Ann Thorac Surg 2004;77:720-721
© 2004 The Society of Thoracic Surgeons
Case report
Successful biventricular assistance after heart transplantation
Jose M. Arribas, MDa*,
Domingo A. Pascual, MDb,
Francisco Gutiérrez, MDa,
Víctor Ray, MDa,
Julio García-Puente, MDa,
Mariano Valdés, MDb,
Ramón Arcas, MDa
a Department of Cardiovascular Surgery, University Hospital Virgen de la Arrixaca, Murcia, Spain
b Department of Cardiology, University Hospital V. Arrixaca, Murcia, Spain
Accepted for publication May 2, 2003.
* Address reprint requests to Dr Arribas, C/Azarbe del papel 3, 2°A, 30.007 Murcia, Spain
e-mail: arribasdelpeso{at}telepolis.com
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Abstract
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We present a successful use of biventricular pneumatic assistance during seven days allowing the recovery from a severe primary graft failure that occurred in the operating room. Suboptimal donors are associated with higher rates of immediate graft failure; however proper use of mechanical assistance can help to recover graft function.
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Introduction
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Primary graft failure (PGF) is the main cause of operative mortality in cardiac transplantation. When this dramatic situation appears and does not resolve with inotropic support or changes in preload and afterload, a ventricular assistance device (VAD) must be used in order to support the patient until a retransplantation is done or the graft recovers. Only a few cases of graft recovery have been previously described [1–5].
We present the case of a heart transplant patient who suffered a severe PGF in the operating room. The early use of a biventricular pneumatic assistance device allowed a complete recovery of graft function after five days of support.
The recipient patient was a 25-year-old male affected by end-stage familiar dilated cardiomyopathy in functional NYHA class IV. The patient's blood type was O. His height was 1.85 m and his weight was 87 kg. The echocardiography showed severe systolic dysfunction with left ventricular end-diastolic volume of 460 ml, ejection fraction of 20%, and severe mitral regurgitation. In the right heart catheterization the cardiac index was 1.9 l/min m2, the pulmonary vascular resistance was 3.3 u wood, the capillary wedge pressure was 31 mm Hg, and the transpulmonar gradient was 13 mm Hg.
On a waiting list for heart transplantation he suffered from severe worsening of heart failure and needed hospital admission and intravenous inotropic drugs. Clinical course was complicated by a nosocomial pneumonia with additional hemodynamic deterioration and a need for intensive care unit admission. At this time a donor heart was offered from a 26-year-old male who was dead 12 hours before due to trauma with thoracic and airway crash. The donor patient was located 800 km away. His height was 181 cm and his weight was 80 kg. His blood type was O and he had been receiving intravenous dopamine (14 µg · kg-1 · min-1) and norepinephrine (0.2 µg · kg-1 · min-1). The echocardiography performed under inotropic support was normal showing a left ventricular ejection fraction of more than 65%. The chest roentgenogram presented pulmonary edema and the mb-fraction of creatinine phosphokinase was 62 ng/ml.
Removal of the donor heart was carried out using in situ arrest and cooling with cardioplegia and the graft was transported in ice-cold saline solution. The heart implantation was performed using the standard surgical technique with 180 minutes of total graft ischemic time. However weaning from cardiopulmonary bypass was impossible due to severe contractile dysfunction of graft despite high dose inotropic drugs and an intra-aortic balloon pump. We decided to implant a pneumatic biventricular assistance device using a Medos model (medizintechnik, GMBH Stolberg, Germany) (right chamber 54 mL, left chamber 60 mL). Implantation was successful allowing to reach hemodynamic stability and consequently to wean the patient from cardiopulmonary bypass and to close the chest. Patient was transferred to the intensive care unit where conventional protocol of immunosuppression was continued.
At the arrival to the intensive care unit, the transesophageal echocardiography showed diffuse hypokinesia of left ventricle with ejection fraction of less than 20%. During the first 24 hours the patient remained stable and we decided to wait for short-term evolution. Successive echocardiography studies showed progressive improvement of biventricular contractility until the seventh postoperative day when we were able to remove the VAD in the operating room. Only mild renal failure developed in this patient (creatinine 2 mg/dl). Pulmonary and hepatic function remained normal and no infections, major bleeding, or other complications appeared. Two days later, the intra-aortic balloon pump was removed and inotropic drugs were progressively reduced. On the twelfth day, the first endomyocardial biopsy showed mild focal acute rejection (ISHLT grade 1A). The patient developed mild critical illness neuropathy, with full recovery after physical therapy, and was discharged one month after heart transplantation. Nowadays, the patient is working full time without activity limitation, and the left ventricular ejection fraction is higher than 60% by echocardiography.
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Comment
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The need for mechanical cardiac support after heart transplantation is less than 1%, similar to postcardiotomy [6]. However the results after heart transplantation are worse than that used as bridge to heart transplantation or postcardiotomy, probably because in the first case the device is implanted when the patient is in a more deteriorated situation [6].
Cardiac assistance is indicated after heart transplantation because of right heart failure, primary graft failure, or acute graft rejection. Primary graft failure is the main cause of operative mortality in cardiac transplantation, whereas right heart failure is the most frequent clinical situation. Election of VAD is influenced by the etiology and the expected duration of assistance. A key decision during the evaluation of a potential VAD recipient relates to univentricular versus biventricular support. In our case we preferred biventricular support because the indication was the failure to separate from cardiopulmonary bypass due to biventricular graft dysfunction. Moreover an isolated left ventricular support could cause a severe failure of donor right ventricle in a recipient with high pulmonary vascular resistance.
The etiology of PGF is usually a multifactorial problem including donor age and inotropic support, weight mismatch, ischemic time and graft preservation, pulmonary vascular resistance, and clinical status of recipient. In our case there was a long ischemic time and the donor heart had moderate inotropic support and may have suffered from a cardiac contusion and hypoxia due to thoracic trauma with airway entrapment. Moreover the recipient had a high pulmonary vascular resistance. All these factors could influence the appearance of PGF. The use of optimal donor hearts is the main measure for prevention of PGF however the lack of donors and the increased waiting list makes it necessary to accept suboptimal hearts and consequently the risk of PGF is higher.
The use of VAD is associated with possible complications such as multiorganic failure, renal failure, sepsis, bleeding, and neurologic problems [6]. In last years the continuous development of cardiac assistance technology and the greater experience of surgical teams have allowed to make implantation easier with better results and fewer complications rates during longer periods of time. In our case after seven days there were not complications related to the assistance.
Recent studies have illustrated that patients with VAD used as bridge to heart transplantation have better results than patients with only inotropic drugs achieving a greater hemodynamic stability and a better preservation of vital organs [7]. Similarly, we believe that VAD use has an important role in the treatment of PGF in order to get hemodynamic stability and to allow the recovery of graft function. Probably the time of implantation is the key; when this situation appears the assistance should begin early before shock and hypoperfusion cause irreversible organ damage. All about in heart transplant recipients, who present previous damage secondary to end-stage heart failure and chronic low cardiac output. In this context, multiorgan failure is the final cause of death.
This case illustrates a recovery from PGF in absence of a maintained myocardial injury using VAD. In our opinion in similar cases after getting hemodynamic stabilization with VAD, which preserves the viability of vital organs and diminishes graft injuries, we have the option of closely monitoring patient evolution and graft function during 24–48 hours waiting for the graft recovery instead of performing an immediate retransplantation.
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References
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- Emery R.W., Eales F., Joice L.D., et al. Mechanical circulatory assistance after heart transplantation. Ann Thorac Surg 1991;51:43-47.[Abstract]
- Jaggers J., Fullerton D.A., Campbell D.N., et al. Cardiac allograft failure: successful use of biventricular assist device. Ann Thorac Surg 1995;60:1406-1409.[Abstract/Free Full Text]
- Fernandez A.L., Herreros J.M., Llorens R., Martinez A., Panizo A., Manito N. Primary graft failure after heart transplantation. Successful recovery with pneumatic biventricular assistance. Int J Artif Organs 1996;19:307-310.[Medline]
- Albes J.M., Eckstein F.S., Heinemann M.K., Ziemer G. Successful weaning of a transplanted heart from biventricular assist device. Ann Thorac Surg 2000;70:277-278.[Abstract/Free Full Text]
- Hooper T.L., Odom N.J., Tetherson G.J., Waterhouse P., Hilton C.J., Dark J.H. Successful use of left ventricular assist device for primary graft failure after heart transplantation. J Heart Transplant 1988;7:385-387.[Medline]
- Minev P.A., El-Banayosy A., Minami K., Körtke H., Kizner L., Körfer R. Differential indication for mechanical circulatory support following heart transplantation. Intensive Care Med 2001;27:1321-1327.[Medline]
- Aaronson K.D., Eppinger M.J., Dyke D.B., Wright S., Pagani F.D. Left ventricular assist device therapy improves utilization of donor hearts. J Am Coll Cardiol 2002;39:1247-1254.[Abstract/Free Full Text]
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Abstract
Introduction
