ATS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kumpati, G. S.
Right arrow Articles by Hoercher, K. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kumpati, G. S.
Right arrow Articles by Hoercher, K. J.
Related Collections
Right arrow Mechanical Circulatory Assistance

Ann Thorac Surg 2001;71:S103-S108
© 2001 The Society of Thoracic Surgeons

Session 2: bridging to transplant and alternatives to transplant

Left ventricular assist device bridge to recovery: a review of the current status

Ganesh S. Kumpati, MDa, Patrick M. McCarthy, MDa, Katherine J. Hoercher, MSa

a George M. and Linda H. Kaufman Center for Heart Failure, Department of Thoracic and Cardiovascular Surgery, The Cleveland Clinic Foundation, Cleveland, Ohio, USA

Address reprint requests to Dr McCarthy, George M. and Linda H. Kaufman Center for Heart Failure, Department of Thoracic and Cardiovascular Surgery, The Cleveland Clinic Foundation, 9500 Euclid Ave, F25, Cleveland, OH 44195
e-mail: mccartp{at}ccf.org

Presented at the Fifth International Conference on Circulatory Support Devices for Severe Cardiac Failure, New York, NY, Sept 15–17, 2000.

Abstract

The use of the left ventricular assist device as a bridge to recovery represents a new phenomenon. This article focuses on bridge-to-recovery in the settings of myocarditis and dilated cardiomyopathy with a review of the hemodynamic, neurohormonal, physiologic, cellular, and molecular changes of recovery during left ventricular assist device support. Despite numerous markers of success, there is a disconnect from the limited clinical successes that are reviewed. The current status and future options to increase the chances of success are highlighted.

Within the epidemic of heart failure, ventricular assist devices have become an accepted means of support for patients with severe, refractory heart failure. The first application of a ventricular assist system was in 1963 by DeBakey [1] for support of postoperative cardiogenic shock, with later successful device removal after 1 week of support with improvement of cardiac function. In 1968 Cooley and associates [2] first used a circulatory assist device as temporary support until cardiac transplantation. Since that time, ventricular assist devices have been applied as an assist to recovery for postcardiotomy support, the experience of which has been documented in multiple studies [3, 4]. In these experiences, approximately 45% of supported patients were weaned from device support, with approximately half of that group surviving to hospital discharge, subsequently achieving good long-term survival [3, 4].

With the advances in cardiac transplantation during the 1980s, ventricular assist systems were used as left ventricular assist devices (LVADs) or as biventricular assist devices for salvage of patients with profound heart failure accompanied by shock and multiple organ dysfunction, with the goal of future transplantation. With evolution of the LVAD, four major devices have been used as a bridge to transplant (ABIOMED, Thoratec, Novacor, and Heartmate). Large experiences with each LVAD type have been described [5–8]. With each device type, a proportion of patients was noted to have significant improvement in left ventricular (LV) function, especially in patients with myocarditis and dilated cardiomyopathy.

In a small subset of these patients, the LVAD was removed after demonstrated LV functional improvement, either after a short duration of support such as with myocarditis, or for device complications in patients receiving longer support for cardiomyopathy. Subsequently, some of these patients did well in the long term, with maintenance of improved cardiac function. Thus, the concept of LVAD as a bridge to cardiac recovery was born. This review will focus on bridge to recovery in patients with myocarditis and dilated cardiomyopathy. We excluded patients who had postcardiotomy or postinfarction shock.

Hemodynamic changes, neurohormonal changes, and remodeling with heart failure

Central to the understanding of bridge to recovery is the current understanding of severe heart failure. Heart failure is the end product of multiple mechanisms, including changes in pumping capacity (LV function, geometry) and neurohormonal changes (salt and water retention, vasoconstriction, and so forth) [9]. Acute and chronic heart failure can occur after ischemic insults (myocardial infarction), myocarditis, and a variety of other disorders (familial, viral, congenital, idiopathic).

The progression from mild to severe heart failure represents an area of ongoing study relevant to bridge to recovery. The alterations in ventricular morphology, structure, and function that occur with heart failure progression have been termed ventricular remodeling [10]. From the organ level to the molecular level, a series of pathologic changes have been described. At the organ level, dilatation of the left ventricle has been widely described. The physiologic consequences of this, including altered end-diastolic pressure–volume and decreased end-systolic pressure–volume relationships have been described in detail. These correlate with imaging findings (decreased ejection fraction [EF], massive dilated ventricular chamber, decreased stroke volume) and hemodynamic findings (decreased cardiac output, elevated pulmonary capillary wedge and central venous pressures). Changes in ventricular geometry include progression to a more spherical chamber size, increased wall tension, and wall thinning [10].

At the cellular level, myocyte necrosis, myocyte apoptosis, fiber hypertrophy, cellular stretching, and matrix fibrosis have all been noted in patients with severe ventricular dysfunction [11]. Myocyte necrosis has been correlated with a variety of neurohormonal mediators, including elevated myocardial angiotensin II, norepinephrine, and tumor necrosis factor-{alpha} content [12].

Also, at the cellular level, multiple changes leading to decreased contractility have been described. Down-regulation of ß receptors [13] and abnormal intracellular calcium metabolism have all been described [14]. In addition, cytoskeleton protein alterations have been described, including myofilament loss [15] and myosin isomer changes [10].

Within neurohormonal changes, elevation in angiotensin II, plasma norepinephrine, and vasopressin have all been noted in severe heart failure. These correlate with peripheral vasoconstriction and salt and water accumulation in severe heart failure. The treatment of hypertension and the use of angiotensin-converting enzyme inhibitors illustrate this [11].

Physiologic basis and correlates of recovery

After LVAD placement, most patients have multiple hemodynamic changes, with improved native left and right ventricular function. Immediately after weaning from cardiopulmonary bypass to LVAD support, the left ventricle has a decreased end-diastolic diameter, demonstrating unloading [16]. In most patients, immediately after device placement, the aortic valve rarely opens, indicative of the LVAD performing most of the hemodynamic support [17, 18]. Subsequently, after support with LVAD, multiple series have demonstrated improvements in LV measurements [16–19]. Patients after LVAD placement were noted to have decreased LV end-diastolic diameter (Fig 1), improved EF, decreased pulmonary capillary wedge pressure, and decreased pulmonary vascular resistance [16]. In explanted hearts with dilated cardiomyopathy that were supported with an LVAD, the end-diastolic pressure–volume relationship was noted to be markedly improved, as compared with explanted dilated cardiomyopathy hearts without LVAD support [19].



View larger version (72K):
[in this window]
[in a new window]
  		Fig 1. Two months after left ventricular assist device implant, this patient with dilated cardiomyopathy (left) demonstrated a striking reduction in heart size (right). Studies with echocardiography in patients have demonstrated an immediate reduction of left ventricular dimensions that is sustained during left ventricular assist device support. (Reprinted from Frazier OH, Rose EA, McCarthy PM, et al. Improved mortality and rehabilitation of transplant candidates treated with a long-term implantable left ventricular assist system. Ann Surg 1995;222:327–38 with permission from Lippincott Williams & Wilkins.)

 
During exercise studies of patients with LVAD support, peak oxygen consumption during maximal exercise demonstrated progressive improvement with time [20]. In another exercise study, patients with LVADs had appropriate rise in heart rate and cardiac output with exercise [21–23].

Cellular and molecular basis of recovery

The cellular and molecular basis of bridge to recovery spans two related areas: resolution of the primary pathologic process, and reverse remodeling. Resolution of the primary pathologic process is most applicable to acute myocarditis. Patients with acute myocarditis have myocyte damage with inflammatory infiltrates, without fibrosis. Resolution of this, with or without subsequent fibrosis, leads to improved cellular function [24]. For patients with idiopathic dilated cardiomyopathy and patients with extensive scar from previous ischemic insults, resolution of the primary process is less straightforward.

Most attention in molecular aspects of recovery in dilated cardiomyopathy has focused on molecular changes collectively grouped together as reverse remodeling. This includes alterations noted at the tissue level, cellular structure, and cellular function, akin to those noted in heart failure pathophysiology. Many of the investigations in this area have used heart muscle from the ventricular core excised at the time of LVAD placement, and then compared this with heart muscle at the time of LVAD explantation during transplantation after a variable period of circulatory support [18].

At the tissue level, myocardial contraction (measured in isolated endocardial trabeculae) was noted to have resolution of force decline with high-frequency contraction after LVAD support compared with before LVAD (indicating contraction performance). In the same model, myocardial contraction had improved responsiveness to isoproterenol stimulation [17]. In isolated myocyte models, LVAD-supported heart myocytes had greater magnitude of contraction, improved relaxation, and more response to ß agonists than myocytes from nondevice-supported failing hearts [25]. Also, using tissue histology, multiple investigations have noted decreased myocardial necrosis in histologic specimens [18, 26]; decreased hypertrophy [27]; reductions in cellular length and width [27]; varying degrees of increase in interstitial fibrosis [18, 26], and reductions in number of wavy fibers and contraction band necrosis [18, 26] in both dilated and ischemic cardiomyopathy (Table 1).


View this table:
[in this window]
[in a new window]
  		Table 1. Histologic Alterations in Myocardium After Left Ventricular Assist Device Support

 
At the cellular level (Table 2), transmural ventricular muscle at LVAD explantation showed decreased immunoreactivity to atrial natriuretic polypeptide and brain natriuretic polypeptide, which correlated with echocardiographic indicators of ventricular improvement [29]. Left ventricular cellular mitochondrial function, as measured by use of Krebs cycle intermediates in an isolated mitochondria model, was improved in the LVAD-supported group compared with before device placement [30]. Alterations in intracellular calcium metabolism, as measured by alterations in calcium cycling proteins (decreased G{propto}q inhibitors, increased sarcoplasmic reticulum calcium adenosine triphosphatase, and so forth) before and after LVAD placement, have also been described [31]. Decreased levels of myocardial tumor necrosis factor-{alpha} were noted after LVAD versus before LVAD [32]. Levels of matrix metalloproteinase, important in matrix remodeling, decreased after LVAD support [33]. Myocardial gene transcription alterations have also been noted. The mRNA levels for genes mediating calcium cycling proteins (increased sarcoplasmic reticulum calcium adenosine triphosphatase mRNA levels and decreased sodium-calcium exchanger mRNA levels) changed after LVAD support [34]. The levels of mRNA for apoptosis inhibiting proteins have been noted to increase after LVAD support [34, 35], along with decreased myocardial apoptosis after LVAD support [36].


View this table:
[in this window]
[in a new window]
  		Table 2. Summary of Alterations at Cellular Level

 
Multiple neurohormonal alterations have been described. Improvement in LV function after LVAD placement has been associated with decreased anti-ß1 adrenoreceptor autoantibodies [37]. Left ventricular assist device placement is associated with decreased systemic levels of interleukins 6 and 8 (mediators correlated with systemic inflammatory response, shock, and multiple organ dysfunction) [38]. Decreased plasma norepinephrine, renin, atrial natriuretic polypeptide, aldosterone, cortisol, and vasopressin have also been noted (Table 3) [39–41].


View this table:
[in this window]
[in a new window]
  		Table 3. Neurohormone Levels at Baseline and Explant

 
Clinical situations: myocarditis, dilated cardiomyopathy

Clinical experience with bridge to recovery in myocarditis has been described by multiple investigators [24, 42–49]. In these series, patients were supported with various devices (pulsatile, most recently axial flow) either as LVAD or biventricular assist device for short-term to medium-term use with documented improvement or recovery in EF.

Clinical experience with bridge to recovery in the setting of dilated cardiomyopathy has been less widespread and, overall, makes up a small fraction of LVAD patients. Experience exists with all device types [50–54]. From our own experience at the Cleveland Clinic, only 2 patients of 250 who had LVAD placement subsequently had device explantation after cardiac recovery. These cases are briefly described below.

Case 1
A 34-year-old man with dilated cardiomyopathy had decompensated biventricular heart failure in 1996. He underwent Heartmate LVAD placement for cardiogenic shock as a bridge to transplant. Before LVAD placement, LVEF was 10% to 15%. One month after the operation, an infection with Staphylococcus aureus developed in the patient’s pump pocket, requiring debridement of the pocket and intravenous vancomycin. Two months after the operation, recurrent bacteremia from LVAD infection with S. aureus developed in the patient. At 3 months postoperatively, the patient continued to have intermittent bacteremia related to this infection despite continuous antibiotics. By this time, the patient had rehabilitated, and the LVEF had increased to 30%. Subsequently the LVAD was explanted and a partial left ventriculotomy was performed. The patient did well and was discharged to home as New York Heart Association class I. Eight months after discharge, he suddenly decompensated and was admitted to another hospital. After initial stabilization of his congestive heart failure, he died of hyperkalemic arrest.

Case 2
A 46-year-old man with dilated cardiomyopathy with progressive heart failure underwent partial left ventriculotomy and mitral valve repair in 1996. He initially did well after this operation, but 1 week after the operation had fever, hypotension, and subsequent cardiovascular collapse, requiring rapid extracorporeal membrane oxygenation and intraaortic balloon pump placement for stabilization. He could not be weaned from extracorporeal membrane oxygenation and intraaortic balloon pump, and received a Heartmate LVAD. He recovered and did well. By 4 months after LVAD placement, LVEF had increased to greater than 45%. The decision was made to proceed with device removal. In the operating room, with the device turned off, the patient maintained normal hemodynamic status and underwent LVAD removal. Gradually during 2 years, the patient had a decrease of LVEF to 30% to 35%, and deteriorated to a New York Heart Association class III level. He had multiple admissions for congestive heart failure, exacerbated by severe medication noncompliance. Because of noncompliance, he was not reactivated for transplantation. Four years later, the patient died of gastrointestinal hemorrhage, aspiration pneumonia, and sepsis.

From other institutions, 5 of 111 LVAD placements from the Columbia-Presbyterian experience [50, 51] and 5 patients from the Texas Heart Institute experience [52] had explantation for recovery. The largest published series is from the German Heart Institute [53], where 19 patients had LVAD explantation for recovery. Device removal occurred after a variable length of support, ranging from 30 days to almost 800 days of support [51, 53, 55].

Predictors of successful recovery and device explantation

Among patients with myocarditis, a proportion of patients had poor recovery of function, requiring subsequent transplantation [24, 45]. The histologic predictors of recovery are not clear [24].

Among patients with dilated cardiomyopathy who had device explantation for recovery, a variable number (up to 30% to 50%) had recurrent failure after device removal, requiring relisting for transplant or repeat LVAD placement [53, 55]. In the above series, criteria for device removal were normalization of LV measurements and maintenance of stable hemodynamics with the pump turned off for short periods of time [51–53, 56]. Factors that could influence success include weaning protocols, medical therapy after device explantation, and any of the cellular and biochemical factors previously mentioned. Some investigators noted a disappearance of anti-ß1 receptor antibodies in patients who recovered [37, 53, 56]. These clinical series were not designed to address the role of length of support and the role of serial cellular and biochemical analysis in the decision to remove the LVAD. The experience with bridge to recovery for dilated cardiomyopathy remains anecdotal.

Device weaning and removal

The optimum weaning protocol has yet to be determined. In the Columbia-Presbyterian series (with Heartmate LVAD), patients were assessed with exercise studies in the auto mode and, if tolerated, switched from the auto mode to a fixed mode at 20 cycles/min for assessment [51]. Maintenance of normal hemodynamic status with the device turned off for short periods in the operating room is also necessary to assess tolerance to device removal.

Device removal procedures have been described for ABIOMED, Thoratec, Heartmate, and Novacor device types. For Heartmate and Novacor devices, explantation involves either ligating and leaving the outflow and inflow conduit in situ as an off-pump procedure or sternotomy for removing the inflow graft with concomitant partial left ventriculotomy on cardiopulmonary bypass [52, 53]. ABIOMED and Thoratec devices require sternotomy for cannula removal [43].

Future horizons: applications and research

Left ventricular assist device as a bridge to recovery represents an intriguing phenomenon in heart failure, but currently there is a frustrating disconnect between the cellular recovery and rare sustained clinical recovery. With the use of an LVAD, selected patients who had severe cardiac failure with multiple organ dysfunction demonstrated recovery of cardiac function to the point that the LVAD could be explanted successfully. Multiple studies have begun to elucidate the basis for this phenomenon. Future studies need to focus on the impact of (1) the primary cardiomyopathy process, (2) the timing of initiating LVAD support in the course of the disease process, (3) medical therapy (eg, angiotensin-converting enzyme inhibitors, ß-blockers) that may improve the opportunity for recovery, (4) LVAD weaning protocols, (5) imaging and functional studies to determine LV function during weaning and periods with the pump turned off, (6) the safest operative technique and LVAD design for LVAD explant, and (7) additional measures that may ensure a sustained recovery (eg, additional surgery such as coronary artery bypass grafting or mitral valve replacement, new medical therapy such as matrix metalloproteinase inhibitors, cell therapy such as myoblast transfer, and gene therapy for heart failure). This area poses a formidable challenge, but in this era of worsening donor shortages, is research that should be well supported.

References

  1. DeBakey M.E. Left ventricular bypass pump for cardiac assistance. Am J Card 1971;27:3-11.
  2. Cooley D.A., Liotta D., Hallman G.L., Bloodwell R.D., Leachman R.D., Milam J.P. Orthotopic cardiac prosthesis for two-staged cardiac replacement. Am J Cardiol 1969;24:723-730.[Medline]
  3. Pennington D.G., Bernhard W.F., Golding L.R., Berger R.L., Khuri S.F., Watson J.T. Long-term follow up of postcardiotomy patients with profound cardiogenic shock treated with ventricular assist device. Circulation 1985;72:216-226.
  4. Pae W.E., Miller C.A., Matthews Y., Pierce W.S. Ventricular assist devices for post cardiotomy cardiogenic shock. J Thorac Cardiovasc Surg 1992;104:541-553.[Abstract]
  5. McCarthy P.M., Portner P.M., Tobler H.G., Starnes V.A., Ramasamy N., Oyer P.E. Clinical experience with the Novacor ventricular assist system. J Thorac Cardiovasc Surg 1991;102:578-587.[Abstract]
  6. McCarthy P.M., Smedira N.O., Vargo R.L., et al. One hundred patients with the HeartMate left ventricular assist device: evolving concepts and technology. J Thorac Cardiovasc Surg 1998;115:904-912.[Abstract/Free Full Text]
  7. Sun B.C., Catanese K.A., Spanier T.B., et al. 100 long-term implantable left ventricular assist devices: the Columbia-Presbyterian interim experience. Ann Thorac Surg 1999;68:688-694.[Abstract/Free Full Text]
  8. Parameshwar J., Wallwork J. Left ventricular assist devices: current status and future applications. Int J Cardiol 1997;62(Suppl 1):S23-S27.
  9. Mann D.L. Mechanisms and models in heart failure: a combinatorial approach. Circulation 1999;100:999-1008.[Free Full Text]
  10. Kurrelmeyer K., Kalra D., Bozkurt B., et al. Cardiac remodeling as a consequence and cause of progressive heart failure. Clin Cardiol 1998;21(Suppl 1):I14-I19.[Medline]
  11. Goldstein S., Ali A.S., Sabbah H. Ventricular remodeling-mechanisms and prevention. Cardiol Clin 1998;16:623-631.[Medline]
  12. Kapadia S., Dibbs Z., Kurrelmeyer K., et al. The role of cytokines in the failing human heart. Cardiol Clin 1998;16:645-656.[Medline]
  13. Bristow M.R., Ginsburg R., Umans V., et al. ß1- and ß2-adrenergic-receptor subpopulations in nonfailing and failing human myocardium: coupling of both receptor subtypes and selective ß1-receptor down-regulation in heart failure. Circ Res 1986;59:297-309.[Abstract/Free Full Text]
  14. Gwathmey J.K., Copelas L., MacKinnon R., et al. Abnormal intracellular calcium handling in myocardium from patients with end-stage heart failure. Circ Res 1987;61:70-76.[Abstract/Free Full Text]
  15. Heling A., Zimmerman R., Kostin S., et al. Increased expression of cytoskeletal, linkage, and extracellular proteins in failing human myocardium. Circ Res 2000;86:846-853.[Abstract/Free Full Text]
  16. Frazier O.H., Benedict C.R., Radovancevic B., et al. Improved ventricular function after chronic left ventricular unloading. Ann Thorac Surg 1996;62:675-682.[Abstract/Free Full Text]
  17. Burkhoff D., Holmes J.W., Madigan J., Barbone A., Oz M.C. Left ventricular assist device–induced reverse ventricular remodeling. Prog Cardiovasc Dis 2000;43:19-26.[Medline]
  18. Nakatani S., McCarthy P.M., Kottke-Marchant K., et al. Left ventricular echocardiographic and histologic changes: impact of chronic unloading by an implantable ventricular assist device. J Am Coll Cardiol 1996;27:894-901.[Abstract]
  19. Levin H.R., Oz M.C., Chen J.M., Packer M., Rose E.A., Burkhoff D. Reversal of chronic ventricular dilation in patients with end stage cardiomyopathy by prolonged mechanical unloading. Circulation 1995;91:2717-2720.[Abstract/Free Full Text]
  20. Nishimura M., Radovancevic B., Odegaard P., Myers T., Springer W., Frazier O.H. Exercise capacity recovers slowly but fully in patients with a left ventricular assist device. ASAIO J 1996;42:M568-M570.[Medline]
  21. Jaski B.E., Branch K.R., Adamson R., et al. Exercise hemodynamics during long-term implantation of a left ventricular assist device in patients awaiting heart transplantation. J Am Coll Cardiol 1993;22:1574-1580.[Abstract]
  22. Jaski B.E., Kim J., Maly R.S., et al. Effects of exercise during long-term support with a left ventricular assist device. Circulation 1997;95:2401-2406.[Abstract/Free Full Text]
  23. Jaski B.E., Lingle R.J., Kim J., et al. Comparison of functional capacity in patients with end-stage heart failure following implantation of a left ventricular assist device versus heart transplantation: results of the experience with left ventricular assist device with exercise trial. J Heart Lung Transplant 1999;18:1031-1040.[Medline]
  24. Houel R., Vermes E., Tixier D.B., Le Besnarais P., Benhaiem-Sigaux N., Loisance D.Y. Myocardial recovery after mechanical support for acute myocarditis: is sustained recovery predictable?. Ann Thorac Surg 1999;68:2177-2180.[Abstract/Free Full Text]
  25. Dipla K., Mattielo J.A., Jeevanandam V., Houser S.R., Margulies K.B. Myocyte recovery after mechanical circulatory support in humans with end-stage heart failure. Circulation 1998:2316-2322.
  26. Scheinin S.A., Capek P., Radovancevic B., Duncan J.M., McAllister H.A., Frazier O.H. The effect of prolonged left ventricular support on myocardial histopathology in patients with end-stage cardiomyopathy. ASAIO J 1992;38:M271-M274.[Medline]
  27. Zafeiridis A., Jeevanandam V., Houser S.R., Margulies K.B. Regression of cellular hypertrophy after left ventricular assist device support. Circulation 1998;98:656-662.[Abstract/Free Full Text]
  28. McCarthy P.M., Nakatani S., Vargo R., et al. Structural and left ventricular histologic changes after implantable LVAD insertion. Ann Thorac Surg 1995;59:609-613.[Abstract/Free Full Text]
  29. Altemose G.T., Gritsus V., Jeevanandam V., Goldman B., Margulies K.B. Altered myocardial phenotype after mechanical support in human beings with advanced cardiomyopathy. J Heart Lung Transplant 1997;16:765-773.[Medline]
  30. Lee S.H., Doliba N., Osbakken M., Oz M., Mancini D. Improvement of myocardial mitochondrial function after hemodynamic support with left ventricular assist devices in patients with heart failure. J Thorac Cardiovasc Surg 1998;116:344-349.[Abstract/Free Full Text]
  31. Takeishi Y., Jalili T., Hoit B., et al. Alterations in calcium cycling proteins and G{alpha}q signaling after left ventricular assist device support in failing human hearts. Cardiovasc Res 2000;45:883-888.[Abstract/Free Full Text]
  32. Torre-Amione G., Stetson S., Youker K.A., et al. Decreased expression of tumor necrosis factor-{alpha} in failing human myocardium after mechanical circulatory support: a potential mechanism for cardiac recovery. Circulation 1999;100:1189-1193.[Abstract/Free Full Text]
  33. Belland S.E., Jeevanandam V., Eisen H.J. Reduced myocardial matrix metalloproteinase expression as a result of sustained mechanical support with left ventricular assist devices in patients with severe dilated cardiomyopathy. J Heart Lung Transplant 1998;17:84.
  34. Milting H., Bartling B., Schumann H., et al. Altered levels of mRNA of apoptosis mediating genes after mid-term mechanical ventricular support in dilative cardiomyopathy—first results of the Halle assist induced recovery study (HAIR). Thorac Cardiovasc Surg 1999;47:48-50.[Medline]
  35. Milting H., Bartling B., Schumann H., et al. Myocardial gene expression of regulators of myocyte apoptosis and myocyte calcium homeostasis during hemodynamic unloading by ventricular assist devices in patients with end-stage heart failure. Circulation 1999;100(Suppl 2):II216-II223.
  36. Belland S.E., Grunstein R., Jeevanandam V., Eisen H.J. The effect of sustained mechanical support with left ventricular assist devices on myocardial apoptosis in patients with severe dilated cardiomyopathy. J Heart Lung Transplant 1998;17:83.
  37. Spanier T.B., Choudhri A.F., Rose E.A., et al. Anti-ß1-adrenoreceptor autoantibodies. A marker of ventricular recovery in patients with left ventricular assist devices. J Heart Lung Transplant 1997;16:80.
  38. Goldstein D.J., Moazami N., Seldomridge J.A., et al. Circulatory resuscitation with left ventricular assist device support reduces interleukins 6 and 8 levels. Ann Thorac Surg 1997;63:971-974.[Abstract/Free Full Text]
  39. Delgado R., Radovancevic B., Massin E.K., Frazier O.H., Benedict C. Neurohormonal changes after implantation of a left ventricular assist system. ASAIO J 1998;44:299-302.[Medline]
  40. James K., McCarthy P.M., Thomas J.D., et al. Effect of the implantable left ventricular assist device on neuroendocrine activation in heart failure. Circulation 1995;92(Suppl 2):II191-II195.
  41. Noirhomme P., Jacquet L., Underwood M., El Khoury G., Goenen M., Dion R. The effect of chronic mechanical circulatory support on neuroendocrine activation in patients with end-stage heart failure. Eur J Cardiothoracic Surg 1999;16:63-67.[Abstract/Free Full Text]
  42. Holman W.L., Bourge R.C., Kirklin J.K. Case report: circulatory support for seventy days with resolution of acute heart failure. J Thorac Cardiovasc Surg 1991;102:932-933.[Medline]
  43. Rockman H.A., Adamson R.M., Dembitsky W.P., Bonar J.W., Jaski B.E. Acute fulminant myocarditis: long-term follow-up after circulatory support with left ventricular device. Am Heart J 1991;121:922-926.[Medline]
  44. Kesler K.A., Pruitt A.L., Turrentine M.W., Heimansohm A., Brown J.W. Temporary left-sided mechanical cardiac support during acute myocarditis. J Heart Lung Transplant 1994;13:268-270.[Medline]
  45. Reiss N., El-Banayosy A., Posival H., Morshuis M., Minami K., Korfer R. management of acute fulminant myocarditis using circulatory support systems. Artif Organs 1996;20:964-970.[Medline]
  46. Ueno T., Bergin P., Richardson M., Esmore D.S. Bridge to recovery with a left ventricular assist device for fulminant acute myocarditis. Ann Thorac Surg 2000;69:284-286.[Abstract/Free Full Text]
  47. Martin J., Sarai K., Schindler M., van de Loo A., Yoshitake M., Beyersdorf F. MEDOS HIA-VAD biventricular assist device for bridge to recovery in fulminant myocarditis. Ann Thorac Surg 1997;63:1145-1146.[Abstract/Free Full Text]
  48. Marelli D., Laks H., Amsel B., et al. Temporary mechanical support with BVS 5000 assist device during treatment of acute myocarditis. J Card Surg 1997;12:55-59.[Medline]
  49. Westaby S., Katsumata T., Pigott D., et al. Mechanical bridge to recovery in fulminant myocarditis. Ann Thorac Surg 2000;70:278-283.[Abstract/Free Full Text]
  50. Levin H.R., Oz M.C., Catanese K.A., Rose E.A., Burkhoff D. Transient normalization of systolic and diastolic function after support with a left ventricular assist device in a patient with dilated cardiomyopathy. J Heart Lung Transplant 1996;15:840-842.[Medline]
  51. Mancini D.M., Beniaminovitz A., Levin H., et al. Low incidence of myocardial recovery after left ventricular assist device implantation in patients with chronic heart failure. Circulation 1998:2383-2389.
  52. Frazier O.H., Myers T.J. Left ventricular assist system as a bridge to myocardial recovery. Ann Thorac Surg 1999;68:734-741.[Abstract/Free Full Text]
  53. Hetzer R., Muller J., Weng Y., et al. Cardiac recovery in dilated cardiomyopathy by unloading with a left ventricular assist device. Ann Thorac Surg 1999;68:742-749.[Abstract/Free Full Text]
  54. Westaby S., Jin X.Y., Katsumata T., Taggart D.P., Coats A.J.S., Frazier O.H. Mechanical support in dilated cardiomyopathy: signs of early cardiac recovery. Ann Thorac Surg 1997;64:1303-1308.[Abstract/Free Full Text]
  55. Loebe M., Weng Y., Muller J., et al. Successful mechanical circulatory support for more than two years with a ventricular assist device in a patient with dilated cardiomyopathy. J Heart Lung Transplant 1997;16:1176-1179.[Medline]
  56. Muller J., Loebe M., Weng Y., et al. Weaning from mechanical cardiac support in patients with dilated cardiomyopathy. Circulation 1997;96:542-549.[Abstract/Free Full Text]



This article has been cited by other articles:


Home page
 Asian Cardiovasc. Thorac. Ann.Home page
Y. Oishi, M. Masuda, K.-i. Imasaka, S. Morita, and H. Yasui
Limitation of Venoarterial Bypass. Early Predictor and Optimal Conversion
Asian Cardiovasc Thorac Ann, June 1, 2005; 13(2): 167 - 171.
[Abstract] [Full Text] [PDF]

Home page
 Card Surg AdultHome page
F. J. Schoen and R. F. Padera Jr.
Cardiac Surgical Pathology
Card. Surg. Adult, January 1, 2003; 2(2003): 119 - 185.
[Full Text]

Home page
 Card Surg AdultHome page
V. Badhwar and S. F. Bolling
Nontransplant Surgical Options for Heart Failure
Card. Surg. Adult, January 1, 2003; 2(2003): 1515 - 1526.
[Full Text]

Home page
 Eur. J. Cardiothorac. Surg.Home page
S. Westaby, O.H. Frazier, F. Beyersdorf, S. Saito, M. P. Siegenthaler, D. W. Pigott, P. A. Catarino, and R. Jarvik
The Jarvik 2000 Heart. Clinical validation of the intraventricular position
Eur. J. Cardiothorac. Surg., August 1, 2002; 22(2): 228 - 232.
[Abstract] [Full Text] [PDF]

Home page
 J. Thorac. Cardiovasc. Surg.Home page
P. Tansley and M. Yacoub
Minimally invasive explantation of implantable left ventricular assist devices
J. Thorac. Cardiovasc. Surg., July 1, 2002; 124(1): 189 - 191.
[Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kumpati, G. S.
Right arrow Articles by Hoercher, K. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kumpati, G. S.
Right arrow Articles by Hoercher, K. J.
Related Collections
Right arrow Mechanical Circulatory Assistance

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS