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Cardiac transplantation

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A heart transplant, or a cardiac transplant, is a surgical transplant procedure performed on patients with end-stage heart failure or severe coronary artery disease. As of 2008 the most common procedure is to take a working heart from a recently deceased organ donor (cadaveric allograft) and implant it into the patient. The patient's own heart is either removed (orthotopic procedure) or, less commonly, left in place to support the donor heart (heterotopic procedure). Post-operation survival periods average 15 years. Heart transplantation is not considered to be a cure for heart disease, but a life-saving treatment intended to improve the quality of life for recipients

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Cardiac transplantation

  1. 1. CARDIAC TRANSPLANTATION DR VISHWANATH HESARUR DEPARTMENT OF CARDIOLOGY JNMC, BELGAUM.
  2. 2. HISTORY OF HEART TRANSPLANTATION  The innovative French surgeon Alexis Carrel performed the first heterotopic canine heart transplant with Charles Guthrie in 1905.  Frank Mann at the Mayo Clinic further explored the idea of heterotopic heart transplantation in the 1930s  In 1946, after unsuccessful attempts in the inguinal region, Vladimir Demikhov of the Soviet Union successfully implanted the first intrathoracic heterotopic heart allograft.  The first human cardiac transplant was a chimpanzee xenograft performed at the University of Mississippi by James Hardy in 1964.
  3. 3.  In 1967 – on December 3, Christiaan Barnard performed the first human-to-human heart transplant at the Groote Schuur Hospital in Cape Town, South Africa.
  4. 4. Denise Darvall - Donor Louis Washkansky - Recipient
  5. 5.  Adrian Kantrowitz performed the first pediatric heart transplant in the world on December 6, 1967 at Maimonides Hospital in Brooklyn, New York barely 3 days after Christiaan Barnard.
  6. 6.  The pioneering efforts of Shumway and his colleagues at Stanford eventually paved the way for the re-emergence of cardiac transplantation in the late 1970s.  Over the next several years, poor early clinical results led to a moratorium on heart transplantation, with only the most dedicated centers continuing experimental and clinical work in the field.
  7. 7.  He is widely regarded as the father of heart transplantation although the world's first adult human heart transplant was performed by Christiaan Barnard in South Africa utilizing the techniques developed and perfected by Norman Shumway & Lower.  The introduction of transvenous endomyocardial biopsy by Philip Caves in 1973 finally provided a reliable means for monitoring allograft rejection.  The advent of the immuno-suppressive agent cyclosporine dramatically increased patient survival and marked the beginning of the modern era of successful cardiac transplantation in 1981.
  8. 8.  Heart transplantation is now a widely accepted therapeutic option for end-stage cardiac failure, with more than 2,700 procedures performed annually.
  9. 9. CARDIAC TRANSPLANT IN INDIA  Organ transplantation act in India came in 1994  Dr. Venugopal led a team of doctors to perform the first successful heart transplant in India on 3 August 1994.  This was the first of the 26 heart transplant procedures performed by Dr. Venugopal
  10. 10. LIST OF APPROVED HOSPITALS FOR HEART TRANSPLANTATION IN INDIA
  11. 11. RECIPIENT SELECTION AND MANAGEMENT Indications  Systolic heart failure (defined by LVEF <35%) with severe functional limitations and/or refractory symptoms despite maximal medical therapy  New York Heart Association Functional Class III–IV  Maximal oxygen uptake (O2 max) of 12–14 mL/kg/min exercise testing  Cardiogenic shock not expected to recover  Ischemic heart disease with intractable angina not amenable to surgical or percutaneous revascularization and refractory to maximal medical therapy  Intractable ventricular arrhythmias, uncontrolled with standard antiarrhythmic therapy, device therapy, and/or ablative therapy  Severe symptomatic hypertrophic or restrictive cardiomyopathy  Congenital heart disease in which severe fixed pulmonary hypertension is not a complication  Cardiac tumors with low likelihood of metastasis
  12. 12.  Cardiomyopathy (ie, dilated, hypertrophic, or restrictive)  Anatomically uncorrectable congenital heart disease (eg, HLHS, pulmonary atresia with intact ventricular septum plus sinusoids, congenitally corrected transposition of the great arteries with single ventricle and heart block, and severely unbalanced atrioventricular septal defects)  Potentially correctable congenital heart disease associated with greatly increased operative risk (eg, severe Shone complex, interrupted aortic arch and severe subaortic stenosis, critical aortic stenosis with severe endocardial fibroelastosis, and Ebstein anomaly in a symptomatic newborn)  Refractory heart failure after previous cardiac surgery  Significant cardiac allograft vasculopathy or chronic graft dysfunction of a previous heart transplant
  13. 13. Role of Exercise Testing  In patients undergoing transplant evaluation, measurement of peak oxygen consumption (O2) during cardiopulmonary exercise testing provides an objective assessment of functional capacity and is more useful than NYHA classification, ejection fraction, or other markers of heart failure severity, for assessing prognosis and determining the optimal timing of listing for transplantation.  Patients with a peak O2 of more than 14 mL/kg/min have 1- and 2-year survival rates that are comparable or better than those achieved with transplantation, and patients should be medically managed and undergo serial exercise testing.
  14. 14.  Patients with a peak O2 between 10 and 14 mL/kg/min constitute an intermediate risk group in which continued medical therapy may offer a survival benefit similar to heart transplantation among selected patients that are able to tolerate beta blockers, have low-risk Heart Failure Survival Scores (HFSS's), and have the protection of an internal defibrillator
  15. 15.  The HFSS is a predictive model calculated from seven prognostic variables that are commonly obtained during the transplant evaluation process.  In patients tolerating beta blockers, a peak O2 of <12 mL/kg/min has been suggested as an appropriate threshold to identify individuals that are likely to derive a survival benefit from transplantation.  Patients with a peak O2 of 10 mL/kg/min, regardless of beta blocker use, have significantly reduced survival rates with medical therapy compared to cardiac transplantation, and these patients should be listed for transplantation.
  16. 16. Contraindications  Irreversible severe pulmonary arterial hypertension  Pulmonary vascular resistance (PVR) >5 Wood units  Pulmonary vascular resistance index (PVRI) >6  Transpulmonary gradient >16–20 mmHg  PA systolic pressure >50–60 mmHg or >50% of systemic pressures  Advanced age (>70 years)  Active systemic infection  Active malignancy or recent malignancy with high risk of recurrence  Diabetes mellitus with:  End-organ damage (neuropathy, nephropathy, proliferative retinopathy)  Poor glycemic control (HbA1c >7.5)
  17. 17.  Marked obesity (BMI >30 kg/m2 or >140% of ideal body weight)  Severe peripheral arterial disease not amenable to revascularization  Systemic process with high probability of recurrence in the transplanted heart  Amyloidosis  Sarcoidosis  Hemochromatosis  Irreversible severe renal, hepatic, or pulmonary disease  Psychosocial factors that may impact on patient's ability to comply with complex medical regimen  History of poor medical compliance  Uncontrolled psychiatric illness (anxiety, depression, psychosis)  Active or recent substance abuse (alcohol, tobacco, or illicit drugs)
  18. 18. DONOR SELECTION AND MANAGEMENT  Acceptance of the concept of irreversible brain death, both legally and medically  Patients with irreversible brain injury accompanied by the intent to withdraw life support are considered to be potential organ donors.
  19. 19. CRITERIA FOR DETERMINING BRAIN DEATH Clinical Evaluation  Mechanism of brain injury is sufficient to account for irreversible loss of brain function  Absence of reversible causes of CNS depression  CNS depressant drugs  Hypothermia (<32°C [85°F])  Hypotension (MAP <55 mmHg)  Absence of neuromuscular blocking drugs that may confound the results of the neurologic exam  No spontaneous movements, motor responses, or posturing  No gag or cough reflexes  No corneal or pupillary light reflexes  No oculovestibular reflex (cold calorics)
  20. 20. Confirmatory Tests  Apnea test for minimum of five minutes showing:  No respiratory movements  PCO2 >55 mmHg  pH <7.40  No intracranial blood flow
  21. 21. DONOR SELECTION CRITERIA  Age <55 y  Absence of significant structural abnormalities  Left ventricular hypertrophy (wall thickness >13 mm by echocardiography)  Significant valvular dysfunction  Significant congenital cardiac abnormality  Significant coronary artery disease
  22. 22.  Adequate physiologic function of donor heart  Left ventricular ejection fraction (LVEF) ≥45% or  Achievement of target hemodynamic criteria after hormonal resuscitation and hemodynamic management  Mean arterial pressure (MAP) >60 mmHg  Pulmonary capillary wedge pressure (PCWP) 8–12 mmHg  Cardiac index >2.4 L/min x m2  Central venous pressure 4–12 mmHg  Systemic vascular resistance 800–1200 dyne/seccm5  Dopamine or dobutamine requirement <10 g/kg/min  Negative hepatitis C antibody, hepatitis B surface antigen, and HIV serologies  Absence of active malignancy or overwhelming infection
  23. 23. Donor Evaluation  Once a potential donor is identified, the procurement process is initiated by contacting the local, or host, organ procurement organization (OPO).  The host OPO is responsible for obtaining consent for organ donation, verifying pronouncement of death, evaluating and managing the donor, and equitably allocating the donor organs.  Suggested cardiac donor evaluation  Past medical history and physical examination  Electrocardiogram  Chest roentgenogram  Arterial blood gases  Laboratory tests (ABO, HIV, HBV, HCV)  Echocardiogram, pulmonary artery catheter evaluation, and in selected cases, coronary angiogram
  24. 24. Donor Management  The main goals of organ donor management are to ensure optimal organ function by providing  Volume resuscitation  Optimizing cardiac output  Normalizing systemic vascular resistance  Maintaining adequate oxygenation  Correcting anemia, acid base, and electrolyte abnormalities, and  Correcting hormonal imbalances that occur after brain death and that can impair circulatory function.
  25. 25.  Standardized algorithms incorporating early use of invasive hemodynamic monitoring along with aggressive hemodynamic management and hormonal resuscitation with insulin, corticosteroids, triiodothyronine, and arginine vasopressin have been proposed to improve cardiac donor management and maximize organ use, particularly in patients with a left ventricular ejection fraction of <45 percent on initial echocardiography.  Currently, most donor hearts are harvested from the donor by a transplant donor team from the transplantation center and transported back to the center for implantation.  A cold ischemic period of 4 to 6 hours in adult hearts is generally considered safe
  26. 26. Continuous Heart Transplant Perfusion
  27. 27. MATCHING DONORS & RECIPIENTS Matching is based upon:  ABO blood group  Body size compatibility (± 20% body weight)  Antibody screen - of preformed reactive anti- HLA antibodies (PRA)  No HLA prospective matching done unless high levels of pre-formed antibodies on screening (PRA > 10-20%) Allocation is determined by:  Recipient’s priority on waiting list  Status code (1A, 1B, 2)  Time accrued within a status
  28. 28.  Because ischemic time during cardiac transplantation is crucial, donor recipient matching is based primarily not on HLA typing but on the severity of illness, ABO blood type (match or compatible), response to PRA, donor weight to recipient ratio (must be 75% to 125%), geographic location relative to donor, and length of time at current status.  The PRA is a rapid measurement of preformed reactive anti-HLA antibodies in the transplant recipient.  In general PRA < 10 to 20% then no cross-match is necessary. If PRA is > 20% then a T and B-cell cross-match should be performed.  Patients with elevated PRA will need plasmapheresis, immunoglobulins, or immunosuppresive agents to lower PRA.
  29. 29. SURGICAL TRANSPLANTATION TECHNIQUES Orthotopic transplantation is the most common – it involves complete explantation of the native heart. Biatrial anastomosis:  The ischemic time is shorter.  Complications include atrial dysfunction due to size mismatch of atrial remnants and arrhythmia (sinus node dysfunction, bradyarrhythmias, and AV conduction disturbances) that necessitate PPM implantation in 10-20% of patients. Bicaval anastomosis:  Decreases incidence of arrhythmias, the need for a pacemaker, and risk for mitral or tricuspid regurgitation.  However narrowing of the SVC and IVC make biopsy surveillance difficult and ischemic times can be prolonged.
  30. 30. Heterotopic implantation is an alternative technique in which the donor heart functions in parallel with the recipient’s heart.  It accounts of less than 0.3% of heart transplants.  Herteropic transplantation is beneficial if the patient :  Has pulmonary hypertension that would exclude orthotopic transplantation.  Has heart failure that is potentially reversible (myocarditis) allowing future removal of the transplant.  The negative aspects of this approach include:  A difficult operation.  No anginal relief.  Need for anticoagulation (the native heart can cease to function and thrombose).  Contraindicated if the native heart has significant tricuspid or mitral regurgitation.
  31. 31. 'Living organ' transplant  In February 2006, at the Bad Oeynhausen Clinic for Thorax and Cardiovascular Surgery, Germany, surgeons successfully transplanted a 'beating heart' into a patient.  Rather than cooling the heart, the living organ procedure keeps it at body temperature and connects it to a special machine called an Organ Care System that allows it to continue pumping warm, oxygenated blood.  This technique can maintain the heart in a suitable condition for much longer than the traditional method.
  32. 32. Dead heart transplant  In October 2014, Australian surgeons have recently successfully transplanted dead hearts into patients for the first time.  According to Surgeon Kumud Dhital, the incredible development of the preservation solution with this technology of being able to preserve heart, resuscitate it and to assess the function of heart has made this possible.
  33. 33. From: NEJM (2007) 356:e6
  34. 34. PHYSIOLOGIC CONCERNS OF TRANSPLANT  Biatrial connection means less atrial contribution to stroke volume.  Resting heart rate is faster (95 to 110 bpm) and acceleration of heart rate is slower during exercise because of denervation.  Diurnal changes in blood pressure are abolished.  Diastolic dysfunction is very common because the myocardium is stiff from some degree of rejection and possibly from denervation.
  35. 35. PHYSIOLOGY OF THE TRANSPLANTED HEART  The transplanted heart is initially completely denervated.  Following recovery of donor sinus node function within the first 2 to 3 postoperative days, the denervated donor heart exhibits a faster resting heart rate usually between 95 to 110 beats/min caused by the intrinsic tachycardic rate of the sinus node and absence of the counter- regulatory effects of the parasympathetic system.  Cardiac denervation has several important clinical manifestations.  First, the cardiac allograft is slower to increase its heart rate in response to exercise and exhibits a slower heart rate recovery.
  36. 36.  Second, many heart transplant patients will not experience angina with ischemia of the cardiac allograft and may present instead with congestive heart failure caused by graft dysfunction, myocardial infarction, or sudden death.  Third, drugs that act primarily through the autonomic nervous system will have little to no effect on the denervated heart. For example, atropine works via a vagolytic mechanism to increase heart rate and is ineffective when used to increase heart rate in the transplanted heart. Isoproterenol is better suited for this purpose because of its direct effect on receptors, causing both increased chronotropy and inotropy.  Reinnervation of the cardiac allograft is felt to occur after the first year, but the timing and degree of reinnervation is highly variable.
  37. 37.  Electrical activity cannot cross suture line  Recipient atrial activity present but not conducted  Donor atrium denervated but source of electrophysiologic response  Loss of SNS, PNS innervation to donor heart  Vagal stimulation has no effect on sinus and AV nodes  No reflex tachycardia in response to hypovolemia, hypotension  ECG has 2 P waves  Indirect sympathomimetic agents have no effect  Anticholinergics, anticholinesterases, pancuronium, ephedrine  Direct acting sympathomimetics work  isoproterenol, NE, epi, phenylephrine, dopamine
  38. 38. POSTOPERATIVE COMPLICATIONS Surgical complications  Most common - Pericardial effusion with or without tamponade. Early graft dysfunction 1. Left ventricular systolic dysfunction.  It is common for transplant recipients to require inotropic support as they come off cardiopulmonary bypass. The most commonly used inotropic agents in this setting are dobutamine, milrinone, and isoproterenol, used alone or in combination. 2. Left ventricular diastolic dysfunction  Results from reversible ischemia or reperfusion injury to the donor organ or donor-recipient mismatch and usually resolves over a period of days to weeks.
  39. 39. 3. Right ventricular dysfunction  In patients with preexisting pulmonary hypertension.  Right ventricle is subjected to similar ischemic or reperfusion injury risks as the left ventricle.  Right ventricular dilation and the failure of coaptation of the tricuspid valve leaflets, leading to severe tricuspid regurgitation.  The treatment for perioperative right ventricular dysfunction is usually intravenous milrinone and nitrates to increase cardiac output and lower the PVR improve over a period of days to weeks.
  40. 40. Cardiac arrhythmias.  Most transplant recipients require perioperative temporary atrioventricular pacing.  Sinus node dysfunction is very common, probably because of a combination of surgical trauma, ischemia or reperfusion injury, and denervation.  Reduced by the bicaval anastomosis technique  With time, the sinus node usually recovers, and a permanent pacemaker is unnecessary. Renal dysfunction.  Preoperatively, many transplant recipients have some degree of impaired renal function. There is a risk of worsening renal function perioperatively.  This risk is compounded by the fact that the major immunosuppressive agents (i.e., cyclosporine and tacrolimus) are nephrotoxic.
  41. 41. SYSTEMIC IMMUNOSUPPRESSION.  Triple-therapy, which constitutes the cornerstone of modern immunosuppressive regimens in cardiac transplantation, includes  Calcineurin inhibitor (such as cyclosporine or tacrolimus),  Antiproliferative agent (such as MMF or azathioprine), and  Corticosteroids Steroids  A dose of 500 to 1000 mg of IV Solu-Medrol is usually given before being brought to the operating room, and then 125 to 150 mg is usually repeated every 8 hours, for a total of three more doses.  If the patient is extubated, oral prednisone 1 mg/kg/day for 8-9 weeks and then wean .
  42. 42.  Some centers continue to advocate the indefinite use of low-dose prednisone (2.5 to 5 mg daily).  If a decision is made to withdraw steroids completely, it should be done approximately 1 month before the next scheduled biopsy to ensure continued lack of acute cellular rejection  If a patient has acute cellular rejection associated with hemodynamic compromise, 1 g of intravenous Solu-Medrol daily for 3 days, and If no hemodynamic compromise , 100 mg of oral prednisone daily for 3 days is usually sufficient, followed by repeat biopsy, at most 2 weeks later to ensure resolution.
  43. 43. Calcineurin inhibitors Cyclosporine  Variable pattern of bioavailability  Narrow therapeutic range , monitoring serum levels important to prevent toxicity  Nephrotoxicity is the most important side effect and is related to renal afferent arteriolar vasoconstriction and the resultant reduced renal perfusion.  Other side effects include systemic hypertension, gingival hyperplasia, and tremors.  Postoperatively, once the patient is hemodynamically stable with good urine output, cyclosporine is initiated via continuous infusion at 1 mg/hour & then orally 100 mg twice daily, with adjustments in the dose based on serum trough levels
  44. 44. Tacrolimus  The dose of tacrolimus is 0.01 mg/kg per day administed by continuous infusion & then changed to 0.5 to 2 mg twice daily, with dose adjustment based on serum levels.  Side effects - nephrotoxicity and neurotoxicity (most commonly tremor). Mycophenolate mofetil  Selectively inhibits lymphocyte proliferation  1 g taken twice daily  SE- gastrointestinal symptoms (nausea, vomiting, and diarrhea) and myelosuppression.
  45. 45. Azathioprine  Purine analogue that works by nonspecific suppression of T and B-cell lymphocyte proliferation.  Dosage is 1 to 2 mg/kg per day.  Side effects - bone marrow suppression (dose related), increased incidence of skin cancer (use sunscreen), cutaneous fungal infections, and rarely liver toxicity and pancreatitis. Inhibitors of the target of rapamycin (TOR) enzyme: sirolimus and everolimus  Block the cellular response cytokines.  Inhibit vascular smooth muscle cell growth and proliferation in response to various growth factors  Dosage . Sirolimus -1 to 5 mg/day, and for everolimus, it is 1.5 to 3 mg/day  Sirolimus appears to lower the incidence of acute cellular rejection in humans and to slow the progression of transplant vasculopathy
  46. 46. Antilymphocyte globulin  Horse polyclonal antibody designed to inhibit T cells by binding to surface antigens.  Dosage is 10 to 15 mg/kg qd through a central venous catheter.  Goal is to keep T lymphocyte count ~200cells/microL.  Side effects include fevers, chills, urticaria, serum sickness, and thrombocytopenia. Muromonab-CD3 (OKT3)  A murine monoclonal antibody to the CD3 complex on the T-cell lymphocyte designed for selective T-cell depletion.  Usual dose is 5 mg/d IV bolus over 10 to 14 days.  Side effects - cytokine release syndrome (fever, chills, nausea, vomiting, mylagia, diarrhea, weakness, bronchospasm, and hypotension), pulmonary edema
  47. 47. REJECTION  According to ISHLT registry , 30% rejection during first yr. Hyperacute Rejection:  Caused by preforemd antibodies against the donor in the recipient.  It occurs within minutes to hours and is uniformly fatal.  PRA screening is the best method in avoiding hyperacute rejection. Acute Cellular Rejection:  Most common form and occurs at least once in about 50% of cardiac transplant recipients.  Half of all episodes occur within the first 2 to 3 months.  It is rarely observed beyond 12 months unless immunosuppression has been decreased.
  48. 48.  Rejection of the cardiac allograft is usually clinically silent unless it is accompanied by significant hemodynamic compromise (i.e., congestive heart failure).  As a result, endomyocardial biopsies are routinely performed for rejection surveillance.  Biopsy grades ≥ 2R warrant accentuation of immunosupression
  49. 49. INFECTIOUS DISEASE AFTER TRANSPLANTATION
  50. 50. CHRONIC COMPLICATIONS Cardiac Allograft Vasculopathy (Cav)  Progressive, neointimal proliferative process in the epicardial coronary vasculature and the microcirculation.  It is common with incidence of 20%,30% & > 50% at 3,5 & 10 yrs after transplant  It is a significant cause of mortality beyond the first year after transplantation, accounting for 30% to 50% of deaths at 5 years.  The pathophysiology of CAV is not completely understood.  Chronic, subclinical, immune-mediated injury at the level of the donor coronary endothelium creates a chronic inflammatory milieu.
  51. 51.  Because donor hearts are denervated at explantation, the transplant recipient typically will not experience cardiac angina from advanced allograft coronary vasculopathy.  Owing to the usually asymptomatic nature of vasculopathy, transplant recipients have frequent surveillance studies to detect significant vasculopathy, including coronary angiography with or without intravascular ultrasound (IVUS), cardiac perfusion magnetic resonance imaging, and dobutamine echocardiography.  Statins - improve survival, regardless of the patient's lipid profile  The antiproliferative effects of TOR inhibitors (sirolimus and everolimus) suggest a significant reduction in coronary neointimal proliferation and, therefore, transplantation coronary vasculopathy.  In severe, advanced CAV, frequently the only viable option is repeat transplantation.
  52. 52. Malignancy  Transplant recipients have a 100-fold increase in the prevalence of malignant tumors as compared with age-matched controls.  Most common tumor is posttransplantation lymphoproliferative disorder (PTLD), a type of non-Hodgkin’s lymphoma believed to be related to EBV.  Treatment involves reduction of immunosuppressive agents, administration of acyclovir, and chemotherapy for widespread disease.  Skin cancer is common with azathioprine use. Hypertension  As many as 75% of transplant recipients treated with cyclosporine or corticosteroids eventialy develop hypertension.  Treatment is empiric with a diuretic added to a calcium channel blocker, B-blocker, or Ace inhibitor.
  53. 53. OUTCOMES AFTER CARDIAC TRANSPLANTATION  The survival rate according to the United States Scientific Registry for Organ Transplantation reports the 1-year survival rate to be 82% and 3 year survival rate to be 74%. However ,10-year survival after cardiac transplantation is only 50%.  The most common cause of mortality was cardiac allograft vasculopathy.
  54. 54. SOME FAMOUS PERSONALITY  Tony Huesman was the world's longest living heart transplant recipient, having survived for 30 years, 11 months and 10 days, before dying of cancer.  As of December 2013, the record holder for longest living heart recipient is Englishman John McCafferty, 71. He received his heart on 20 October 1982  Kelly Perkins climbs mountains around the world to promote positive awareness of organ donation. Perkins was the first recipient to climb the peaks of Mt. Fuji, Mt. Kilimanjaro,  Twenty-two years after Dwight Kroening s heart transplant, he was the first recipient to finish an Ironman competition.
  55. 55.  Fiona Coote was the second Australian to receive a heart transplant in 1984 (at age 14) and the youngest Australian. In the 24 years after her transplant she became involved in publicity and charity work for the Red Cross, and promoted organ donation in Australia.  Race car driver and manufacturer Carroll Shelby received a heart transplant in 1990. Mr Shelby died on May 10, 2012, making him one of the longest living heart recipients.  Golfer Erik Compton qualified for the PGA Tour at age 32, after his second heart transplant.  Former Vice President of the United States Dick Cheney received a heart transplant on March 24, 2012

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