Electroconvulsive therapy in a patient with hypertrophic obstructive cardiomyopathy

To the Editor

This case describes considerations for electroconvulsive therapy (ECT) in a patient with hypertrophic obstructive cardiomyopathy (HOCM) and major depression. ‘A’ was a 62-year-old woman admitted to a regional psychiatric facility for treatment of major depression with psychosis. She responded poorly to Olanzapine 5 mg nocte, Mirtazapine 45 mg nocte and Duloxetine 30 mg mane, and had poor oral intake and deconditioning. Hypotension and pre-syncope complicated her presentation and restricted pharmacological up-titration. Echocardiography revealed HOCM, with increased septal thickness and severe left ventricular outflow tract (LVOT) obstruction. ‘A’ was transferred to a tertiary hospital under cardiology for assessment of symptomatic LVOT obstruction, risks of ventricular arrhythmias and sudden cardiac death (SCD). Duloxetine was ceased due to dysrhythymogenic effects.

Surgical myectomy would relieve LVOT obstruction but would require post-operative cardiac rehabilitation. ‘A’ was unlikely to participate due to depression. Therefore, options for expedient treatment of depression were discussed including risks and benefits. Psychiatry, in consultation with ‘A’, her husband, cardiology and anaesthetics, recommended ECT.

In HOCM, events that acutely increase outflow obstruction including tachycardia can precipitate acute haemodynamic collapse. Patients are at increased risk of arrhythmias and SCD. After the electrical stimulus in ECT, there are haemodynamic changes in the tonic phase including bradycardia, hypotension and asystole. A catecholamine surge in the clonic phase can cause tachycardia, hypertension and transient depression in ejection fraction (Tess and Smetana, 2009). Bifrontal ECT was chosen, as it has been associated with less severe bradycardia and lower incidence of prolonged asystole than bitemporal or right unilateral electrode placement (Stewart et al., 2011).

Standard pulse-width bifrontal ECT (1.5× seizure threshold) was commenced three times weekly. Olanzapine and Mirtazapine doses were unchanged. Intravenous prehydration was administered to avoid worsening LVOT obstruction periprocedurally. Metaraminol was used to minimise hypotensive effects of induction agents, Remifentanil and Esmolol to control the sympathetic effects of ECT during the seizure and external defibrillator pads were attached should arrhythmias occur. Depressive symptoms improved after four uncomplicated treatments. ‘A’ was transferred to her regional hospital and discharged home after two further ECT treatments.

There is one prior report of ECT use in 92-year-old woman with HOCM and depression (Robinson et al., 2011). She had continuous transthoracic echocardiography while successfully receiving bitemporal ECT. Anaesthesia similarly included beta-blockade. Monitoring revealed decreased LVOT pressure gradient during ECT.

Our case demonstrates how consideration of electrode placement and anaesthetic techniques may reduce the risks of ECT in patients with HOCM.