HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Stephen Westaby Takahiro Katsumata David P. Taggart Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Westaby, S. Articles by Frazier, O. H. Search for Related Content PubMed PubMed Citation Articles by Westaby, S. Articles by Frazier, O. H.

Ann Thorac Surg 1997;64:1303-1308
© 1997 The Society of Thoracic Surgeons

---

Original Articles: Cardiovascular

Mechanical Support in Dilated Cardiomyopathy: Signs of Early Left Ventricular Recovery

Department of Cardiac Surgery, Oxford Heart Centre, John Radcliffe Hospital, Oxford, England

Accepted for publication May 7, 1997.

	Abstract

Top Footnotes Abstract Introduction Patients and Methods Results Comment Acknowledgments References

 
Background. Recent reports have documented left ventricular recovery in patients with dilated cardiomyopathy off-loaded long term with a left ventricular assist device. We sought to document the natural history of left ventricular recovery.

Methods. We implanted the TCI left ventricular assist device without the intention to perform transplantation in 2 patients with dilated cardiomyopathy who had been rejected for transplantation. Both were in New York Heart Association functional class IV and had renal failure. One was a diabetic. We studied left ventricular function with detailed echocardiography at 4, 6, and 8 weeks postoperatively.

Results. With the left ventricular assist device turned off, we observed a progressive increase in myocardial contractility beginning as early as 4 weeks after implantation and improving progressively. Histologic examination showed resolution of myocytolysis in both patients.

Conclusions. Left ventricular recovery begins earlier than was previously suspected. Mechanical bridge to myocardial recovery is a potential approach to therapy for such patients.

	Introduction

Top Footnotes Abstract Introduction Patients and Methods Results Comment Acknowledgments References

 
Heart failure resistant to medical treatment consumes an increasing amount of health care resources. Meanwhile surgical intervention has reached a watershed. Outcomes after cardiac transplantation are limited by the morbidity and mortality associated with long-term immunosuppressive therapy [1]. Because of the severely restricted donor pool and a 5-year mortality of 40%, conventional transplantation is not adequately addressing the problem [2]. Transplantation may also result in the discarding of some hearts with potentially reversible contractile dysfunction in patients with viral myocarditis, dilated cardiomyopathy, or ischemic cardiomyopathy.

Two surgical procedures are currently available to support the failing heart. The first, skeletal muscle dynamic cardiomyoplasty, may prevent further cardiac dilation but provides little in the way of increased stroke volume or cardiac output [3]. Its long-term effects are also unproved. The second is the implantation of a left ventricular assist device (LVAD), which has been used to sustain the circulation in critically ill patients pending transplantation [4, 5]. The paucity of suitable donor hearts has led to long-term LVAD support, with up to 2 years of complete mechanical off-loading [6]. Although full physiologic rehabilitation improves the outcome after transplantation, examination of the discarded heart has shown that there may be some resolution of the pathologic changes [7, 8]. These findings have led to the suggestion that LVAD implantation may even be an alternative to transplantation by providing a "mechanical bridge to myocardial recovery" [7]. A small number of patients with dilated cardiomyopathy have now undergone elective LVAD removal without transplantation.

Although left ventricular function is known to improve eventually in such patients, the time course of this recovery and its predictors remain undetermined. Consequently we prospectively studied 2 patients with dilated cardiomyopathy and advanced heart failure in whom an LVAD was implanted without the intention to perform transplantation.

	Patients and Methods

Top Footnotes Abstract Introduction Patients and Methods Results Comment Acknowledgments References

 
Both patients were male and 64 years of age and had been turned down for cardiac transplantation because of impaired renal function. Patient 2 had insulin-dependent diabetes with microvascular complications despite continuous intensive medical treatment. Both patients had had multiple previous hospital admissions to treat exacerbations of heart failure (New York Heart Association functional class IV). There were no other treatment options. Preoperative indices of myocardial function are given in Table 1. Both patients were referred for LVAD insertion from a specialized heart failure unit to a surgical center in a different hospital. A purposefully constituted ethics committee was assembled to consider the treatment strategy and gave approval to the procedure.

Initial recovery was uneventful in both patients, who were mobilized on the first postoperative day. Patient 1 was anticoagulated with warfarin on day 2 for the treatment of atrial fibrillation but suffered a cerebral hemorrhage (confirmed by computed tomography) into an old occipital infarct on the fourth postoperative day. The warfarin was discontinued, and apart from a visual field defect, he made a complete neurologic recovery, reverted to sinus rhythm, and was rehabilitated. During the first 6 weeks he also suffered four episodes of ventricular fibrillation. These were detected clinically by a decrease in the LVAD output that resulted from right heart failure. After electrocardiographic (ECG) confirmation, sinus rhythm was restored by a direct current shock. Patient 2 was not anticoagulated at any time and was discharged from the hospital 3 weeks after the operation. Right ventricular failure and dysrhythmias in both patients were managed pharmacologically and resolved with time. Renal function returned to normal limits in both patients.

Left ventricular function was assessed by serial M-mode and two-dimensional echocardiography performed before and 4, 6, and 8 weeks after operation in both patients. M-mode echocardiography was used to measure left ventricular minor axis dimensions. We also performed Doppler echocardiography preoperatively and postoperatively to make serial measurements of flow velocity at the tip of the mitral valve (with both patients in sinus rhythm). In addition, we serially recorded carotid artery pulse waves using simultaneous ECG and phonocardiography before LVAD insertion and at 4, 6, and 8 weeks postoperatively.

When patient 1 suffered a contained hemorrhage from the outflow graft of the LVAD at 5.5 months, left ventricular function was again studied echocardiographically to determine the feasibility of LVAD removal. During and after LVAD removal, transesophageal echocardiography was performed to further document left ventricular function.

	Results

Top Footnotes Abstract Introduction Patients and Methods Results Comment Acknowledgments References

 
Both patients experienced complete resolution of left and right ventricular failure with progressive reductions in body weight, heart size, and drug therapy. No diuretics were required by 6 weeks. ß-Blockers were used for the treatment of hypertension and digoxin for the management of the unsupported right ventricle. Figure 1 shows the serial recordings of the carotid pulse wave in patient 2 obtained using simultaneous ECG and phonocardiography before LVAD insertion and at 4, 6, and 8 weeks postoperatively. The findings in patient 1 were similar. Before operation there was a pronounced respiratory swing imposed on the pulse wave amplitude. At 4 weeks the arterial pulse wave corresponded only with the LVAD ejection independent of the ECG, as confirmed by phonocardiography. The aortic valve remained closed at this stage with no ejection from the native left ventricular outflow tract. At 6 weeks the arterial pulse wave still corresponded predominantly with the LVAD stroke volume, but there were also pulse waves of lesser amplitude corresponding with the ECG and systolic ejection from the left ventricle, which intermittently opened the aortic valve. By 8 weeks ejection from the native left ventricle was more pronounced (as shown by the consistent relationship of the arterial pressure waves with the ECG). This reflects an early and progressive improvement in left ventricular systolic function with the restoration of ejection through the left ventricular outflow tract.

View larger version (38K): [in this window] [in a new window]   Fig 1. . Serial recordings of the carotid artery pulse with simultaneous electrocardiography (ECG) and phonocardiography (PCG) were obtained from 1 day before to 8 weeks after the implantation of the TCI left ventricular assist device (LVAD). Note that a significant influence from respiration was imposed on the amplitude of the arterial pulse before the implantation of the LVAD. Four weeks after implantation of the LVAD the arterial pulse entirely follows the output of the LVAD (as indicated by the phonocardiogram), with no input from the native left ventricle. By 6 weeks the arterial pulse remains dominated by the LVAD; however, there are small pulse waves occurring between the LVAD output. At 8 weeks, in addition to the dominant pulse wave from the LVAD, there is significant output from the native left ventricle with a consistent relationship to the electrocardiogram.

View larger version (53K): [in this window] [in a new window]   Fig 2. . Serial recordings of mitral flow velocity obtained by Doppler echocardiography were made from 1 day before to 8 weeks after implantation of the left ventricular assist device (LVAD). Note that before implantation there is a single spiked summation wave of filling velocity (less than 200 ms), which indicates a very restrictive filling pattern. At 8 weeks the filling velocity after atrial systole has become dominant and the filling time has lengthened to 600 ms. This suggests a greatly improved left ventricular filling profile. (ECG = electrocardiography; PCG = phonocardiography.)

View larger version (70K): [in this window] [in a new window]   Fig 3. . Serial recordings of left ventricular minor axis dimension obtained by M-mode echocardiography from 1 day before to 8 weeks after implantation of the left ventricular assist device (LVAD). Note that before implantation there was a very dilated and hypokinetic left ventricle. Four weeks after implantation the end-diastolic dimension has decreased from the original 8.5 cm to 5.5 cm and has remained at this level at 8 weeks. Meanwhile the posterior wall inward motion and the reversal of septal wall motion (after the electrocardiogram) progressively increased from 4 weeks to 8 weeks. This suggests an improvement in native left ventricular systolic function. (ECG = electrocardiography; PCG = phonocardiography.)

View larger version (73K): [in this window] [in a new window]   Fig 4. . With the left ventricular assist device (LVAD) switched off at 8 weeks after implantation, there was a significant increase in the left ventricular outflow tract flow velocity with well-sustained left ventricular cavity dimensions, wall motion pattern, and ventricular filling pattern. The arterial pulse and pulmonary flow velocity are well maintained. (ECG = electrocardiography; LV = left ventricular; PCG = phonocardiography.)

At 5 months postoperatively patient 2 was readmitted from home because of fever, general malaise, and a Staphylococcus epidermidis drive line infection. Candida albicans was grown in blood cultures, and he was treated with intravenous amphotericin. The Candida disappeared from the blood, and his clinical state improved. Abnormalities of liver function persisted, and a liver biopsy was advised. There was no sign of hepatic Candida infection or heart failure, but he died of a bleeding complication of the procedure. Autopsy showed a comparative reduction in the size and intracavitary volume of the left ventricle compared with the dimensions at the time of operation. His heart weight was 765 g, and histological studies showed resolution of the myocytolysis.

	Comment

Top Footnotes Abstract Introduction Patients and Methods Results Comment Acknowledgments References

 
Although both our patients died of device-related complications, there is accumulating evidence that mechanical circulatory support with chronic off-loading of the left ventricle is a potential therapeutic option for heart failure in some categories of patients. Given the scope of this approach it is important to identify the time course of ventricular remodeling and determine whether functional recovery is sustainable. Our findings indicate that, with complete mechanical off-loading in dilated cardiomyopathy, the ventricle begins to recover within 4 to 6 weeks of implantation of the LVAD.

Until recently the structural changes that occur in end-stage cardiomyopathy have been considered irreversible. Chronic left ventricular failure results in adaptive remodeling of the myocardium, consisting of alterations in the geometry of the left ventricle and in the orientation of the cardiac myocytes, as well as disturbances in the biochemical function of the cellular organelles [9]. The neurohormonal changes that occur in heart failure (increased levels of angiotensin and norepinephrine) modify the phenotypic characteristics of the myocyte and fibroblast, leading to hypertrophy and changes in the extracellular matrix [10]. Although some aspects of remodeling are beneficial, left ventricular dilatation is a maladaptive response which increases wall stress and imparts a mechanical disadvantage to the myofibrils. This is reflected in shifts in the end-diastolic pressure-volume relationship toward larger volumes [11].

Thirty years ago, Burch and DePasquale [12] reported that one could achieve a degree of left ventricular recovery in patients with congestive heart failure by maximally reducing the workload of the dilated heart through prolonged bed rest. This approach was not pursued, however, because of the codependent effects of prolonged recumbency on other organ systems. Recently angiotensin-converting enzyme inhibitors and nitroglycerin have been shown to attenuate left ventricular enlargement after myocardial infarction, indicating that a reduction in wall stress may allow remodeling to occur [13, 14]. Long-term ß-blockade also reduces ventricular mass and may normalize left ventricular geometry [15]. In some cases pharmacologically induced unloading has resulted in a decrease in norepinephrine levels, a reliable indicator of the severity of heart failure.

In contrast with the modest pharmacologically induced reductions in ventricular filling pressure and volume, mechanical blood pumps provide substantial off-loading and the capacity to rest the heart while the patient remains active. The experience from bridge to cardiac transplantation programs has shown dramatic physiologic rehabilitation of patients with multisystem organ failure and greatly improved survival after transplantation. Besides causing hepatic and renal failure to resolve, prolonged circulatory support reverses the neurohormonal effects of chronic heart failure. Specifically, the serum aldosterone levels, plasma renin activity, and levels of atrial natriuretic peptide and norepinephrine revert to normal [8].

During cardiac transplantation after mechanical support for many months, it was noted that the hearts of patients with end-stage idiopathic cardiomyopathy had reverted toward a normal size and weight [7, 8]. In many patients indices of left ventricular function approached normal values by the time a donor organ became available. This stimulated the performance of studies of left ventricular recovery at two major transplant centers. Levin and associates [7] studied the end-diastolic pressure-volume relationships in seven excised hearts from transplant recipients with idiopathic dilated cardiomyopathy. Four had received optimal medical therapy, and 3 whose condition had deteriorated during medical treatment underwent LVAD support for 4 months [7]. The seven hearts were compared with three normal human hearts that had been harvested but were technically unsuitable for transplantation. Prolonged LVAD use was found to have reduced the left ventricular end-diastolic dimensions and pulmonary capillary wedge pressure. Hearts from the medically treated patients, however, had end-diastolic pressure-volume relationships with much larger volumes than those of the normal hearts. After LVAD support for 127 ± 20 days the end-diastolic pressure-volume relationships were shifted toward much lower volumes (similar to those of normal hearts) and ventricular mass was reduced. The study findings indicated that the severe left ventricular dilatation in idiopathic cardiomyopathy could be substantially reversed.

Frazier and associates [8] retrospectively analyzed radiographic and echocardiographic data from patients with idiopathic or ischemic cardiomyopathy who had been supported for more than 30 days (mean, 137 days; range, 31 to 505 days) with the TCI HeartMate LVAD [8]. The patients had been in heart failure for an average of 33.5 ± 39 months before implantation of the device. Tissue samples from the core of the left ventricular apex removed at the time of implantation were compared with myocardium from the explanted heart at the time of transplantation. These were examined for the extent of myocytolysis, and calcium uptake and binding studies were performed on isolated sarcoplasmic reticulum vesicles. Echocardiography performed with the pump off showed a significant decrease in the left ventricular end-diastolic dimension and an improvement in the ejection fraction cardiac index. The plasma norepinephrine levels were found to have decreased to near normal. The histologic studies showed a marked reduction in the extent of myocytolysis, and the deranged calcium uptake and binding rates in the sarcoplasmic reticulum were found to have normalized. When 1 of Frazier's patients died of a stroke after 505 days of support, the LVAD was turned off but the native heart continued to maintain the circulation with satisfactory blood pressure and cardiac output until ventilation was discontinued.

Our own experience in patients with dilated cardiomyopathy suggests that recovery begins much sooner than anticipated (though we acknowledge that changes in ventricular morphology do not necessarily convey a permanent improvement in left ventricular function). Although in the United States it has been mandatory to perform transplantation in a patient after committal to mechanical bridging with an LVAD, these restrictions do not apply elsewhere. In Berlin myocardial recovery has been sustained for periods of up to 14 months in 4 patients with dilated cardiomyopathy who underwent explantation after 160, 244, 331, and 347 days [16]. In Osaka 4 patients underwent explantation after 26 to 94 days of LVAD support [17]. Two patients with dilated cardiomyopathy are well 20 months afterwards, whereas 2 patients with ischemic cardiomyopathy have died.

There is considerable scope for a mechanical bridge to recovery as opposed to transplantation for patients with either acute or chronic left ventricular failure, depending on the cause. The Berlin group has already used a miniaturized extracorporeal biventricular support system in 2 children (age, 4 and 5 years) with acute myocarditis and cardiogenic shock [16]. The duration of support was 25 and 31 days, respectively. During cardiac off-loading the left ventricular ejection fraction increased from less than 0.15 in both to 0.55 and 0.65. This improvement was sustained after the device was removed. Transplantation would have discarded these potentially recoverable hearts and substituted the problems of immunosuppression.

Myocardial recovery through mechanical off-loading of the left ventricle is an exciting prospect for the future treatment of heart failure. There are two basic requirements for a bridge to recovery. First, reliable biochemical markers are needed to indicate whether recovery is sustainable. Hetzer's group [16] in Berlin have used the disappearance from serum of the autoantibody against the ß-adrenergic receptor. They consider that the presence of the autoantibody indicates the presence of an immune process that produces cardiac dilatation and functional impairment [16]. The Texas Heart group have suggested normalization of the norepinephrine levels as an indicator [8]. The second requirement is a user-friendly LVAD that can be removed easily or simply switched off. Efforts are now directed toward the design of small axial-flow impeller pumps that can fit within the failing left ventricle. The most advanced of these is the Jarvik 2000 (currently under development in Oxford and at the Texas Heart Institute), which can deliver a flow of up to 10 L/min. The device is silent, hemolysis is insignificant, and the propensity for thrombosis is low, even in sheep without anticoagulation. Use of the device also does not preclude transplantation.

The capacity for ventricular recovery indicates a new approach to the treatment of advanced heart failure. Unlike the human donor heart, LVADs are available from the shelf and should not be withheld until the patient is moribund. Our findings suggest that the process of myocardial recovery begins earlier than expected and that further efforts should be made to promote myocardial recovery in preference to transplantation.

	Acknowledgments

Top Footnotes Abstract Introduction Patients and Methods Results Comment Acknowledgments References

 
We thank Dr Heinrich Taegtmeyer for his help with the manuscript.

	Footnotes

Top Footnotes Abstract Introduction Patients and Methods Results Comment Acknowledgments References

 
Address reprint requests to Mr Westaby, Department of Cardiac Surgery, Oxford Heart Centre, John Radcliffe Hospital, Oxford OX3 9DU, England.

	References

Top Footnotes Abstract Introduction Patients and Methods Results Comment Acknowledgments References

 

1. Westaby S. The need for artificial hearts. Heart 1996;76:200–6.[Abstract/Free Full Text]
2. Kaye MP. The Registry of the International Society for Heart and Lung Transplantation: tenth official report—1993. J Heart Lung Transplant 1993;12:541–8.[Medline]
3. Bellotti G, Moraes A, Bocchi E, et al. Late effects of cardiomyoplasty on left ventricular mechanics and diastolic filling. Circulation 1993;88:304–8.
4. McCarthy PM. Heartmate implantable left ventricular assist device: bridge to transplantation and future applications. Ann Thorac Surg 1995;59:846–51.
5. Frazier OH, Rose EA, McCarthy P, et al. Improved mortality and rehabilitation of transplant candidates treated with a long term implantable left ventricular assist system. Ann Thorac Surg 1995;222:327–38.
6. Levin HR, Chen JM, Oz MC, et al. Potential of left ventricular assist devices as outpatient therapy while awaiting transplantation. Ann Thorac Surg 1994;58:1515–20.[Abstract]
7. Levin HR, Oz MC, Chen JM, Packer M, Rose EA, Burkhoff D. Reversal of chronic ventricular dilation in patients with end stage cardiomyopathy by prolonged mechanical offloading. Circulation 1995;91:2717–20.[Abstract/Free Full Text]
8. Frazier OH, Benedict CR, Radovancevic B, et al. Improved left ventricular function after chronic left ventricular offloading. Ann Thorac Surg 1996;62:675–82.[Abstract/Free Full Text]
9. Pfeffer MA, Braunwald E. Ventricular remodelling after myocardial infarction: experimental observations and clinical implications. Circulation 1990;81:1161–72.[Abstract/Free Full Text]
10. Packer M. Neurohormonal interactions and adaptations in congestive heart failure. Circulation 1988;77:721–30.[Free Full Text]
11. Burkhoff D, Flaherty JT, Yue DT, et al. In vitro studies of isolated supported human hearts. Heart Vessels 1988;4:185–96.[Medline]
12. Burch GE, DePasquale NP. On resting the human heart. Am J Med 1968;44:165–7.[Medline]
13. Pfeffer MA, Lamas G, Vaughan D, Parisi A, Braunwald E. Effect of captopril on progressive ventricular dilatation after anterior myocardial infarction. N Engl J Med 1988;319:80–6.[Abstract]
14. Jugutt BL, Warnica JW. Intravenous nitroglycerin therapy to limit myocardial infarct size, expansion and complications: effect of timing, dosage and infarct location. Circulation 1988;78:906–19.[Abstract/Free Full Text]
15. Hall S, Cigassoa C, Marcouz L, et al. Regression of hypertrophy and alteration in left ventricular geometry in patients with congestive heart failure treated with beta-adrenergic blockade [Abstract].Circulation1994;90 (suppl 1)1:543.
16. Mueller J, Wallukat G, Weng Y, Hetzer R. Recovery from dilated cardiomyopathy and anti-ß₁-adrenoceptor autoantibodies. In: Akutsu T, Koyanagi H, eds. Artificial heart 6. Tokyo: Springer-Verlag (in press).
17. Nakatani T, Sasako Y, Kosakai T, et al. Influence of long-term support upon the severely failed left ventricle. In: Akutsu T, Koyanagi H, eds. Artificial heart 6. Tokyo: Springer-Verlag (in press).

This article has been cited by other articles:

				S. Klotz, A. Barbone, S. Reiken, J. W. Holmes, Y. Naka, M. C. Oz, A. R. Marks, and D. Burkhoff Left ventricular assist device support normalizes left and right ventricular beta-adrenergic pathway properties J. Am. Coll. Cardiol., March 1, 2005; 45(5): 668 - 676. [Abstract] [Full Text] [PDF]

				N. de Jonge, D. F. van Wichen, M. E. I. Schipper, J. R. Lahpor, F. H. J. Gmelig-Meyling, E. O. Robles de Medina, and R. A. de Weger Left ventricular assist device in end-stage heart failure: persistence of structural myocyte damage after unloading: An immunohistochemical analysis of the contractile myofilaments J. Am. Coll. Cardiol., March 20, 2002; 39(6): 963 - 969. [Abstract] [Full Text] [PDF]

				A. Barbone, J. W. Holmes, P. M. Heerdt, A. H.S. The', Y. Naka, N. Joshi, M. Daines, A. R. Marks, M. C. Oz, and D. Burkhoff Comparison of Right and Left Ventricular Responses to Left Ventricular Assist Device Support in Patients With Severe Heart Failure: A Primary Role of Mechanical Unloading Underlying Reverse Remodeling Circulation, August 7, 2001; 104(6): 670 - 675. [Abstract] [Full Text] [PDF]

				G. S. Kumpati, P. M. McCarthy, and K. J. Hoercher Left ventricular assist device bridge to recovery: a review of the current status Ann. Thorac. Surg., March 1, 2001; 71 (2007): S103 - S108. [Abstract] [Full Text] [PDF]

				E. Vermes, R. Houel, M. Simon, P. Le Besnerais, and D. Loisance Doppler tissue imaging to predict myocardial recovery during mechanical circulatory support Ann. Thorac. Surg., December 1, 2000; 70(6): 2149 - 2151. [Abstract] [Full Text] [PDF]

				H. Suma, T. Isomura, T. Horii, T. Sato, N. Kikuchi, K. Iwahashi, and J. Hosokawa NONTRANSPLANT CARDIAC SURGERY FOR END-STAGE CARDIOMYOPATHY J. Thorac. Cardiovasc. Surg., June 1, 2000; 119(6): 1233 - 1245. [Abstract] [Full Text] [PDF]

				T. Isomura, H. Suma, T. Horii, T. Sato, and N. Kikuchi Partial left ventriculectomy, ventriculoplasty or valvular surgery for idiopathic dilated cardiomyopathy - the role of intra-operative echocardiography Eur. J. Cardiothorac. Surg., March 1, 2000; 17(3): 239 - 245. [Abstract] [Full Text] [PDF]

				R. Houel, E. Vermes, D. B. Tixier, P. Le Besnerais, N. Benhaiem-Sigaux, and D. Y. Loisance Myocardial recovery after mechanical support for acute myocarditis: is sustained recovery predictable? Ann. Thorac. Surg., December 1, 1999; 68(6): 2177 - 2180. [Abstract] [Full Text] [PDF]

				P. M. Dohmen, H. Laube, K. de Jonge, G. Baumann, and W. Konertz MECHANICAL CIRCULATORY SUPPORT FOR ONE THOUSAND DAYS OR MORE WITH THE NOVACOR N100 LEFT VENTRICULAR ASSIST DEVICE J. Thorac. Cardiovasc. Surg., May 1, 1999; 117(5): 1029 - 1030. [Full Text] [PDF]

				S. Westaby, T. Katsumata, R. Houel, R. Evans, D. Pigott, O. H. Frazier, and R. Jarvik Jarvik 2000 Heart : Potential for Bridge to Myocyte Recovery Circulation, October 13, 1998; 98(15): 1568 - 1574. [Abstract] [Full Text] [PDF]

				R. Jarvik, S. Westaby, T. Katsumata, D. Pigott, and R. D. Evans LVAD Power Delivery: A Percutaneous Approach to Avoid Infection Ann. Thorac. Surg., February 1, 1998; 65(2): 470 - 473. [Abstract] [Full Text] [PDF]

This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Stephen Westaby Takahiro Katsumata David P. Taggart Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Westaby, S. Articles by Frazier, O. H. Search for Related Content PubMed PubMed Citation Articles by Westaby, S. Articles by Frazier, O. H.