Volume 199 - Issue 10

Sotalol-associated cardiogenic shock in a patient with asymptomatic transient rate-related cardiomyopathy

Author:  Simon D Leslie

Med J Aust 2013; 199 (10): 658-659. || doi: 10.5694/mja12.11678
Published online: 18 November 2013
The prescribing information for sotalol does not warn of the risk of life-threatening cardiogenic shock when this drug is used in patients with left ventricular dysfunction, and should probably be amended.

To the Editor: An 80 kg, 73-year-old man with type 2 diabetes managed with gliclazide and metformin was discharged on a dose of 40 mg twice daily of sotalol and a therapeutic dose of warfarin after an admission for atrial flutter. Transoesophageal echocardiography during his admission showed normal left ventricular (LV) size with mild to moderate global systolic dysfunction and moderate mitral incompetence.

Two weeks later, he developed generalised weakness, malaise, diaphoresis, nausea and dull left-sided chest pain, progressing to severe shock within 45 minutes of onset, evident on arrival at a hospital emergency department. Two hours before onset, he had taken a planned increase in his oral dose of sotalol to 80 mg.

His systolic blood pressure was 74 mmHg without evidence of respiratory compromise. Results of an arterial blood gas analysis were consistent with severe tissue hypoperfusion. Electrocardiography showed a sinus rhythm of 60 beats per minute, normal conduction, a lengthened QTc interval (510 ms), and anterolateral T-wave inversion without ST-segment abnormalities. Results of bedside ultrasonography suggested global LV dysfunction.

The patient was given 2 litres of fluids and high doses of noradrenaline and adrenaline intravenously, but his condition did not improve. Intravenous calcium chloride (10 mmol) and glucagon (2 mg) restored his blood pressure to 120/70 mmHg, maintained with adrenaline (5 μg/min) alone. The initial relative bradycardia, prolonged QTc interval and response to calcium and glucagon were consistent with cardiogenic shock secondary to sotalol therapy. Other investigations excluded circulatory, cardiac, pulmonary, infective and drug causes of sudden cardiovascular collapse. The patient’s initial mild to moderate LV systolic dysfunction abated after adequate rate control, consistent with a transient rate-related cardiomyopathy. Echocardiography showed normal LV function 2 months after discharge.

This is the first reported case of acute cardiogenic shock associated with low-dose sotalol alone (note that therapeutic doses range up to 640 mg/day). Cardiogenic shock has been reported in a patient taking a combination of sotalol and diltiazem,1 and in another patient taking digoxin, sotalol and verapamil.2 I have seen a similar case of reversible life-threatening cardiovascular collapse after sotalol (40 mg) was given orally to a 26-year-old with known atrial fibrillation. In that case, non-compliance with digoxin therapy resulted in an unrecognised rate-related cardiomyopathy.

As with all β-blockers, the official prescribing information for sotalol in 2013 cautions about use in patients with known LV dysfunction, but does not warn of the risk of life-threatening cardiogenic shock. It is contraindicated only in “uncontrolled congestive heart failure”. “Hypo-tension” is considered a side effect.3

Research is indicated to determine whether rate-related cardiomyopathy is an independent risk factor for sotalol-induced cardiogenic shock and/or sudden death. Prescribing information for commencing sotalol or increasing the dose may need to be amended to warn of the risk of cardiogenic shock in this subset of patients.