A 70-year-old woman with depression, quiescent polycythemia rubra vera, and previously treated (with curative intent) carcinoma breast with no residual complications was admitted following a drug overdose. She was assessed to be suicidal in the setting of recalcitrant depression and was scheduled for electroconvulsive therapy (ECT). Her current medications were aspirin 150 mg mane on alternative days, quetiapine 50 mg BD, nitrazepam 60 mg nocte, and aperients as needed. Her baseline electrocardiograph (ECG) showed sinus rhythm, left-axis deviation, normal PR & QT intervals, and normal QRS and T wave morphology (Figure 1).

At her first session she was administered bifrontal 50% ECT under anaesthetic supervision using IV propofol 120 mg and IV succinylcholine 50 mg. Immediately following ECT, a 22-second motor seizure was noted and on electroencephalograph (EEG), seizure activity lasting 34 seconds was recorded. The patient then developed atrial fibrillation with a rapid ventricular rate of 130 bpm with deep (up to 4 mm) T-wave inversion in leads I, aVL, II, III, aVF, and V3-V6. She was treated with 135 mg IV esmolol and IV magnesium sulphate 30 mg and reverted to sinus rhythm, but the diffuse T-wave inversion persisted (Figure 2).

She denied chest pain and demonstrated no symptoms or signs of cardiopulmonary or haemodynamic compromise. She was afebrile with a respiratory rate of 24/minute, arterial oxygen saturations of 94% on room air, pulse of 90/minute, blood pressure of 130/70 mmHg, and clear chest on auscultation. A formal neurological examination was unremarkable. Given her past smoking history of 200-pack years and previously reported cases of critical stenosis of the left anterior descending coronary artery presenting with similar ECG changes,1 she was commenced on IV heparin and admitted to the medical ward for serial ECGs and troponin I measurements. Over the next 48 hours, she remained stable with no elevation in serial troponin I measurements, although her ECG changes persisted.

An inpatient dipyridamole stress perfusion scan performed on day 8 showed a small reversible apical perfusion defect, with the gated SPECT (Single Photon Emission Computed Tomography) study showing normal wall motion and contractility with left ventricular ejection fraction of 60%. The patient was transferred back to the psychogeriatric service and remained psychologically stable. Repeat ECG on day 5 showed persistence of T-wave inversion.

Sudden onset of new diffuse ECG changes not reflective of myocardial ischaemia but secondary to other aetiologies is well documented. A familiar example are the ECG changes induced by acute subarachnoid haemorrhage (SAH) which, it is hypothesised, reflect non-uniform myocardial repolarisation secondary to increased amounts of noradrenaline release from the hypothalamus.2 Typical findings are nonspecific ST and T-wave changes, prolonged QRS duration, U waves, and increased QT intervals. However, about 20% of cases of SAH are associated with myocardial ischaemia as a result of increased systemic levels of catecholamines.3

Although ECG changes are known to occur following ECT, such occurrences are not well described in the literature—one possible reason being that physician consultations to patients undergoing ECT are relatively few in number.4 In the presence of negative results of noninvasive cardiac testing for myocardial ischaemia, the most likely cause for the abnormal ECG changes of widespread T-wave inversion is increased sympathetic activity associated with ECT,5 which is supported by the finding of decreased T-wave amplitude following injection of IV adrenaline.6

Prospective studies suggest that this phenomenon may be seen in up to 4% of patients treated with ECT5. In our patient, the normal ECG a month prior to ECT along with negative cardiac testing is reassuring in that the ECG changes do not reflect myocardial ischaemia secondary to underlying widespread obstructive coronary disease which may have been induced by psychotropic and/or anaesthetic medications.

ECT has a recognised therapeutic role in the management of severe depression resistant to medical treatment,7,8 and has been shown to be a safe procedure, even in older patients with known cardiovascular disease.9 However, cardiac complications can occur which include arrhythmias, particularly ventricular ectopy, transient ST-segment depression, and transient wall motion abnormalities on echocardiography.10–14 Not surprisingly, these are seen more often in patients with underlying cardiac disease and related to ECT-associated systemic hypertension and tachycardia which increase myocardial oxygen demand resulting in myocardial ischemia.10,11

Of interest is a prospective review of 53 patients where ECT was found to lead to transient decrease in left ventricular systolic function in patients without underlying cardiac disease.14 Fortunately, multiple ECT sessions did not have a cumulative deleterious effect on left ventricular function which suggests that tolerance to ECT can develop.14

Despite the fact that ECG changes can be detected following ECT, as seen in this case and reported by others, it may still be prudent to investigate for coronary artery disease in patients with cardiovascular risk factors. It is not clearly defined on how long the abnormal ECG changes following ECT may persist but it was seen to last for 3 weeks in one report.5 On current evidence the long-term outcome in patients with such changes remains unknown.

Seshasayee Narasimhan
Cardiology Registrar, John Hunter Hospital
NSW, Australia
(seshnarasimhan@yahoo.com.au)