Chemical formula: C₁₂H₂₀N₂O₃S Molecular mass: 272.364 g/mol PubChem compound: 5253
Sotalol interacts in the following cases:
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.
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.
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.
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.
Hyperglycaemia may occur, and the dosage of antidiabetic drugs may require adjustment. Symptoms of hypoglycaemia (tachycardia) may be masked by beta-blocking agents.
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.
The concomitant use of other beta-blocking agents with sotalol may result in additive Class II effects.
Concurrent administration of beta-blocking agents and calcium channel blockers has resulted in hypotension, bradycardia, conduction defects, and cardiac failure.
The neuromuscular blockade is prolonged by beta-blocking agents.
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.
Co-administration of sotalol with artemether may cause additional QT prolongation.
Co-administration of sotalol with cisapride may increase the risk of cardiotoxicity and arrhythmia.
Co-administration of sotalol with clarithromycin may increase the risk of cardiotoxicity and arrhythmia.
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.
Co-administration of sotalol with dihydroergotamine may cause ischemia with a risk of gangrene.
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.
Co-administration of sotalol with epinephrine may initially cause hypertension and then bradycardia.
Concomitant use of ergotamine with sotalol may cause ischemia with the risk of gangrene.
Co-administration of sotalol with erythromycin may increase the risk of cardiotoxicity and arrhythmia.
Co-administration of somalol with fenoterol induces antagonistic action.
Beta-adrenergic blocking agents may impede the compensatory cardiovascular reactions associated with hypotension or shock that may be induced by floctafenine.
Co-administration of somalol with formoterol causes antagonistic action.
Concomitant use of somatolol with gatifloxacin may increase the risk of cardiotoxicity and arrhythmia.
Co-administration of sotalol with grepafloxacin may increase the risk of cardiotoxicity and arrhythmia.
Co-administration of sotalol with ibuprofen may inhibit the secretion of renal prostaglandins.
Co-administration of sotalol with indomethacin may inhibit the secretion of renal prostaglandins.
Co-administration of sotalol with levofloxacin may increase the risk of cardiotoxicity and arrhythmia.
Co-administration of sotalol with lumefantrine may cause additional QT prolongation.
Co-administration of sotalol with mesoridazine may increase the risk of cardiotoxicity and arrhythmia.
Co-administration of somalol with methysergide may cause ischemia with a risk of gangrene.
Co-administration of sotalol with moxifloxacin may increase the risk of cardiotoxicity and arrhythmia.
Co-administration of sotalol with orciprenaline has antagonistic action.
Co-administration of sotalol with pirobromane has antagonistic action.
Co-administration of sotalol with piroxicam may inhibit the secretion of renal prostaglandins.
Co-administration of sotalol with ranolazine may cause additional QT prolongation.
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.
An additional prolongation of the QT interval may be induced when sotalol is co-administered with tacrolimus.
Co-administration of sotalol with telithromycin may cause additional QT prolongation.
Co-administration of somalol with terbutaline has antagonistic effect.
Co-administration of sotalol with terfenadine may increase the risk of cardiotoxicity and arrhythmia.
Co-administration of sotalol with theophylline induces antagonistic activity and increases theophylline activity.
Co-administration of sotalol with thioridazine may increase the risk of cardiotoxicity and arrhythmia.
An additional prolongation of the QT interval may be induced when co-administering sotalol with thiothixene.
Co-administration of sotalol with toremifene may cause additional QT prolongation.
Co-administration of sotalol with trimipramine may cause additional prolongation of the QT interval.
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.
Co-administration of sotalol with vorinostat may cause additional QT prolongation.
Co-administration of sotalol with ziprasidone may cause additional QT prolongation.
Co-administration of sotalol with zuclopenthixol may cause additional QT prolongation.
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.
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.
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.
Beta-blocking drugs have been reported rarely to exacerbate the symptoms of psoriasis vulgaris.
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.
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.
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.
There are no data available, but the occasional occurrence of side effects such as dizziness and fatigue should be taken into account.
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.
Common: Bradycardia, dyspnoea, chest pain, palpitations, oedema, ECG abnormalities, hypotension, arrhythmia, syncope, heart failure, presyncope
Common: Rash
Common: Nausea, vomiting, diarrhoea, dyspepsia, abdominal pain, flatulence
Common: Muscle spasms
Common: Fatigue, dizziness, asthenia, lightheadedness, headache, paresthesia, dysgeusia
Common: Sleep disorder, mood altered, depression, anxiety
Common: Sexual dysfunction
Common: Visual disturbances
Common: Hearing disturbances
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 Pointes | 4.1% | 1.0% | 1.4% |
Sustained VT/VF | 1.2% | 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:
Fatigue | 4% |
Bradycardia (<50 bpm) | 3% |
Dyspnoea | 3% |
Proarrythmia | 2% |
Asthenia | 2% |
Dizziness | 2% |
Cold and cyanotic extremities, Raynaud’s phenomenon, increase in existing intermittent claudication and dry eyes have been seen in association with other beta-blockers.
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