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Keywords:

  • Cardiovascular physiology;
  • Heart failure;
  • Transplant;
  • Ventricular assist devices

Abstract

  1. Top of page
  2. Abstract
  3. Introduction
  4. Background
  5. Types of LVADs
  6. Bridge to Transplantation
  7. Destination Therapy
  8. Bridge to Recovery
  9. Adverse Events
  10. Management of Acute Complications
  11. Cost-Effectiveness of LVAD Support
  12. Future Directions
  13. Conclusion
  14. Conflict of Interest
  15. References

Ventricular assist devices are an important therapeutic option for advanced congestive heart failure. A left ventricular assist device (LVAD) can be implanted as a bridge to transplantation or for the purpose of destination therapy. LVADs improve end-organ function and reduce morbidity and mortality in appropriately selected patients. The development of axial flow pumps has overcome many of the limitations of the first-generation pulsatile flow LVADs. However, many complications of LVAD therapy remain. Treating these complications requires an understanding of LVAD physiology. Ongoing research is directed at reducing the incidence of many of these complications and may allow for wider use of LVADs.


Introduction

  1. Top of page
  2. Abstract
  3. Introduction
  4. Background
  5. Types of LVADs
  6. Bridge to Transplantation
  7. Destination Therapy
  8. Bridge to Recovery
  9. Adverse Events
  10. Management of Acute Complications
  11. Cost-Effectiveness of LVAD Support
  12. Future Directions
  13. Conclusion
  14. Conflict of Interest
  15. References

The burden of congestive heart failure (CHF) continues to grow, with over 500,000 new cases annually. Fortunately, increased understanding of the disease process as well as of the advances in pharmacological and pacemaker-based therapies have led to significant improvements in survival for patients with CHF over the past two decades [1]. For example, 1-year mortality in subjects with New York Heart Association (NYHA) association class IV CHF participating in clinical trials investigating angiotensin converting enzyme (ACE) inhibitors, beta-blockers, and aldosterone antagonists has decreased from approximately 50% in 1986 to less than 15% in 2002 [2–4]. However, many patients with advanced CHF continue to have significant symptoms despite these interventions. For these patients, prognosis remains very poor, with 1-year mortality rates approaching 75%[5].

When CHF is refractory to medical therapy, then in appropriate candidates, cardiac transplantation is the most effective treatment modality. Refinement in techniques and immunosuppressive regimens has produced 1-year survival rates of approximately 90%[6,7]. However, the number of transplants performed annually in the United States has plateaued at 2200 because of a limited number of donor organs (Figure 1), and because many patients die while waiting for a transplant [8].

image

Figure 1. Number of heart transplants performed annually in the United States, 1970–2005. Reproduced from reference [8] with permission. Copyright 2007 American Heart Association. All rights reserved. 254 × 190 mm (96 × 96 DPI).

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In the last 15 years, left ventricular assist devices (LVADs) have emerged as a method to prolong the survival of these patients as they wait for a suitable donor heart. By mechanically unloading the failing heart and improving systemic end-organ perfusion, LVADs can reverse the systemic abnormalities seen in advanced CHF, improving survival and quality of life. Advances in design and clinical experience have significantly reduced the morbidity and mortality associated with LVADs and have led to the continual spread of this technology [9]. Further advances are currently under evaluation and promise to make LVADs available to a greater number of patients. Importantly, the use of LVADs is no longer limited to subjects waiting for heart transplants, but is now approved to treat end-stage heart failure refractory to medical therapy in patients not suitable for transplantation because of age and/or comorbidities. This review discusses the evolution of LVAD devices, the current uses of this therapy, and its potential future applications.

Background

  1. Top of page
  2. Abstract
  3. Introduction
  4. Background
  5. Types of LVADs
  6. Bridge to Transplantation
  7. Destination Therapy
  8. Bridge to Recovery
  9. Adverse Events
  10. Management of Acute Complications
  11. Cost-Effectiveness of LVAD Support
  12. Future Directions
  13. Conclusion
  14. Conflict of Interest
  15. References

Mechanical circulatory support devices were initially developed in the 1960s as a means to assist patients who could not be weaned from cardiopulmonary bypass following cardiac surgery and Dr. Michael E. DeBakey implanted the first device in 1963 to treat cardiogenic shock following aortic valve surgery. Although the patient did not survive up to hospital discharge, this operation proved the feasibility of mechanical circulatory assistance [10]. Through the 1960s and 1970s, researchers developed several devices for investigational use. These “early” LVADs caused significant hemolysis and had high rates of bleeding and infection because of their size and extracorporeal location. Furthermore, patients with otherwise good clinical recovery remained significantly limited in their mobility because of the large power consoles (Figure 2).

image

Figure 2. The ABIOMED BVS 5000 extracorporeal ventricular assist device. Reproduced with permission. Copyright 2007 ABIOMED. All rights reserved. 254 × 190 mm (96 × 96 DPI).

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The limitations of the early devices, however, provided the impetus for the development of an intracorporeal LVAD powered from an external source through a percutaneous driveline. Situating the pump inside the body provided patients with greater independence, allowed discharge from the hospital, and substantially improved the quality of life [11]. In addition, outpatient LVAD management led to significant cost savings over prolonged inpatient stays [12]. Consequently, the Heartmate 1000 IP (Thoratec Corporation, Pleasanton, CA, USA) received the FDA approval as a “bridge-to-transplantation device” in 1994. The power console of this pneumatic LVAD was smaller than that of earlier pumps, but its size remained a significant limitation. Further research produced an electric power source connected to a wearable battery pack. An LVAD using this technology, the Heartmate Vented Electric (VE) (Thoratec Corporation), was approved by the FDA in 1998 (Figure 3).

image

Figure 3. Intracorporeal LVADs. (A) The Heartmate VE left ventricular assist system. Reproduced from reference [5] with permission. Copyright 2001 Massachusetts Medical Society. All rights reserved. (B) The Novacor left ventricular assist system. Reproduced with permission. Copyright World Heart Corporation. All rights reserved. 254 × 190 mm (96 × 96 DPI).

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Types of LVADs

  1. Top of page
  2. Abstract
  3. Introduction
  4. Background
  5. Types of LVADs
  6. Bridge to Transplantation
  7. Destination Therapy
  8. Bridge to Recovery
  9. Adverse Events
  10. Management of Acute Complications
  11. Cost-Effectiveness of LVAD Support
  12. Future Directions
  13. Conclusion
  14. Conflict of Interest
  15. References

Pulsatile Flow Pumps

The first generation of LVADs includes the Heartmate I and the Novacor. (World Heart Corporation, Ottawa, Ontario, Canada). Both are surgically implanted in a pocket in the abdominal wall (Figure 3). An inflow conduit is attached to the left ventricular apex, and an outflow conduit is anastamosed to the ascending aorta. Bioprosthetic valves ensure unidirectional blood flow. The blood is expelled by electrically powered pusher plates that contract a polyurethane diaphragm and provide pulsatile flow to the aorta. The devices can pump blood at rates up to 10 L/min. Each device is connected to a wearable battery pack through a percutaneous line that also houses the venting system.

First-generation devices have several significant drawbacks. Their size is a source of patient discomfort, and implantation requires a large operation, increasing the risk of both bleeding and infection. The pump is noisy and subject to failure because of the presence of wearing mechanical parts. Valves inside the pump decay over time. The percutaneous driveline is a major source of infection.

Continous Flow Pumps

As blood moves through the systemic circulation, the initial pulsatile flow in the aorta is progressively dampened, transforming into continuous flow at the level of the capillary (Figure 4). Accordingly, a pulsatile flow may not be necessary for humans. An understanding of this particular aspect of circulatory physiology fueled the development of axial flow pumps [13]. These LVADs propel blood forward in a continuous fashion with a rotary impeller (Figure 5). With this design, the device has only one moving part and does not require valves, reducing the long-term risk of mechanical failure. Axial flow pumps are also smaller and lighter than the first-generation LVADs and function in virtual silence. Early concerns about the adverse effects of continuous flow on end organs have been alleviated with successful long-term use of these devices [14].

image

Figure 4. Pressure and volume distribution in the systemic circulation. Adapted with permission from Smith JJ, Kampine JP. Circulatory physiology: The essentials, 3rd Edition. Baltimore, MD: Williams & Wilkins, 1990. Copyright 2005 Lippincott Williams & Wilkins. All rights reserved. 254 × 190 mm (96 × 96 DPI).

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image

Figure 5. The interior of the Micromed–DeBakey axial flow left ventricular assist device. Reproduced with permission. Copyright Micromed Cardiovascular, Inc. All rights reserved. 254 × 190 mm (96 × 96 DPI).

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Currently, the Heartmate II (Thoratec Corporation) is the only FDA-approved axial flow pump. Three other devices are in advanced stages of clinical testing (Figure 6): the Micromed–DeBakey VAD (Micromed Cardiovascular, Inc., Houston, TX, USA), the Jarvik 2000 (Jarvik Heart, Inc., New York, NY, USA), and the VentrAssist (Ventracor, Inc., Foster City, CA, USA).

image

Figure 6. Axial flow ventricular assist devices (VAD). (A) Thoratec Heartmate II. Reproduced with permission. Copyright 2007 Thoratec Corporation. All rights reserved. (B) Micromed–Debakey VAD. Reproduced with permission. Copyright Micromed Cardiovascular. All rights reserved. (C) Jarvik 2000. Reproduced with permission. Copyright 2004 Jarvik Heart. All rights reserved. 254 × 190 mm (96 × 96 DPI).

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Bridge to Transplantation

  1. Top of page
  2. Abstract
  3. Introduction
  4. Background
  5. Types of LVADs
  6. Bridge to Transplantation
  7. Destination Therapy
  8. Bridge to Recovery
  9. Adverse Events
  10. Management of Acute Complications
  11. Cost-Effectiveness of LVAD Support
  12. Future Directions
  13. Conclusion
  14. Conflict of Interest
  15. References

The Heartmate I, Novacor, and Heartmate II are all approved for use in bridge to transplantation. When implanted in patients refractory to medical therapy, LVADs lead to improved renal function, right heart function, and overall physical conditioning [15,16]. By taking over the work of the left ventricle, the LVAD markedly decreases filling pressures and increases cardiac output. Decreased end-diastolic pressure in the left ventricle results in lower pulmonary vascular resistance and a reduction in afterload for the right ventricle. Additionally, the increase in cardiac output provides additional preload for the right ventricle, further enhancing its function. The combination of effective native right ventricular function and mechanical replacement of left ventricular output results in more efficient delivery of oxygen to end-organ tissues. As a result, the presence of the LVAD can partially or totally reverse functional impairment of these organs. This is most clearly seen in the kidneys, in which renal failure can resolve following the implantation of an LVAD. All organ systems benefit from the increase in perfusion, allowing sick patients to stabilize or improve as they wait for a heart transplant.

Multiple studies have shown that LVADs can be successfully used as a bridge to transplantation [16–21], with one prospective series showing an increase in survival up to transplant from 33% to 71% with the use of the Heartmate LVAD (when compared with historical controls managed with medical therapy alone) [18]. In addition to providing an increased length of time on the organ waiting list, LVADs improve outcomes by significantly reducing patients’ comorbidities at the time of transplant, making them better transplant candidates and improving their posttransplant outcomes [18,19].

Although most commonly implanted into patients with symptoms of class IV CHF that are refractory to medical therapy, intracorporeal LVADs have also been used for the treatment of postcardiotomy shock, myocardial infarction complicated by cardiogenic shock, myocarditis, and primary graft failure following cardiac transplantation [22–25]. The following criteria should generally be met prior to consideration of LVAD implant: clinical evidence of impaired end-organ perfusion with cardiac index <2 L/min/m2, pulmonary capillary wedge pressure >20 mmHg, and systolic blood pressure <80 mmHg despite maximal medical support, including inotropes and an intraaortic balloon pump, if indicated [26]. Although it is important to meet these criteria, LVAD implantation needs to be performed prior to extensive end-organ damage for maximal chance of success [27].

Clinical data suggest that the axial flow devices have comparable, if not higher, success in bridge to transplantation as that of pulsatile flow devices [28–31]. The axial flow devices have fewer perioperative complications, with less bleeding and a shorter duration of intensive care [30,32]. By nature of their small size, these devices eliminate the infections associated with a large abdominal pocket and also reduce the incidence of driveline infections [31–33]. Mechanical failure is less frequent as well [34]. On the other hand, thromboembolism has been a significant issue, and all axial flow pumps require systemic anticoagulation [31,34,35].

Destination Therapy

  1. Top of page
  2. Abstract
  3. Introduction
  4. Background
  5. Types of LVADs
  6. Bridge to Transplantation
  7. Destination Therapy
  8. Bridge to Recovery
  9. Adverse Events
  10. Management of Acute Complications
  11. Cost-Effectiveness of LVAD Support
  12. Future Directions
  13. Conclusion
  14. Conflict of Interest
  15. References

As patients with LVADs survived for longer periods of time prior to transplantation, the concept of using LVADs as “destination therapy” arose. In the late 1990s, researchers conducted the Randomized Evaluation of Mechanical Assistance for the Treatment of Congestive Heart Failure (REMATCH) study, a randomized, controlled, clinical trial of LVADs compared with optimal medical management [5]. One hundred and twenty-nine subjects with NYHA class IV CHF who were not candidates for transplantation were followed for 2 years. The results showed a 48% reduction in the risk of all-cause mortality at 2 years with LVAD therapy. In the LVAD group, the primary causes of mortality were sepsis and device failure, whereas in the medical management cohort, almost all patients died from progressive heart failure. REMATCH must be considered a seminal study, as it conclusively demonstrated that subjects in the most advanced stages of CHF (nearly all of them were inotrope-dependent) can survive a major cardiac operation, and that the small increase in short-term mortality due to perioperative deaths is significantly outweighed by the long-term benefits of device therapy. Indeed, patients in this cohort who were on inotropic therapy at randomization derived the largest benefit [36]. In addition to reduced mortality, patients with LVADs spent fewer days in the hospital and had a higher quality of life. Following the publication of REMATCH, the Heartmate LVAD received the FDA approval for use as destination therapy in 2002. As with bridge to transplantation, employment of destination therapy early in the clinical course is recommended, as high-risk patients have significantly worse survival than low-risk patients [37].

Despite the superiority of LVADs to medical therapy for this group of patients (Figure 7), the absolute mortality rate for LVAD patients in REMATCH was still 48% at 1 year and 75% at 2 years. These statistics indicate the severity of illness in the REMATCH cohort and emphasize the need for further improvements in pump design and management. Since REMATCH, further clinical experience with destination therapy has produced lower complication rates, and the 2-year mortality in REMATCH-type patients has been reduced to 60% at experienced centers [38]. Only the Heartmate I is currently approved for destination therapy. A clinical trial that will provide the first head-to-head comparison of pulsatile (Heartmate I) and axial flow pumps (Heartmate II) was recently stopped early by the Data Safety and Monitoring Board because of better outcomes with the Heartmate II. Details on this direct comparison will soon be available and likely establish continuous flow pumps as a first-line therapy for destination candidates.

image

Figure 7. Kaplan–Meier survival curves from the REMATCH trial. Reproduced with permission from reference [5]. Copyright 2001 Massachusetts Medical Society. All rights reserved. 254 × 190 mm (96 × 96 DPI).

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Bridge to Recovery

  1. Top of page
  2. Abstract
  3. Introduction
  4. Background
  5. Types of LVADs
  6. Bridge to Transplantation
  7. Destination Therapy
  8. Bridge to Recovery
  9. Adverse Events
  10. Management of Acute Complications
  11. Cost-Effectiveness of LVAD Support
  12. Future Directions
  13. Conclusion
  14. Conflict of Interest
  15. References

The ability of LVADs to support an acutely failing heart while it recovers function, as in the cases of myocarditis or postcardiotomy failure, is well documented [22,23,39]. However, observations have also noted the potential for myocardial recovery in patients with chronic heart failure. Researchers have documented that the unloaded left ventricle undergoes a process of reverse remodeling, as categorized by multiple different indices. An early report noted a decrease in left ventricular size [40]. Building on this finding, an examination of pressure–volume relationships in explanted hearts has shown that the curves of patients with LVADs normalize as compared with the curves of patients with chronic heart failure [41]. Cellular structure and function also revert toward normal [42–45]. Thus, the reduction in left ventricular volumes is not just a function of the unloading provided by the LVAD but actually reflects alterations in the dynamics of myocyte function. A more detailed investigation has found that increases in the expression of genes promote calcium handling [46,47], downregulation of pathologic cytokines [48], and upregulation of β-adrenergic receptors [49,50]. All of these processes contribute to reverse remodeling of the left ventricle. Clinically, left ventricular function improves, and patients have a dramatic increase in their exercise capacity following LVAD implantation [51–53].

These findings encouraged the explantation of LVADs in select patients who had demonstrated sufficient recovery of myocardial function. To date, clinical results are mixed, with some groups finding substantial numbers of patients who demonstrate prolonged cardiac recovery, whereas other groups report a frequent recurrence of heart failure [54,55]. Recovery is less likely in patients with ischemic cardiomyopathy, and most data have shown that few patients achieve enough recovery of function to allow explantation [56–58]. Recently, physicians in Harefield, England, have reported provocative findings using high-dose neurohormonal blockade and clembuterol, a β2 adrenergic receptor agonist, to promote myocardial recovery in LVAD patients. With this protocol, 73% of patients were explanted, and 73% of these patients demonstrated sustained recovery over 4 years (Figure 8) [59]. A multicenter trial is ongoing in the United States to confirm these results.

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Figure 8. Long-term freedom from recurrent heart failure following treatment with Harefield protocol and LVAD explantation. Reproduced from reference [51] with permission. Copyright 2006 Massachusetts Medical Society. All rights reserved. 254 × 190 mm (96 × 96 DPI).

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Adverse Events

  1. Top of page
  2. Abstract
  3. Introduction
  4. Background
  5. Types of LVADs
  6. Bridge to Transplantation
  7. Destination Therapy
  8. Bridge to Recovery
  9. Adverse Events
  10. Management of Acute Complications
  11. Cost-Effectiveness of LVAD Support
  12. Future Directions
  13. Conclusion
  14. Conflict of Interest
  15. References

Table 1 shows the most commonly encountered adverse events in patients who receive LVADs as a bridge to transplantation. Different complications are seen in the early period following LVAD implantation and the later period following prolonged use.

Table 1.  Adverse events in patients with the Heartmate VE when used as a bridge to transplantation (adapted from references [16,18,30,31]) 254 × 190 mm (96 × 96 DPI)
EventFrequency
Bleeding48%
Infection18–59%
Neurological event10–27%
RV failure7–11%
Thromboembolism12%
Device failure12.8%

The two major perioperative complications are bleeding and right ventricular (RV) failure. Bleeding causes significant morbidity and mortality and often requires exploration of the surgical site. The degree of RV failure is difficult to predict prior to LVAD implantation, although the presence of elevated central venous pressure (CVP), high pulmonary vascular resistance, and significant RV dilatation raise concern that additional RV support may be required postoperatively. The importance of the right ventricle in the management of LVAD patients cannot be underestimated. With a functioning LVAD in place, cardiac output is dependent on the ability of the right ventricle to provide sufficient preload to the left side of the heart. Postsurgical RV dysfunction can compound underlying contractile weakness and cause right heart failure, which is correlated with worse outcomes [60,61]. The treatment consists of pharmacological augmentation of RV contractility and reduction of pulmonary vascular resistance. In our practice, RV work conditions are optimized at the time of LVAD implantation with the routine use of milrinone (providing contractility enhancement as well as afterload reduction through pulmonary vasodilation) and inhaled nitric oxide if the pulmonary artery pressure remains over 45 mmHg after the initiation of milrinone. Occasionally, refractory RV failure dictates placement of a right ventricular assist device (RVAD).

With intermediate- and long-term use, the most common complication is infection, occurring in up to 59% of patients [62–65]. The relative immunosuppression of critical illness as well as the presence of large amounts of foreign material leaves LVAD patients particularly susceptible to infectious complications. Infections can occur in the device pocket or surrounding surgical area, along the percutaneous drivelines, and inside the device itself. Prevention efforts, including enhanced prophylactic antibiotic regimens, new surgical techniques, improved driveline design, and attention to drive line management, are critical in reducing the overall infection rate [38].

With prolonged use, device failure can occur. Most commonly, this is due to deterioration of the device inflow valves and resultant regurgitation. Bearings attached to the motor are also subject to decay due to the repetitive wearing motion of the pump. Additionally, the electrical system can malfunction, causing abrupt cessation of LVAD function. These complications are medical emergencies and often necessitate explantation or replacement of the device.

The risk of thromboembolism and neurological events has been significantly reduced by the introduction of the Heartmate LVAD. The Heartmate I has a unique, textured design that promotes the formation of an endothelial layer on its blood-contacting surfaces. This “natural” surface has low thrombogenicity, and the Heartmate therefore does not require systemic anticoagulation [66]. With other devices, thrombotic complications remain prevalent and necessitate anticoagulation.

Management of Acute Complications

  1. Top of page
  2. Abstract
  3. Introduction
  4. Background
  5. Types of LVADs
  6. Bridge to Transplantation
  7. Destination Therapy
  8. Bridge to Recovery
  9. Adverse Events
  10. Management of Acute Complications
  11. Cost-Effectiveness of LVAD Support
  12. Future Directions
  13. Conclusion
  14. Conflict of Interest
  15. References

Figure 9 shows cardiac physiology following LVAD implantation and identifies causes of decreased cardiac output, which can be divided into three general categories:

image

Figure 9. Cardiac pathophysiology following left ventricular assist device implantation. Red lettering and lines indicate the causes of poor cardiac output and systemic hypoperfusion. LV, left ventricle; RV, right ventricle; LVAD, left ventricular assist device; PVR, pulmonary vascular resistance. 254 × 190 mm (96 × 96 DPI).

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  • 1
    decreased pump preload,
  • 2
    increased pump afterload, and
  • 3
    intrinsic pump malfunction

Decreased Preload

Reduced filling of the LVAD chamber can be device-related (inflow cannula obstruction, usually in the early postoperative period and secondary to malpositioning against the ventricular septum) or patient-related. RV failure is the most common cause of low pump flows and is managed best by early initiation of inotropic therapy and maximal RV afterload reduction with inhaled nitric oxide. Hypovolemia from any cause also presents with decreased preload and can worsen underlying RV dysfunction.

Increased Afterload

An inability to fully empty the LVAD chamber can occur with the obstruction of the outflow cannula by mechanical kinks and infections. Injection of radioopaque dye may be used to identify the source of the problem, and LVAD replacement is the primary solution to outflow cannula obstruction. Systemic hypertension can also prevent complete emptying of the LVAD chamber, and afterload reduction is crucial to maintaining adequate LVAD blood flow.

Pump Malfunction

Disruption of the LVAD's motor or electrical system is usually evident to both the patient and the physician. Pulsatile flow LVADs can be attached to a pneumatic hand pump and manually operated until the source of the problem can be found. This option is not available for axial flow pumps. Replacement of the battery pack is often sufficient to repair electrical failures. Worn bearings or a malfunctioning motor require replacement of the entire LVAD.

Right heart catheterization can differentiate causes of low pump output (Table 2). Low CVP and low pulmonary capillary wedge pressure (PCWP) indicate hypovolemia. A finding of elevated CVP with a low PCWP is most likely due to RV dysfunction. Elevated CVP and PCWP are seen with inflow cannula obstruction, pump malfunction, and outflow cannula obstruction. Echocardiography can pinpoint the source of the problem.

Table 2.  Differentiation of the etiology of hypotension in the LVAD patient using intracardiac pressure measurements. 254 × 190 mm (96 × 96 DPI)
 CVPPCWPLVAD outputCardiac output
Hypovolemia[DOWNWARDS ARROW][DOWNWARDS ARROW][DOWNWARDS ARROW][DOWNWARDS ARROW]
Sepsis[DOWNWARDS ARROW][DOWNWARDS ARROW][UPWARDS ARROW][UPWARDS ARROW]
RV failure[UPWARDS ARROW][DOWNWARDS ARROW][DOWNWARDS ARROW][DOWNWARDS ARROW]
Pump failure or cannula obstruction[UPWARDS ARROW][UPWARDS ARROW][DOWNWARDS ARROW][DOWNWARDS ARROW]
Valvular regurgitation[UPWARDS ARROW][UPWARDS ARROW][UPWARDS ARROW][DOWNWARDS ARROW]

Hypotension or poor systemic perfusion can also be seen in the setting of normal or elevated pump flows. Vasodilation due to sepsis is the most likely cause in these situations, and an infectious source should be sought aggressively. Infections within the pump itself often necessitate explantation of the device. In the absence of infection, the patient with hypoperfusion and preserved device flow should be evaluated for valvular incompetence. If the cardiac output obtained from the Swan–Ganz catheter is low and the cardiac output reported by the pump is high, the most likely cause is regurgitation through either the native aortic valve or one of the valves within the LVAD. Echocardiography can localize the culprit valve.

Cost-Effectiveness of LVAD Support

  1. Top of page
  2. Abstract
  3. Introduction
  4. Background
  5. Types of LVADs
  6. Bridge to Transplantation
  7. Destination Therapy
  8. Bridge to Recovery
  9. Adverse Events
  10. Management of Acute Complications
  11. Cost-Effectiveness of LVAD Support
  12. Future Directions
  13. Conclusion
  14. Conflict of Interest
  15. References

The rapid spread of LVAD use has focused attention on the expense of this technology. An analysis from the REMATCH trial found an initial hospitalization cost of approximately $200,000 [67]. When these costs are applied to the bridge-to-transplant population, the cost-effectiveness of the LVAD depends on a comparison with the cost of medically managing these patients while they wait for a heart to become available. Typically, this management involves prolonged intensive care unit stays and the use of other costly technologies. Among the destination therapy population, the alternatives such as home inotrope therapy are typically significantly less costly, but have dismal outcomes. Thus, for LVADs to be cost-effective for these patients, they need to demonstrate a substantial improvement in efficacy over optimal medical management. A recent review of cost-effectiveness studies found a range of $48,000–86,000 per life-year saved for bridge-to-transplant patients. For destination therapy, the cost per quality-adjusted life-year (QALY) was $36,000–60,000 [68].

Future Directions

  1. Top of page
  2. Abstract
  3. Introduction
  4. Background
  5. Types of LVADs
  6. Bridge to Transplantation
  7. Destination Therapy
  8. Bridge to Recovery
  9. Adverse Events
  10. Management of Acute Complications
  11. Cost-Effectiveness of LVAD Support
  12. Future Directions
  13. Conclusion
  14. Conflict of Interest
  15. References

With the advent of the continuous flow pumps and improved operative experience, the risk associated with LVAD implantation has decreased substantially. The Jarvik 2000 allows placement through a lateral thoracotomy rather than through the traditional median sternotomy, allowing the surgery to be performed without cardiopulmonary bypass and substantially reducing recovery time [69]. As more advances such as this are incorporated into the design of subsequent devices, we believe that LVAD implantation will increasingly be used earlier in the clinical course, in the same way that valve surgery is most therapeutic when performed at the beginning, not end, of a downward spiral. Further refinements may ultimately allow these devices to be used to improve the quality of life for patients with earlier stages of heart failure.

The two primary obstacles left to conquer are driveline infections and the risk of thromboembolism with the continuous flow pumps. A transcutaneous energy transfer system that would replace the percutaneous driveline is in early stages of clinical testing. Increasing clinical experience with the anticoagulation regimens needed in continuous flow pump recipients should prove successful at reducing the thromboembolic complications. Finally, third-generation devices are entering the clinical trial phase of development [70]. These pumps feature electromagnetically levitated impellers that eliminate the need for bearings and thus reduce the risk of device failure.

Conclusion

  1. Top of page
  2. Abstract
  3. Introduction
  4. Background
  5. Types of LVADs
  6. Bridge to Transplantation
  7. Destination Therapy
  8. Bridge to Recovery
  9. Adverse Events
  10. Management of Acute Complications
  11. Cost-Effectiveness of LVAD Support
  12. Future Directions
  13. Conclusion
  14. Conflict of Interest
  15. References

Ventricular assist device therapy has made tremendous progress since the first devices were tested in the 1960s. The success of the LVAD as a bridge to transplantation and as destination therapy provides cardiologists and cardiothoracic surgeons with a new tool for the management of advanced heart failure. The current devices offer significant benefits to patients’ quality and quantity of life. With continued device improvement and clinical experience, LVADs may not only become a viable alternative to transplantation but also be used to improve the quality of life of patients in earlier stages of advanced CHF. The application of the LVAD as a bridge to recovery is an exciting development, with significant potential to alter physicians’ approach to the management of CHF.

References

  1. Top of page
  2. Abstract
  3. Introduction
  4. Background
  5. Types of LVADs
  6. Bridge to Transplantation
  7. Destination Therapy
  8. Bridge to Recovery
  9. Adverse Events
  10. Management of Acute Complications
  11. Cost-Effectiveness of LVAD Support
  12. Future Directions
  13. Conclusion
  14. Conflict of Interest
  15. References
  • 1
    Cleland JG, Dewbert JC, Erdman E, et al. The effect of cardiac resynchronization on morbidity and mortality in heart failure. N Engl J Med 2005;352:15391549.
  • 2
    Effects of enalapril on mortality in severe congestive heart failure. Results of the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS). The CONSENSUS Trial Study Group. N Engl J Med 1987;316:14291435.
  • 3
    Packer M, Fowler MB, Roecker EB, et al. Effect of carvedilol on the morbidity of patients with severe chronic heart failure: Results of the carvedilol prospective randomized cumulative survival (COPERNICUS) study. Circulation 2002;106:21942199.
  • 4
    Pitt B, Zannad F, Remme WJ, et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators. N Engl J Med 1999;341:709717.
  • 5
    Rose EA, Gelijns AC, Moskowitz AJ, et al. Long-term mechanical left ventricular assistance for end-stage heart failure. N Engl J Med 2001;345:14351443.
  • 6
    Morgan JA, John R, Weinberg AD, et al. Heart transplantation in diabetic recipients: A decade review of 161 patients at Columbia Presbyterian. J Thorac Cardiovasc Surg 2004;127:14861492.
  • 7
    Taylor DO, Edwards LB, Boucek MM, et al. Registry of the International Society for Heart and Lung Transplantation: twenty-third official adult heart transplantation report–2006. J Heart Lung Transplant 2006;25:869879.
  • 8
    Rosamond W, Flegal K, Friday G, et al. Heart disease and stroke statistics–2007 update: A report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 2007;115:e69e171.
  • 9
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