by determining ejection fraction before and after surgical intervention loses sight of the fact that the actual goal of any intervention for heart failure is to improve cardiac output and end-organ perfusion. Since the ventricular end-diastolic volume (EDV) is automatically reduced by this method, ejection fraction (EF) will increase with no improvement in stroke volume.

EF = SV/EDV

Fourth, there is no way to predict how much gain in cardiac output may be obtained, if any, for a given surgical intervention. Fifth, this model ignores the fact that ventricular failure results from actual molecular events occurring in the cardiac myocyte, thus if any benefit is derived, it would be expected to be short-lived. Despite these immediately obvious limitations, surgical attempts at remodeling the ventricle have provided some benefits for a select number of patients. However, the evidence that this approach can be successful leads one to believe that a better understanding of the mechanisms by which some of the surgical techniques improve ventricular function may lead to better patient selection, better prediction of the true benefit that each patient may expect to receive, and simpler techniques to guarantee success. The following section reviews the more common procedures.

Ventricular Aneurysmectomy and the "Dor Procedure"

Aneurysm surgery has been known to be beneficial for quite some time 30. Early studies demonstrated that excision of scarred myocardium could improve long-term survival, symptoms and ventricular function. However, results with the original linear repair techniques were inconsistent 31. As a result of these inconsistent findings and in light of the geometric considerations discussed above, surgeons have looked for ways to preserve left ventricular shape with the hope of improving or at least preserving function 32. Dor introduced the technique known as endoventricular circular patch plasty, which avoided the alteration in ventricular shape produced by simple linear closure. The original linear resection involved scar excision leaving a rim to sew directly to and allow closure in a straightforward linear manner. The technique proposed by Dor uses a patch in order to preserve the shape of the ventricular wall after scar excision. Several studies have shown more consistent improvement in survival, ventricular function and symptoms with the "Dor Porcedure" 26;33. The mechanisms by which anterior aneurysmectomy excision confer benefit to patients have still to be completely elucidated. Certainly, there is benefit to removal of thrombogenic and arrhythmogenic myocardium 34. Yet concepts based on a simple application of Laplace's Law do not explain why the "Dor Procedure" should confer any advantage over linear closure. Some intriguing mechanisms have been brought forth. Fantini et al. (1999) 35 have proposed that maintaining the ventricular geometry with patch closure allows the remaining nonischemic myocardial fibers to gain some mechanical advantage through alterations in loading conditions and ventricular pressure waveform, resulting in improved ventriculoarterial coupling. No actual improvement in contractility is demonstrated. Hadland et al. (1997) 36 developed an experimental model that makes an important distinction between a dyskinetic and an akinetic aneurysm. An akinetic aneurysm does not produce a mechanical disadvantage, while a dyskinetic aneurysm will produce a loss of energy by allowing contraction to fill or distort the aneurysmal sac. In light of the improvements noted in aneurysmal scar excisions, others have proposed that large areas of wall motion abnormalities in patients with ischemic disease should be treated in a manner similar to those with definitive transmural scars 37. Mickleborough and others have proposed an expanded definition of a ventricular aneurysm not limited to areas of scarred myocardium and suggest that operative intervention should be offered prior to the development of severe failure 38.

The "Batista" Operation

A natural progression of the above rationale led Batista to hypothesize that patients with large dilated ventricles (end-diastolic dimensions greater than 65mm) might benefit from partial ventriculectomy39;40. The group of patients considered for this intervention had global left ventricular dysfunction and, as a result of the extreme dilatation, severe mitral regurgitation. The operation involves resecting a portion of the left ventricle between the papillary muscles with repair, replacement or preservation of the mitral valve. This operation received much media coverage and was transiently advertised as the operation to replace heart transplantation. A large experience was obtained at the Cleveland Clinic and, recently, 41 review of their data has confirmed that not enough lasting benefit has been obtained to recommend wide use of this technique. As predicted earlier, heart failure returns in the majority. By three years, 75% of the patients who had had some benefit, developed recurrent NYHA class IV symptoms, required transplantation, or died. 42

Surgery for Mitral Regurgitation in Patients
with Severe Left Ventricular Dysfunction

The experience with partial ventriculectomy raises the question of the significance of correcting the mitral valve regurgitation. Repairing the severe mitral valve regurgitation alone in patients with end-stage ventricular dysfunction may provide mechanical advantage as well as chronic volume unloading, allowing the ventricle to work at smaller end-diastolic volumes. Bolling 43 has had intermediate results at 1 and 2 years comparable with partial ventriculectomy. 44 This area still requires further investigation.

Skeletal Muscle Pumps

The use of skeletal muscle to provide ventricular support is an exciting idea. Various approaches have been tried and suggested. The basic approaches are as follows: One, cardiomyoplasty, the use of skeletal muscle for ventricular augmentation by wrapping the ventricle; two, aortomyoplasty, the use of skeletal muscle as a counterpulsation technique; three, the use of skeletal muscle as a ventricle; and four, the use of skeletal muscle as a power source for an assist device. The immediate benefits would be several. Using skeletal muscle may avoid the use of  foreign tissue and thus eliminate the need for immunosuppression. Furthermore, the difficulty of implanting long-term power supplies needed for mechanical support would be replaced by less energy-demanding muscle stimulators and pacers. Early studies in the 1960s attempted to use a hemidiaphragm as a cardiomyoplasty technique 45. Little was known at that time about some of the essential differences between skeletal and cardiac muscle. Skeletal muscle is limited without preconditioning to fatigue and does not exhibit the "all or none" properties typical of cardiac muscle. Skeletal muscle requires appropriate stimulation to produce a maximal contraction. This early experience highlighted the many differences between skeletal and cardiac muscle physiology. The use of a hemidiaphragm would be difficult to justify as most patients are tenuous and may not tolerate the decreased respiratory drive. Carpentier et al. (1985) 46 has investigated extensively the possibility of transferring cardiac muscle properties to skeletal muscle and specifically looked at the latissimus dorsi muscle. His group and others47 have looked extensively at the ability to overcome the fatigability of skeletal muscle and have investigated the use of skeletal muscle as a cardiac assist (cardiomyoplasty)48-50, as a counterpulsation aortomyoplasty51 and as a neoventricle.52-55 Clinical data with cardiomyoplasty techniques have been inconsistent between centers, but this may reflect limited experience at many centers. Aortomyoplasty and the creation of a neoventricle is primarily in the laboratory stages, although limited clinical worldwide data is encouraging. All three techniques offer hope as simpler and more cost-effective surgical ways of treating end-stage heart failure. Some laboratory data and no clinical data are available in the use of the skeletal muscle as a power source for an assist device. Research continues in this area.56;57

Mechanical Circulatory Support

The use of mechanical circulatory assist has always been an area of general excitement for the media and lay public. This subject elicits images and dreams of highly sophisticated, completely internal pumps replacing a patient's dying heart and makes one recall the days of Barney Clark and the enormous console he was attached to for many days. However, mechanical circulatory support includes a variety of devices and is used to accomplish different goals.

Patients require either short-term support or chronic long-term support. Patients requiring acute support are those who may have suffered an acute cardiac event such as a myocardial infarction, an acute myocarditis, or who have had difficulty coming off cardiopulmonary bypass after open heart surgery. These patients may need left or right heart support for less than a week to 10 days. Patients requiring long-term support are suffering from chronic heart failure and will clearly not survive until a heart becomes available for transplantation. Thus, the currently accepted use of long-term support is as a "bridge to transplant." No device has, as of yet, been approved for end-therapy. Devices are specifically designed for either short-term or long-term support and thus have different strengths and weaknesses in different clinical scenarios. These devices are referred to as LVADs or RVADs based on whether they are used to support the left (left ventricular assist device) or right heart. They do not require oxygenators as they either drain blood from the right atrium or ventricle (RVAD) and pump into the pulmonary artery, or from the left atrium or ventricle (LVAD) and pump into the aorta. When used to support the left and right simultaneously, they are referred to as BiVADs (biventricular). These devices are not helpful in the setting of acute lung injury and inability to oxygenate. Extracorporeal membrane oxygenation (ECMO) is needed in those patients and, in concept, is a form of cardiopulmonary bypass with an oxygenator that can be used for several days.

Short-Term Support

The most commonly used cardiac assist device is the intra-aortic balloon pump. This device is a balloon that inflates and deflates at a specified rate that is determined by the electrocardiogram or the arterial blood pressure waveform. The balloon is programmed to provide counterpulsation, thus, the balloon inflates during diastole to aid coronary flow and deflates during systole to decrease the workload on the ventricle. The overall effect is to decrease the peak systolic pressure generated by the ventricle and increase the diastolic coronary artery perfusion pressure. This relatively simple device highlights the importance of the interaction between the heart and the peripheral arterial circulation and demonstrates how changes in the characteristics of the arterial tree can improve cardiac output. The balloon pump was first used clinically in the late 1960s58 and has the benefit of being easily placed percutaneously via the femoral arteries. It can be placed at the bedside or catheterization laboratory with the position confirmed by x-ray. It can also be placed by the surgeon directly into the thoracic aorta in patients with severe peripheral vascular disease. Its main drawbacks are the inability to increase overall peripheral perfusion by more than 10-15%, and the risk of limb ischemia caused by the catheter and sheath obstructing blood flow to an extremity. Though widely used in the acute setting, it is not helpful with chronically ill patients awaiting transplant.

The most common acute setting in which the surgeon will need to offer a patient short-term support is post-cardiotomy ventricular failure. The decision of when to insert a device can vary from one center to another, but needs to be based on a definition of what constitutes maximal medical support. A patient on several inotropic agents and an intra-aortic balloon pump needs to be considered for mechanical circulatory support in order to assure adequate end-organ perfusion, not necessarily provided by an adequate systemic pressure.

Until recently, non-pulsatile centrifugal pumps were the most widely available temporary support devices. The advantages of these pumps are their ease of surgical implantation and of use in the intensive care unit. However, these devices require immediate anti-coagulation, can cause severe hemolysis over several days, and require a cardiac perfusionist available on site at all times. In addition, patients on this device require continued ventilator support, sedation and bedrest. More recently, a simple device made by Abiomed, the BVS-5000,59 allows for short-term pulsatile support. This device uses cannulas to drain blood from the atrium or ventricle and synthetic grafts sewn onto the aorta or pulmonary artery to provide outflow. The blood drains by gravity into two flexible reservoirs in series contained in rigid compartments. Filling of the second reservoir triggers a CO2 pump that fills the rigid compartment and thus compresses the flexible reservoir. One-way valves control the direction of blood flow. The advantages to this device are several, including its ease of implantation. Anticoagulation can be reversed in the first 12 hours, thus bleeding can be controlled prior to transfer out of the operating room. A cardiac perfusionist is not required and the device can be managed by the intensive care unit nurses. Patients can be extubated and some can be mobilized and exercised. However, doing so is awkward with this device and not often feasible. The Abiomed BVS-5000 can be used by non-transplant centers and allows for easy transport of patients to a transplant center. It is not ideal for long-term support. If long-term support will be clearly needed then a different device should be considered.

Bridge to Transplant

Various ventricular assist devices are available for long-term use. The Thoratec system, the Heartmate and the Novacor have been the most widely used. All are based on a system of drainage cannulas and outflow grafts, and a pulsatile pump that lies internally in the abdomen (Heartmate and Novacor) or extracorporeally (Thoratec). They differ in the mechanical details of the pumps, the power source and the blood-device interface. All parts of the Heartmate and Novacor are internalized except for the drive lines that traverse the skin. Patients cannot be smaller than 1.5m2 as the pumps are too large. Thus, these pumps are not useful in small adults or in pediatric heart failure. However, since these pumps are completely internalized except for the drive-lines, patients are able to be discharged from the hospital after they have been completely rehabilitated. The appropriate outpatient support systems must be in place to make this feasible. The Thoratec uses extracorporeal pumps, thus the inflow and outflow cannulas draining and delivering blood must traverse the skin. This system allows for a wider use in patients of differing sizes and also allows for RVAD or BiVAD support. However, these patients cannot be discharged from the hospital until after transplantation.

More interest has grown over the last few years in non-pulsatile cardiac assist devices. Investigators have debated for many years the physiologic consequences of non-pulsatile versus pulsatile devices.60 Clearly, the natural biology would seem to dictate that an advantage must exist in pulsatile flow. Pulsatile flow is a natural consequence of the very nature of sarcomere shortening and relengthening. An immediate efficient system is created whereby a pulsatile heart ejects into a compliant arterial tree which, by its elastic properties, helps propel blood forward even after the aortic valve has closed. The renewed interest stems from major advantages over non-pulsatile pumps, including the smaller size required for the device, the elimination of the need for valves, and the energy needed to power the device.61;62 These devices rely on a rotating or centrifugal system to propel the blood. Since they do not require a capacitance chamber, they can be significantly smaller than standard pulsatile implantable devices. They do not necessarily dictate that there will be no pulsatility in the vascular system since, by maintaining the recipient heart in situ, some pulsatile flow can continue. One such device, the continuous-flow DeBakey VAD (weighing only 93 grams) has been used successfully in patients and has sparked much excitement.62 The use of continuous-flow pumps leads one to regain interest in the concept of "bridge to recovery." No significant recovery has ever been obtained in patients with chronic heart failure. By unloading the ventricle, these devices may allow for remodeling and healing. By being small, they are more easily considered for use as end therapy and are more likely to be considered in patients who would otherwise not be considered for transplantation.

Totally Implantable Mechanical Hearts

Ultimately, the goal is to design a device that is completely implantable, with no cables or cannulas traversing
the skin. Clearly, no device will ever be considered as end-therapy if this is not the case and even as a "bridge to transplant," such a device would provide significant improvement in quality of life and decreased infection rate. One such device has been in the media recently and is showing compelling promise, the Abiocor, developed by ABIOMED, inc.63 The Abiocor is a completely implantable pulsatile device that replaces the recipient right and left heart. The recipient heart is excised and the artificial one sewn in its place. No cables or cannulas traverse the skin and power is provided by a wireless transcutaneous system. Animal studies and the initial clinical results are encouraging. Although not advertised in the media as such, this device offers the possibility of becoming an end therapy. The ultimate64;65 test of this device and all future devices will rest on the ability to minimize cerebrovascular accidents, infections and mechanical failures.

Heart Transplantation

Heart transplantation is undoubtedly the best long-term solution available for patients in chronic heart failure. As of the year 2000, a total of 57,818 heart transplants had been entered in the registry of the International Society of Heart and Lung Transplantation worldwide since 1982.8 It is well known that the first human-to-human heart transplant was performed in 1967 by Professor Christian Barnard in Cape Town, South Africa. However, not until the clinical use of cyclosporin in the early 1980s did heart transplantation become a clinically viable alternative. The one-year survival is currently 80%, with a 10-year survival of approximately 50% overall for all patients since 1982. However, if one compares 5-year survival from the years between1980-1987 with the years since 1987, there has been significant increased survival from 60% to almost 70%.8 The major indications for adult heart transplantation are ischemic heart disease and cardiomyopathy. The development of cardiac graft vasculopathy remains as the major long-term morbidity determining graft survival. The causes of graft vasculopathy are not well understood but several immune and non-immune mechansisms are implicated.66 Clearly, a history of coronary artery disease in the recipient is a key risk factor. The limited donor supply remains as the primary factor preventing many from being able to receive a transplant.

Conclusions

Heart failure is a global health problem representing a major emotional and financial burden on society. Treatments include several medical and surgical options to improve the quality of life and survival of patients suffering from heart failure. The continued investigation of the many possible therapies will help tailor appropriate treatment to the needs of the patient. All hospitals performing open heart surgery need to be able to provide a form of acute support for a failing heart in order to allow time for the heart to recover or to transfer the patient to a transplant center. Heart transplantation remains the best alternative for some patients with end-stage heart disease. Currently, mechanical circulatory assist offers methods to bridge patients for transplant who would otherwise die on the waiting list. Soon, mechanical support may offer end therapy without the need to go on to transplantation. The use of skeletal muscle as a pump or as a cardiac assist and the use of surgical revascularization, remodeling and mitral valve repair may offer less expensive alternatives eliminating the need for large power supplies and immunosuppression.

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  • For an excellent review of this topic see Vol 43, No. 5 of Progress in Cardiovascular Diseases, March/April 2001.
Jacksonville Medicine / February, 2002

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