(Circulation. 1995;91:2717-2720.)
© 1995 American Heart Association, Inc.
Articles |
Reversal of Chronic Ventricular Dilation in Patients With End-Stage Cardiomyopathy by Prolonged Mechanical Unloading
From the Division of Circulatory Physiology, Department of Medicine, and the Division of Cardiothoracic Surgery, Department of Surgery, College of Physicians and Surgeons, Columbia University, New York, NY.
Correspondence to Howard R. Levin, MD, Columbia-Presbyterian Medical Center, Division of Circulatory Physiology, 177 Fort Washington Ave, Milstein 5-435, New York, NY 10032.
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Abstract |
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 Top Abstract IntroductionMethods Results Discussion References |
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Background Ventricular dilation, indexed by marked shifts toward larger volumes of the end-diastolic pressure-volume relation (EDPVR), has been considered to represent an irreversible aspect of ventricular remodeling in end-stage heart failure. However, we hypothesized that such dilation could be reversed with sufficient hemodynamic unloading, such as can be provided by a left ventricular assist device (LVAD).
Methods and Results The EDPVRs of hearts from seven patients with
end-stage idiopathic cardiomyopathy and comparable
baseline hemodynamics were measured ex vivo at the time of cardiac
transplantation; these were compared with EDPVRs from three normal
human hearts that were technically unsuitable for transplantation. Four
of the patients received optimal medical therapy; three of the
patients, who deteriorated on optimal therapy, underwent LVAD support
for 
4 months. Compared with the normal hearts, EDPVRs of hearts from
medically treated patients were shifted toward markedly larger volumes.
In contrast, EDPVRs of hearts from LVAD patients were similar to those
of normal hearts.
Conclusions Chronic hemodynamic unloading of sufficient magnitude and duration can result in reversal of chamber enlargement and normalization of cardiac structure as indexed by the EDPVR, both important aspects of remodeling, even in the most advanced stages of heart failure.
Key Words: diastole • heart failure • ventricles • cardiac volume
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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Biochemical composition of the ventricular wall, orientation of cardiac muscle fibers, and geometry of the ventricular chamber are all modified in states of chronic heart failure. Remodeling is the term commonly used to describe these facets of cardiac adaptation in disease. While some aspects of the remodeling process may be beneficial to overall heart function in disease, other aspects are likely to be maladaptive in the long run. One notable maladaptive aspect of remodeling is left ventricular dilation, which is characterized not only by an increase in ventricular end-diastolic volume but also by shifts of the end-diastolic pressure-volume relation (EDPVR) toward larger volumes.1 Ventricular dilation increases wall stress and imparts mechanical disadvantage to the myofibrils; therefore, it is a critical event in the disease process.
Accordingly, there has been significant interest in understanding the mechanisms of ventricular dilation and in developing interventions to prevent and reverse this process. Both angiotensin-converting enzyme inhibitors and nitroglycerin have been shown to attenuate ventricular enlargement after myocardial infarction, suggesting, at least in part, that reduction of wall stress may be an important factor.2 3 Preliminary studies also suggest that chronic ß-blocker therapy reduces ventricular mass and normalizes left ventricular shape in patients with heart failure.4 Thus, while previous studies suggest that the remodeling process may be reversed to some degree by pharmacological interventions, the extent to which this could be achieved with adequate hemodynamic unloading is unclear. Accordingly, it is generally considered that ventricular dilation due to remodeling in advanced heart failure is an irreversible process.
Mechanical left ventricular assist devices (LVADs), which have been used in critically ill patients awaiting heart transplantation, can provide hemodynamic unloading of the left ventricle that is much greater than can be achieved by pharmacological agents. The goal of the present study was to test whether prolonged mechanical unloading of the ventricle by an LVAD in end-stage idiopathic dilated cardiomyopathy would lead to a reversal of the dilation process and normalization of the EDPVR.
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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Patient Population
Hearts explanted from seven patients with New York Heart Association class IV heart failure due to idiopathic dilated cardiomyopathy were studied at the time of cardiac transplantation. Four patients received optimal medical therapy with digitalis, diuretics, and a converting enzyme inhibitor, whereas three patients who continued to deteriorate despite optimal medical therapy underwent mechanical support with the Thermo Cardiosystems Heartmate 1000 IP LVAD5 (Thermo Cardiosystems, Inc) for 127±20 (mean±SD) days as a bridge to cardiac transplantation. All patients had comparable baseline hemodynamic characteristics, as summarized in the Table
. Three normal human hearts not suitable for
transplantation for technical reasons were also available for study.
Two hearts were from male donors and one was from a female donor, with
ages ranging between 30 and 45 years. In all cases, the hearts were
given cardioplegia and explanted, and their diastolic mechanical
properties were studied as detailed below.
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Principles of LVAD Operation
The Heartmate 1000 IP LVAD is a
pneumatic device of pusher-plate
design5 that sits over the abdominal cavity between the
muscles and fatty layers of the abdominal wall. The inflow conduit
connects with the LV chamber through a 1-in.-diameter hole created near
the LV apex. The outflow conduit passes through the diaphragm, back
into the thoracic cavity, and next to the heart to reach the ascending
aorta with an end-to-side anastomosis. During normal operation, blood
flows from the left ventricle into the LVAD chamber and out to the
aorta. Since the ventricle generally empties into the compliant LVAD
pumping chamber, LV volume and pressure are low. The degree of volume
unloading was assessed by echocardiography performed during normal
operation and during temporary (30- to 60-second) cessation of LVAD
pumping. The degree of diastolic pressure unloading and hemodynamic
support provided by the LVAD was assessed at 30 days after implantation
by measurement of cardiac output, pulmonary capillary wedge pressure,
and systemic blood pressure. Comparisons between hemodynamic
measurements before and 30 days after LVAD implantation were performed
with a Student's paired t test; P<.05 was
considered significant.
Isolated Heart Experiment
The principal measure of LV size
and structure examined in the
present study was the EDPVR. The EDPVR was measured in all hearts
in a state of cold cardioplegia (4°C, hypocalcemic, hyperkalemic
solution) by methods similar to those described
previously.1 Hearts from LVAD patients and transplant
patients were studied within 1 hour of explantation; two of the normal
hearts were studied after 2 hours and the third after 4 hours of
explantation. Briefly, a compliant water-filled latex balloon was
placed within the LV chamber and held in place by a metal adapter
sutured to the mitral annulus; a clamp was placed around the remnants
of the aortic root. The volume within the balloon was varied in steps
from the volume that provided an intracavitary pressure of 0 mm Hg to
the volume needed to obtain an end-diastolic pressure of at
least 20 mm Hg. The resulting pressure at each volume was measured by
a high-fidelity micromanometer placed in the intraventricular balloon.
LV EDPVRs were then constructed by plotting the corresponding pressures
and volumes.
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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LVAD Provides Pressure and Volume Unloading
Volume unloading by the LVAD is demonstrated by the echocardiograms, obtained from a patient 7 days after implantation, shown in Fig 1
, which is typical of those obtained from
the other patients. Whereas end-diastolic dimension was >6
cm with the device temporarily turned off (top), it decreased to <3 cm
during mechanical support (bottom). This pronounced degree of
ventricular volume unloading was accompanied by a marked degree of
pressure unloading, as evidenced by a reduction in the pulmonary
capillary wedge pressure from a baseline of 29±4 mm Hg to 3±2
mm Hg
(P<.001) measured 30 days after implantation. Despite
ventricular pressure and volume unloading, there was an increase in
cardiac output (from 2.2±0.4 to 5.1±0.3 L/min,
P<.001)
and an increase in mean systemic blood pressure (from 71±9 to
93±10
mm Hg, P<.001) also measured 30 days after implantation.
All of these hemodynamic benefits have been shown previously to be
realized immediately after LVAD implantation and to be maintained for
the duration of LVAD support.6 Another piece of indirect
evidence suggesting systolic pressure unloading of the LV by the LVAD
is obtained from echocardiography, which reveals that during normal
LVAD operation, the aortic valve almost always remains closed; this
implies that peak LV pressure generation is generally less than
diastolic aortic pressure. Thus, the LVAD provides both pressure and
volume unloading of the left ventricle while maintaining adequate
systemic perfusion.
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EDPVR Normalizes After Prolonged LVAD Support
The EDPVRs
measured from all hearts studied are shown in Fig 2. Hearts
from the medically treated patients (open
circles) had EDPVRs that were shifted toward much larger volumes
compared with those of the normal hearts (diamonds). Since the
preoperative end-diastolic dimensions and hemodynamic
profiles of the LVAD patients were similar to those of the medically
treated patients (Table
), it would be expected that the EDPVRs
in the
LVAD group would have been similar to the medical treatment group
before LVAD implantation. However, after LVAD support for 127±20 days,
the EDPVRs of these hearts (filled circles) were shifted toward much
lower volumes compared with those of the medically treated heart
failure patients and were similar to those obtained from the normal
hearts. Accompanying the leftward shift of the EDPVR was a trend for
heart mass (combined LV and RV mass) to decrease: normal hearts weigh
between 250 and 350 g; heart failure hearts weighed 393, 668, 487, and
905 g; and LVAD-supported heart failure hearts weighed only 270, 390,
and 300 g.
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), three heart failure patients after prolonged left ventricular
assist device (LVAD) support (
), and three normal subjects
(
). Whereas EDPVRs of hearts from medically treated patients were
shifted far to the right of the normal hearts, EDPVRs from the LVAD
groups were close to normal. x axis shows volume in
milliliters; y axis, pressure in mm Hg. |
Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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Ventricular remodeling is the result of many factors, including the initial degree of myocardial impairment, the efficacy of endogenous repair mechanisms, and the balance of distending versus restorative mechanical forces.7 In addition, the neurohormonal milieu in heart failure8 (increased levels of angiotensin, norepinephrine, etc) substantially alters the phenotypic characteristics of myocytes and nonmyocytes (fibroblasts) that lead to hypertrophy and modifications in the extracellular matrix.9 10 11 It is hypothesized that these physical stresses and alterations in biochemical composition set up an environment that fosters structural rearrangement and dilation of the failing heart. These intrinsic structural changes are reflected grossly as shifts of the EDPVR. This chronic change in structure differs from acute, reversible increases in ventricular end-diastolic dimension (as occurs, for example, during acute heart failure or exercise) that simply represent a stretching of muscles and interstitial components along a fixed EDPVR. In contrast, the changes in ventricular composition and structure in patients with end-stage cardiomyopathy have generally been considered to be irreversible.
Recently, there has been some evidence from both experimental and clinical heart failure that angiotensin-converting enzyme inhibitors can limit or reverse remodeling to a small degree.3 12 13 14 However, such pharmacological therapies have been less effective than the mechanical assist device in normalizing ventricular size as reported in this study, perhaps because such agents produce only modest reductions in ventricular filling pressure and volume.13 15 Although larger doses of vasodilator drugs may result in more pronounced ventricular unloading, the accompanying reduction in vital organ perfusion would limit the ultimate degree of unloading that could be achieved by these means. The results of the present study provide the first evidence that severe ventricular dilation due to idiopathic cardiomyopathy can be substantially reversed, even in the most advanced stages of heart failure.
Previous reports have suggested that restoration of other aspects of ventricular structure may also occur during long-term support with various types of ventricular assist devices. The most notable of these are normalization of fiber orientation16 and regression of myocyte hypertrophy (ie, normalization of myocyte dimensions)17 ; the latter observation is consistent with the marked reduction of ventricular mass also observed in the present study. More recently, Frazier18 observed a reduction in heart size, improved ejection fraction, and the ability of the native heart to support cardiac output and blood pressure after the LVAD was turned off in one patient who died of a thromboembolic event after 505 days of LVAD support.
The findings reported in this study are observational and do not elucidate the specific components or mechanisms involved in reverse remodeling. The marked hemodynamic unloading of the left ventricle by the LVAD may be the primary factor responsible for this dramatic change in heart structure. However, we must also consider that plasma concentration of several neurohormones that regulate myocardial growth (aldosterone, renin, norepinephrine) normalize during LVAD support,6 and accordingly, these may contribute to the observed phenomenon. Independent of the mechanism, the findings are striking and raise several points that may contribute to future thinking about the nature of end-stage heart failure. First, the results challenge a long-held view regarding the irreversible nature of ventricular dilation in end-stage heart failure. In retrospect, this view was based on limitations of previously available therapies and not on an intrinsic inability of heart structure to be restored if the stimuli for dilation are withdrawn. In this regard, it will be important to examine separately changes in myocyte properties and changes in nonmyocyte properties in response to the unloading; the former may reveal important information pertaining to the processes involved in regression of hypertrophy, and the latter may reveal information pertaining to the regulation of extracellular matrix composition. Improved understanding of the hemodynamic, neurohormonal, and molecular events involved in reverse remodeling may lead to new strategies to attain the same goal by pharmacological means.
It is also important to recognize that normalization of ventricular structure does not mean normalization of ventricular function. While reduction of chamber size will lead to a stronger pump (via Laplace's law),7 prolonged unloading of the heart is not expected to reverse intrinsic (perhaps genetically based) defects in muscle contractile properties. Thus, in thinking about future therapies for heart failure, restoration of heart size is only one, albeit an important, factor that needs to be addressed. One can imagine, as the era of cellular and gene therapy in cardiology approaches, that the circulation can be supported and the failing heart restored to normal size by temporary use of a mechanical support device while another therapy is applied to remedy the underlying molecular defect responsible for contractile dysfunction of the muscles.
In summary, long-term LV unloading by mechanical circulatory support results in normalization of the EDPVR in patients with idiopathic dilated cardiomyopathy. Whether this reversal of the remodeling process truly represents restoration of detailed aspects of cardiac chamber ultrastructure with normalization of the biochemical and cellular makeup of the chamber wall, as well as the permanence of the normalization, remains to be elucidated. Nevertheless, these findings are consistent with the concept that if sufficient ventricular unloading can be achieved, at least some aspects of cardiac remodeling, even when advanced, can be reversed.
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Acknowledgments |
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This work was supported in part by grant 1R29-HL-51885-01 from the NIH Heart, Lung, and Blood Institute and by the Lowy Foundation. Dr Burkhoff was supported by an Investigatorship award from the American Heart Association, New York City Affiliate, and from the Whitaker Foundation.
Received January 26, 1995; revision received April 3, 1995; accepted April 3, 1995.
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G. D. Buckberg Imaging, models, and reality: A basis for anatomic-physiologic planning J. Thorac. Cardiovasc. Surg., February 1, 2005; 129(2): 243 - 245. [Full Text] [PDF]
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S. Klotz, M. C. Deng, J. Stypmann, J. Roetker, M. J. Wilhelm, D. Hammel, H. H. Scheld, and C. Schmid Left ventricular pressure and volume unloading during pulsatile versus nonpulsatile left ventricular assist device support Ann. Thorac. Surg., January 1, 2004; 77(1): 143 - 149. [Abstract] [Full Text] [PDF]
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N. A. Nussmeier, C. B. Probert, D. Hirsch, J. R. Cooper Jr., I. D. Gregoric, T. J. Myers, and O. H. Frazier Anesthetic Management for Implantation of the Jarvik 2000TM Left Ventricular Assist System Anesth. Analg., October 1, 2003; 97(4): 964 - 971. [Abstract] [Full Text] [PDF]
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K.-l. He, J. Shimizu, G.-h. Yi, A. Gu, M. A. Kashem, D. L. Crabbe, S. Popilskis, E. X. Wu, W. P. Santamore, D. Melvin, et al. Left ventricular systolic performance in failing heart improved acutely by left ventricular reshaping J. Thorac. Cardiovasc. Surg., July 1, 2003; 126(1): 56 - 65. [Abstract] [Full Text] [PDF]
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B. S. McGowan, C. B. Scott, A. Mu, R. J. McCormick, D. P. Thomas, and K. B. Margulies Unloading-induced remodeling in the normal and hypertrophic left ventricle Am J Physiol Heart Circ Physiol, June 1, 2003; 284(6): H2061 - H2068. [Abstract] [Full Text] [PDF]
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S. Reiken, X. H.T. Wehrens, J. A. Vest, A. Barbone, S. Klotz, D. Mancini, D. Burkhoff, and A. R. Marks {beta}-Blockers Restore Calcium Release Channel Function and Improve Cardiac Muscle Performance in Human Heart Failure Circulation, May 20, 2003; 107(19): 2459 - 2466. [Abstract] [Full Text] [PDF]
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B. C. Blaxall, B. M. Tschannen-Moran, C. A. Milano, and W. J. Koch Differential gene expression and genomic patient stratification following left ventricular assist device support J. Am. Coll. Cardiol., April 2, 2003; 41(7): 1096 - 1106. [Abstract] [Full Text] [PDF]
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M. R. Bristow Microarray measurements of gene expression before and after left ventricular assist device placement J. Am. Coll. Cardiol., April 2, 2003; 41(7): 1107 - 1108. [Full Text] [PDF]
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D. Burkhoff New heart failure therapy: The shape of things to come? J. Thorac. Cardiovasc. Surg., March 1, 2003; 125(90030): S50 - 52. [Full Text] [PDF]
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N.E. Bowles The molecular biology of dilated cardiomyopathy Eur. Heart J. Suppl., December 1, 2002; 4(suppl_I): I2 - I7. [Abstract] [PDF]
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M. S. Joharchi, U. Neiser, U. Lenschow, J. Schubert, W. Kienast, G. Noeldge-Schomburg, and G. Steinhoff Thoratec left ventricular assist device for bridging to recovery in fulminant acute myocarditis Ann. Thorac. Surg., July 1, 2002; 74(1): 234 - 235. [Abstract] [Full Text] [PDF]
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W. F. Saavedra, R. S. Tunin, N. Paolocci, T. Mishima, G. Suzuki, C. W. Emala, P. A. Chaudhry, P. Anagnostopoulos, R. C. Gupta, H. N. Sabbah, et al. Reverse remodeling and enhancedadrenergic reserve from passive externalsupport in experimental dilated heart failure J. Am. Coll. Cardiol., June 19, 2002; 39(12): 2069 - 2076. [Abstract] [Full Text] [PDF]
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B. W. Duncan Mechanical circulatory support for infants and children with cardiac disease Ann. Thorac. Surg., May 1, 2002; 73(5): 1670 - 1677. [Abstract] [Full Text] [PDF]
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P. M. Heerdt, M. Schlame, R. Jehle, A. Barbone, D. Burkhoff, and T. J.J. Blanck Disease-specific remodeling of cardiac mitochondria after a left ventricular assist device Ann. Thorac. Surg., April 1, 2002; 73(4): 1216 - 1221. [Abstract] [Full Text] [PDF]
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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]
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P. M. L. Janssen, G. Hasenfuss, O. Zeitz, S. E. Lehnart, J. Prestle, D. Darmer, J. Holtz, and H. Schumann Load-dependent induction of apoptosis in multicellular myocardial preparations Am J Physiol Heart Circ Physiol, January 1, 2002; 282(1): H349 - H356. [Abstract] [Full Text] [PDF]
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A. Barbone, M. C. Oz, D. Burkhoff, and J. W. Holmes Normalized Diastolic Properties After Left Ventricular Assist Result From Reverse Remodeling of Chamber Geometry Circulation, September 18, 2001; 104 (2009): I-229 - I-232. [Abstract] [Full Text] [PDF]
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D. L. Mann and H. Taegtmeyer Dynamic Regulation of the Extracellular Matrix After Mechanical Unloading of the Failing Human Heart: Recovering the Missing Link in Left Ventricular Remodeling Circulation, September 4, 2001; 104(10): 1089 - 1091. [Full Text] [PDF]
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Y. Y. Li, Y. Feng, C. F. McTiernan, W. Pei, C. S. Moravec, P. Wang, W. Rosenblum, R. L. Kormos, and A. M. Feldman Downregulation of Matrix Metalloproteinases and Reduction in Collagen Damage in the Failing Human Heart After Support With Left Ventricular Assist Devices Circulation, September 4, 2001; 104(10): 1147 - 1152. [Abstract] [Full Text] [PDF]
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D. Burkhoff New heart failure therapy: The shape of things to come? J. Thorac. Cardiovasc. Surg., September 1, 2001; 122(3): 421 - 423. [Full Text] [PDF]
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B. W. Duncan, D. J. Bohn, A. M. Atz, J. W. French, P. C. Laussen, and D. L. Wessel Mechanical circulatory support for the treatment of children with acute fulminant myocarditis J. Thorac. Cardiovasc. Surg., September 1, 2001; 122(3): 440 - 448. [Abstract] [Full Text] [PDF]
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M. L. Ogletree-Hughes, L. B. Stull, W. E. Sweet, N. G. Smedira, P. M. McCarthy, and C. S. Moravec Mechanical Unloading Restores {beta}-Adrenergic Responsiveness and Reverses Receptor Downregulation in the Failing Human Heart Circulation, August 21, 2001; 104(8): 881 - 886. [Abstract] [Full Text] [PDF]
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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]
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N. W. Guldner, P. Klapproth, M. Gro{beta}herr, A. Brugge, A. Sheikhzadeh, R. Tolg, E. Rumpel, R. Noel, and H.-H. Sievers Biomechanical Hearts: Muscular Blood Pumps, Performed in a 1-Step Operation, and Trained Under Support of Clenbuterol Circulation, August 7, 2001; 104(6): 717 - 722. [Abstract] [Full Text] [PDF]
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J. D. Madigan, A. Barbone, A. F. Choudhri, D. L. S. Morales, B. Cai, M. C. Oz, and D. Burkhoff Time course of reverse remodeling of the left ventricle during support with a left ventricular assist device J. Thorac. Cardiovasc. Surg., May 1, 2001; 121(5): 902 - 908. [Abstract] [Full Text] [PDF]
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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]
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G. L. Brower and J. S. Janicki Contribution of ventricular remodeling to pathogenesis of heart failure in rats Am J Physiol Heart Circ Physiol, February 1, 2001; 280(2): H674 - H683. [Abstract] [Full Text] [PDF]
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M. S. Slaughter, M. A. Silver, D. J. Farrar, A. J. Tatooles, and P. S. Pappas A new method of monitoring recovery and weaning the thoratec left ventricular assist device Ann. Thorac. Surg., January 1, 2001; 71(1): 215 - 218. [Abstract] [Full Text] [PDF]
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P. M. Heerdt, J. W. Holmes, B. Cai, A. Barbone, J. D. Madigan, S. Reiken, D. L. Lee, M. C. Oz, A. R. Marks, and D. Burkhoff Chronic Unloading by Left Ventricular Assist Device Reverses Contractile Dysfunction and Alters Gene Expression in End-Stage Heart Failure Circulation, November 28, 2000; 102(22): 2713 - 2719. [Abstract] [Full Text] [PDF]
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S. Mital, K. E. Loke, L. J. Addonizio, M. C. Oz, and T. H. Hintze Left ventricular assist device implantation augments nitric oxide dependent control of mitochondrial respiration in failing human hearts J. Am. Coll. Cardiol., November 15, 2000; 36(6): 1897 - 1902. [Abstract] [Full Text] [PDF]
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R. Hetzer, J. H. Muller, Y.-G. Weng, M. Loebe, and G. Wallukat Midterm follow-up of patients who underwent removal of a left ventricular assist device after cardiac recovery from end-stage dilated cardiomyopathy J. Thorac. Cardiovasc. Surg., November 1, 2000; 120(5): 843 - 855. [Abstract] [Full Text] [PDF]
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E. A.K. Beyer, D. M. McMullan, R. Delgado, I. Gregoric, B. Radovancevic, and O.H. Frazier Normalization of native heart function years after heterotopic transplantation Ann. Thorac. Surg., November 1, 2000; 70(5): 1690 - 1691. [Abstract] [Full Text] [PDF]
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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]
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Y. Takeishi, T. Jalili, B. D. Hoit, D. L. Kirkpatrick, L. E. Wagoner, W. T. Abraham, and R. A. Walsh Alterations in Ca2+ cycling proteins and G{alpha}q signaling after left ventricular assist device support in failing human hearts Cardiovasc Res, March 1, 2000; 45(4): 883 - 888. [Abstract] [Full Text] [PDF]
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A. S. Shah, R. E. Lilly, A. P. Kypson, O. Tai, J. A. Hata, A. Pippen, S. C. Silvestry, R. J. Lefkowitz, D. D. Glower, and W. J. Koch Intracoronary Adenovirus-Mediated Delivery and Overexpression of the {beta}2-Adrenergic Receptor in the Heart : Prospects for Molecular Ventricular Assistance Circulation, February 1, 2000; 101(4): 408 - 414. [Abstract] [Full Text] [PDF]
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B. Bartling, H. Milting, H. Schumann, D. Darmer, L. Arusoglu, M. M. Koerner, A. El-Banayosy, R. Koerfer, J. Holtz, and H.-R. Zerkowski 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, November 9, 1999; 100 (2009): II-216 - II-223. [Abstract] [Full Text] [PDF]
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D. L. Mann Mechanisms and Models in Heart Failure : A Combinatorial Approach Circulation, August 31, 1999; 100(9): 999 - 1008. [Full Text] [PDF]
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B. C. Sun, K. A. Catanese, T. B. Spanier, M. R. Flannery, M. T. Gardocki, L. S. Marcus, H. R. Levin, E. A. Rose, and M. C. Oz 100 long-term implantable left ventricular assist devices: the Columbia Presbyterian interim experience Ann. Thorac. Surg., August 1, 1999; 68(2): 688 - 694. [Abstract] [Full Text] [PDF]
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R. Hetzer, J. Muller, Y. Weng, G. Wallukat, S. Spiegelsberger, and M. Loebe Cardiac recovery in dilated cardiomyopathy by unloading with a left ventricular assist device Ann. Thorac. Surg., August 1, 1999; 68(2): 742 - 749. [Abstract] [Full Text] [PDF]
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J. M. Chen, J. J. DeRose, J. P. Slater, T. B. Spanier, T. M. Dewey, K. A. Catanese, M. A. Flannery, and M. C. Oz Improved survival rates support left ventricular assist device implantation early after myocardial infarction J. Am. Coll. Cardiol., June 1, 1999; 33(7): 1903 - 1908. [Abstract] [Full Text] [PDF]
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D. L. Mann and J. T. Willerson Left Ventricular Assist Devices and the Failing Heart : A Bridge to Recovery, a Permanent Assist Device, or a Bridge Too Far? Circulation, December 1, 1998; 98(22): 2367 - 2369. [Full Text] [PDF]
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D. M. Mancini, A. Beniaminovitz, H. Levin, K. Catanese, M. Flannery, M. DiTullio, S. Savin, M. E. Cordisco, E. Rose, and M. Oz Low Incidence of Myocardial Recovery After Left Ventricular Assist Device Implantation in Patients With Chronic Heart Failure Circulation, December 1, 1998; 98(22): 2383 - 2389. [Abstract] [Full Text] [PDF]
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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]
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W. E. Pae Jr, J. M. Anderson, E. H. Blackstone, H. S. Boroevetz, A. Ciarkowski, J. G. Copeland III, M. R. Costanzo-Nordin, K. Daase, M. A. Dew, M. J. Domanski, et al. Bethesda conference: conference for the design of clinical trials to study circulatory support devices for chronic heart failure Ann. Thorac. Surg., October 1, 1998; 66(4): 1452 - 1465. [Full Text] [PDF]
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A. Zafeiridis, V. Jeevanandam, S. R. Houser, and K. B. Margulies Regression of Cellular Hypertrophy After Left Ventricular Assist Device Support Circulation, August 18, 1998; 98(7): 656 - 662. [Abstract] [Full Text] [PDF]
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L. Pietsch, H. Laube, G. Baumann, and W. Konertz Recovery from end-stage ischemic cardiomyopathy during long-term LVAD support Ann. Thorac. Surg., August 1, 1998; 66(2): 555 - 557. [Abstract] [Full Text] [PDF]
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S. H. Lee, N. Doliba, M. Osbakken, M. Oz, and D. Mancini Improvement of myocardial mitochondrial function after hemodynamic support with left ventricular assist devices in patients with heart failure J. Thorac. Cardiovasc. Surg., August 1, 1998; 116(2): 344 - 349. [Abstract] [Full Text] [PDF]
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K. Dipla, J. A. Mattiello, V. Jeevanandam, S. R. Houser, and K. B. Margulies Myocyte Recovery After Mechanical Circulatory Support in Humans With End-Stage Heart Failure Circulation, June 16, 1998; 97(23): 2316 - 2322. [Abstract] [Full Text] [PDF]
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L. F. P. Moreira, N. A. G. Stolf, E. A. Bocchi, F. Bacal, M. C. P. Giorgi, J. R. Parga, and A. D. Jatene Partial left ventriculectomy with mitral valve preservation in the treatment of patients with dilated cardiomyopathy J. Thorac. Cardiovasc. Surg., April 1, 1998; 115(4): 800 - 807. [Abstract] [Full Text] [PDF]
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N. Moazami, M. Argenziano, T. Kohomoto, S. Yazdani, E. A. Rose, D. Burkhoff, and M. C. Oz Inflow Valve Regurgitation During Left Ventricular Assist Device Support May Interfere With Reverse Ventricular Remodeling Ann. Thorac. Surg., March 1, 1998; 65(3): 628 - 631. [Abstract] [Full Text] [PDF]
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M. Komeda, A. DeAnda Jr, J. R. Glasson, A. F. Bolger, G. T. Daughters II, N. B. Ingels Jr, and D. C. Miller Complete Unloading Alone May Not Adequately Protect the Left Ventricle Ann. Thorac. Surg., November 1, 1997; 64(5): 1250 - 1255. [Abstract] [Full Text]
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S. Westaby, X. Y. Jin, T. Katsumata, D. P. Taggart, A. J. S. Coats, and O. H. Frazier Mechanical Support in Dilated Cardiomyopathy: Signs of Early Left Ventricular Recovery Ann. Thorac. Surg., November 1, 1997; 64(5): 1303 - 1308. [Abstract] [Full Text]
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S. Westaby, T. Katsumata, R. Evans, D. Pigott, D. P. Taggart, and R. K. Jarvik THE JARVIK 2000 OXFORD SYSTEM: INCREASING THE SCOPE OF MECHANICAL CIRCULATORY SUPPORT J. Thorac. Cardiovasc. Surg., September 1, 1997; 114(3): 467 - 474. [Abstract] [Full Text]
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J. Muller, G. Wallukat, Y.-G. Weng, M. Dandel, S. Spiegelsberger, S. Semrau, K. Brandes, V. Theodoridis, M. Loebe, R. Meyer, et al. Weaning From Mechanical Cardiac Support in Patients With Idiopathic Dilated Cardiomyopathy Circulation, July 15, 1997; 96(2): 542 - 549. [Abstract] [Full Text]
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H. R. Levin and M. L. Weisfeldt Deep Thoughts on Tin Men: Fact, Fallacy, and Future of Mechanical Circulatory Support Circulation, May 20, 1997; 95(10): 2340 - 2343. [Full Text]
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B. E. Jaski, J. Kim, R. S. Maly, K. R. Branch, R. Adamson, L. K. Favrot, S. C. Smith Jr, and W. P. Dembitsky Effects of Exercise During Long-term Support With a Left Ventricular Assist Device : Results of the Experience With Left Ventricular Assist Device With Exercise (EVADE) Pilot Trial Circulation, May 20, 1997; 95(10): 2401 - 2406. [Abstract] [Full Text]
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MehmetC. Oz, M. Argenziano, K. A. Catanese, M. T. Gardocki, D. J. Goldstein, R. C. Ashton, A. C. Gelijns, E. A. Rose, and H. R. Levin Bridge Experience With Long-term Implantable Left Ventricular Assist Devices: Are They an Alternative to Transplantation? Circulation, April 1, 1997; 95(7): 1844 - 1852. [Abstract] [Full Text]
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O. H. Frazier, C. R. Benedict, B. Radovancevic, R. J. Bick, P. Capek, W. E. Springer, M. P. Macris, R. Delgado, and L. M. Buja Improved Left Ventricular Function After Chronic Left Ventricular Unloading Ann. Thorac. Surg., September 1, 1996; 62(3): 675 - 681. [Abstract] [Full Text]
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