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Heart Transplantation Medication

  • Author: Donald M Botta, Jr, MD; Chief Editor: John Geibel, MD, DSc, MSc, MA  more...
 
Updated: Feb 26, 2016
 

Medication Summary

The goals of pharmacotherapy are to prevent complications, to reduce morbidity, and to reduce the chances for organ rejection.

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Immunosuppressants

Class Summary

Immunosuppression is started soon after surgery. Transplant recipients are maintained on an immunosuppression regimen that includes 1-3 drugs. Generally, the drugs fall into 3 categories: steroids, antimetabolites, and other immunosuppressants.Several regimens can be used, including pretransplantation induction therapy and simple postoperative maintenance therapy; the choice of regimen depends on the training and experience of the transplantation center.[10, 11]

Cyclosporine (Neoral, Sandimmune, GENGRAF)

 

Cyclosporine is a cyclic polypeptide that suppresses some humoral immunity and, to a greater extent, cell-mediated immune reactions such as delayed hypersensitivity, allograft rejection, experimental allergic encephalomyelitis, and graft versus host disease for various organs.

For children and adults, base dosing on ideal body weight. Maintaining appropriate levels of the drug in the bloodstream is crucial to the maintenance of the allograft. Foods can alter the level of the drug and time of administration. Medication must be taken at the same time every day.

Neoral is the capsular form of cyclosporine, available in 25- and 100-mg capsules. Sandimmune is the liquid form. GENGRAF is the branded generic form, available in 25- and 100-mg capsules.

Prednisone

 

Prednisone is an immunosuppressant used for the treatment of autoimmune disorders. It may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear (PMN) leukocyte activity. It is an oral steroid with approximately 5 times the potency of endogenous steroids. Minimal to no oral prednisone should be given for the first 21 days after transplantation unless rejection occurs.

Methylprednisolone (Medrol, Solu-Medrol, A-Methapred)

 

Methylprednisolone is an immunosuppressant used to treat autoimmune disorders. It may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. It is the intravenous (IV) form of prednisone.

Tacrolimus (Prograf)

 

Tacrolimus suppresses humoral immunity (T-cell activity). It is a calcineurin inhibitor with 2-3 times the potency of cyclosporine. Tacrolimus can be used at lower doses than cyclosporine, but it has severe adverse effects, including renal dysfunction, diabetes, and pancreatitis. Levels are adjusted according to renal function, hepatic function, and adverse effects.

Mycophenolate mofetil (CellCept, Myfortic)

 

Mycophenolate mofetil inhibits inosine monophosphate dehydrogenase (IMPDH) and suppresses de novo purine synthesis by lymphocytes, thus inhibiting their proliferation. It inhibits antibody production.

Azathioprine (Imuran, Azasan)

 

Azathioprine antagonizes purine metabolism and inhibits synthesis of DNA, RNA, and proteins. It may decrease proliferation of immune cells, which results in lower autoimmune activity. Antimetabolites are used to block the uptake of vital nutrients needed by the cells. As implied, these drugs affect not only the cells of the immune system but also other cells of the body. The potency of therapy is dose dependent. Azathioprine is not effective treatment for acute rejection episodes but remains an economical choice for long-term immunosuppression.

Sirolimus (Rapamune)

 

Sirolimus, also known as rapamycin, is a macrocyclic lactone produced by Streptomyces hygroscopicus. It is a potent immunosuppressant that inhibits T-cell activation and proliferation by a mechanism that is distinct from those of all other immunosuppressants. This inhibition suppresses cytokine-driven T-cell proliferation by inhibiting progression from the G1 phase to the S phase in the cell cycle.

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Inotropic Agents

Class Summary

After the procedure, the patient is maintained on a combination of pressor agents while the donor heart regains energy stores. Once stabilized, the patient is rapidly weaned from the ventilator and the pressors. The chosen combination depends on the training and experience of the center.

Dopamine

 

Dopamine is a naturally occurring endogenous catecholamine that stimulates beta1-and alpha1-adrenergic and dopaminergic receptors in a dose-dependent fashion. It stimulates the release of norepinephrine.

In low doses (2-5 μg/kg/min), dopamine acts on dopaminergic receptors in renal and splanchnic vascular beds, causing vasodilatation in these beds. In midrange doses (5-15 μg/kg/min), it acts on beta-adrenergic receptors to increase heart rate and contractility. In high doses (15-20 μg/kg/min), it acts on alpha-adrenergic receptors to increase systemic vascular resistance and raise blood pressure.

Dobutamine

 

Dobutamine is a sympathomimetic amine with stronger beta than alpha effects. It increases the inotropic state. Vasopressors augment the coronary and cerebral blood flow during the low-flow state associated with severe hypotension.

Dopamine and dobutamine are the drugs of choice to improve cardiac contractility, with dopamine the preferred agent in hypotensive patients. Higher dosages may cause an increase in heart rate, exacerbating myocardial ischemia.

Epinephrine (Adrenalin)

 

Its alpha-agonist effects include increased peripheral vascular resistance, reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. Its beta2-agonist effects include bronchodilation, chronotropic cardiac activity, and positive inotropic effects.

Norepinephrine (Levophed)

 

Norepinephrine stimulates beta1- and alpha-adrenergic receptors, increasing cardiac muscle contractility and heart rate, as well as vasoconstriction; this results in systemic blood pressure and coronary blood flow increases. After obtaining a response, the rate of flow should be adjusted and maintained at a low-normal blood pressure, such as 80-100 mm Hg systolic, sufficient to perfuse vital organs.

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Contributor Information and Disclosures
Author

Donald M Botta, Jr, MD Assistant Professor, Department of Surgery, Section of Cardiac Surgery, Surgical Director, Cardiac Transplantation, Director of Mechanical Circulatory Support, Yale University School of Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Mary C Mancini, MD, PhD, MMM Professor and Chief of Cardiothoracic Surgery, Department of Surgery, Louisiana State University School of Medicine in Shreveport

Mary C Mancini, MD, PhD, MMM is a member of the following medical societies: American Association for Thoracic Surgery, American College of Surgeons, American Surgical Association, Society of Thoracic Surgeons, Phi Beta Kappa

Disclosure: Nothing to disclose.

Chief Editor

John Geibel, MD, DSc, MSc, MA Vice Chair and Professor, Department of Surgery, Section of Gastrointestinal Medicine, and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director, Surgical Research, Department of Surgery, Yale-New Haven Hospital; American Gastroenterological Association Fellow

John Geibel, MD, DSc, MSc, MA is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, Society for Surgery of the Alimentary Tract

Disclosure: Received royalty from AMGEN for consulting; Received ownership interest from Ardelyx for consulting.

Acknowledgements

Deepak M Gangahar, MBBS, MD Professor, Department of Surgery, Chief, Section of Cardiovascular and Thoracic Surgery, Surgical Director, Heart Transplant and VAD Services, University of Nebraska Medical Center

Deepak M Gangahar, MBBS, MD is a member of the following medical societies: American College of Cardiology, American College of Chest Physicians, American College of Surgeons, American Medical Association, International Society for Heart and Lung Transplantation, International Society for Minimally Invasive Cardiothoracic Surgery, Nebraska Medical Association, and Society of Thoracic Surgeons

Disclosure: Nothing to disclose.

Shreekanth V Karwande, MBBS Chair, Professor, Department of Surgery, Division of Cardiothoracic Surgery, University of Utah School of Medicine and Medical Center

Shreekanth V Karwande, MBBS is a member of the following medical societies: American Association for Thoracic Surgery, American College of Chest Physicians, American College of Surgeons, American Heart Association, Society of Critical Care Medicine, Society of Thoracic Surgeons, and Western Thoracic Surgical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Richard Thurer, MD B and Donald Carlin Professor of Thoracic Surgical Oncology, University of Miami, Leonard M Miller School of Medicine

Richard Thurer, MD is a member of the following medical societies: American Association for Thoracic Surgery, American College of Chest Physicians, American College of Surgeons, American Medical Association, American Thoracic Society, Florida Medical Association, Society of Surgical Oncology, and Society of Thoracic Surgeons

Disclosure: Nothing to disclose.

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View of the recipient's chest after the heart is removed, with the patient on cardiopulmonary bypass.
Suturing of the donor heart. Note that the left atrial anastomosis is performed first.
Completed operation. Note suture lines on now-implanted heart.
Heterotopic transplantation.
View after cardiectomy, showing cuffs for bicaval anastomosis.
Completed bicaval transplantation technique.
 
 
 
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