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Ann Thorac Surg 1995;59:609-613
© 1995 The Society of Thoracic Surgeons
Departments of Thoracic and Cardiovascular Surgery, Cardiology, Clinical Pathology and Cell Biology, Biomedical Engineering, and Cardiothoracic Anesthesia, The Cleveland Clinic Foundation, Cleveland, Ohio
Accepted for publication November 1, 1994.
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Abstract |
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Introduction |
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The implantable left ventricular assist device (LVAD) provides excellent hemodynamic support [1–3]. While the patient is on support it has been noted that the patient's heart undergoes ``remodeling'', with a decrease in the cardiothoracic ratio [4, 5]. With typical function of the device in the early postimplantation period the left ventricle is unloaded and the aortic valve does not open [6]. Several other pertinent clinical observations have been made regarding patients on long-term LVAD support. First, during brief periods with the pump off (``venting'' the pump), the patient's own heart ejects and the patient is hemodynamically stable [2]. With exercise the patient's own heart may eject in addition to the output that is being supplied by the LVAD [7]. In 1 patient in whom brain death developed after prolonged support (>1 year), the patient's own heart supported the circulation with normal hemodynamic function for more than 24 hours after the LVAD was turned off (personal communication, O. H. Frazier, MD, Houston, TX). Finally, histologic improvement of the left ventricular muscle has been described after chronic left ventricular support [8].
These multiple clinical observations eventually led to a clinical question: after chronic LVAD support, can the assist device be safely removed with subsequent patient survival and acceptable functional capacity [5]? If patients on chronic LVAD support can be weaned with subsequent successful pump removal, it would be an important new treatment modality for patients with heart failure. The objective of this study was to retrospectively analyze the Cleveland Clinic pneumatic HeartMate LVAD patient population to assess histologic and structural changes during HeartMate LVAD support. This information will be interpreted in regard to the clinical question relating to the feasibility of removal of the LVAD after long-term left ventricular (LV) support.
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Material and Methods |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentReferences |
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Patients and Methods
Twenty-five patients received the HeartMate 1000 IP device between December 1991 and March 1994 [10]. All patients were in cardiogenic shock and on inotropic agents before LVAD insertion; 7 (28%) were on extracorporeal membrane oxygenation as a ``bridge-to-bridge'' device and 21 patients (84%) were also on an intraaortic balloon pump. Six patients progressed with multiple organ failure and subsequently died. Nineteen patients (76%) were transferred out of the intensive care unit, were rehabilitated, and underwent subsequent cardiac transplantation. The mean age was 50 years (range, 35 to 62 years); 68% had ischemic cardiomyopathy and 32% had dilated cardiomyopathy. All patients were in New York Heart Association functional classes I or II before transplantation. All transplant recipients are alive.
Transesophageal Echocardiographic Studies
Transesophageal echocardiographic studies were obtained at three specific time intervals: (1) in the operating room immediately before LVAD insertion (baseline), (2) in the operating room after the patient had been weaned from cardiopulmonary bypass and the patient was stable on LVAD support, and (3) intraoperatively at the time of LVAD explantation and heart transplantation. Images were recorded using a Hewlett-Packard SONOS OR and SONOS 1500 (Hewlett-Packard, Andover, MA) or Acuson 128 XP (Acuson, Mt. View, CA). Acoustic quantification techniques also were used to determine right ventricular fractional area of change (equivalent to ejection fraction) using automatic boundary detection [6, 11]. Transgastric or basal views were used to measure left ventricular diastolic (LVD) and systolic (LVS) diameters, and LV wall thickness. Fractional shortening was calculated as: (LVD - LVS)/LVD.
Histologic Examination
Specimens were available for histologic examination at two times. The first specimen consisted of the left ventricular apical core removed during LVAD insertion. These specimens were compared with specimens taken from areas close to the left ventricular apex of the explanted heart at transplantation. Specimens were fixed in buffered formalin, embedded in paraffin, cut into 4-µm sections, stained with hematoxylin and eosin, and examined by light microscopy. The examination included qualitative (0 to 3 scale) assessment of wavy fibers, contraction band necrosis, and fibrosis as a measure of myocardial injury [12]. In addition, minimal myocyte diameter across the nucleus was measured at a magnification of x1,000 using the Bioquant system (W. Nuchsbaum, Inc, McHenry, IL) connected to a personal computer (Gateway 4D-X-66U; Gateway, North Sioux City, SD) [13]. An average of 100 myocytes were analyzed per section. Right ventricular biopsy specimens were not taken at LVAD insertion because of clinical concerns that we might produce bleeding or perforation.
Statistical Analysis
Not all data points were available for analysis. Transesophageal echocardiographic studies were reviewed retrospectively and were not included unless images were very clear. In addition, in 2 patients who underwent emergency LVAD insertion we were not able to perform baseline and immediate post-LVAD studies. Data are expressed as mean ± standard deviation. Comparison of differences between the three times was performed using analysis of variance and Student's t tests with Bonferroni's correction. The results were considered significant when the p value was less than 0.05.
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Results |
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). The cardiothoracic ratio decreased, most notably in patients with dilated cardiomyopathy (Fig 1). Right ventricular volumes (as determined using an REF catheter, Baxter Healthcare, Irvine, CA) showed decreased volumes early after LVAD insertion, and these decreased further by the time of explantation. In addition, the right ventricular ejection fraction rose (see Table 1), and this correlated with the change seen using acoustic quantification.
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). Left ventricular fractional shortening was markedly decreased in all patients. Before device insertion, LV fractional shortening was 0.07 ± 0.03. There was no significant change when fractional shortening was evaluated immediately after device insertion (0.11 ± 0.10) or at the time of device explantation (0.11 ± 0.09). Intraoperative echocardiography confirmed that the aortic valve was not opening during device function and therefore the left ventricle was unloaded.
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) in histologic measures of cardiac myocyte damage, with a decrease in the numbers of wavy fibers (p < 0.001) and contraction band necrosis (p < 0.01). However, there was an increase in the amount of myocardial fibrosis (p < 0.05) during the time of LVAD support. The increase in fibrosis was most marked for patients with dilated cardiomyopathy (0.8 ± 0.8 at implantation versus 1.7 ± 0.8 at explantation; p < 0.05). There was no significant change in myocyte diameter during support, although a slight increase in size approached significance (p = 0.07). Myocyte diameter was minimally increased at both time periods (normal, 10 to 15 µm [13]).
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Comment |
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). Our findings include the documentation of immediate changes in right ventricular volumes and left ventricular structure. Both of these changes were seen in the operating room after LVAD insertion and were sustained throughout the period of support. If comparisons were only made from before LVAD insertion until before LVAD explantation, then the significant changes may be inferred to be gradual. The change in cardiothoracic ratio [5] fails to detect the immediate post-LVAD changes in the left ventricle documented in our study by transesophageal echocardiography. Histologic markers for myocyte damage also improved, with a significant reduction in contraction band necrosis and wavy fibers. Similar histologic findings have been reported by others [5, 8]. These pathologic findings reflect the acute decompensation of patients in cardiogenic shock, and would be expected to improve in patients stable on chronic support.
Other measurements showed no improvement in left ventricular function during support. Left ventricular fractional shortening did not increase during the period of support. However, this measurement is dependent on loading conditions and therefore should not be used alone as an indication of LV function. Ventricular fibrosis increased during LVAD support, particularly in the subgroup with dilated cardiomyopathy. Finally, LV echocardiographic studies showed very early changes after the initiation of LVAD support, but later decreases in LV volume were not seen. These structural findings indicate that changes were not related to ``recovery'', but were secondary to immediate changes in loading conditions with LVAD support (left atrial pressure dropped in the operating room from 23 ± 2 mm Hg to 11 ± 1 mm Hg).
We made no attempt to compare the 6 LVAD nonsurvivors with survivors, and we did not obtain ``baseline'' right ventricular biopsy specimens before LVAD insertion. We thought that right ventricular biopsies could be dangerous in this clinical setting. Also in this retrospective study we did not try to ``wean'' the LVAD or to repeat preexplantation studies with the LVAD off. We did not examine the nonsurvivor group because we could not obtain the same histologic and transesophageal echocardiographic information. Furthermore, the nonsurvivor group did not address the clinical question, ``Can the LVAD be removed successfully?''
Once myocytes die, they cannot be salvaged, they do not regenerate, and eventually they are replaced by fibrosis [14]. Therefore, one generally would not expect to find LV improvement in patients with ischemic cardiomyopathy or after extensive acute myocardial infarction (eg, left main occlusion). Exceptions may exist for patients with ``borderline'' areas of ischemia and edema, who may be salvaged on LVAD support. For patients with a treated reversible disorder (such as myocarditis), the left ventricle may truly recover during LVAD support [15]. Patients with idiopathic dilated cardiomyopathy may appear to have improved (because of the decreased cardiothoracic ratio, decreased chamber size, and improved acute histologic pattern) and some may tolerate LVAD removal. However, the unanswered question is, ``how long will these improvements be sustained''? It may be that after a period off LVAD support, the ventricle may redilate and the improvement may be reversed.
We envision three clinical situations that justify implantable LVAD removal. The first is in patients with a treatable underlying disorder (myocarditis) in whom cardiac recovery has occurred and will be sustained after LVAD removal. The second would be in patients in whom intractable LVAD device infection develops in whom there has been cardiac improvement (dilated cardiomyopathy patients). Treating these infections sometimes will require removal of the LVAD. After intensive antibiotic therapy, theoretically a patient then could undergo LVAD reinsertion. Third, we will soon start implanting the LVAD for permanent outpatient support as an alternative to transplantation. These patients should be on support for a period of years. Eventually the pump may reach ``end-of-life'' and a decision would have to be made whether to replace the LVAD, or for selected patients, the pump could be removed and the patients followed up closely.
In summary, although our study did not include patients with very extended periods of support (>1 year), and it is still a small number of patients from which to draw conclusions, we think the clinical situations that would allow successful LVAD removal after chronic support are rare. As we expand our clinical experience and implant the device earlier in the patients' course, the prospects for this approach may become more practical.
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K. B. James, P. M. McCarthy, S. Jaalouk, E. L. Bravo, A. Betkowski, J. D. Thomas, S. Nakatani, and F. M. Fouad-Tarazi Plasma Volume and Its Regulatory Factors in Congestive Heart Failure After Implantation of Long-term Left Ventricular Assist Devices Circulation, April 15, 1996; 93(8): 1515 - 1519. [Abstract] [Full Text]
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K. B. James, P. M. McCarthy, J. D. Thomas, R. Vargo, R. E. Hobbs, S. Sapp, and E. Bravo Effect of the Implantable Left Ventricular Assist Device on Neuroendocrine Activation in Heart Failure Circulation, November 1, 1995; 92(9): 191 - 195. [Abstract] [Full Text]
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