(Circulation. 1997;96:542-549.)
© 1997 American Heart Association, Inc.
Articles |
Weaning From Mechanical Cardiac Support in Patients With Idiopathic Dilated Cardiomyopathy
From the German Heart Institute Berlin, Department of Cardiac and Vascular Surgery, and the Max-Delbrück-Center, Berlin, Germany (G.W.).
Correspondence to Johannes Müller, MD, German Heart Institute Berlin, Augustenburger Platz #1, 13353 Berlin, Germany.
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionFollow-upReferences |
|---|
Background Implantation of mechanical cardiac support systems (MCSS) in patients with idiopathic dilated cardiomyopathy (IDC) may improve cardiac function and allow explantation of the device. We report of long-term effects of ventricular unloading on cardiac function, humoral anti-ß1-adrenoceptor autoantibodies (A-ß1-AABs), and myocardial fibrosis.
Methods and Results Seventeen patients in New York Heart Association functional class IV with nonischemic IDC received MCSS. All had a cardiac index of <1.6 L · min-1 · m-2 of body surface area, a left ventricular ejection fraction (LVEF) of <16%, and a left ventricular internal diameter in diastole (LVIDd) of >68 mm and tested positive for A-ß1-AABs. Echocardiographic evaluation, serum tests for A-ß1-AABs, and histological assessment of myocardial fibrosis were performed before and after MCSS implantation. The mean support duration was 230±201 days. Six patients died, four were transplanted, and two are still on MCSS. Five patients with significant cardiac recovery (mean LVIDd, 54±2.3 mm; LVEF, 47±3.7%) were weaned after 160 to 794 days and are now device free for 51 to 592 days. A-ß1-AABs disappeared gradually during MCSS without increase after weaning; cardiac function and volume density of fibrosis remained normal. Nine patients' cardiac function hardly improved during ventricular unloading.
Conclusions Cardiac function can be normalized in selected patients with end-stage IDC by MCSS. The degree of preoperative myocardial fibrosis may be an indicator for outcome; A-ß1-AABs can be used to monitor myocyte recovery. Weaning from MCSS offers an alternative to cardiac transplantation in certain patients.
Key Words: cardiomyopathy • assist devices • implantation
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionFollow-upReferences |
|---|
When a donor heart is not available, implantation of a mechanical assist device often is the only possible means of supporting patients with end-stage heart failure in the form of bridging to transplantation. As of 1994, this method had been performed 584 times worldwide, with an increasing trend.1 2 3 4 About two thirds of the patients who receive a cardiac assist device have IDC.5
The bridge-to-transplantation concept may be life-saving for the individual patient, but it does not solve the basic problem, which is acute donor organ shortage. Possible alternatives could be the permanent use of mechanical systems or their temporary application with the goal of durable heart recovery. Success with the latter approach has been reported in isolated cases of acute onset of cardiac enlargement or myocarditis and postcardiotomic heart failure.2 6 7 8 9
Observations made in several institutions have supported the opinion that in certain patients with IDC, the heart may indeed shrink considerably in size during MCSS therapy and even regain normal contractility; however, it seems that these effects prevail only as long as the ventricle is unloaded.10 11 12 13 14
The questions of how and to what extent such an observation may express a healing process occurring in an individual IDC heart and whether this would be long lasting have to be approached in the context of the wide field of IDC pathophysiological research and theory. It is generally accepted that at least a few of the heart ailments within the spectrum of what is termed idiopathic cardiomyopathy are related to immunological processes.15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31
The A-ß1-AAB levels found in the sera of 80% of the patients with IDC were selected for a pilot study, originally with the intention to see whether some of the patients with MCSS might qualify for immunosuppressive treatment.26 During this pilot study, it became apparent that the process of normalization of the function of the heart in association with the support system was accompanied by a simultaneous decrease and, finally, disappearance of the A-ß1-AABs. The next logical step, which is to explant the pump once the heart function had been shown to be normal for a certain period, was controversially discussed in our group, with the main focus on the question of the persistence of the cardiac function achieved after pump explantation. The decision in favor of pump explantation was then eased by two additional events.
First, a 34-year-old patient with IDC (LVIDd, 71 mm; LVEF, 15%) was implanted with a left ventricular assist device. Twelve weeks after implantation, he sustained massive cerebral bleeding, such that neurosurgical intervention had to be carried out. For this procedure, all anticoagulation had to be interrupted, with the consequence that the device had to be turned off because of the risk of thromboembolic events. Before implantation of the device, the serum of this patient had been positive for A-ß1-AABs. At the time of the cerebral bleeding, however, these antibodies could no longer be detected, and his left heart had improved to a near-normal function (LVIDd, 52 mm; LVEF, 50%), remaining stable with a trend toward further improvement over a period of 5 days until he eventually died from the effects of cerebral hemorrhage.
Second, a 38-year-old patient had a thromboembolic event with paresis of the left oculomotor nerve 158 days after implantation of an MCSS. At the time of embolism, he had near-normal cardiac function and no detectable A-ß1-AABs, which had previously been high. Not to expose the patient to further emboli, we decided to explant the pump.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionFollow-upReferences |
|---|
Patients
Between January 1994 and May 1995, 31 patients with end-stage cardiac insufficiency were implanted with an MCSS. Seventeen patients had an IDC and were selected as our study group. All 17 patients were male and between the ages of 32 and 67 years (mean, 49±11 years) with a body surface area of 2.1±0.2 m2 (range, 1.7 to 2.4 m2). At the time of implantation, all patients fulfilled the established criteria defining cardiogenic shock and required positive inotropic support of dobutamine, dopamine, and phosphodiesterase inhibitors.33 The cardiac index was <1.6 L · min-1 · m-2, LVEF was <16% (because of an increasing error with decreasing area LVEF, values of <16% are not explicitly quoted in our institution), and LVIDd >68 mm; it was necessary to increase the positive inotropic support for the duration of 1 week.
Myocardial tissue specimens did not reveal sufficient evidence that a virus could have caused the IDC: Polymerase chain reactions for cytomegalovirus, enterovirus, and adenoviruses were negative. In situ hybridization for the same viruses as well as for coxsackievirus, Epstein-Barr virus, and herpes viruses were also negative. Infiltration of CD2-, CD3-, CD4-, CD5-, CD11-, CD14-, CD19-, CD25-, or CD57-positive cells was <1.5 cells/hpf. One patient (patient 5) was suspected of having had excessive alcohol intake as a cause of IDC, but this could not be confirmed by auto- and social anamnesis.
LVEF and LVIDd were measured by echocardiography before MCSS implantation and once a week thereafter with the pump turned off for 4 minutes. All examinations were conducted by the same examiner to ensure a minimum of variability in the echocardiographic parameters. Of these 17 patients, 5 demonstrated recovery of their natural heart function, and the pump was explanted.
Informed consent was obtained from each patient, and the project was approved by the Ethics Committee of Humboldt University, Berlin, Germany.
Cardiac Assist Devices
The assist devices (Baxter Healthcare Corporation, Novacor
Division: 11 patients; Thermo Cardiosystems Inc.,: 6 patients) were
implanted anterior to the fascia musculi recti abdominis posterioris in
the left upper abdominal quadrant. The inflow conduit was anastomosed
to the apex of the left ventricle and the outflow conduit to the
ascending aorta in an end-to-side position. All implantations were
performed under extracorporeal circulation.34 35
To avoid postoperative thrombus formation, the patients with the Novacor N100 device were anticoagulated with warfarin (coumarin), with the aim of a prothrombin time in the international normalized ratio of 2.5, whereas patients with the TCI HeartMate were administered 100 mg acetylsalicylic acid PO and 225 mg dipyridamole PO per day.
Postimplant and Postexplant Management
Early postimplantation management of cardiac assist patients was
similar to that of any other critically ill post–cardiac surgery
patient. Invasive postoperative monitoring included a thermodilution
pulmonary artery catheter and a left atrial line. Pump output
and stroke volume and pulmonary and radial arterial
and central venous pressures were continuously monitored during the
initial postoperative phase. In addition to the standard postsurgical
care of cardiac patients, postoperative management of the assisted
patients included percutaneous exit-side care and a
device-specific anticoagulant regimen. All patient problems and the
handling of decisions regarding mechanical assist management were under
the care of a specially trained mechanical support team.
By the time cardiac function had recovered and the patients had become accustomed to living with their device, they were either discharged home (4 patients) or to a residence with daily medical observation near the German Heart Institute (7 patients). They were seen here as outpatients at least every 3 weeks.
Medical treatment consisted of ß-blockers, low-dose diuretics
(thiazides and loop diuretics), ACE inhibitors, and
nitrates with an aim of a systolic arterial blood
pressure of 
110 mm Hg. For oxidative stress reduction, every
patient got an additional moderate dosage of different vitamins,
vitaminoids, minerals, and trace elements (OrthoCor Plus; Orthomol
GmbH) as a nutritional supplement and enzymes (Phlogenzym; Mucos GmbH).
This medication as well as nutritional supplements were continued with
only dosage adjustments after weaning.
Within the first year after explantation, the patients came in for outpatient follow-up at least every 2 months. Thereafter, they were seen three times a year.
Blood Samples
Blood samples were taken during routine clinic visits
immediately before implantation and once a week; thereafter, samples of
10 mL of peripheral blood were drawn in a serum syringe
without additives and treated in accordance with established clinical
guidelines. To obtain the sera for determination of
A-ß1-AABs by bioassay, the blood was centrifuged
at 3600 rpm.
Bioassay
An exact description of the bioassay for the
A-ß1-AAB scan has been previously
published.23 36 The underlying principle is the
registration of the stimulating effect of A-ß1-AABs on
single myocytes dissociated from minced ventricles after the IgG
fraction has been isolated and the precipitates dialyzed from the sera.
The incremental change of myocytal undulation in a 15-second interval
was used to quantify the amount of functionally effective
autoantibodies present (LU).
Morphometry
Myocardial full-thickness samples taken during insertion of the
device and biopsy specimens taken 
1 year after explantation of the
support system were fixed in 10% formalin followed by paraffin
embedding and sectioned at 5-µm thickness. Domagk stain was used for
visualization of the connective tissue and morphometry of fibrosis. The
volume fraction of fibrosis was determined using the method of Weibel
et al.37 A 100-point grid with an area of 400 Tm was used.
All points counted in tissue that was occupied by fibrosis were
expressed as a percentage (volume density, percent) of the entire
tissue sample (after subtraction of points occupied by empty area,
arterioles, and veins). Interstitial tissue volume density
was evaluated at a magnification x400 by light microscopy. It was
calculated that 20 adjacent fields should be analyzed per
specimen to ensure a standard error of an average of 5%. For
assessment of collagen type III, the sections were deparaffinized,
rehydrated, and treated with pepsin before immunohistochemical staining
was performed with a polyclonal antibody (Quartett
Immundiagnostica & Biotechnologie) specific to human
placental collagen type III. Assessment of collagen content was
performed semiquantitatively on the basis of a five-grade ranking
scale.
The Weaned
All weaned patients had at least a 4-year history of dilated
cardiomyopathy with two or more episodes of cardiac
decompensation before being admitted here in cardiogenic shock. We saw
patients with severe biventricular cardiac insufficiency,
tachypnea, and sinus tachycardia exhibiting all the signs
of chronic low-output syndrome, most requiring oxygen via nasal tube.
Humoral A-ß1-AABs were detected in all. A left
ventricular assist device was implanted on the day of
admission or 1 day later. Patients 1, 2, 3, and 5 received the Novacor
N100 system; patient 4 received the TCI HeartMate. Detailed
patient-specific hemodynamic data at the time of device
implantation are listed in Table 1
.
|
In patient 1, systemic transient thromboembolism suggested pump explantation to preclude recurrence of this complication; patient 3 had a persistent purulent wound infection prohibiting later transplantation; and patients 2, 4, and 5 voluntarily insisted on pump removal when postexplantation success in patient 1 became apparent. All patients were fully aware of the lack of long-term experience with this treatment and of their roles as pioneers; therefore, they remain under close long-term observation.
Weaning Procedure
In the patients who chose the option of being weaned from the
pump, the drive unit was programmed in an asynchronous mode (a fixed
pumping rate mode) for 3 consecutive weeks to test the stability of the
recovered cardiac function. The fixed-rate mode leads to a dissociation
in the coordination between the moment of maximum cardiac ejection and
that of optimum filling of the pump, a discrepancy that tends to
increase left ventricular afterload. When this occurs,
synchronization between heart and pump is random at best.
Pump Explantation
Explantation was performed by opening the pouch containing the
device and ligating both inflow and outflow conduits from below the
diaphragm in the patients with the Novacor system and via a left
thoracotomy to the inflow cannula in the patient with the TCI.
Statistical Analysis
All data summary and statistical analyses were performed
using SPSS for Windows 95, version 7.0. To assess the significance of
the differences between individual groups, the
nonparametric Mann-Whitney two-sample test was applied.
Paired data were analyzed by the Wilcoxon signed rank
test. A value of P<.05 was considered to indicate
statistical significance.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionFollow-upReferences |
|---|
Presentation of the results concentrates on the clinical progression of LVIDd, LVEF, volume density of replacement fibrosis, and the A-ß1-AAB levels found in 17 patients who received either a Novacor (11 patients) or a TCI (6 patients) as a consequence of IDC. Three patients died from bleeding complications between days 59 and 75 postoperatively. One patient died from multiorgan failure on the 93rd postoperative day, and 2 died from technical pump-related problems leading to massive bleeding on the 37th and 183rd postoperative day, respectively. Presently, 2 patients continue to receive support for periods totaling to date 491 and 496 days, respectively. Four patients were transplanted after 95, 123, 225, and 236 days, and 5 additional patients were weaned from the device 160, 243, 347, 200, and 794 days, respectively, after insertion. These patients have been device free since 592, 510, 502, 395, and 51 days (as of October 31, 1996). The mean duration of support for all 17 patients was 230±201 days (range, 37 to 794 days).
All sera tested positive for A-ß1-AABs with a mean value of 6.5±0.8 LU (range, 5.2 to 7.5 LU) before implantation. After assist implantation, A-ß1-AABs decreased in all patients and ultimately disappeared at 12±5 weeks (range, 8 to 25 weeks) in all the 14 patients who survived long enough after implant and could not be detected at any later time.
At follow-up evaluations, echocardiographic
examinations of the 14 patients who survived at least until
A-ß1-AABs had disappeared showed an improvement in LVIDd
and LVEF from a mean value of 77±7 mm (range, 69 to 95 mm)
to 64±10 mm (range, 52 to 81 mm) and from <16% to a mean
value of 31±14% (range, 15 to 50%), respectively (Fig 1).
|
The cardiothoracic ratio showed an improvement from a mean value of 0.69±0.03 (range, 0.62 to 0.74) to a mean value of 0.59±0.11 (range, 0. 43 to 0.70) (P<.05).
When these 14 patients were divided into two groups—one (A) of 9 patients with an LVIDd of >74 mm and one (B) of 5 patients with an LVIDd of <75 mm before implantation—certain differences became apparent: In group A, LVIDd decreased from a mean value of 81±7 mm (range, 75 to 95 mm) before implantation to 69±8 mm (range, 62 to 81 mm), and LVEF rose to a mean value of 22±7% (range, 15% to 34%) at the time after implantation (when the A-ß1-AABs had disappeared), whereas patients in group B showed a better recovery of LVIDd from a mean value of 71±2 mm (range, 69 to 74 mm) to 54±2 mm (range, 52 to 58 mm) and an increase of LVEF to a mean value of 47±4% (range, 41% to 50%). All the weaned were in group B.
A detailed breakdown of this group's hemodynamic and
functional data immediately after explantation is listed in Table 1
.
The mean volume density of replacement fibrosis calculated from
myocardial full-thickness samples of all 17 patients taken at the time
of device insertion showed a mean value of 30±5% (range, 19% to
36%) (Fig 2, Table 2).
Although the myocardial histology of patients of group A showed a mean
value of 34±2% (range, 30% to 36%), group B exhibited a mean value
of 24±4% (range, 19% to 28%). Specimens taken >1 year after
explantation (from the first 4 weaned patients) showed a mean value of
5±3% (range, 3% to 8%) (Fig 3, Table 2). Furthermore, collagen subtype III was
semiquantitatively graded. All patients had been highly positive at the
time of insertion. One year after explantation, collagen III was
histologically no longer detectable in 2 patients. In
1, it was slightly positive, and in another it was just positive (Table 3).
|
|
|
|
Since explantation of the assist pumps, all 5 patients have remained in a stable physical and circulatory condition. Invariably, they have been in New York Heart Association functional class IA. One patient (patient 2) has fully returned to his professional occupation, 1 (patient 1) has entered an employment retraining course, and 2 (patients 3 and 4) are permanently retired. Patient 5 is planning to go back to his work as a roofer. The follow-up echo data (LVIDd <58 mm and LVEF >41% in all patients as of October 31, 1996) demonstrate a persistently stable cardiac function with no trend toward deterioration over a period of 2 to 20 months. All patients have been given the aforementioned medication.
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionFollow-upReferences |
|---|
It was shown that MCSS could be effectively used in selected patients with end-stage IDC as a tool to normalize cardiac function. By their use, the initially planned cardiac transplantation became unnecessary. Weaning patients with advanced IDC from MCSS after >160 days of left ventricular unloading is a new and hitherto unknown procedure of which the success could not be anticipated with certainty. A complete recovery to normal cardiac function could not be expected because of the persistent trauma associated with the implantation of the inflow cannula into the left ventricular apex. However, after a cumulative observation period of nearly 6 years, it can now be assumed that this treatment will succeed.
This result is contrary to the expectations of many authors who have considered a long-lasting improvement of cardiac function in patients with end-stage IDC to be most unlikely or who failed with a similar trial.10 12 32
The decision to choose this method of treatment as opposed to carrying out the originally planned transplantation was facilitated by either the occurrence of device-related complications or by patient option on the one hand and the observation of functional cardiac recovery and the persistent disappearance of A-ß1-AABs as a sign of myocyte recovery on the other. In view of the fact that during mid-term follow-up observation both cardiac function and A-ß1-AAB levels have not pointed toward relapse, our experience with this concept, though still limited, would seem to indicate new avenues of treatment, at least for some of those patients otherwise destined for transplantation, and may also ignite new discussions concerning the pathophysiology of IDC. It was in any case possible to wean 29% (5 of 17) of the patients and 45% (5 of 11) of the surviving patients in this study.
The idea that hearts ravaged by advanced stages of chronic IDC may indeed profit from long-term unloading dates back to previous cardiologists who saw substantial improvements in such patients after prolonged periods of strict bed rest. However, those patients did not depend on high doses of positive inotropic medication before they began bed rest therapy.38 39 In the era of assist devices, there have been rare unpublished studies of unexpectedly good heart function after longer assist periods. To our knowledge, there has been no report about planned assist explantation, not to mention accounts of successful patient progress after explantation in chronic IDC. Success of this nature was achieved in patients with acute heart failure caused by ischemic heart disease and acute myocarditis.6 8
A wide spectrum of autoimmune antibodies is currently being discussed as playing a role in the development of IDC. Because it was not the primary intention of this study to enter into the discussion about which individual antibody or set of antibodies would provide the most meaningful marker for IDC and improvement of myocyte function, we adhered exclusively to A-ß1-AABs, as these antibodies have been detected in >80% of patients with IDC.26 A-ß1-AABs were found in all of our 17 nonselected patients at the time of assist implantation, whereas this antibody was never present in patients with exclusive ischemic cardiomyopathy. Other autoantigens, such as the mitochondrial ADP/ATP carrier, branched-chain keto acid dehydrogenase, the cardiac myosin heavy chain, and laminin, are found less frequently in patients with IDC.20 29 30 40 41
The detection of A-ß1-AABs by bioassay is based on their
stimulating effect on myocytes, an effect that can be inhibited in the
assay by ß-blockers. This supports the hypothesis that
A-ß1-AABs may also have a chronically stimulating effect
on the heart rate of patients with IDC and may indeed initiate or
accelerate the further course of IDC. This view is in turn supported by
animal experiments in which chronic stimulation over a period of 3
weeks with abnormally high heart rates (240 bpm) has been seen to
induce dilated cardiomyopathy.42 43
Matsui et al44 could prove for the first time a causative
linkage between the effect of A-ß1-AABs and development
of IDC. A-ß1-AABs seem to act as a primary trigger of
cardiac dilatation and reduction of wall thickness in their animal
setting.44
As we know, ß1-adrenoceptors are not limited to the heart. We tend to assume that the antibodies monitored in our patients resulted from the antigenicity of cardiac structures, which would explain the surprising parallelism of antibody decrease and the increase in ventricular function. Another factor favoring this assumption is the fact that A-ß1-AABs have been described only in patients with heart diseases.23 24 25 31 Nevertheless, the reason why long-term left ventricular unloading leads to a disappearance of A-ß1-AABs remains unexplored. A similar but inverse process was observed in an experimental setting; exercise in subjects with known autoimmune myocarditis resulted in an augmentation of autoimmunity associated with cardiac dilatation.45
There were variations in cardiac functional improvement within the group of patients whose A-ß1-AABs disappeared in relation to cardiac diameter. We did not examine the reason for less-than-complete improvement, but it is conspicuous that more extensively dilated hearts (LVIDd >74 mm) and those with a higher degree of replacement fibrosis showed less functional improvement. This may be because such hearts with considerably more structural changes may need more time to recover or, indeed, will never reach acceptable functional values. The LVIDd values of the weaned patients were all within the lower range of left ventricular diameters measured in this study. An analysis of the distribution of fibrosis observed in these patients seems to confirm this hypothesis. The hearts with a low grade of improvement showed significantly more myocardial fibrosis at the time of insertion than the myocardium of the weaned patients.
The morphometric analyses of the biopsy specimens taken from patients >1 year after explantation exhibited a quasinormal myocardial histology. Fibrosis had been reduced to normal myocardial volume density. We unfortunately did not perform biopsies at the time of explantation. Literature data describe increased fibrosis at the time of transplantation compared with fibrosis at the time of insertion.11 46 47 48 49 We therefore hypothesize that the process of fibrosis reduction may continue even after explantation.
Patient 5 was on the device for 794 days. His heart showed the highest level of fibrosis within the group of weaned patients. However, even his cardiac function improved in parallel the disappearance of A-ß1-AABs until he reached a LVEF of 35%. This seemed to us to be insufficient for device removal at that time. To reach 41% he required almost 2 additional years of unloading. Therefore, we speculate that the process of normalization depends on both improvement of myocyte function and the reduction of connective tissue thereafter. This process may be additionally supported by deactivation of the neuroendocrine axis.50
Although the importance of A-ß1-AABs is still an open question and will require further intensive study, we do see as confirmation of our clinical strategy the fact that all 5 patients between 51 and 594 days after explantation of the device continually exhibit unchanged cardiac functional parameters and do not show a reincrease of A-ß1-AABs. Echocardiographic examinations and screening for A-ß1-AABs in patients with IDC provide a possibility to assess the earliest moment for explantation.
Thus, weaning from the assist device saves donor hearts and improves the quality and hopefully the life prospects for these patients compared with those who undergo transplantation. The possibility of weaning compels reflection on the best moment for implantation of an assist device to avoid overextensive impairment of cardiac function. It may offer a favorable new outlook for a certain group of patients with IDC.
|
Follow-up |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionFollow-upReferences |
|---|
Since we concluded this study, we successfully weaned 5 additional patients with end-stage IDC from the device (as of February 3). They all met the aforementioned criteria for the described patient group B.
|
Selected Abbreviations and Acronyms |
|---|
|
|
|
Acknowledgments |
|---|
This work was supported by Berliner Sparkassenstiftung Medizin. The authors would like to express their appreciation for the editorial assistance of Dr L.O. Thompson, German Heart Institute Berlin, Berlin, Germany.
Received December 5, 1996; revision received March 10, 1997; accepted March 18, 1997.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionFollow-upReferences |
|---|
1. Mehta SM, Aufiero TX, Pae WE Jr, Miller CA, Pierce WS. Combined registry for the clinical use of mechanical ventricular assist pumps and the total artificial heart in conjunction with heart transplantation: sixth official report-1994. J Heart Lung Transplant. 1995;14:584-593.
2. Pae WE Jr. Ventricular assist devices and total artificial hearts: a combined registry experience. Ann Thorac Surg. 1993;55:295-298.[Abstract]
3. Hetzer R, Hennig E, Schiessler A, Friedel N, Warnecke H, Adt M. Mechanical circulatory support and heart transplantation. J Heart Lung Transplant. 1992;11:S175-S181.[Medline] [Order article via Infotrieve]
4. Magovern GL, Golding LA, Oyer PE, Cabrol C. Circulatory support-1988: weaning and bridging. Ann Thorac Surg. 1989;47:102-107.[Abstract]
5. Pae WE Jr, Miller CA, Matthews Y, Pierce WS. Ventricular assist devices for postcardiotomy cardiogenic shock: a combined registry experience. J Thorac Cardiovasc Surg. 1992;104:541-553.[Abstract]
6. Holman WL, Bourge RC, Kirklin JK. Case report: circulatory support for seventy days with resolution of acute heart failure. J Thorac Cardiovasc Surg. 1991;102:932-934.[Medline] [Order article via Infotrieve]
7. Portner PM. A totally implantable heart assist system: the Novacor program. In: Akutsu T, Koyanagi H, eds. Heart Replacement: Artificial Heart 4. Tokyo, Japan: Springer-Verlag; 1993:71-82.
8. Noon GP. Clinical use of cardiac assist devices. In: Akutzu T, Koyanagi H, eds. Heart Replacement: Artificial Heart 4. Tokyo, Japan: Springer-Verlag; 1993:195-205.
9. Nakatani T, Sasako Y, Kumon K, Nagata S, Kosakai Y, Isobe F, Nakano K, Kobayashi J, Eishi K, Takano H, Kito Y, Kawashima Y. Long-term circulatory support to promote recovery from pro found heart failure. ASAIO J. 1995;41:M526-M530.[Medline] [Order article via Infotrieve]
10. Levin HR, Oz MC, Catanese KA, Rose EA, Burkhoff D. Transient normalisation 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] [Order article via Infotrieve]
11.
McCarthy PM, Nakatani S, Vargo R, Kottke-Marchant K,
Harasaki H, James KB, Savage RM, Thomas JD. Structural and
left ventricular histologic changes after implantable LVAD
insertion. Ann Thorac Surg. 1995;59:609-613.
12. Levin HR. Invited commentary to: McCarthy PM, Nakatani S, Vargo R, Kottke-Marchant K, Harasaki H, James KB, Savage RM, Thomas JD. Structural and left ventricular histologic changes after implantable LVAD insertion. Ann Thorac Surg. 1995;59:609-613.
13.
Levin HR, Oz MC, Chen JM, Packer M, Rose EA, Burkhoff
D. Reversal of chronic ventricular dilatation in
patients with end-stage cardiomyopathy by prolonged
mechanical unloading. Circulation. 1995;91:2717-2720.
14.
Frazier OH, Benedect CR, Radovancevic B, Bick RJ, Capek
P, Springer WE, Macris MP, Delgado R, Buja M. Improved left
ventricular function after chronic left
ventricular unloading. Ann Thorac Surg. 1996;62:675-682.
15. Krehl L. Beitrag zur Kenntnis der idiopathischen Herzmuskelerkrankung. Deutsch Arch F Klin Med. 1891;48:414-431.
16. Abelmann WH. Myocarditis as a cause of dilated cardiomyopathy. In: Engelmeier BS, O'Connel JB, eds. Drug Therapy in Dilated Cardiomyopathy and Myocarditis. New York, NY: Marcel Dekker; 1988:221-231.
17.
Dec GW, Fuster V. Idiopathic dilated
cardiomyopathy. N Engl J
Med. 1994;331:1564-1575.
18. Maisch B, Berg PA, Kochsiek K. Immunological parameters in patients congestive cardiomyopathy. Basic Res Cardiol. 1980;75:221-222.[Medline] [Order article via Infotrieve]
19. Maisch B, Deeg P, Liebau G, Kochsiek K. Diagnostic relevance of humoral and cytoxic immune reactions in primary and secondary dilated cardiomyopathy. Am J Cardiol. 1983;52:1072-1078.[Medline] [Order article via Infotrieve]
20. Schultheiss H-P. The significance of autoantibodies against ADP/ATP carrier for the pathogenesis of myocarditis and dilated cardiomyopathy: clinical and experimental data. Springer Semin Immunopathol. 1989;11:15-30.[Medline] [Order article via Infotrieve]
21. Schultheiss H-P. Disturbance of the myocardial energy metabolism in dilated cardiomyopathy due to autoimmunological mechanisms. Circulation. 1993;87(suppl IV):IV-43-IV-48.
22. Caforio AL, Bonifacio E, Stewart JT, Neglia D, Parodi O, Bottazzo GF, McKenna WJ. Novel organ-specific circulating cardiac auto-antibodies in dilated cardiomyopathy. J Am Coll Cardiol. 1990;15:1527-1534.[Abstract]
23. Wallukat G, Wollenberger A. Effects of serum gamma globulin fractions of patients with allergic asthma and dilated cardiomyopathy on chronotropic ß-adrenoceptor function in cultured neonatal rat heart myocytes. Biomed Biochim Acta. 1987;46:634-639.
24.
Limas CJ, Goldenberg IF, Limas C. Autoantibodies
against beta-adrenoceptors in human dilated
cardiomyopathy. Circ Res. 1989;64:97-103.
25.
Magnusson Y, Wallukat G, Waagstein F, Hjalmarson Å,
Hoebeke J. Autoimmunity in idiopathic dilated
cardiomyopathy: characterization of antibodies
against the ß1-adrenoceptor with positive chronotropic
effect. Circulation. 1994;89:2760-2767.
26. Wallukat G, Morwinski R, Magnusson Y, Hoebeke J, Wollenberger A. Autoantikörper gegen den ß1-adrenergen Rezeptor bei Myokarditis und dilatativer Kardiomyopathie: Lokalisation von zwei Epitopen. Z Kardiol. 1992;81(suppl 4):79-83.
27. Ansari AA, Neckelmann N, Wang Y-C, Gravenis MC, Sell KW, Herskowitz A. Immunologic dialogue between cardiac myocytes, endothelial cells and mononuclear cells. Clin Immunol Immunopathol. 1993;68:208-214.[Medline] [Order article via Infotrieve]
28. Taha TH, Mazelka P, Oakley CM, Maisch B. Cardiac-specific antibodies in dilated cardiomyopathy. J Am Coll Cardiol. 1991;18:644-645.[Medline] [Order article via Infotrieve]
29. Rose NR, Beisel KW, Herskowitz A. Cardiac myosin and autoimmune myocarditis. Ciba Found Sympos. 1987;129:3-24.
30. Wolff PG, Schulteis H-P. Laminin distribution and autoantibodies to laminin in dilated cardiomyopathy and myocarditis. Am Heart J. 1989;117(6):1303-1309.
31. Borda ES, Pascual J, Cossio PM, Vega M, Arana RM, Sterin-Borda L. Circulating IgG in chagas disease which binds to ß-adrenoceptor of myocardium and modulates its activity. Clin Exp Immunol. 1984;57:679-686.[Medline] [Order article via Infotrieve]
32. Tayama E, Nose Y. Can we treat dilated cardiomyopathy using a left ventricular assist device? Artif Organs. 1996;20:197-201. Editorial.[Medline] [Order article via Infotrieve]
33. Nomenclature and Criteria for Diagnosis of Diseases of the Heart and Great Vessels, 9th ed. In: Dolgin M, ed. Boston, Mass: Little, Brown and Co; 1994:240.
34.
Pennington DG, McBride LR, Swartz MT.
Implantation technique for the Novacor left ventricular
assist system. J Thorac Cardiovasc Surg. 1994;108:604-608.
35. Radovancevic B, Frazier OH, Michael JM. Implantation technique for the HeartMate left ventricular assist device. J Card Surg. 1992;7(3):203-207.
36. Wallukat G, Wollenberger A. Die kultivierte Herzmuskelzelle. Ein funktionelles Testsystem zum Nachweis von Autoantikörpern gegen den ß-adrenergen Rezeptor. Acta Histochem. 1988:(suppl XXXV);145-149.
37.
Weibel ER, Kistler GS, Scherle WF. Practical
stereological methods for morphometric cytology. J Cell
Biol. 1966;30:23-38.
38. Burch GE. On resting the human heart. Am Heart J. 1966;71:422.[Medline] [Order article via Infotrieve]
39. Burch GE, McDonald CD, Walsh JJ. The effect of prolonged bed rest on postpartal cardiomyopathy. Am Heart J. 1971;81:186-201.[Medline] [Order article via Infotrieve]
40. Ansari AA, Wang Y-C, Danner DJ, Gravanis MB, Mayne A, Neckelmann N, Sell KW, Herskowitz A. Abnormal expression of histocompatibility and mitochondrial antigens by cardiac tissue from patients with myocarditis and dilated cardiomyopathy. Am J Pathol. 1991;139:337-354.[Abstract]
41. Maisch B, Wedekind U, Kochsiek K. Quantitative assessment of antilaminin antibodies in myocarditis and perimyocarditis. Eur Heart J. 1987;8(suppl I):233-235.
42.
Spinale FG, Zellner JL, Tomita M, Crawford FA,
Zile MR. Relation between ventricular and myocyte
remodeling with the development and regression of
supraventricular tachycardia-induced
cardiomyopathy. Circ Res. 1991;69:1058-1067.
43. Spinale FG, Tomita M, Zellner JL, Cook JC, Crawford FA, Zile MR. Collagen remodeling and changes in LV function during development and recovery from supraventricular tachycardia. Am J Physiol. 1991;261(2 Pt 2):H308-H318.
44. Matsui S, Fu MLX, Katsuda S, Hayase M, Yamaguchi N, Teraoka K, Kurihara T, Takekoshi N, Murakami E, Hoebeke J, Hjalmarson Å. Peptides derived from cardiovascular G-protein-coupled receptors induce morphological cardiomyopathy changes in immunized rabbits. JMCC. 1997; in press.
45. Hosenpud JD, Campbell SM, Niles NR, Lee J, Mendelson D, Hart MV. Exercise induced augmentation of cellular and humoral autoimmunity associated with increased cardiac dilatation in experimental autoimmune myocarditis. Cardiovasc Res. 1987;21:217-222.[Medline] [Order article via Infotrieve]
46. Nakatani S, McCathy PM, Kottke-Marchant K, Harasaki H, James KB, Savage RM, Thomas JD. 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]
47. Scheinin SA, Capek P, Radovancevic B, Duncan JM, McAllister HA, Frazier OH. The effect of prolonged left ventricular support on myocardial histopathology in patients with end-stage cardiomyopathy. ASAIO J. 1992;38:M271-M274.[Medline] [Order article via Infotrieve]
48.
Kinoshita M, Takano H, Takaichi S, Taenaka Y, Nakatani
T. Influence of prolonged ventricular assistance on
myocardial histopathology in intact heart. Ann Thorac
Surg. 1996;61:640-645.
49. Tomantek RJ, Cooper G. Morphological changes in the mechanically unloaded myocardial cell. Anat Record. 1981;200:271-280.[Medline] [Order article via Infotrieve]
50. James KB, McCarthy PM, Thomas JD, Vargo R, Hobbs RE, Sapp S, Bravo E. Effect of the implantable assist ventricular device on neuroendocrine activation in heart failure. Circulation. 1995;92(suppl II):II-191-II-195.
This article has been cited by other articles:
 |
|
 |
|
  H. Brinks, H. Tevaearai, C. Muhlfeld, D. Bertschi, B. Gahl, T. Carrel, and M.-N. Giraud Contractile function is preserved in unloaded hearts despite atrophic remodeling. J. Thorac. Cardiovasc. Surg., March 1, 2009; 137(3): 742 - 746. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Wang, M. Tsukashita, T. Nishina, A. Marui, E. Yoshikawa, H. Muranaka, S. Matsuoka, and T. Ikeda Chronic partial unloading restores beta-adrenergic responsiveness and reverses receptor downregulation in failing rat hearts. J. Thorac. Cardiovasc. Surg., February 1, 2009; 137(2): 465 - 470. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Dandel, Y. Weng, H. Siniawski, E. Potapov, T. Drews, H. B. Lehmkuhl, C. Knosalla, and R. Hetzer Prediction of Cardiac Stability After Weaning From Left Ventricular Assist Devices in Patients With Idiopathic Dilated Cardiomyopathy Circulation, September 30, 2008; 118(14_suppl_1): S94 - S105. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. K. Yang, B. Y. Choi, Y.-H. Lee, Y.-G. Kim, M.-C. Cho, S.-E. Hong, D. H. Kim, R. J. Hajjar, and W. J. Park Gene profiling during regression of pressure overload-induced cardiac hypertrophy Physiol Genomics, June 19, 2007; 30(1): 1 - 7. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Liden, K. Karason, C.-H. Bergh, F. Nilsson, B. Koul, and L. Wiklund The feasibility of left ventricular mechanical support as a bridge to cardiac recovery Eur J Heart Fail, May 1, 2007; 9(5): 525 - 530. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Suzuki, T.-S. Li, A. Mikamo, M. Takahashi, M. Ohshima, M. Kubo, H. Ito, and K. Hamano The reduction of hemodynamic loading assists self-regeneration of the injured heart by increasing cell proliferation, inhibiting cell apoptosis, and inducing stem-cell recruitment J. Thorac. Cardiovasc. Surg., April 1, 2007; 133(4): 1051 - 1058. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Hetzer, M. Dandel, C. Knosalla, J. G. Burniston, V. G. Florea, D. Rott, D. Leibowitz, G. J. Vanderwilt, M. H. Yacoub, and E. J. Birks Left Ventricular Assist Devices and Drug Therapy in Heart Failure N. Engl. J. Med., February 22, 2007; 356(8): 869 - 872. [Full Text] [PDF]
|
|
|
|
 |
|
 H. Bugger, S. Leippert, D. Blum, P. Kahle, B. Barleon, D. Marme, and T. Doenst Subtractive hybridization for differential gene expression in mechanically unloaded rat heart Am J Physiol Heart Circ Physiol, December 1, 2006; 291(6): H2714 - H2722. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Klotz, J. Stypmann, H. Welp, C. Schmid, G. Drees, A. Rukosujew, and H. H. Scheld Does Continuous Flow Left Ventricular Assist Device Technology Have a Positive Impact on Outcome Pretransplant and Posttransplant? Ann. Thorac. Surg., November 1, 2006; 82(5): 1774 - 1778. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Kilic, T. Li, T. D.C. Nolan, J. R. Nash, S. Li, D. J. Prastein, G. Schwartzbauer, S. L. Moainie, G. K. Yankey, C. DeFilippi, et al. Strain-related regional alterations of calcium-handling proteins in myocardial remodeling J. Thorac. Cardiovasc. Surg., October 1, 2006; 132(4): 900 - 908. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. J. Wilhelm, C. Schmid, and H. H. Scheld Reply to the Editor: J. Thorac. Cardiovasc. Surg., July 1, 2006; 132(1): 210 - 211. [Full Text] [PDF]
|
|
|
|
|
|
H. Liang, H. Lin, Y. Weng, M. Dandel, and R. Hetzer Prediction of cardiac function after weaning from ventricular assist devices J. Thorac. Cardiovasc. Surg., December 1, 2005; 130(6): 1555 - 1560. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Wohlschlaeger, K. J. Schmitz, C. Schmid, K. W. Schmid, P. Keul, A. Takeda, S. Weis, B. Levkau, and H. A. Baba Reverse remodeling following insertion of left ventricular assist devices (LVAD): A review of the morphological and molecular changes Cardiovasc Res, December 1, 2005; 68(3): 376 - 386. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Matsumiya, O. Monta, N. Fukushima, Y. Sawa, T. Funatsu, K. Toda, and H. Matsuda Who would be a candidate for bridge to recovery during prolonged mechanical left ventricular support in idiopathic dilated cardiomyopathy? J. Thorac. Cardiovasc. Surg., September 1, 2005; 130(3): 699 - 704. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Dandel, Y. Weng, H. Siniawski, E. Potapov, H. B. Lehmkuhl, and R. Hetzer Long-Term Results in Patients With Idiopathic Dilated Cardiomyopathy After Weaning From Left Ventricular Assist Devices Circulation, August 30, 2005; 112(9_suppl): I-37 - I-45. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Mancini and D. Burkhoff Mechanical Device-Based Methods of Managing and Treating Heart Failure Circulation, July 19, 2005; 112(3): 438 - 448. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. E. DeBakey Development of Mechanical Heart Devices Ann. Thorac. Surg., June 1, 2005; 79(6): S2228 - S2231. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 O. Lisy, M. M. Redfield, J. A. Schirger, and J. C. Burnett Jr. Atrial BNP endocrine function during chronic unloading of the normal canine heart Am J Physiol Regulatory Integrative Comp Physiol, January 1, 2005; 288(1): R158 - R162. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Schmid, C. Etz, H. Welp, M. Rothenburger, H. Reinecke, M. Schafers, Ch. Schmidt, and H.H. Scheld Clinical situations demanding weaning from long-term ventricular assist devices Eur. J. Cardiothorac. Surg., October 1, 2004; 26(4): 730 - 735. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Pieske Reverse remodeling in heart failure - fact or fiction? Eur. Heart J. Suppl., August 1, 2004; 6(suppl_D): D66 - D78. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|
|
|
 |
|
 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]
|
|
|
|
|
|
H. A. Baba, J. Stypmann, F. Grabellus, P. Kirchhof, A. Sokoll, M. Schafers, A. Takeda, M. J. Wilhelm, H. H. Scheld, N. Takeda, et al. Dynamic regulation of MEK/Erks and Akt/GSK-3{beta} in human end-stage heart failure after left ventricular mechanical support: myocardial mechanotransduction-sensitivity as a possible molecular mechanism Cardiovasc Res, August 1, 2003; 59(2): 390 - 399. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. G. Nabavi, J. Stockmann, C. Schmid, M. Schneider, D. Hammel, H. H. Scheld, and E. B. Ringelstein Doppler microembolic load predicts risk of thromboembolic complications in Novacor patients J. Thorac. Cardiovasc. Surg., July 1, 2003; 126(1): 160 - 167. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 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]
|
|
|
|
 |
|
 F Duru, R Candinas, M Lachat, M Rahn, G Noll, T.F Luscher, and M Turina Electrical and mechanical support in advanced heart failure. Rationale and feasibility of a combined management strategy Eur. Heart J., July 1, 2002; 23(13): 1005 - 1010. [Full Text] [PDF]
|
|
|
|
|
|
S. Westaby, A. P. Banning, S. Saito, D. W. Pigott, X. Y. Jin, P. A. Catarino, D. Robson, N. Moorjani, A. Kardos, P. A. Poole-Wilson, et al. Circulatory Support for Long-Term Treatment of Heart Failure: Experience With an Intraventricular Continuous Flow Pump Circulation, June 4, 2002; 105(22): 2588 - 2591. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|
|
|
|
|
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]
|
|
|
|
|
|
R. Gradaus, S. Kerber, D. Bocker, H. H. Scheld, G. Breithardt, and M. C. Deng Therapeutic options and heart failure survival score predictability in an academic heart failure center: an analysis of 120 consecutive patients during a 1-year period Eur J Heart Fail, March 1, 2002; 4(2): 207 - 214. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Grabellus, B. Levkau, A. Sokoll, H. Welp, C. Schmid, M. C Deng, A. Takeda, G. Breithardt, and H. A Baba Reversible activation of nuclear factor-{kappa}B in human end-stage heart failure after left ventricular mechanical support Cardiovasc Res, January 1, 2002; 53(1): 124 - 130. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Sodian, M. Loebe, C. Schmitt, E. V. Potapov, H. Siniawski, J. Muller, H. Hausmann, H. R. Zurbruegg, Y. Weng, and R. Hetzer Decreased plasma concentration of brain natriuretic peptide as a potential indicator of cardiac recovery in patients supported by mechanical circulatory assist systems J. Am. Coll. Cardiol., December 1, 2001; 38(7): 1942 - 1949. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Razeghi, M. Mukhopadhyay, T. J. Myers, J. N. Williams, C. S. Moravec, O. H. Frazier, and H. Taegtmeyer Myocardial tumor necrosis factor-{alpha} expression does not correlate with clinical indices of heart failure in patients on left ventricular assist device support Ann. Thorac. Surg., December 1, 2001; 72(6): 2044 - 2050. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Korfer, A. El Banayosy, and H. Milting Invited commentary Ann. Thorac. Surg., December 1, 2001; 72(6): 2050 - 2050. [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|
|
|
 |
|
 K. Minami Surgical Treatments for Endstage Heart Failure Due to Dilated Cardiomyopathy Asian Cardiovasc Thorac Ann, September 1, 2001; 9(3): 159 - 166. [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|
|
|
|
|
A. Staudt, F. Schaper, V. Stangl, A. Plagemann, M. Bohm, K. Merkel, G. Wallukat, K. D. Wernecke, K. Stangl, G. Baumann, et al. Immunohistological Changes in Dilated Cardiomyopathy Induced by Immunoadsorption Therapy and Subsequent Immunoglobulin Substitution Circulation, June 5, 2001; 103(22): 2681 - 2686. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|
|
|
 |
|
 A. Y. Schure, P. C. Laussen, and F. X. McGowan JR Mechanical Cardiopulmonary Support of Infants and Children With Congenital Heart Disease Seminars in Cardiothoracic and Vascular Anesthesia, March 1, 2001; 5(1): 46 - 54. [Abstract] [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]
|
|
|
|
|
|
R. Hetzer, J. H. Muller, Y.-g. Weng, R. Meyer, and M. Dandel Bridging-to-recovery Ann. Thorac. Surg., March 1, 2001; 71 (2007): S109 - S113. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. C. Deng, M. Loebe, A. El-Banayosy, E. Gronda, P. G. M. Jansen, M. Vigano, G. M. Wieselthaler, B. Reichart, E. Vitali, A. Pavie, et al. Mechanical Circulatory Support for Advanced Heart Failure : Effect of Patient Selection on Outcome Circulation, January 16, 2001; 103(2): 231 - 237. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|
|
|
|
|
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]
|
|
|
|
|
|
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]
|
|
|
|
|
|
D. N. Helman, S. W. Maybaum, D. L.S. Morales, M. R. Williams, A. Beniaminovitz, N. M. Edwards, D. M. Mancini, and M. C. Oz Recurrent remodeling after ventricular assistance: is long-term myocardial recovery attainable? Ann. Thorac. Surg., October 1, 2000; 70(4): 1255 - 1258. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. G. Rose, S. J. Park, A. J. Bank, and L. W. Miller Partial aortic valve fusion induced by left ventricular assist device Ann. Thorac. Surg., October 1, 2000; 70(4): 1270 - 1274. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A K Mahmood, J M Courtney, S Westaby, M Akdis, and H Reul Critical review of current left ventricular assist devices Perfusion, September 1, 2000; 15(5): 399 - 420. [PDF]
|
|
|
|
|
|
D. Y. Loisance, P. G.M. Jansen, D. R. Wheeldon, and P. M. Portner Long-term mechanical circulatory support with the wearable Novacor left ventricular assist system Eur. J. Cardiothorac. Surg., August 1, 2000; 18(2): 220 - 224. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. B. Felix, A. Staudt, W. V. Dorffel, V. Stangl, K. Merkel, M. Pohl, W. D. Docke, S. Morgera, H. H. Neumayer, K. D. Wernecke, et al. Hemodynamic effects of immunoadsorption and subsequent immunoglobulin substitution in dilated cardiomyopathy: Three-month results from a randomized study J. Am. Coll. Cardiol., May 1, 2000; 35(6): 1590 - 1598. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Westaby HEART FAILURE: Non-transplant surgery for heart failure Heart, May 1, 2000; 83(5): 603 - 603. [Full Text]
|
|
|
|
|
|
S. J. Park, D. Q. Nguyen, A. J. Bank, S. Ormaza, and R. M. Bolman III Left ventricular assist device bridge therapy for acute myocardial infarction Ann. Thorac. Surg., April 1, 2000; 69(4): 1146 - 1151. [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]
|
|
|
|
|
|
U. W. Kjellman, P. Hallgren, C.-H. Bergh, J. Lycke, A. Oldfors, and L. Wiklund Weaning from mechanical support in a patient with acute heart failure and multiple sclerosis Ann. Thorac. Surg., February 1, 2000; 69(2): 628 - 630. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Muller, G. Wallukat, M. Dandel, H. Bieda, K. Brandes, S. Spiegelsberger, E. Nissen, R. Kunze, and R. Hetzer Immunoglobulin Adsorption in Patients With Idiopathic Dilated Cardiomyopathy Circulation, February 1, 2000; 101(4): 385 - 391. [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]
|
|
|
|
|
|
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]
|
|
|
|
|
|
G. Torre-Amione, S. J. Stetson, K. A. Youker, J.-B. Durand, B. Radovancevic, R. M. Delgado, O. H. Frazier, M. L. Entman, and G. P. Noon Decreased Expression of Tumor Necrosis Factor-{alpha} in Failing Human Myocardium After Mechanical Circulatory Support : A Potential Mechanism for Cardiac Recovery Circulation, September 14, 1999; 100(11): 1189 - 1193. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S Westaby, O Franklin, and M Burch New developments in the treatment of cardiac failure Arch. Dis. Child., September 1, 1999; 81(3): 276 - 277. [Full Text]
|
|
|
|
|
|
M. C. Deng, T. D.T. Tjan, B. Asfour, and H. H. Scheld Left ventricular assist devices -- reasons to be enthusiastic Eur J Heart Fail, August 31, 1999; 1(3): 289 - 291. [Full Text] [PDF]
|
|
|
|
|
|
M. E. DeBakey A miniature implantable axial flow ventricular assist device Ann. Thorac. Surg., August 1, 1999; 68(2): 637 - 640. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|
|
|
|
|
B Stiller, I Dahnert, Y G Weng, E Hennig, R Hetzer, and P E Lange Children may survive severe myocarditis with prolonged use of biventricular assist devices Heart, August 1, 1999; 82(2): 237 - 240. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. El-Banayosy, M. Deng, D.Y. Loisance, H. Vetter, E. Gronda, M. Loebe, and M. Vigano The European experience of Novacor left ventricular assist (LVAS) therapy as a bridge to transplant: a retrospective multi-centre study Eur. J. Cardiothorac. Surg., June 1, 1999; 15(6): 835 - 841. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. J. Thomas and A. T. Harvey BRIDGE TO RECOVERY WITH THE ABIOMED BVS-5000 DEVICE IN A PATIENT WITH INTRACTABLE VENTRICULAR TACHYCARDIA J. Thorac. Cardiovasc. Surg., April 1, 1999; 117(4): 831 - 832. [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|
|
|
|
|
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]
|
|
|
|
|
|
S. Podlowski, H. P. Luther, R. Morwinski, J. Muller, and G. Wallukat Agonistic Anti-ß1-Adrenergic Receptor Autoantibodies From Cardiomyopathy Patients Reduce the ß1-Adrenergic Receptor Expression in Neonatal Rat Cardiomyocytes Circulation, December 1, 1998; 98(22): 2470 - 2476. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. J. Goldstein, M. C. Oz, and E. A. Rose Implantable Left Ventricular Assist Devices N. Engl. J. Med., November 19, 1998; 339(21): 1522 - 1533. [Full Text] [PDF]
|
|
|
|
|
|
R. Hetzer, M. Loebe, E. V. Potapov, Y. Weng, B. Stiller, E. Hennig, V. Alexi-Meskishvili, and P. E. Lange Circulatory support with pneumatic paracorporeal ventricular assist device in infants and children Ann. Thorac. Surg., November 1, 1998; 66(5): 1498 - 1506. [Abstract] [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]
|
|
|
|
|
|
S. A. Hunt and O.H. Frazier Mechanical Circulatory Support and Cardiac Transplantation Circulation, May 26, 1998; 97(20): 2079 - 2090. [Full Text] [PDF]
|
|
|
|
|
|
P. M. McCarthy, N. O. Smedira, R. L. Vargo, M. Goormastic, R. E. Hobbs, R. C. Starling, and J. B. Young One hundred patients with the HeartMate left ventricular assist device: evolving concepts and technology J. Thorac. Cardiovasc. Surg., April 1, 1998; 115(4): 904 - 912. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||