Sotalol

Chemical formula: C₁₂H₂₀N₂O₃S  Molecular mass: 272.364 g/mol  PubChem compound: 5253

Interactions

Sotalol interacts in the following cases:

Drugs inducing ventricular tachycardia torsades de pointes

Sotalol should be given with extreme caution in conjunction with other drugs known to have an increased risk for torsades de pointes such as erythromycin IV, halofantrine, pentamidine, and quinolone antibiotics.

Drugs known to prolong the QT-interval

Sotalol should be given with extreme caution in conjunction with other drugs known to prolong the QT-interval such as phenothiazines, tricyclic antidepressants, terfenadine and astemizole.

Renal failure stage 3 (GFR: 30-59 mL/min/1.73 m²)

Because sotalol is excreted mainly in urine, the dosage should be reduced when GFR: 30-59 mL/min/1.73 m² to the ½ of recommended dose.

Renal failure stage 4 (GFR: 15-29 mL/min/1.73 m²)

Because sotalol is excreted mainly in urine, the dosage should be reduced when GFR: 15-29 mL/min/1.73 m² to the ¼ of recommended dose.

Antidiabetic drugs

Hyperglycaemia may occur, and the dosage of antidiabetic drugs may require adjustment. Symptoms of hypoglycaemia (tachycardia) may be masked by beta-blocking agents.

Digitalis glycosides

Single and multiple doses of sotalol do not significantly affect serum digoxin levels. Proarrhythmic events were more common in sotalol treated patients also receiving digitalis glycosides; however, this may be related to the presence of CHF, a known risk factor for proarrhythmia, in patients receiving digitalis glycosides. Association of digitalis glycosides with beta-blockers may increase auriculo-ventricular conduction time.

beta-blocking agents

The concomitant use of other beta-blocking agents with sotalol may result in additive Class II effects.

Calcium channel blockers

Concurrent administration of beta-blocking agents and calcium channel blockers has resulted in hypotension, bradycardia, conduction defects, and cardiac failure.

Neuromuscular blocking agents

The neuromuscular blockade is prolonged by beta-blocking agents.

beta-agonists

Patients in need of beta-agonists should not normally receive sotalol. However, if concomitant therapy is necessary beta-agonists may have to be administered in increased dosages.

Artemether

Co-administration of sotalol with artemether may cause additional QT prolongation.

Cisapride

Co-administration of sotalol with cisapride may increase the risk of cardiotoxicity and arrhythmia.

Clarithromycin

Co-administration of sotalol with clarithromycin may increase the risk of cardiotoxicity and arrhythmia.

Clonidine

Beta-blocking drugs may potentiate the rebound hypertension sometimes observed after discontinuation of clonidine; therefore, the beta-blocker should be discontinued slowly several days before the gradual withdrawal of clonidine.

Dihydroergotamine

Co-administration of sotalol with dihydroergotamine may cause ischemia with a risk of gangrene.

Disopyramide, quinidine, procainamide, amiodarone, bepridil

Class 1a antiarrhythmic drugs, such as disopyramide, quinidine and procainamide and other antiarrhythmic drugs such as amiodarone and bepridil are not recommended as concomitant therapy with sotalol, because of their potential to prolong refractoriness.

Epinephrine

Co-administration of sotalol with epinephrine may initially cause hypertension and then bradycardia.

Ergotamine

Concomitant use of ergotamine with sotalol may cause ischemia with the risk of gangrene.

Erythromycin

Co-administration of sotalol with erythromycin may increase the risk of cardiotoxicity and arrhythmia.

Fenoterol

Co-administration of somalol with fenoterol induces antagonistic action.

Floctafenine

Beta-adrenergic blocking agents may impede the compensatory cardiovascular reactions associated with hypotension or shock that may be induced by floctafenine.

Formoterol

Co-administration of somalol with formoterol causes antagonistic action.

Gatifloxacin

Concomitant use of somatolol with gatifloxacin may increase the risk of cardiotoxicity and arrhythmia.

Grepafloxacin

Co-administration of sotalol with grepafloxacin may increase the risk of cardiotoxicity and arrhythmia.

Ibuprofen

Co-administration of sotalol with ibuprofen may inhibit the secretion of renal prostaglandins.

Indometacin

Co-administration of sotalol with indomethacin may inhibit the secretion of renal prostaglandins.

Levofloxacin

Co-administration of sotalol with levofloxacin may increase the risk of cardiotoxicity and arrhythmia.

Lumefantrine

Co-administration of sotalol with lumefantrine may cause additional QT prolongation.

Mesoridazine

Co-administration of sotalol with mesoridazine may increase the risk of cardiotoxicity and arrhythmia.

Methysergide

Co-administration of somalol with methysergide may cause ischemia with a risk of gangrene.

Moxifloxacin

Co-administration of sotalol with moxifloxacin may increase the risk of cardiotoxicity and arrhythmia.

Orciprenaline

Co-administration of sotalol with orciprenaline has antagonistic action.

Pipobroman

Co-administration of sotalol with pirobromane has antagonistic action.

Piroxicam

Co-administration of sotalol with piroxicam may inhibit the secretion of renal prostaglandins.

Ranolazine

Co-administration of sotalol with ranolazine may cause additional QT prolongation.

Reserpine, guanethidine, alpha methyldopa

Concomitant use of catecholamine-depleting drugs, such as reserpine, guanethidine, or alpha methyldopa, with a beta-blocker may produce an excessive reduction of resting sympathetic nervous tone. Patients should be closely monitored for evidence of hypotension and/or marked bradycardia which may produce syncope.

Tacrolimus

An additional prolongation of the QT interval may be induced when sotalol is co-administered with tacrolimus.

Telithromycin

Co-administration of sotalol with telithromycin may cause additional QT prolongation.

Terbutaline

Co-administration of somalol with terbutaline has antagonistic effect.

Terfenadine

Co-administration of sotalol with terfenadine may increase the risk of cardiotoxicity and arrhythmia.

Theophylline

Co-administration of sotalol with theophylline induces antagonistic activity and increases theophylline activity.

Thioridazine

Co-administration of sotalol with thioridazine may increase the risk of cardiotoxicity and arrhythmia.

Thiothixene

An additional prolongation of the QT interval may be induced when co-administering sotalol with thiothixene.

Toremifene

Co-administration of sotalol with toremifene may cause additional QT prolongation.

Trimipramine

Co-administration of sotalol with trimipramine may cause additional prolongation of the QT interval.

Verapamil, diltiazem

Beta-blockers should be avoided in combination with cardiodepressant calcium-channel blockers such as verapamil and diltiazem because of the additive effects on atrioventricular conduction, and ventricular function.

Vorinostat

Co-administration of sotalol with vorinostat may cause additional QT prolongation.

Ziprasidone

Co-administration of sotalol with ziprasidone may cause additional QT prolongation.

Zuclopenthixol

Co-administration of sotalol with zuclopenthixol may cause additional QT prolongation.

Anaphylaxis

Patients with a history of anaphylactic reaction to a variety of allergens may have a more severe reaction on repeated challenge while taking beta-blockers. Such patients may be unresponsive to the usual doses of adrenaline used to treat the allergic reaction.

Anaesthesia

As with other beta-blocking agents, sotalol should be used with caution in patients undergoing surgery and in association with anaesthetics that cause myocardial depression, such as cyclopropane or trichloroethylene.

Diabetes mellitus

Sotalol should be used with caution in patients with diabetes (especially labile diabetes) or with a history of episodes of spontaneous hypoglycaemia, since beta-blockade may mask some important signs of the onset of acute hypoglycaemia, e.g. tachycardia.

Psoriasis

Beta-blocking drugs have been reported rarely to exacerbate the symptoms of psoriasis vulgaris.

Thyrotoxicosis

Beta-blockade may mask certain clinical signs of hyperthyroidism (e.g. tachycardia). Patients suspected of developing thyrotoxicosis should be managed carefully to avoid abrupt withdrawal of beta-blockade which might be followed by an exacerbation of symptoms of hyperthyroidism, including thyroid storm.

Pregnancy

Animal studies with sotalol have shown no evidence of teratogenicity or other harmful effects on the foetus.

Although there are no adequate and well-controlled studies in pregnant women, sotalol has been shown to cross the placenta and is found in amniotic fluid. Beta-blockers reduce placental perfusion, which may result in intrauterine foetal death, immature and premature deliveries. In addition, adverse effects (especially hypoglycaemia and bradycardia) may occur in foetus and neonate.

There is an increased risk of cardiac and pulmonary complications in the neonate in the postnatal period. Therefore, sotalol should be used in pregnancy only if the potential benefits outweigh the possible risk to the foetus.

The neonate should be monitored very carefully for 48-72 hours after delivery if it was not possible to interrupt maternal therapy with sotalol 2-3 days before the birthdate.

Nursing mothers

Most beta-blockers, particularly lipophilic compounds, will pass into breast milk although to a variable extent. Breast-feeding is therefore not recommended during administration of these compounds.

Effects on ability to drive and use machines

There are no data available, but the occasional occurrence of side effects such as dizziness and fatigue should be taken into account.

Adverse reactions


Sotalol is well tolerated in the majority of patients, with the most frequent adverse effects arising from its beta-blockade properties. Adverse effects are usually transient in nature and rarely necessitate interruption of, or withdrawal from treatment. These include dyspnoea, fatigue, dizziness, headache, fever, excessive bradycardia and/or hypotension. If they do occur, they usually disappear when the dosage is reduced. The most significant adverse effects, however, are those due to proarrhythmia, including torsades de pointes.

Frequency is defines using the following convention: very common (≥1/10); common (≥1/100, <1/10); uncommon (≥1/1,000, <1/100); rare (≥1/10,000, <1/1,000); very rare (<1/10,000) including isolated reports.

The following are adverse events considered related to therapy, occurring in 1% or more of patients treated with sotalol.

Cardiovascular disorders

Common: Bradycardia, dyspnoea, chest pain, palpitations, oedema, ECG abnormalities, hypotension, arrhythmia, syncope, heart failure, presyncope

Skin and subcutaneous tissue disorders

Common: Rash

Gastro-intestinal disorders

Common: Nausea, vomiting, diarrhoea, dyspepsia, abdominal pain, flatulence

Musculoskeletal, connective tissue and bone disorders

Common: Muscle spasms

Nervous system disorders

Common: Fatigue, dizziness, asthenia, lightheadedness, headache, paresthesia, dysgeusia

Psychiatric disorders

Common: Sleep disorder, mood altered, depression, anxiety

Reproductive system and breast disorders

Common: Sexual dysfunction

Eye disorders

Common: Visual disturbances

Ear and labyrinth disorders

Common: Hearing disturbances

General disorders and administration site conditions

Common: Pyrexia

In clinical trials, 3256 patients with cardiac arrhythmias (1,363 with sustained ventricular tachycardia) received oral sotalol, of whom 2,451 received the drug for at least 2 weeks.

The most significant adverse events were torsade de pointes and other serious new ventricular arrhythmias, which occurred at the following rates:

Patient Populations
 VT/VF (n=1,363) NSVT/PVC (n=946) SVA (n=947)
Torsade de Pointes4.1%1.0%1.4%
Sustained VT/VF1.2%0.7%0.3%

VT = ventricular tachycardia; VF = ventricular fibrillation; NSVT = nonsustained ventricular tachycardia; PVC = premature ventricular contractions; SVA = supraventricular arrhythmia.

Overall, discontinuation because of unacceptable adverse events was necessary in 18% of all patients in cardiac arrhythmia trials.

The most common adverse events leading to discontinuation of sotalol are listed in the table below:

Fatigue4%
Bradycardia (<50 bpm) 3%
Dyspnoea3%
Proarrythmia2%
Asthenia2%
Dizziness2%

Cold and cyanotic extremities, Raynaud’s phenomenon, increase in existing intermittent claudication and dry eyes have been seen in association with other beta-blockers.

Cross-check medications

Review your medication to ensure that there are no potentially harmful drug interactions or contraindications.

Ask the Reasoner

Related medicines

© All content on this website, including data entry, data processing, decision support tools, "RxReasoner" logo and graphics, is the intellectual property of RxReasoner and is protected by copyright laws. Unauthorized reproduction or distribution of any part of this content without explicit written permission from RxReasoner is strictly prohibited. Any third-party content used on this site is acknowledged and utilized under fair use principles.