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| Trade names | Betapace, Sorine, Sotylize, others[1] |
| AHFS/Drugs.com | Monograph |
| MedlinePlus | a693010 |
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| Routes of administration | By mouth |
| Drug class | Beta blocker |
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| Pharmacokinetic data | |
| Bioavailability | 90–100%[2] |
| Metabolism | Not metabolized[2] |
| Eliminationhalf-life | 12 hours[2] |
| Excretion | Kidney Mammary gland (In lactating individuals)[2] |
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| Chemical and physical data | |
| Formula | C12H20N2O3S |
| Molar mass | 272.36 g·mol−1 |
| 3D model (JSmol) | |
| Chirality | Racemic mixture |
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Sotalol, sold under the brand nameBetapace among others, is a medication used to treat and preventabnormal heart rhythms.[1] Evidence does not support a decreased risk of death with long term use.[1] It is takenby mouth or given byinjection into a vein.[1]
Common side effects include aslow heart rate,chest pain,low blood pressure, feeling tired, dizziness, shortness of breath, problems seeing, vomiting, andswelling.[1] Other serious side effects may includeQT prolongation,heart failure, orbronchospasm.[3] Sotalol is a non-selectiveβ-adrenergic receptor blocker which has bothclass II andclass III antiarrhythmic properties.[1]
Sotalol was first described in 1964 and came into medical use in 1974.[4] It is available as ageneric medication.[3] In 2020, it was the 296th most commonly prescribed medication in the United States, with more than 1 million prescriptions.[5][6]
According to the U.S.Food and Drug Administration (FDA), sotalol can bevalidly used to maintain a normalheart rhythm in people with life-threateningventricular arrhythmias (e.g.,ventricular tachycardia), or very symptomaticatrial fibrillation orflutter.[7] Due to the risk of serious side effects, the FDA states that sotalol should generally be reserved for people whose ventricular arrhythmias are life-threatening, or whose fibrillation/flutter cannot be resolved using theValsalva maneuver or another simple method.[7] Sotalol has shown some potential efficacy against symptoms ofessential tremor due to its binding to theβ2-adrenergic receptor but this remains anoff-label use.[8]
According to the FDA, sotalol should not be used in people with a waking heart rate lower than 50 beats per minute.[7] It should not be used in people withsick sinus syndrome,long QT syndrome,cardiogenic shock, uncontrolledheart failure,asthma or a related bronchospastic condition, or people with serumpotassium below 4 meq/L.[7] It should only be used in people with a second and third degreeAV block if a functioningpacemaker is present.[7]
Since sotalol is removed from the body through the kidneys, it should not be used in people with acreatinine clearance rate below 40 mL/min.[7] It is also excreted inbreast milk, so mothers should notbreastfeed while taking sotalol.[7]
Since sotalol prolongs theQT interval, the FDA recommends against using it in conjunction with other medications that prolong the QT interval.[7] Studies have found serious side effects to be more common in individuals also takingdigoxin, possibly because of pre-existing heart failure in those people.[7] As with other beta blockers, it mayinteract withcalcium channel blockers,catecholamine-depleting drugs,insulin or antidiabetic drugs,β2-adrenergic receptor agonists, andclonidine.[7]
Some evidence suggests that sotalol should be avoided in the setting of heart failure with a reducedejection fraction (resulting in the heart squeezing little blood out into the circulation with each pump) due to an increased risk of death.[9]
Over 10% of oral sotalol users experiencefatigue,dizziness,lightheadedness,headache,weakness,nausea,shortness of breath,bradycardia (slow heart rate),a sensation of the heart beating too hard, fast, or irregularly, orchest pain. Higher doses of sotalol increase the risk for all of these possible side effects.[2]
In rare cases, theQT prolongation caused by sotalol can lead to the development of life-threateningtorsade de pointes (TdP) polymorphic ventricular tachycardia. Across severalclinical trials, 0.6% of oral sotalol patients with supraventricular abnormal heart rhythms (such as atrial fibrillation) developed TdP.[2] For patients who had a history ofsustained ventricular tachycardia (abnormal rhythm lasting more than 30 seconds), 4% developed TdP. Risk increases with dosage, female sex, or having a history of anenlarged heart orcongestive heart failure.[2] Theincidence of TdP for sustained ventricular tachycardia patients was 0% with an 80 mg daily dose, 0.5% at 160 mg, 1.6% at 320 mg, 4.4% at 480 mg, 3.7% at 640 mg, and 5.8% at doses greater than 640 mg.[2] Due to this risk, the U.S. Food and Drug Administration requires affected individuals to be hospitalized for at least three days in a facility that can provide cardiac resuscitation and continuous electrocardiographic monitoring upon starting or restarting sotalol.[2]
Sotalol is abeta blocker andnon-selectively binds to bothβ1- andβ2-adrenergic receptors preventing activation of the receptors by their stimulatory ligand (catecholamines).[10][11] It has nointrinsic sympathomimetic activity.[11]
Without the binding of catecholamines to the β-adrenergic receptor, theG protein complex associated with the receptor cannot activate production ofcyclic AMP, which is responsible for turning on calcium inflow channels.[12] A decrease in activation of calcium channels will therefore result in a decrease in intracellular calcium. In heart cells, calcium is important in generating electrical signals for heart muscle contraction, as well as generating force for this contraction.[13] In consideration of these important properties of calcium, two conclusions can be drawn. First, with less calcium in the cell, there is a decrease in electrical signals for contraction, thus allowing time for the heart's natural pacemaker to rectify arrhythmic contractions.[14] Secondly, lower calcium means a decrease in strength and rate of the contractions, which can be helpful in treatment of abnormally fast heart rates.[14]
Sotalol also acts onpotassium channels and causes a delay in relaxation of the ventricles.[15] By blocking these potassium channels, sotalol inhibits efflux of K+ ions, which results in an increase in the time before another electrical signal can be generated in ventricular myocytes.[13] This increase in the period before a new signal for contraction is generated, helps to correct arrhythmias by reducing the potential for premature or abnormal contraction of the ventricles but also prolongs the frequency of ventricular contraction to help treat tachycardia.[medical citation needed]
Sotalol is classified as a beta blocker with lowlipophilicity and hence lower potential for crossing theblood–brain barrier.[11] This in turn may result in fewer effects in thecentral nervous system as well as a lower risk ofneuropsychiatric side effects.[11]
The experimentallog P of sotalol is 1.1 and its predicted log P ranges from -0.42 to 0.85.[16][17][18][19] It is ahydrophilic or low-lipophilicity beta blocker.[19]
Sotalol was firstsynthesized in 1960 by A. A. Larsen of Mead-Johnson Pharmaceutical.[20] It was originally recognized for itsblood pressure lowering effects and its ability toreduce the symptoms of angina.[21] It was made available in theUnited Kingdom andFrance in 1974,Germany in 1975, andSweden in 1979.[21] It became widely used in the 1980s.[14] In the 1980s, its antiarrhythmic properties were discovered.[21] The United States approved the drug in 1992.[22]
Trade names for Sotalol include Betapace and Betapace AF (Berlex Laboratories),[23] Sotalex and Sotacor (Bristol-Myers Squibb), and Sotylize (Arbor Pharmaceuticals).[7]
