SOTACOR

What it is

SOTACOR contains sotalol hydrochloride 80 mg or 160 mg per tablet. The 80 mg tablets are light blue, biconvex, capsule-shaped tablets with 'S', '80' and a break bar engraved on one side, while the 160 mg tablets are identically shaped with 'S', '160' and a break bar engraved.

Approved indications

— Prevention and treatment of supraventricular arrhythmias — Prevention and treatment of ventricular arrhythmias

Dosing overview

SOTACOR should be taken preferably 1–2 hours before meals, with oral dosage adjusted gradually allowing 2–3 days between dosing increments to attain steady-state and allow monitoring of QT intervals. The recommended initial oral dosing schedule is 160 mg daily, given in two divided doses at approximately 12 hour intervals, which may be increased if necessary after appropriate evaluation to 240 or 320 mg per day, with most patients obtaining a therapeutic response at a total daily dose of 160–320 mg per day given in 2 divided doses. Some patients with life-threatening refractory ventricular arrhythmias may require doses as high as 480–640 mg per day; however, these doses should only be prescribed when the potential benefit outweighs the increased risk of adverse events particularly proarrhythmias. As sotalol is primarily excreted by the kidneys, dosage adjustment should be made in patients with impaired renal function.

Key safety warnings

No antiarrhythmic drug has been shown to reduce the incidence of sudden death in patients with supraventricular or asymptomatic ventricular arrhythmias, and since most antiarrhythmic drugs have the potential to cause proarrhythmias or increase the incidence of sudden death, physicians should carefully consider the risks and benefits of antiarrhythmic therapy in these patients. The most dangerous adverse effect of antiarrhythmic drugs is the aggravation of preexisting arrhythmias or the provocation of new arrhythmias, and drugs that prolong the QT interval may cause torsades de pointes, a polymorphic ventricular tachycardia associated with prolongation of the QT interval. The risk of torsades de pointes is associated with prolongation of the QT interval, reduction in heart rate, reduction in serum potassium and magnesium (for example as a consequence of diuretic use), high plasma drug concentrations (for example as a consequence of overdosage or renal insufficiency), and concomitant use of sotalol and other medications such as antidepressants and Class I antiarrhythmics which have been associated with torsades de pointes. Females appear to be at increased risk of developing torsades de pointes. During clinical trials, 4.3% of 3257 patients with arrhythmias experienced a new or worsened ventricular arrhythmia, including sustained ventricular tachycardia (approximately 1%) and torsades de pointes (2.4%), and in approximately 1% of patients, deaths were considered possibly drug-related. Proarrhythmic events must be anticipated not only on initiating therapy, but with every upward dose adjustment; events tend to occur within 7 days of initiating therapy or with an increase in dose, and initiating therapy at 80 mg twice daily with gradual upward dose titration thereafter reduces the risk of proarrhythmia. Beta-blockade depresses myocardial contractility and may precipitate cardiac failure in some patients with a history of cardiac failure, chronic myocardial insufficiency, or unsuspected cardiomyopathy, and patients with congestive heart failure have a higher risk of torsade de pointes. In patients with controlled congestive heart failure, sotalol should be administered cautiously, and caution is advised when initiating therapy in patients with left ventricular dysfunction controlled by therapy with a low initial dose and careful dose titration. Sotalol should not be used in patients with hypokalaemia or hypomagnesaemia prior to correction of imbalance; these conditions can exaggerate the degree of QT prolongation and increase the potential for torsades de pointes, and prior to starting treatment with sotalol, serum electrolytes should be obtained and any electrolyte imbalance corrected. Care should be taken if beta-blockers have to be discontinued abruptly in patients with coronary artery disease, as hypersensitivity to catecholamines is observed in patients withdrawn from beta-blocker therapy, and severe exacerbation of angina pectoris and precipitation of myocardial infarction and ventricular arrhythmias have occurred following abrupt discontinuation of beta-blockade in patients with ischaemic heart disease.

Contraindications

SOTACOR is contraindicated in bronchospasm (for example bronchial asthma or chronic obstructive airway disease) and allergic disorders (including allergic rhinitis) which may suggest a predisposition to bronchospasm. SOTACOR is contraindicated in sinus bradycardia (less than 45–50 beats per minute) and second and third degree AV block or sick sinus syndrome unless a functioning pacemaker is present. SOTACOR is contraindicated in uncontrolled congestive heart failure, severe renal impairment (CrCl < 10 mL/min), and congenital or acquired long QT syndromes. SOTACOR is contraindicated in hypersensitivity to sotalol hydrochloride, other beta blockers, sulfonamides or the excipients. SOTACOR is contraindicated in hypomagnesaemia, hypotension, metabolic acidosis, torsades de pointes, and hypokalaemia.

PBS listing

No source document provides information about PBS listing for SOTACOR.

Regulatory history

SOTACOR sotalol hydrochloride 80 mg and 160 mg tablets were first listed on the ARTG on 16 November 1999.