Complications Of Heart
Transplantation
The initial complications of heart
transplantation relate to donor events, damage due to cold ischaemia,
reperfusion injury, technical complications and the haemodynamic challenge
facing the new heart in the recipient.
· Bradycardia – related to cold
ischaemia, damage to the sinoatrial node or pre-transplant treatment with
amiodarone. Treatment comprises either isoproterenol (isoprenaline) or
temporary atrioventricular pacing.
· Atrial fibrillation or flutter occurs in up to a fifth of patients.
· Right ventricular failure – due to pre-existing pulmonary hypertension and high pulmonary vascular
resistance. Isoproterenol is a pulmonary vasodilator as well as a chronotrope,
and is used routinely. Inhaled nitric oxide can be a useful addition to reduce
pulmonary artery pressure.
· Systemic hypotension may be due to impaired left ventricular function, which may recover.
Reduction in peripheral vascular resistance may occur due to acidosis and
vasoconstricting inotropes such as noradrenaline or vasopressin may be
required.
· Valvular dysfunction. Tricuspid regurgitation is more common and may relate to dilatation of the
tricuspid valve ring due to high pulmonary pressures. It typically recovers
within 12 months.
· Bleeding resulting in
tamponade may occur.
· Pericardial effusion may also occur and sometimes requires treatment, although it usually
resolves within 6 weeks.
· Renal dysfunction is
very common, particularly in patients with pre-existing renal impairment, those
requiring prolonged bypass (retransplants, previous congenital heart disease)
and as a consequence of calcineurin inhibitor immunosuppression. Short-term
haemofiltration should be started early and does not confer any late
disadvantage.
Immunosuppression
A typical immunosuppressive regimen would
comprise an induction agent such as antithymocyte globulin or basiliximab, with
maintenance therapy with tacrolimus, mycophenolate and steroids. In addition,
statins such as pravastatin are also used in the early post-transplant period,
regardless of serum cholesterol level.
Rejection
Hyperacute rejection
Hyperacute rejection is very uncommon. The
short ischaemic tolerance of the heart means that formal cross-matching cannot
usually be performed, and virtual cross-matching must be relied on.
Transplantation in the presence of donor-specific antibody predicts less good
outcome, with antibody-mediated rejection (AMR).
Acute rejection
Signs and symptoms of rejection are few, and
the first presentation maybe with an arrhythmia. For this reason evidence of
rejection is sought using frequent endocardial biospies. These are performed by
passing fine biopsy forceps down the internal jugular vein and into the heart.
Most rejection is acute cellular rejection,
which responds to pulsed high-dose steroids; AMR is increasingly being
recognised.
Cardiac allograft vasculopathy
Cardiac allograft vasculopathy (CAV) is the
main cause of graft loss after the first year, with an incidence of around 50%
at 10 years. It manifests as a diffuse accelerated form of atherosclerosis
affecting the entire coronary arterial tree circumferentially, rather than
appearing as the eccentric plaques in the large arteries that is typical of
normal coronary artery disease.
Since the transplanted heart is denervated
the recipient tends not to feel pain due to progressive ischaemia. Instead CAV
is detected either on routine coronary angiography or the patient presents with
new onset heart failure, arrhythmias, syncope or death. More recently
intravascular ultrasound is being used to monitor the coronary arteries.
Treatment of CAV is preventative. Factors
that might contrib- ute to vascular disease, such as smoking, hypertension,
diabetes and hyperlipidaemia are treated aggressively. In addition there is
some evidence that the mTOR inhibitor immunosuppressants sirolimus and
everolimus may prevent its occurrence.
Outcomes of heart transplantation
Current 1-year patient survival after a first
heart transplant is 83%, with 60% surviving 10 years. The shortage of donor
hearts, and the increased morbidity and mortality following retransplantation,
means that most patients will not be considered for a second heart once the
first heart fails.
