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Cardiac Transplantation: Hera Fatima, BPT 4th Year Centre For Physiotherapy and Rehabilitation Jamia Millia Islamia

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0% found this document useful (0 votes)
42 views54 pages

Cardiac Transplantation: Hera Fatima, BPT 4th Year Centre For Physiotherapy and Rehabilitation Jamia Millia Islamia

Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as KEY, PDF, TXT or read online on Scribd

Cardiac

Transplantation

Hera Fatima, BPT 4th


year
Centre for
Physiotherapy and
Rehabilitation
Jamia Millia Islamia
Introduction

There are only about 2500 heart donors


yearly.
Scarcity of donors is complicated by the
use of single organs, heart injury with
common brain-death injuries, difficulty
with ex-vivo preservation, heart disease
among donors, and the complexity of the
operation.
Class I Indications for Cardiac
Transplantation
Cardiogenic shock requiring mechanical assistance.
Refractory heart failure with continuous inotropic infusion.
NYHA functional class 3 and 4 with a poor 12 month
prognosis.
Progressive symptoms with maximal therapy.
Severe symptomatic hypertrophic or restrictive
cardiomyopathy.
Medically refractory angina with unsuitable anatomy for
revascularization.
Life-threatening ventricular arrhythmias despite
aggressive medical and device interventions.
Cardiac tumors with low likelihood of metastasis.
Hypoplastic left heart and complex congenital heart
disease.
Indications of Cardiac
Transplantation
Patients should receive maximal medical therapy
before being considered for transplantation. They
should also be considered for alternative surgical
therapies including CABG, valve repair /
replacement, cardiac septalplasty, etc.
VO2 has been used as a reproducible way to
evaluate potential transplant candidates and their
long term risk. Generally a peak VO2
>14ml/kg/min has been considered “too well” for
transplant as transplantation has not been shown
to improve survival over conventional medical
therapy. Peak VO2 10 to 14 ml/kg/min had some
survival benefit, and peak VO2 <10 had the
greatest survival benefit.
Contraindications to Cardiac
Transplantation
Evaluation of Cardiac
Transplantation Recipient
Right and Left Heart Catheterization.
Cardiopulmonary testing.
Labs including BMP, CBC, LFT, UA, coags, TSH,
UDS, ETOH level, HIV, Hepatitis panel, PPD, CMV
IgG, RPR / VDRL, PRA (panel of reactive
antibodies), ABO and Rh blood type, lipids.
CXR, PFT’s including DLCO, EKG.
Substance abuse history and evidence of
abstinence for at least 6 months and enrollment
in formal rehabilitation.
Mental health evaluation including substance
abuse hx and social support.
Financial support.
Weight no more than 140% of ideal body weight.
Status Listing
Once accepted as a transplant candidate,
a patient is entered on the list and given a
status based upon severity of illness.
If status changes, time accrual starts over.
Status I heart recipients are given
preference over status I heart / lung
recipients who are given preference over
status II heart recipients.
Zones are established to give local priority
to recipients within 500 to 1000 mile
radius centered on donor site.
Status Listings
Status I.
Cardiac Assistance
Total artificial heart
Ventricular assist devices
Intraaotic balloon pump
Ventilator
Inotrope dependent for maintaining cardiac output and
in hospital intensive care unit
Younger than 6 months
Status II. Patients not status I according to
criteria
Status VII. Patients improved and not in
immediate need of transplantation or with new
complication making transplantation
contraindicated.
Cardiac Donor

Brain death is necessary for any cadaveric


organ donation. This is defined as absent
cerebral function and brainstem reflexes
with apnea during hypercapnea in the
absence of any central nervous system
depression.
There should be no hypothermia,
hypotension, metabolic abnormalities, or
drug intoxication.
If brain death is uncertain, confirmation
tests using EEG, cerebral flow imaging, or
cerebral angiography are indicated.
Cardiac Donor – Exclusion
Criteria
Age older than 55 years.
Serologic results (+) for HIV, Hepatitis B or C.
Systemic Infection.
Malignant tumors with metastatic potential (except
primary brain tumors)
Systemic comorbidity (diabetes mellitus, collagen
vascular disease)
Cardiac disease or trauma
Coronary artery disease
Allograft ischemic time estimated to be > than 4-5 hours
LVH or LV dysfunction on echocardiography
Death of carbon monoxide poisoning
IV drug abuse.
Care of Donor Before
Transplantation
Contact local organ procurement organization
(OPO).
Obtain patient’s height and weight.
Collect CBC, CMP, ABO / Rh testing, HIV,
Hepatitis panel, and CMV Ab.
EKG.
Echocardiogram. (Fellow should be paid for
this, especially if after hours)
Consider cardiac catheterization if man over
40-45 or woman over 45-50.
Insert arterial line and right heart catheter.
Care of Donor Before
Transplantation
Donors with beating hearts are often volume
depleted because of therapy directed at reducing
cerebral edema.
As soon as consent for organ transplantation is
obtained (usually by OPO), normal saline should
be started or sparingly blood.
A goal CVP should be 5 to 10 and PCWP of 10 to
16.
Arterial systolic BP should be maintained at least
100mmHg. If CVP and PCWP are adequate and
hypotension persists dopamine and / or
dobutamine should be initiated.
Care of Donor Before
Transplantation
Diabetes Insipidus should be suspected if urine
output is >300cc/hr or if hypernatremia begins to
develop. Vasopressin and hypotonic solutions
can be used in this setting.
Electrolytes should be measured and corrected
hourly until organ procurement. Hypertension as
a result of sympathetic discharge can be
managed with IV NTG.
Hyperpyrexia or hypothermia should be
addressed with surveillance cultures, empiric
broad-spectrum antibiotics, cooling / warming
blankets.
Care of Donor Before
Transplantation
Metabolic acidosis from loss of adrenal and
thyroid hormone secretion of brain death
can depress myocardial contractility and
cause vasodilatation. Acidosis should be
corrected.
Ventricular dysfunction sometimes
responds to levothyroxine 4
micrograms/kg/hr and methylprednisolone
100mg IV qhr and can be tried in this
situation. Some recommend empiric
treatment with these agents.
Care of Donor Before
Transplantation
Echo should be performed as soon as possible
on the donor heart for assessment of LV
function. If unexpected dysfunction is found in
a young person, LVEDD and wall thickness
should be measured. If dimensions are normal
then corticosteroid and thyroid replacement
should begin and any acidosis should be
corrected.
Particular attention should be paid to wall
motion abnormalities (especially in individuals
with more advanced age), aortic stenosis, and
significant mitral valve abnormalities.
Care of Donor Before
Transplantation
Coronary angiography should be performed on
men older than 45 and women older than 50.
Precise definition of coronary anatomy is not
the goal! Quick exclusion of severe lesions is!
The sheath should be sutured in place for ICU
monitoring and blood sampling. Removal may
also be complicated by coagulopathy.
Risk to potential donor kidneys necessitates
limiting contrast exposure. Use non-ionic
contrast and <25cc’s if possible. No LVgram
unless absolutely necessary.
Matching Donor and Recipient
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.
Surgical Transplantation
Techniques
Orthotopic implantation is the most
common – it involves complete
explantation of the native heart.
Biatrial anastomosis: Most common because
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.
Surgical Transplantation
Techniques
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.
This procedure can be considered if the donor heart is
small enough to fit into the mediastinum without
physical restriction of function.
Hypertopic 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.
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.
Postoperative Complications
Surgical
Aortic pseudoaneurism or rupture at cannulation
site
Hemorrhagic pericardial effusion due to bleeding
or coagulopathy
Medical
Severe tricuspid regurgitation
RV failure
Pulmonary artery compression
Pulmonary hypertension
LV failure
Ischemia
Operative Injury
Acute rejection
Postoperative Complications
Rhythm disturbances
Asystole
Complete heart block.
Sinus node dysfunction with bradyarrhythmias (25%
permanent but most resolve within 1-2 weeks).
Atrial fibrillation.
Ventricular tachycardia.
Coagulopathy induced by cardiopulmonary
bypass
Respiratory failure
Cardiogenic pulmonary edema.
Noncardiogenic pulmonary edema.
Infection.
Renal or hepatic insufficiency
Drugs.
CHF.
Treatment of Postoperative
Complications
Treatment is directed at maintaining organ perfusion,
oxygenation, acid-base balance, avoiding RV failure,
and managing arrhythmias.
If needed drugs to maintain perfusion include
dopamine, milrinone, NTG, Nitroprusside,
isoproterenonol.
Managing RV failure is difficult.
Improve hypoxemia, acidosis, uremia, and electrolyte
imbalance.
Keep transpulmonary gradient <10mmHg and PVR < 6 woods
units
If vasodilators, volume reduction with diuretics and
ultrafiltration, and inotropic agents fail to improve RV function,
then RVAD can be considered.
Treatment of Postoperative
Complications
Arrhythmias – may signify acute rejection.
Bradyarrhythmias
Isoproterenol 0.01 to 0.02 micrograms/kg/min.
AV sequetial pacing.
Most resolve in 1 to 2 weeks.
AV disturbances in the early postoperative period
may indicate incomplete myocardial preservation,
pulmonary hypertension, acute rejection, or cardiac
edema.
Tachyarrhythmias
Amiodarone, Lidocaine, B-blockers, etc.
Postoperative Management

Initiation of medications, particularly


immunosuppressive agents begins on the
day of the operation.
Cyclosporin started IV on day of the surgery
and usually continued until day 3 at which time
converted to po. Usual IV dose is 0.5 mg/kg at
2 mg/min qd
Azathioprine 2 mg/kg IV qd until day 3 and
then converted to po.
Solumedrol 125mg IV q8h until tolerating po
and then Prednisone 0.6 mg/kg/day.
+/- Muromonab-CD3 (OKT3) started on postop
day 1 at 5mg IV qd.
Postoperative Management
Pneumocystis carinii prophylaxis is started within
the first week after transplant.
If patient or donor is CMV positive then
ganciclovir is started on postop day 2.
Endomyocardial biopsy is performed on postop
day 4 and steroids can begin to be tapered if
there is no rejection greater than grade 2b.
Anticoagulation is started if heterotopic
transplantation has been performed.
Amylase and lipase are measured on day 3 to
detect pancreatitis.
ECG’s are obtained qday.
Long-term Management
Endomycardial biopsy is performed once a week for the
first month and then less frequently depending on the
presence or absence of rejection (usual regimen is qweek x
4 weeks, qmonth x 3 months, q3months in 1st year,
q4months in 2nd year, 1 to 2 times per year subsequently).
If the donor was CMV positive a Hickman or peripherally
inserted central catheter is placed for IV gangciclovir
(5mg/kg IV bid x 14 days then 6mg/kg IV qd x 14 days. If
the recipient was CMV negative then oral acyclovir is
admisitered orally. If the recipient is CMV seropositive then
the antiviral agent can be discontinued. If seroconversion
occurs during treatment (and check at 1, 2, 3, and 6 month
intervals), then ganciclovir is initiated for at least an
additional 2 week period.
Long-term Management

Cyclosporine levels are checked


periodically by individual center protocols.
Echocardiography is useful periodically
and as an adjunct to endomyocardial
biopsy.
Cardiac catheterization is performed
annually for early detection of allograft
vasculopathy.
There is probably no need for routine
exercise or nuclear stress testing.
Immunosuppressive Agents

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 are bone marrow suppression (dose
related), increased incidence of skin cancer (use
sunscreen), cutaneous fungal infections, and rarely
liver toxicity and pancreatitis.
Drug interactions: allopurinol (decrease dose by
75%) and TMP/Sulfa (worsens thrombocytopenia).
Immunosuppressive Agents

Cyclosporin: inhibits T-cell lymphokine


production. Highly lipophilic.
Dosage is 8 to 10mg/kg/day in 2 divided doses. IV doses are
1/3 of oral doses in a continuous infusion.
Drug levels are frequently measured for dosage and toxicity,
but levels are not highly predictive of actual
immunosuppressive effect. Drug levels are reflected for 5 to
10 days because of a long half life.
Side effects: nephrotoxicity caused by afferent arteriolar
constriction and manifested by oliguria. Loop diuretics may
exacerbate this side effect. Dosage adjustments should only
be made if creatinine level is >3.0mg/dL (some renal
insufficiency is expected). Other side effects include
hypertension, hypertrichosis, tremor, hyperkalemia,
hyperlipidemia, and hyperuricemia.
Multiple drug interactions.
Immunosuppressive Agents

Corticosteroids: immunosuppressives of
uncertain mechanism. Used for
maintenance of immunosuppression and
to manage acute rejections.
High doses used initially tapered over the 1st 6
months to 5 to 15mg/d prednisone.
Side effects include mood and sleep disturbances,
acne, weight gain, obesity, hypertension, osteopenia,
and hyperglycemia.
Immunosuppressive Agents

Mycophenolate mofetil: selectively inhibits


lymphocyte proliferation.
Dosage is 2g/d po.
Side effects include GI disturbances. Does not cause
significant bone marrow suppression.
FK-506 (tacrolimus): Lymphophilic
macrolide that inhibits lymphokine
production similar to cyclosporine.
More toxic than cyclosporine.
Side effects include nephrotoxicity and neuotoxicity.
Immunosuppressive Agents

Antilymphocyte globulin: Horse polyclonal


antibody designed to inhibit T cells by
binding to surface antigens.
It is generally used at the time of transplantation for
induction therapy or during acute rejections.
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.
Immunosuppressive Agents
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 5mg/d IV bolus over 10 to 14 days.
CD3 cells are monitored with goal <25cells/mL.
Used in patients with renal insufficiency.
Side effects include cytokine release syndrome (fever,
chills, nausea, vomiting, mylagia, diarrhea, weakness,
bronchospasm, and hypotension), pulmonary edema.
Rapamycin: Similar mechanism of action of FK-
506 except that it antagonizes the proliferation of
nonimmune cells such as endothelial cells,
fibroblasts, and smooth muscle cells.
Not routinely used at present.
May have a roal in prevention of immunologically mediated
Basic Drug Regimen
Immunosuppressives
Antibiotic prophylaxis
PCP: TMP/Sulfa or Dapsone or Pentamidine aerosols.
CMV infection: Ganglyclovir, acyclovir.
Fungal infections: Nystatin.
Antihypertensives
Diuretics as needed
Potassium and Magnesium replacement (cyclosporin leads to
wasting of thes electrolytes.
Lipid-lowering agents. (Avoid allograft vasculopathy).
Glucose lowering agents (DM and steroids)
Anticoagulation if transplant heterotopic.
Cyclosporin dose lowering meds (Diltiazem / Verapamil /
Theophyilline)
Complications - Rejection

Avoidance with preoperative therapy with


cyclosporin, corticosteroids, and azathioprine.
If rejection is suspected then workup should
include: measurement of cyclosporine level
CKMB level, echocardiography for LV
function, and endomyocardial biopsy.
Signs and symptoms of rejection only
manifest in the late stages and usually as
CHF (rarely arrhythmias). Due to close
surveillance, most rejection is picked up in
asymptomatic patients.
Complications - Rejection

Hyperacute Rejection: Caused by preformed


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.
Complications - Rejection

Vascular (humoral) Rejection: not well


defined.
Characterized by immunoglobulin and
complement in the microvasculature with little
cellular infiltrate.
It is associated with positive cross match,
sensitization to OKT3, female sex, and younger
recipient age.
It is more difficult to treat than acute cellular
rejection, is associated with hemodynamic
instability, and carries a worse prognosis.
Staging of Acute Rejection
If acute rejection is found, histologic review of
endomyocardial biopsy is performed to determine the
grade of rejection.
Grade 0 — no evidence of cellular rejection
Grade 1A — focal perivascular or interstitial infiltrate
without myocyte injury.
Grade 1B — multifocal or diffuse sparse infiltrate without
myocyte injury.
Grade 2 — single focus of dense infiltrate with myocyte
injury.
Grade 3A — multifocal dense infiltrates with myocyte injury.
Grade 3B — diffuse, dense infiltrates with myocyte injury.
Grade 4 — diffuse and extensive polymorphous infiltrate
with myocyte injury; may have hemorrhage, edema, and
microvascular injury.
Treatment of Acute Rejection

Grade 1A and Grade 1B: No treatment is necessary.


Grade 2: Probably no treatment is necessary. Short course
of steriods (Prednisone 100mg qd x 3 days) is optional.
Grade 3A and Grade 3B: High dose corticosteroids
(Solumedrol 1mg/kg IV). If no response then ATGAM (OTK3
also an option, but causes more intense cytokine reaction).
Grade 3 with hemodynamic compromise or Grade 4: High
dose corticosteriods plus ATGAM or OTK3.
It is critical that an endomyocardial biopsy be performed to
document reversal of rejection after treatment. Otherwise
additional agents will need to be added. A biopsy is
obtained 1 week after initial biopsy showed rejection and
then 1 week after therapy complete. If ATGAM or OTK3 is
used biopsy should be obtained at the end of a course of
therapy (usually 7 to 14 days) and then again 1 week later
off therapy.
Complications - Rejection
Allograft vasculopathy (Chronic rejection): Transplant
coronary artery disease that is the leading cause of
death in patients more than 1 year after transplantation.
Likely a result of a proliferative response to
immunologically mediated endothelial injury (chronic
humoral rejection).
It differs from native CAD in that it is manifested by
concentric stenoses, predominately subendocardial
location, lack of calcification, can be rapidly progressive
and lack of angina pectoris.
Risk factors include degree of histocompatibility,
hypertension, hyperlipidemia, obesity, and CMV
infection.
Complications – Rejection
Allograft Vasculopathy
Treatment is mainly prevention with statins,
diltiazem, and antioxidant vitamins. Rapamycin is
an agent that has shown promise in preventing
this complication.
Treatment with percutaneous interventions and
CABG is limited due to its diffuse nature and
subendocardial locations.
Retransplantation for this disorder is an option,
but retrospective analysis have shown this
approach does not improve mortality as patients
do significantly worse with a second transplant as
compared with the first.
Complications - Infection

There are two peak infection periods after


transplantation:
The first 30 days postoperatively: nosocomial infections
related to indwelling catheters and wound infections.
Two to six months postoperatively: opportunistic
immunosuppresive-related infections.
There is considerable overlap, however as fungal
infections and toxoplasmosis can be seen during
the first month.
It is important to remember that
immunosuppressed transplant patients can
develop severe infections in unusual locations and
remain afebrile.
Opportunistic Infections

CMV: most common infection transmitted


donor to recipient.
Manifested by fever, malaise, and anorexia. Severe
infection can affect the lungs, gastrointestinal tract,
and retina.
If donor is CMV positive and the recipient is CMV
negative, prophylaxis with IV ganciclovir or foscarnet
is given for 6 weeks and followed by longterm oral
prophylaxis with acyclovir.
If the recipient is CMV positive a less potent regimen
can be used.
Bone marrow toxicity related to treatment can occur
and be confused with that due to azathioprine
treatment.
Opportunistic Infections

Toxoplasma gondii: Primary infection can be


serious while reactivation is rarely a serious
clinical problem.
Manifested as encephalitis, myocarditis, or pneumonitis.
Treated with pyrimethamine and sulfadiazine.
Pneumocystis carinii: Prophylactic therapy
with TMP/Sulfa is highly effective in preventing
progressive bilateral interstitial pneumonia
caused by this protozoan.
Dapsone (Requires G6PD testing) and pentamidine
aerosols (does not protect lung apices) are quite effective
for those with sulfa allergies.
Opportunistic Infections

Aspergillus organisms: Invasive Aspergillus


infection, typically of the lung or upper
respiratory tract is extremely difficult to
manage.
It is fortunately rare, and usually occurs among
patients who are severely immunocompromised from
use of antilymphocyte antibodies.
Standard treatment is with IV Amphotericin.
Complications - 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.
The incidence is as high as 50% in EBV-negative recipients of EBV-
positive hearts.
Treatment involves reduction of immunosuppressive agents,
administration of acyclovir, and chemotherapy for widespread
disease.
Skin cancer is common with azathioprine use.
Any malignant tumor present before transplantation carries
the risk for growth once immunosuppresion is initiated
because of the negative effects on the function of T-cells.
Complications - Hypertension

As many as 75% of transplant recipients


treated with cyclosporine or
corticosteroids evential develop
hypertension.
Treatment is empiric with a diuretic added
to a calcium channel blocker, B-blocker, or
Ace inhibitor.
If either diltiazem or verapamil is used, the
dosage of cyclosporin should be reduced.
Complications - Dyslipidemia

As many as 80% of transplant recipients


eventually have lipid abnormalities related
to immunosuppression medications.
These dyslipidemias have been linked to
accelerated allograft arteriopathy.
These disorders should be treated
aggressively with statins and fibrates to
hopefully alleviate transplant coronary
vasculopathy.
Complications – Tricuspid
Regurgitation
A rare complication is tricuspid
regurgitation caused by biotome-induced
trauma to the valve apparatus that rarely
requires valve replacement.
Hospitalization of Transplanted
Patients
If nausea and vomiting prevent
administration of oral medications, the
regimen should be changed to an IV one
i.e. transplant patients should not be
without immunosuppressives for even a
short period of time!!!
Cyclosporin IV dose is 1/3 of oral dose.
If fever develops then the following should
be performed:
Blood, urine and sputum cultures, BMP, CBC
CXR, Echocardiography (for LV function and effusion).
Consider endomyocardial biopsy for rejection.
Outcomes
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%.
The most common cause of mortality was cardiac
allograft vasculopathy.
The UNOS data suggested some group differences
with 3-year survival rate for white persons 75%,
Hispanics 71%, and African Americans 68%
Similar survival rates between men and women.
Lowest survival in patients < age 1 and
approaching age 65.
Outcomes

The typical causes of death in the first


year are due to acute rejection and
infection.
After the 1st year the primary cause of
death is vasculopathy.
In the later stages (after the perioperative
period) arrhythmia may be signs of acute
rejection or of an allograft vasculopathy.
Outcomes

Poor outcomes are associated with the


following risk factors:
Age less than 1 year or approaching age 65.
Ventilator use at time of transplant.
Elevated pulmonary vascular resistance.
Underlying pulmonary disease.
Diffuse atherosclerotic vascular disease.
Small body surface area.
The need for inotropic support pre-transplant.
Diabetes mellitus.
Ischemic time longer than 4 hours of transplanted
heart.
Sarcoidosis or amyloidosis as reason for transplant
(as they may occur in the transplanted heart).

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