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TUTORIAL Table of Contents   
Year : 2009  |  Volume : 12  |  Issue : 1  |  Page : 71-78
Adult cardiac transplantation: A review of perioperative management Part - I

1 Department of Anesthesiology, Cardiothoracic Anesthesiology Division (H.R.), Mayo Clinic, Phoenix
2 Division of Cardiovascular and Thoracic Surgery (D.E.J., F.A.A.), Mayo Clinic, Phoenix, Arizona

Click here for correspondence address and email

Date of Submission24-Oct-2008
Date of Acceptance27-Oct-2008


Cardiac allotransplantation has, over the years, become the established therapeutic modality for patients with end-stage heart failure. Significant advances in immunosuppressive therapy have dramatically improved the outcome of heart transplantation over the past four decades. This review will focus on the anaesthetic challenges involved in the perioperative management of these complex patients as well as some of the proposed alternatives to transplantation.

Keywords: Anaesthetic management, heart failure, heart transplantation

How to cite this article:
Ramakrishna H, Jaroszewski DE, Arabia FA. Adult cardiac transplantation: A review of perioperative management Part - I. Ann Card Anaesth 2009;12:71-8

How to cite this URL:
Ramakrishna H, Jaroszewski DE, Arabia FA. Adult cardiac transplantation: A review of perioperative management Part - I. Ann Card Anaesth [serial online] 2009 [cited 2022 Nov 29];12:71-8. Available from:

   History and Epidemiology Top

From uncertain beginnings more than half a century ago, heart transplantation has evolved into a commonplace reality and the definitive therapy for patients with end-stage cardiomyopathy.

After Carrell and Guthrie first attempted the procedure in dogs in 1905, the next reported heart transplantations were at Mayo Clinic in 1933 by Mann; these canine heart transplants were able to function until the onset of rejection at 8 days. [1] The currently used technique was first described by Lower and Shumway in 1960. [2] Barnard performed the first successful orthotopic heart transplant in1967; the patient succumbed to postoperative pneumonia in less than 4 weeks. The introduction of cyclosporine in 1981 and monoclonal antibody OKT3 in 1983 for heart transplant patients greatly accelerated the progress of organ transplantation. By the year 2000, the registry of the International Society for Heart and Lung Transplantation (ISHLT) reported that 55,359 heart transplants were performed worldwide. [3]

Limitations in the availability of donor organs have served to slow the pace of heart transplantation from the peak period in the mid-1980s. However, the number of patients with end-stage heart disease (ESHD) in need of transplantation has continued to rise. In addition, demographic data indicate that recent patients are in fact sicker than patients in previous eras. The number of patients who are United Network for Organ Sharing (UNOS) status 1 prior to transplantation increased over the past 15 years from 50% to 75%. [4] In the United States, approximately 20-30% of patients will die before a donor heart is found and of all patients listed, approximately only 35% will eventually receive transplants, with children and patients with UNOS 2 status being especially affected. [5] Survival after heart transplantation has progressively improved since its inception over 35 years ago, with 1-year survival approaching 90% and 7-year survival approaching 75%. [4]

   Indications for Heart Transplantation Top

The indications and contraindications have been considerably revised since the early days of heart transplantation. [6],[7],[8] The classic indication has been severe, end-stage disease refractory to medical or surgical therapy and in most patients the etiology is ischemic. Severe, irreversible pulmonary hypertension (marked by a calculated pulmonary vascular resistance of >6-8 Wood units that is unresponsive to pulmonary vasodilators) remains one of the few absolute contraindications, and this is related to the increased afterload placed on the donor heart and the possibility of acute right ventricular failure in the recipient [Table 1]. The degree of responsiveness of the pulmonary vasculature is the key in the selection of these patients for heart transplantation. Some centres do consider severe pulmonary hypertension to be a relative contraindication only and do transplant patients with this problem after a long period of medical therapy with pulmonary vasodilators and right ventricular inotropes in an outpatient setting and/or subject them to combined heart-lung transplantation. Studies have shown that patients who do respond to therapy have the same survival rates as patients without severe pulmonary hypertension. [9]

   Pathophysiology of End-Stage Heart Disease Top

The patient with end-stage heart disease (ESHD) presenting for heart transplantation presents formidable anaesthetic challenges. The pathophysiology is one of severe cardiomyopathy marked by varying degrees of both systolic and diastolic dysfunction. The former is reflected by reduced stroke volumes and elevated end diastolic volumes and the latter by chronically elevated diastolic filling pressures. To this picture is added the well-recognised sequelae of heart failure-increased renal salt and water retention secondary to increased renin and aldosterone production, impaired visceral, splanchnic and renal perfusion and increased catecholamine levels, which in time produce significant down regulation of beta receptors and diminished myocardial catecholamine stores.

The heart transplant candidate is maintained on near maximal regimens of conventional (diuretics, beta blockers, calcium channel blockers, nitrates, angiotensin-converting enzyme (ACE) inhibitors, inotropes and vasodilators) and second-line therapies such as phosphodiesterase inhibitors and heart-assist devices for chronic congestive heart failure. [10],[11] It is now well appreciated that the failing heart is preload dependent and afterload sensitive, and these patients do not tolerate even the most trivial perturbations in these and other parameters such as rhythm, heart rate and contractility that the anaesthesiologist is well-versed in manipulating. Many patients are also chronically anti-coagulated in order to prevent pulmonary and systemic embolization.

   Anaesthetic Management of the Donor Top

Perioperative management of the heart transplant donor follows the general principles of brain-dead donor care. [12] Recipient-donor cross matching for ABO compatibility is performed. In 1998, the average donor age was 28 years as per the recent ISHLT data for 2007; the majority of heart donors are in the 18-34 year demographic (UNOS/ISHLTA data as of August 2008), although the relative scarcity of donors is now forcing many centres to accept older donors provided they are free of coronary artery disease. The donor's cardiac history is always of concern, a key issue is the degree of haemodynamic support required to support the donor. Electrocardiography and echocardiography are mandatory. Coronary angiography is recommended for male donors over 45 years of age and females over the age of 50. The heart is also closely examined under direct visualization by the procurement team before donor cardiectomy occurs. In the matching of donor and recipient aside from human leukocyte antigen typing (HLA), ABO blood group compatibility is performed. If ABO barriers are crossed hyperacute or accelerated rejection will result due to the existence of donor-specific antibodies in the recipient. With regard to matching donor and recipient heart sizes, the shortage of donor hearts has made the guidelines less restrictive. The donor heart size should be within 20%-30% of the recipient. Generally, a larger donor heart is chosen in patients with elevated pulmonary vascular resistance, the larger heart being better able to withstand the stress of higher pulmonary afterload.

Crucial to anaesthetic management of the brain dead donor is the maintenance of normovolaemia and normothermia to ensure organ perfusion since the most donors are haemodynamically unstable secondary to derangements in metabolism and intravascular volume. Filling pressures are maintained in the normal to high range, care is taken to avoid hypoxia using high inspired oxygen concentrations and positive end-expiratory pressure (PEEP) if necessary. The oxygen carrying capacity of the blood is maximised using red cell transfusion if needed. Mean arterial pressure should be maintained at 80-90 mmHg with the help of vasopressors, if necessary. The loss of central thermoregulatory mechanisms may lead to hypothermia with resultant arrhythmias. Ventilator management is critical; brain-dead patients frequently develop neurogenic pulmonary oedema or acute respiratory distress syndrome (ARDS). High levels of PEEP are often required. Central diabetes insipidus typically ensues in the brain-dead patient leading to massive diuresis; volume and electrolyte status must be closely monitored.

The surgical details, briefly, are as follows. Following median sternotomy and pericardiotomy, systemic heparinisation is accomplished and the superior vena cava is ligated. The aortic root is then cannulated for the administration of cardioplegia. After ligation of the great veins, the heart is exsanguinated and decompressed. Following the infusion of cardioplegia and cardiac arrest, the aorta is cross-clamped. Topical hypothermia by way of iced slush is sometimes applied to the heart. Donor cardiectomy is then performed leaving remnants of the posterior atrial walls, pulmonary veins and venae cavae intact. At present, conventionally accepted donor heart ischemic time ranges from 3 to 6 hours. Some centres have begun to use innovative methods to avoid the issues limiting successful transplantation, the biggest being cold ischemic time. One such is the TransMedics Portable Warm Blood Perfusion System (Organ Care System, TransMedics Corporation, Andover, MA), which is currently under investigation in the United States. This system is designed to keep the donor heart warm and beating, maintaining pulsatile perfusion. Donor blood is used and the system provides blood oxygenation and flow from an internal gas supply and pulsatile pumping system. This has the advantage of enabling resuscitation of the donor organ, potentially improving its function and increasing the amount of time that an organ can be maintained outside the body in a condition suitable for transplantation by reducing time dependent ischaemic injury. This system has been approved for use in the European Union since mid-2006.

   Anaesthetic Management of the Recipient Top


Heart transplantation is typically urgent, leaving the anaesthesiologist little time for detailed pre-anaesthetic evaluation. An exam focusing on current symptoms, level of activity, medications, prior surgical and anaesthetic history, last oral intake and review of organ systems involved, is performed as is a comprehensive physical and airway evaluation and complete review of blood tests, radiologic and echocardiographic studies. These patients range from completely ambulatory outpatients to critically ill patients on multiple infusions, intra-aortic balloon counterpulsation and ventricular assist devices. [13],[14],[15] Using a fresh sterile breathing circuit is recommended as is the use of a bacterial filter in the circle system. Cytomegalovirus (CMV)-free blood products should be procured for patients lacking antibodies to this ubiquitous organism.


Aside from standard non-invasive monitors, the protocol at Presbyterian Hospital includes radial or femoral arterial pressure monitoring, central venous and pulmonary artery catheters. The right internal jugular venous approach is routinely used, and authors have found that this does not create difficulties with future cannulation for future endomyocardial biopsies. Conventional aseptic technique is used for all line insertions. A long sheath is used for the pulmonary artery (PA) catheter; it is initially advanced to the right atrium for central venous pressure (CVP) measurement. It is advanced into the pulmonary artery following separation from cardiopulmonary bypass (CPB). Factors that make passage of the PA catheter difficult in heart transplant patients prior to transplant include severe orthopnea, cardiac dilatation predisposing to intra-ventricular coiling, cardiac arrhythmias and tricuspid regurgitation. Pulmonary artery catheters capable of monitoring continuous mixed venous oxygen saturation and cardiac output in the authors opinion are particularly useful in the management of heart transplant recipients both intraoperatively as well as in the intensive care unit.

Patients are usually considerably apprehensive and most will have recently eaten, dictating the need for a rapid sequence induction with the preoperative use of agents such as metoclopramide to promote gastric emptying and drugs to raise gastric pH. The induction sequence is of critical importance as these patients are highly dependent on endogenous sympathetic drive and the combination of anaesthetic agents, which ablates the latter combined with drug-induced reductions in heart rate inotropic function, and preload can produce sudden cardiovascular collapse.[16] Regardless of the agents used for the induction of anaesthesia, care must be taken at all times to minimise the effects of negative inotropes, maintain heart rate and intravascular volume, avoid reductions in systemic vascular resistance (SVR) and minimise the ever present risks of aspiration. Opioids are the mainstay of induction; at the authors institute fentanyl 10-15 µg/kg (upto 60-75 µg/kg) is used to maintain the anaesthetic, depending upon the recipient's hepatic and renal function. Amnesia is usually accomplished using titratable doses of midazolam or scopolamine in the moribund patient. Some patients will be able to tolerate small concentrations of volatile anaesthetics as adjuncts in maintenance of anaesthesia.

Transoesophageal echocardiography is routinely employed at the authors institution and is invaluable in assessing ventricular function, contractility, volume status and the detection of intracardiac thrombi as well as aortic atherosclerosis in the pre-bypass period. Manipulation of the heart in the pre-pump phase is minimised to avoid possible embolism of intracardiac thrombus if present. Following individual cannulation of the venae cavae and aorta, CPB is instituted and the diseased heart is excised leaving an atrial cuff containing the cavae, pulmonary veins and remnants of the pulmonary artery and aorta. On CPB, other patients are cooled as for conventional cardiac procedures. The 4 major anastomoses of the procedure are the left and right atrial anastomoses and the end-to-end aortic and pulmonary anastomoses. The majority of procedures employ the classic Lower and Shumway technique; however, the bicaval technique is also used in some situations [Figure 1]. Here, the right atrium of the recipient is excised leaving behind a 2-3 cm cuff around each cava (cavoatrial cuff). The left atrial excision removes the left atrial appendage leaving a small cuff around the 4 pulmonary veins. The donor left atrium is sutured to the recipient left atrium before the inferior vena cava and the superior vena cava are sutured to the recipient cavoatrial cuff. The biggest advantages of this technique are lower incidence of tricuspid regurgitation and conduction disturbances.[17] Heterotopic transplantation is usually indicated in situations characterised by gross disparity in size between donor and recipient hearts and irreversible pulmonary hypertension and involves end-to-side aortic and pulmonary anastomoses and biatrial connections. Standard de-airing manoeuvres are performed; at the author's institution routinely methylprednisolone 1g prior to cross clamp release. Following removal of the cross clamp, some electromechanical activity usually ensues. Rewarming is completed in the usual fashion and the weaning process is begun. Choice of inotrope varies from one institution to the other; some groups advocate the routine use of isoproterenol in doses ranging from 0.005 to 0.05 ug/kg/min to ensure an adequate heart rate and contractility, and some others employ dobutamine 5-15 ug/kg/min. Some patients may need temporary epicardial pacing to wean from bypass and into the immediate postoperative period, indeed long-term transvenous pacing is not uncommon in heart transplant recipients owing to loss of sinus node function.

Right ventricular failure or dysfunction is the most common etiology of failure to wean from CPB, heralded by mean PA pressures often greater than 25-30 mmHg. Management of this situation involves maintaining adequate oxygenation and ventilation, avoiding acidosis, hypercarbia, hypothermia and the use of appropriate pulmonary vasodilators (prostaglandin E1, nitric oxide, nitroglycerine, sodium nitroprusside) and inotropes that support the right ventricle (dobutamine and milrinone), Failure to respond to these measures might indicates the need for mechanical right heart support. [18] Aggressive measures to reduce pulmonary vascular resistance are essential.

The newly transplanted heart needs appropriate filling pressures, being completely preload dependent. However, one must be vigilant to avoid high central venous pressures and right ventricular over distension. The remainder of the post bypass management is essentially similar to other cardiac procedures: maintenance of adequate haemodynamics, reversal of heparinisation, administration of blood products as indicated and preparation for transfer to the intensive care unit. Coagulopathy remains an ever present concern, especially in the redo patient. Aprotinin in the conventional high-dose regimen is frequently used and has been found to significantly reduce the quantity of blood products transfused. [19],[20] However, it has been withdrawn from the market in the United States in 2008 following the results of the Blood Conservation Using Antifibrinolytics in a Randomized Trial (BART) study that found an unacceptably high mortality in patients treated with aprotinin as compared with the lysine analogues. [21] At present, the standard of care is the use of epsilon amino caproic acid or tranexamic acid, which are potent antifibrinolytics instead of aprotinin, with the use of Factor 7a for emergency salvage in the case of uncontrolled bleeding


Postoperative management of the cardiac transplant recipient combines the concerns both of the post-pump as well as the transplant status. [22] Meticulous attention is paid to the maintenance of adequate oxygenation and ventilation, intravascular volume, pulmonary and systemic pressures, normothermia and coagulation. Appropriate antirejection and immunosuppressive regimens are instituted (typically prednisone, tacrolimus, azathioprine and cyclosporine combinations). Most patients are maintained on inotropic and chronotropic support for 36-72 hours. Extubation is typically achieved when haemodynamics is stable and bleeding is no longer a risk. Inotropic support is withdrawn gradually, and invasive monitoring is removed; chest tubes are usually taken out after 24 hours. The uncomplicated patient is usually discharged from the intensive care unit within 72 hours.

   Post-Transplantation Physiology Top

Post-transplantation physiology has assumed greater importance owing to the fact that cardiac allograft recipients are returning to the operating room in higher numbers for non-cardiac procedures. The vast majority seem to be general surgical in nature, resulting in intra-abdominal explorations, the others are related to treating the effects of chronic steroid use and immunosuppression.[23] Cardiac denervation is an inevitable consequence, as the cardiac plexus is divided in the donor, resulting in a denervated donor heart. [24],[25] The atrial remnant of the recipient remains innervated, but no impulses will cross the suture line. As a result, the donor atrium is responsible for heart rate generation. The transplanted heart has a higher intrinsic rate and reduced rate variability. Resting heart rates range from 90 to 110 beats per minute. Normal responses to changes in position, e.g. orthostatic changes, are lost as are the variations in response to stimuli such as the Valsalva manoeuvre, carotid sinus massage as well as normal responses to laryngoscopy and intubation. This has obvious implications for the anaesthesiologist. Intrinsic functions such as cardiac impulse formation and conduction are intact. The Frank-Starling mechanism is also intact. In the innervated heart, the normal acute response to a sudden reduction in intravascular volume is a simultaneous increase in both heart rate and contractility. [26] In the denervated heart, however, the initial response via the Frank-Starling mechanism is an increase in stroke volume dependent on an adequate left ventricular end diastolic volume. The increased contractility secondary to heart rate is a secondary effect and is dependent on circulating catecholamines. The transplanted heart is, therefore, critically preload dependent; higher filling pressures are needed, and this has to be kept in mind before the induction of general and regional anaesthesia. [27]

In terms of altered drug effects, it is now well known that drugs or manoeuvres that act via autonomic nerve fibres are ineffective in the transplanted heart. Vagolytic agents such as pancuronium, atropine and glycopyrollate have no effects on heart rate and may have undesirable effects in heart transplant recipients. The response to anticholinesterases is unpredictable. The heart retains its responsiveness to direct acting agents such as isoproterenol, epinephrine, norepinephrine, dopamine and dobutamine.

Other features noted in the transplanted heart include mild to moderate mitral and tricuspid regurgitation. [28],[29] Some studies have shown that the response to exercise is also submaximal secondary to diminished sympathetic activity. [30],[31]

   Heart Transplantation Outcomes Top

Complications in the early postoperative period include hyperacute and acute rejection, pulmonary and systemic hypertension, cardiac arrhythmias, respiratory failure, renal failure and infection in the immunocompromised patient.

The major limiting factor in the long-term outcome after heart transplantation has been allograft coronary artery disease to the extent that it is the major cause of death after the first year. Its incidence ranges from 10%-20% at 1 year and has been found to be as high as 50% by 5 years post transplant.

This transplant vasculopathy is an insidious process and has been well characterised. [32],[33] In contrast to non-transplant related arteriosclerosis, it is usually diffuse and involves the vessel circumferentially and has no particular predilection for specific vasculature. It is considered to be a panvasculopathy. The exact immunomechanisms of graft arteriopathy are poorly understood.

Some of the factors that predispose to allograft coronary artery disease (CAD) are speculated to be older donor age, male sex, hypertension in the donor, hypertension in the recipient, African-American recipient, immunosuppression and CMV infection.

Overall survival has improved over the past 40 years climbing from a 5-year survival rate of 70% in the early 1990s to 77% in 2004. [4] Post-transplant renal dysfunction is common and is primarily the result of cyclosporine nephrotoxicity. Hypertension is common, occurring in approximately two-thirds of all cardiac transplant recipients, attributed to the use of cyclosporine and corticosteroids -both mainstays of immunosuppressive therapy.

Chronic immunosuppression is associated with an increased incidence of malignant neoplastic disease. It has been estimated that transplant recipients have a 100 times greater risk for developing cancer than the general population. Cancers seen in the heart-transplant recipient include those of the skin as well as post-transplant lymphoproliferative disorders

   Future Directions Top

The imbalance in supply and demand relating to the heart donor has made the consideration of viable alternatives imperative. Worldwide, annual transplantation volumes have plateaued over the past decade. Dramatic improvements in medical therapy as well as the technological improvements in mechanical circulatory support and heart assist devices have also served to slow the pace of transplantation. The following is a brief summary of some potential alternatives, some of which have been proven to be failures.

Xenotransplantation: [34],[35] This refers to the use of organs from other species, specifically porcine and non-human primate hearts. This offers a theoretical alternative to allograft transplantation, but is limited by multiple issues such as the immune responses to xenograft antigens as well as complex ethical and societal dilemmas.

'Cardiac Reduction:' This procedure introduced by Batista, involves reducing the size of the left ventricle by removing a portion of it, usually the lateral wall on the theoretical premise (Laplace's law) that wall tension will be reduced in a smaller chamber and that reducing the mass to diameter ratio of the heart improves pump function. Part of this procedure involves mitral valve repair, which improves the mitral regurgitation associated with severe dilated cardiomyopathy. However, much of the evidence over the past decade has indicated lack of success with this procedure. This procedure was introduced as a potentially promising therapy for patients with dilated cardiomyopathy and congestive heart failure, but multiple studies have shown that the reduction in left ventricular volume is insufficient to restore adequate function, clinical results have been disappointing with event free survival being poor at 2 years. [36],[37]

Dynamic cardiomyoplasty: This entails the use of the latissimus dorsi muscle that is mobilised and wrapped around both ventricles and connected to a pacing device, which causes the muscle to contract synchronously with the heart. Long-term results of this procedure have been limited by high incidences of sudden cardiac death and by the decrease in the power production of the skeletal muscle graft with time. Comparative studies have failed to demonstrate any survival improvement against medical therapy. [38] Other experimental techniques include the use of foetal myoblast cells to replace injured myocardium as well as the use of endothelial and fibroblast growth factors. [39]

   References Top

1.Mann FC, Priestley JT, Markowitz J, Yater WM. Transplantation of the intact mammalian heart. Arch Surg 1933;26:219-24.  Back to cited text no. 1    
2.Lower RR, Shumway NE. Studies on orthotopic homotransplantation of the canine heart. Surg Forum 1960;11:18-9.  Back to cited text no. 2  [PUBMED]  
3.Hosenpud JD, Bennett LE, Keck BM, Boucek MM, Novick RJ. The Registry of the International Society for Heart and Lung Transplantation: Seventeenth official report-2000. J Heart Lung Transplant 2000;19:909-31.  Back to cited text no. 3  [PUBMED]  [FULLTEXT]
4.Taylor DO, Brown RN, Jessup ML, Starling RC, Aaronson KD, Rayburn BK, et al . Progress in heart transplantation: Riskier patients yet better outcomes: A 15 year multi-institutional study. J Heart Lung Transplant 2007;26:S61.  Back to cited text no. 4    
5.Lin HM, Kauffman HM, McBride MA, Davies DB, Rosendale JD, Smith CM, et al . Center-specific graft and patient survival rates: 1997 United Network for Organ Sharing (UNOS) report. JAMA 1998;280:1153-60.  Back to cited text no. 5  [PUBMED]  [FULLTEXT]
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8.Reardon MJ, Letsou GV, Anderson JE, Safi HJ, Espada R, Baldwin JC. Orthotopic cardiac transplantation after minimally invasive direct coronary artery bypass. J Thorac Cardiovasc Surg 1999;117:390-1.  Back to cited text no. 8  [PUBMED]  [FULLTEXT]
9.Nwakarma LU, Weiss ES, Patel ND, Baumgartner WA, Russell SD, Conte JV. Reversible pulmonary hypertension has comparable survival: An analysis of 10,331 heart transplant patients in recent era. Circulation 2007;116:664.  Back to cited text no. 9    
10.Cohn JN, Archibald DG, Ziesche S, Franciosa JA, Harston WE, Tristani FE, et al . Effect of vasodilator therapy on mortality in chronic congestive heart failure; Results of a Veterans Administration Cooperative Study. N Engl J Med 1986;314:1547-52.  Back to cited text no. 10  [PUBMED]  
11.Kalman J, Buchholz C, Steinmetz M, Courtney M, Gass A, Lansman S, et al . Safety and efficacy of beta blockade in patients with chronic congestive heart failure awaiting transplantation. J Heart Lung Transplant 1995;14:1212-7.  Back to cited text no. 11  [PUBMED]  
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13.Hensley FA Jr, Martin DE, Larach DR, Romanoff ME. Anesthetic management for cardiac transplantation in North America--1986 survey. J Cardiothorac Anesth 1987;1:429-37.  Back to cited text no. 13  [PUBMED]  
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17.Schnoor M, Schafer T, Luhmann D, Sievers HH. Bicaval versus standard technique in orthotopic heart transplantation: A systematic review and meta-analysis. J Thorac Cardiovasc Surg 2007;134:1322-31.  Back to cited text no. 17    
18.Fonger JD, Borkon AM, Baumgartner WA, Achuff SC, Augustine S, Reitz BA. Acute right ventricular failure following heart transplantation: Improvement with prostaglandin E1 and right ventricular assist. J Heart Transplant 1986;5:317-21.  Back to cited text no. 18  [PUBMED]  
19.Propst JW, Siegel LC, Feeley TW. Effect of aprotinin on transfusion requirements during repeat sternotomy for cardiac transplantation surgery. Transplant Proc 1994;26:3719-21.  Back to cited text no. 19  [PUBMED]  
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22.Stein KL, Armitage JM, Martich GD. Intensive care of the cardiac transplant recipient. In: Ayres SM, Grenvik A, Holbrook PR, Shoemaker WC, editors. Textbook of Critical Care. 3rd ed. Philadelphia: WB Saunders; 1995. p. 1649.  Back to cited text no. 22    
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26.Schwaiblmair M, von Scheidt W, Uberfuhr P, Ziegler S, Schwaiger M, Reichart B, et al . Functional significance of cardiac reinnervation in heart transplant recipients. J Heart Lung Transplant 1999;18:838-45.  Back to cited text no. 26  [PUBMED]  [FULLTEXT]
27.Fontes M, Rosenbaum S. Noncardiac surgery after heart transplantation. Anesthesiol Clin North Am 1997;15:207-20.  Back to cited text no. 27    
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29.Stevenson LW, Dadourian BJ, Kobashigawa J, Child JS, Clark SH, Laks H. Mitral regurgitation after cardiac transplantation. Am J Cardiol 1987;60:119-22.  Back to cited text no. 29  [PUBMED]  [FULLTEXT]
30.Quigg RJ, Rocco MB, Gauthier DF, Creager MA, Hartley LH, Colucci WS. Mechanism of the attenuated peak heart rate response to exercise after orthotopic cardiac transplantation. J Am Coll Cardiol 1989;14:338-44.  Back to cited text no. 30  [PUBMED]  
31.von Scheidt W, Neudert J, Erdmann E, Kemkes BM, Gokel JM, Autenrieth G. Contractility of the transplanted, denervated human heart. Am Heart J 1991;121:1480-8.  Back to cited text no. 31  [PUBMED]  
32.Labarrere CA. Relationship of fibrin deposition in microvasculature to outcomes in cardiac transplantation. Curr Opin Cardiol 1999;14:133-9.  Back to cited text no. 32  [PUBMED]  [FULLTEXT]
33.Young JB. Editorial. Current Opin Cardiol 1999;14:111-3.  Back to cited text no. 33    
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35.Rose EA, Stevenson LW. Xenotransplantation: Management of end-stage heart disease. Philadelphia: Lippincott-Raven Publishers; 1998.  Back to cited text no. 35    
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Correspondence Address:
Harish Ramakrishna
Department of Anesthesiology, Cardiothoracic Anesthesiology Division (H.R.), Mayo Clinic, Phoenix, Arizona

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DOI: 10.4103/0971-9784.45018

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