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Ann Thorac Surg 2006;81:1107-1109
© 2006 The Society of Thoracic Surgeons

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Case report

Triple Bridge-to-Transplant in a Case of Giant Cell Myocarditis Complicated by Human Leukocyte Antigen Sensitization and Heparin-Induced Thrombocytopenia Type II

Cardiovascular Surgery, Heart Center North Rhine-Westphalia, Bad Oeynhausen, Germany

Accepted for publication December 28, 2004.

^_* Address correspondence to Dr El-Banayosy, Cardiovascular Surgery, Heart Center NRW, Georgstrasse 11, 32545 Bad Oeynhausen, Germany (Email: abanayosy{at}hdz-nrw.de).

	Abstract

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Bridge-to-bridge experience has documented the feasibility of a switch from short-term to long-term mechanical circulatory support until heart transplant. We describe a case of irreversible cardiogenic shock due to giant cell myocarditis treated consecutively with extracorporal membrane oxygenation, bi-ventricular assist device, and total artificial heart. The postoperative course was complicated by human leukocyte antigen sensitization and heparin-induced thrombocytopenia type II. Our patient successfully underwent heart transplant after 10 months of support and was discharged in good condition. This case illustrates suitable device selection for myocarditis and represents two treatable immunological complications.

	Introduction

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Acute myocarditis may require mechanical circulatory assistance if the native heart fails. Suitable device selection depends on the individual clinical situation and may constitute a therapeutic challenge. The present case of giant cell myocarditis with cardiogenic shock illustrates various indications for mechanical assistance and additionally depicts two treatable immunological complications.

A 39-year-old man presented to our institution in severe cardiogenic shock. The patient was referred from another hospital where he had been admitted for acute myocarditis 2 weeks before. At the time of admission, the patient was intubated and ventilated. Mean arterial, central venous, and pulmonary wedge pressure were 61 mm Hg, 17 mm Hg, and 17 mm Hg, respectively, at a cardiac index of 1.5 L/min/m² despite high-dose inotropes (12 µg/kg/min dopamine, 12 µg/kg/min dobutamine, and 0.2 µg/kg/min norepinephrine). Left ventricular ejection fraction was < 10% by echocardiography. Myocardial enzymes and serological markers of common blood-borne pathogens were within normal limits. Ultrasound revealed moderate ascites and bilateral pleural effusions. There was acute renal failure with anuria, yet liver function was normal.

Initially we sought to stabilize the hemodynamics by milrinone and epinephrine, and with insertion of an intraaortic balloon pump. However, the patient rapidly deteriorated necessitating cardiopulmonary resuscitation followed by urgent femoro-femoral extracorporal membrane oxygenation. One day later, the patient was re-evaluated and we elected intermediate-term mechanical circulatory support for bridge-to-recovery anticipating the myocarditis would resolve within the next few weeks. Intraoperatively, we found poorly contracting ventricles with severe inflammation; tissue samples were obtained for histopathology. After implantation of a paracorporal bi-ventricular assist device (BVAD; Thoratec, Pleasanton, CA), the patient left the operating room in a stable condition with left and right pump flows of 4.3 L/min and 4.2 L/min, respectively. Postoperative blood loss was 1,450 mL within 24 hours, and heparin-based anticoagulation was resumed. Unfortunately, cardiac function ceased over the next 3 days as assessed by echocardiography. The heart was entirely akinetic, valve leaflets were immobile, and spontaneous echo contrasts indicated a highly procoagulant state. Histologic evaluation of tissue samples became available and revealed giant cell myocarditis as the underlying pathology. Because myocardial recovery had become unlikely, and devastating thromboembolic events were imminent, we proceeded to long-term cardiac replacement by implantation of the CardioWest Total Artificial Heart (TAH; SynCardia Systems, Tucson, AZ) on day 5 after admission. This operation was uneventful, and once again, the patient left the operating room in stable condition with adequate device support (left and right flows of 5.4 and 5.2 L/min, respectively). Total postoperative blood loss was 930 mL, and heparin-based anticoagulation was re-started.

The postoperative course was protracted, but the patient improved steadily. Assisted ventilation was withdrawn by day 12, and acute renal failure with need for hemofiltration resolved within 3 weeks. Beginning on day 15 after TAH implant, our patient started to ambulate; he was transferred to the regular nursing floor after 4 weeks. Some immunological complications are noteworthy. Heparin-induced thrombocytopenia type II (HIT II) was diagnosed on postoperative day 3 and required switching to r-hirudin followed by phenprocoumon for anticoagulation. Furthermore, human leukocyte antigen (HLA) sensitization developed after 5 months and was treated by plasmapheresis. After 291 days of TAH support, in which no major infection, bleeding, or any thromboembolic event occurred, a donor heart became available for transplant. Surgery and postoperative course were uneventful, and the patient was discharged home in satisfactory condition 25 days posttransplant and 311 days after initial admission to our hospital. Our patient has since returned to work as a businessman, supporting his wife and 2 children.

	Comment

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Our institution began assist device implantation in 1987 [1]. We have 800 patients. This is one of the largest experiences worldwide. The complexity of the current case reveals several aspects pertinent to our device selection criteria for fulminant myocarditis with cardiogenic shock. First, we attempted to balance intravenous inotropes by intraaortic balloon pump insertion. However, as presented here, emergent femoro-femoral extracorporal membrane oxygenation may become necessary to salvage the patient. Versatility and effectiveness of extracorporal membrane oxygenation for acute myocarditis were shown by our group [2] and others [3]. Once there was hemodynamic stability, we elected intermediate-term assist devices if there was potential for myocardial recovery. We prefer the Thoratec device (Thoratec, Pleasanton, CA) and expect recovery from fulminant myocarditis in nearly 50%. If recovery occurs and the Thoratec device is removed, the 5-year transplant-free survival rate approximates 77% [4]. In contrast, if cardiac function does not recover under support, a donor heart is allocated for transplant. The 1-year actuarial survival of patients who were placed on extracorporal membrane oxygenation and survived to long-term support ("bridge-to-bridge") approximates 80% [5] (ie, similar to bridge-to-recovery [1] and other bridge-to-transplant scenarios [6]).

While supported by the Thoratec BVAD, the therapeutic options for this patient were either bridge-to-recovery or bridge-to-transplant. However, this situation changed once the patient's heart ceased to function and became completely akinetic. Giant cell myocarditis may have accounted for the dramatic deterioration, because this entity is often fatal despite treatment [7]. With recovery being unlikely and thromboembolism highly imminent, this represented an absolute indication for removal of the native heart and TAH implantation as a third bridge-to-transplant. Although this strategy is not common, it emphasizes the importance of device selection for myocarditis. Bi-ventricular assist device support is justified when it is safe and the heart can recover. In contrast, TAH implantation with excision of the heart is indicated once the native heart imposes a risk to the patient. The survival to transplant with the CardioWest TAH (SynCardia Systems) approximates 79% [8], justifying its use.

The immunologic complications of this unusual case highlight some current challenges of mechanical circulatory support. The HLA sensitization can be detected in about 10% at the time of heart transplant [9]. Pre-transplant plasmapheresis may be necessary and was successfully used in our patient. Moreover, although reports of the occurrence of heparin-induced thrombocytopenia type II in patients with assist devices are anecdotal [10], this may underestimate its prevalence. In our experience, heparin-induced thrombocytopenia type II may develop in as many as 20% of cases and constitutes a therapeutic obstacle. We substitute r-hirudin for heparin and switch to oral phenprocoumon as soon as it is safe. Using this strategy, neither bleeding nor thromboembolic events were observed in our patient.

Collectively, this report demonstrates not only the treatment of acute myocarditis by feasible device selection, but also the exchange thereof as the clinical course dictates. Furthermore, this case depicts serious immunologic complications one can expect. Thus, successful management requires the integrated efforts of surgeons, cardiologists, hematologists, and dedicated nursing care.

	Acknowledgments

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The authors thank Dr Murray for editorial advice and the Ventricular Assist Device Clinical Team, especially Peter Sarnowski, RN, Daniela Roefe, RN, and Frank Jaschke, RN, for their outstanding care of this patient.

	References

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1. Korfer R, El-Banayosy A. Mechanical circulatory support15 years of experience in the Heart Center North Rhine-Westphalia. Dtsch Med Wochenschr 2004;129(15):800-804.[Medline]
2. Reiss N, El-Banayosy A, Posival H, Morshuis M, Minami K, Korfer R. Management of acute fulminant myocarditis using circulatory support systems Artif Organs 1996;20(8):964-970.[Medline]
3. Kawahito K, Murata S, Yasu T, et al. Usefulness of extracorporeal membrane oxygenation for treatment of fulminant myocarditis and circulatory collapse Am J Cardiol 1998;82(7):910-911.[Medline]
4. Farrar DJ, Holman WR, McBride LR, et al. Long-term follow-up of Thoratec ventricular assist device bridge-to-recovery patients successfully removed from support after recovery of ventricular function J Heart Lung Transplant 2002;21(5):516-521.[Medline]
5. Pagani FD, Aaronson KD, Swaniker F, Bartlett RH. The use of extracorporeal life support in adult patients with primary cardiac failure as a bridge to implantable left ventricular assist device Ann Thorac Surg 2001;71(Suppl 3):S77-S81discussion S82–5.[Medline]
6. Navia JL, McCarthy PM, Hoercher KJ, Smedira NG, Banbury MK, Blackstone EH. Do left ventricular assist device (LVAD) bridge-to-transplantation outcomes predict the results of permanent LVAD implantation? Ann Thorac Surg 2002;74:2051-2062.[Abstract/Free Full Text]
7. Cooper Jr LT, Berry GJ, Shabetai R. Idiopathic giant-cell myocarditis—natural history and treatment. Multicenter Giant Cell Myocarditis Study Group Investigators N Engl J Med 1997;336(26):1860-1866.[Medline]
8. Copeland JG, Smith RG, Arabia FA, et al. Cardiac replacement with a total artificial heart as a bridge to transplantation N Engl J Med 2004;351(9):859-867.[Medline]
9. Massad MG, Cook DJ, Schmitt SK, et al. Factors influencing HLA sensitization in implantable LVAD recipients Ann Thorac Surg 1997;64:1120-1125.[Abstract/Free Full Text]
10. Christiansen S, Jahn UR, Meyer J, et al. Anticoagulative management of patients requiring left ventricular assist device implantation and suffering from heparin-induced thrombocytopenia type II Ann Thorac Surg 2000;69:774-777.[Abstract/Free Full Text]

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