The ECG After Cardiac Transplantation

This may be normal in a transplanted heart, arising as a consequence of autonomic denervation. The heart rate tends to fall over time. A persistently rapid heart rate may lead to tachycardia induced cardiomyopathy. Alternatively, a fast heart rate may be a manifestation of a failing heart.

Recipient p waves:

P waves on the ECG may arise from the atrial remnant of the recipient. They are dissociated from the graft QRS complexes. If they occur in the context of a donor bradycardia, they may lead to heart block being diagnosed incorrectly.

Right bundle branch block

This is a common finding and may reflect elevated right heart pressure or right ventricular dysfunction.

Atrial premature beats (APBs)

APBs are a common finding in transplant ECGs. They may become less frequent over time. An increase in frequency may be associated with graft rejection.

Atrial flutter (AF) or fibrillation

Approximately 18% of transplant patients develop AF or flutter. These rhythm disturbances become more common when rejection occurs. AF may be treated with amiodarone or cardioversion. Digoxin is ineffective. Caution must be exercised in prescribing beta blockers because the graft uses circulating catecholamines to increase cardiac output. Therefore whilst they are effective for achieving rate control, the patient must be observed carefully for signs of clinical deterioration. AF may respond to overdrive pacing or cardioversion. Ablation may also be considered.

Pitfall: Exercise caution using beta blockers in patients with transplants because these patients use circulating catecholamines to increase cardiac output.

Ventricular arrhythmias

These are rare in the early period following transplant. They may occur following the use of antiarrhythmics for atrial rhythm disturbances. In the late period after transplant, VF and VT may be caused by graft coronary disease. This may present as sudden cardiac death.

Sinus node dysfunction

Sinus bradycardia is common immediately after transplant. Sinus node disease is the commonest cause of bradyarrhythmia in the transplanted heart. This may be due to perioperative ischaemia or surgical trauma affecting the sinus node. It tends to improve over time. Permanent pacemakers can be used to treat symptomatic patients. Only about a third of patients receiving a pacemaker will actually pace long term. An isoprenaline infusion may improve the rate whilst pacing is arranged. Atropine is ineffective in transplant bradyarrhythmias because the heart is denervated.

Atrioventricular (AV) block

This is less common than sinus node dysfunction following transplantation. It must be distinguished from recipient p waves giving the appearance of heart block. It is more common in late onset bradyarrhythmias and there may be underlying rejection or graft vasculopathy. A patient with AV block should therefore be further investigated with angiography and biopsy. If the patient is haemodynamically compromised, a permanent pacemaker should be inserted.

The rhythm-related consequences of denervation of the graft heart are (a) a persistent tachycardia, (b) reliance on circulating catecholamines to increase heart rate and (c) atropine is ineffective in treating transplant bradyarrhythmias.

Ischaemic changes

Ischaemia in the transplanted heart may produce conventional ST segment and T wave changes. If a patient is found to have frank ST segment elevation, a working diagnosis of infarction should be made. It may be difficult to establish a time course for this in the likely absence of pain. ST segment depression and T wave inversion should similarly raise the suspicion of ischaemia. However, the ECG in transplant patients must be interpreted with caution. There are case reports of ‘pseudo-infarct’ ECGs of transplant patients who were subsequently found to have neither regional wall motion abnormality on echo nor obstructive coronary disease at angiography [8]. It has been speculated that myocardial oedema and reperfusion injury following surgery may be one cause of such ECG changes. The ECG may normalise with time and this can be associated with a reduction in left ventricular (LV) wall thickness as oedema resolves.

Pitfall: beware ‘pseudo-infarction’ in transplant patients where ST segment elevation may represent myocardial oedema or surgical injury rather than ischaemia.