Sotalol Information
Sotalol (Sotalol hydrochloride)
Sotalol (Sotalol hydrochloride)
Sotalol (Sotalol hydrochloride) Description
Sotalol (Sotalol hydrochloride) hydrochloride is an antiarrhythmic drug with Class II (beta-adrenoreceptor blocking) and Class III (cardiac action potential duration prolongation) properties. It is supplied as a light blue, capsule-shaped tablet for oral administration. Sotalol (Sotalol hydrochloride) hydrochloride is a white, crystalline solid with a molecular weight of 308.8. It is hydrophilic, soluble in water, propylene glycol and ethanol, but is only slightly soluble in chloroform. Chemically, Sotalol (Sotalol hydrochloride) hydrochloride is d,l-N-[4-[1-hydroxy-2-[(1-methylethyl)amino] ethyl]phenyl]methane-sulfonamide monohydrochloride. The molecular formula is CHNOS•HCl and is represented by the following structural formula:
Sotalol (Sotalol hydrochloride) hydrochloride tablets contain 80 mg, 120 mg, 160 mg, or 240 mg Sotalol (Sotalol hydrochloride) hydrochloride. In addition, each tablet contains the following inactive ingredients: anhydrous lactose NF, colloidal silicon dioxide NF, corn starch NF, FD&C blue #2 HT Aluminum Lake, magnesium stearate NF, and microcrystalline cellulose NF.
Sotalol (Sotalol hydrochloride) Clinical Pharmacology
Sotalol (Sotalol hydrochloride) has both beta-adrenoreceptor blocking (Vaughan Williams Class II) and cardiac action potential duration prolongation (Vaughan Williams Class III) antiarrhythmic properties. Sotalol (Sotalol hydrochloride) hydrochloride is a racemic mixture of d- and l-Sotalol (Sotalol hydrochloride) . Both isomers have similar Class III antiarrhythmic effects, while the l-isomer is responsible for virtually all the beta-blocking activity. The beta-blocking effect of Sotalol (Sotalol hydrochloride) is non-cardioselective, half maximal at about 80 mg/day and maximal at doses between 320 and 640 mg/day. Sotalol (Sotalol hydrochloride) does not have partial agonist or membrane stabilizing activity. Although significant beta-blockage occurs at oral doses as low as 25 mg, significant Class III effects are seen only at daily doses of 160 mg and above.
Information related to an electrophysiologic effect in pediatric patients is approved for the Berlex Laboratories Sotalol (Sotalol hydrochloride) hydrochloride tablets. However, due to the Berlex marketing exclusivity rights, this drug product is not labeled for pediatric use.
Sotalol (Sotalol hydrochloride) prolongs the plateau phase of the cardiac action potential in the isolated myocyte, as well as in isolated tissue preparations of ventricular or atrial muscle (Class III activity). In intact animals it slows heart rate, decreases AV nodal conduction and increases the refractory periods of atrial and ventricular muscle and conduction tissue.
In man, the Class II (beta-blockade) electrophysiological effects of Sotalol (Sotalol hydrochloride) are manifested by increased sinus cycle length (slowed heart rate), decreased AV nodal conduction and increased AV nodal refractoriness. The Class III electrophysiological effects in man include prolongation of the atrial and ventricular monophasic action potentials, and effective refractory period prolongation of atrial muscle, ventricular muscle, and atrio-ventricular accessory pathways (where present) in both the anterograde and retrograde directions. With oral doses of 160 to 640 mg/day, the surface ECG shows dose-related mean increases of 40 – 100 msec in QT and 10 – 40 msec in QT. (See for description of relationship between QT and torsade de pointes type arrhythmias). No significant alteration in QRS interval is observed.
In a small study (n = 25) of patients with implanted defibrillators treated concurrently with Sotalol (Sotalol hydrochloride) , the average defibrillatory threshold was 6 joules (range 2 – 15 joules) compared to a mean of 16 joules for a non-randomized comparative group primarily receiving amiodarone.
Pediatric clinical trial information is approved the Berlex Laboratories Sotalol (Sotalol hydrochloride) hydrochloride tablets. However, due to the Berlex marketing exclusivity rights, this drug product is not labeled for pediatric use.
In a study of systemic hemodynamic function measured invasively in 12 patients with a mean LV ejection fraction of 37% and ventricular tachycardia (9 sustained and 3 non-sustained), a median dose of 160 mg twice daily of Sotalol (Sotalol hydrochloride) produced a 28% reduction in heart rate and a 24% decrease in cardiac index at 2 hours post dosing at steady-state. Concurrently, systemic vascular resistance and stroke volume showed non-significant increases of 25% and 8%, respectively. Pulmonary capillary wedge pressure increased significantly from 6.4 mmHg to 11.8 mmHg in the 11 patients who completed the study. One patient was discontinued because of worsening congestive heart failure. Mean arterial pressure, mean pulmonary artery pressure and stroke work index did not significantly change. Exercise and isoproterenol induced tachycardia are antagonized by Sotalol (Sotalol hydrochloride) , and total peripheral resistance increases by a small amount.
In hypertensive patients, Sotalol (Sotalol hydrochloride) produces significant reductions in both systolic and diastolic blood pressures. Although Sotalol (Sotalol hydrochloride) is usually well-tolerated hemodynamically, caution should be exercised in patients with marginal cardiac compensation as deterioration in cardiac performance may occur. (See )
Sotalol (Sotalol hydrochloride) has been studied in life-threatening and less severe arrhythmias. In patients with frequent premature ventricular complexes (VPC), Sotalol (Sotalol hydrochloride) was significantly superior to placebo in reducing VPC's, paired VPC's and non-sustained ventricular tachycardia (NSVT); the response was dose-related through 640 mg/day with 80 – 85% of patients having at least a 75% reduction of VPC's. Sotalol (Sotalol hydrochloride) was also superior, at the doses evaluated, to propranolol (40 – 80 mg TID) and similar to quinidine (200 – 400 mg QID) in reducing VPC's. In patients with life-threatening arrhythmias [sustained ventricular tachycardia/fibrillation (VT/VF)], Sotalol (Sotalol hydrochloride) was studied acutely [by suppression of programmed electrical stimulation (PES) induced VT and by suppression of Holter monitor evidence of sustained VT] and, in acute responders, chronically.
In a double-blind, randomized comparison of Sotalol (Sotalol hydrochloride) and procainamide given intravenously (total of 2 mg/kg Sotalol (Sotalol hydrochloride) hydrochloride vs. 19 mg/kg procainamide over 90 minutes), Sotalol (Sotalol hydrochloride) suppressed PES induction in 30% of patients vs. 20% for procainamide (p=0.2). In a randomized clinical trial [Electrophysiologic Study Versus Electrocardiographic Monitoring (ESVEM) Trial] comparing choice of antiarrhythmic therapy by PES suppression vs. Holter monitor selection (in each case followed by treadmill exercise testing) in patients with a history of sustained VT/VF who are also inducible by PES, the effectiveness acutely and chronically of Sotalol (Sotalol hydrochloride) was compared with 6 other drugs (procainamide, quinidine, mexiletine, propafenone, imipramine and pirmenol). Overall response, limited to first randomized drug, was 39% for Sotalol (Sotalol hydrochloride) and 30% for the pooled other drugs. Acute response rate for first drug randomized using suppression of PES induction was 36% for Sotalol (Sotalol hydrochloride) vs. a mean of 13% for the other drugs. Using the Holter monitoring endpoint (complete suppression of sustained VT, 90% suppression of NSVT, 80% suppression of VPC pairs, and at least 70% suppression of VPCs), Sotalol (Sotalol hydrochloride) yielded 41% response vs. 45% for the other drugs combined. Among responders placed on long-term therapy identified acutely as effective (by either PES or Holter), Sotalol (Sotalol hydrochloride) , when compared to the pool of other drugs, has the lowest two-year mortality (13% vs. 22%), the lowest two-year VT recurrence rate (30% vs. 60%), and the lowest withdrawal rate (38% vs. about 75 – 80%). The most commonly used doses of Sotalol (Sotalol hydrochloride) in this trial were 320 to 480 mg/day (66% of patients), with 16% receiving 240 mg/day or less and 18% receiving 640 mg or more.
It cannot be determined, however, in the absence of a controlled comparison of Sotalol (Sotalol hydrochloride) vs. no pharmacologic treatment (e.g., in patients with implanted defibrillators) whether Sotalol (Sotalol hydrochloride) response causes improved survival or identifies a population with a good prognosis.
In a large, double-blind, placebo controlled secondary prevention (post-infarction) trial (n=1456), Sotalol (Sotalol hydrochloride) was given as a non-titrated initial dose of 320 mg once daily. Sotalol (Sotalol hydrochloride) did not produce a significant increase in survival (7.3% mortality on Sotalol (Sotalol hydrochloride) vs. 8.9% on placebo, p=0.3), but overall did not suggest an adverse effect on survival. There was, however, a suggestion of an early (i.e., first 10 days) excess mortality (3% on Sotalol (Sotalol hydrochloride) vs. 2% on placebo). In a second small trial (n=17 randomized to Sotalol (Sotalol hydrochloride) ) where Sotalol (Sotalol hydrochloride) was administered at high doses (e.g., 320 mg twice daily) to high-risk post-infarction patients (ejection fraction < 40% and either > 10 VPC/hr or VT on Holter), there were 4 fatalities and 3 serious hemodynamic/electrical adverse events within two weeks of initiating Sotalol (Sotalol hydrochloride) .
In healthy subjects, the oral bioavailability of Sotalol (Sotalol hydrochloride) is 90 – 100%. After oral administration, peak plasma concentrations are reached in 2.5 to 4 hours, and steady-state plasma concentrations are attained within 2 – 3 days (i.e., after 5 – 6 doses when administered twice daily). Over the dosage range 160 to 640 mg/day Sotalol (Sotalol hydrochloride) displays dose proportionality with respect to plasma concentrations. Distribution occurs to a central (plasma) and to a peripheral compartment, with a mean elimination half-life of 12 hours. Dosing every 12 hours results in trough plasma concentrations which are approximately one-half of those at peak.
Sotalol (Sotalol hydrochloride) does not bind to plasma proteins and is not metabolized. Sotalol (Sotalol hydrochloride) shows very little intersubject variability in plasma levels. The pharmacokinetics of the d and l enantiomers of Sotalol (Sotalol hydrochloride) are essentially identical. Sotalol (Sotalol hydrochloride) crosses the blood brain barrier poorly. Excretion is predominantly via the kidney in the unchanged form, and therefore lower doses are necessary in conditions of renal impairment (see ). Age per se does not significantly alter the pharmacokinetics of Sotalol (Sotalol hydrochloride) , but impaired renal function in geriatric patients can increase the terminal elimination half-life, resulting in increased drug accumulation. The absorption of Sotalol (Sotalol hydrochloride) was reduced by approximately 20% compared to fasting when it was administered with a standard meal. Since Sotalol (Sotalol hydrochloride) is not subject to first-pass metabolism, patients with hepatic impairment show no alteration in clearance of Sotalol (Sotalol hydrochloride) .
Pediatric pharmacokinetic information is approved for the Berlex Laboratories Sotalol (Sotalol hydrochloride) hydrochloride tablets. However, due to the Berlex marketing exclusivity rights, this drug product is not labeled for pediatric use.
Sotalol (Sotalol hydrochloride) Indications And Usage
Sotalol (Sotalol hydrochloride) hydrochloride is indicated for the treatment of documented ventricular arrhythmias, such as sustained ventricular tachycardia, that in the judgement of the physician are life-threatening. Because of the proarrhythmic effects of Sotalol (Sotalol hydrochloride) (See ), including a 1.5 to 2% rate of torsade de pointes or new VT/VF in patients with either NSVT or supraventricular arrhythmias, its use in patients with less severe arrhythmias, even if the patients are symptomatic, is generally not recommended. Treatment of patients with asymptomatic ventricular premature contractions should be avoided.
Initiation of Sotalol (Sotalol hydrochloride) treatment or increasing doses, as with other antiarrhythmic agents used to treat life-threatening arrhythmias, should be carried out in the hospital. The response to treatment should then be evaluated by a suitable method (e.g., PES or Holter monitoring) prior to continuing the patient on chronic therapy. Various approaches have been used to determine the response by antiarrhythmic therapy, including Sotalol (Sotalol hydrochloride) .
In the ESVEM Trial, response to Holter monitoring was tentatively defined as 100% suppression of ventricular tachycardia, 90% suppression of non-sustained VT, 80% suppression of paired VPCs, and 75% suppression of total VPCs in patients who had at least 10 VPCs/hour at baseline; this tentative response was confirmed if VT lasting 5 or more beats was not observed during treadmill exercise testing using a standard Bruce protocol. The PES protocol utilized a maximum of three extrastimuli at three pacing cycle lengths and two right ventricular pacing sites. Response by PES was defined as prevention of induction of the following: 1) monomorphic VT lasting over 15 seconds; 2) non-sustained polymorphic VT containing more than 15 beats of monomorphic VT in patients with a history of monomorphic VT; 3) polymorphic VT or VF greater than 15 beats in patients with VF or a history of aborted sudden death without monomorphic VT; and 4) two episodes of polymorphic VT or VF of greater than 15 beats in a patient presenting with monomorphic VT. Sustained VT or NSVT producing hypotension during the final treadmill test was considered a drug failure.
In a multicenter open-label long-term study of Sotalol (Sotalol hydrochloride) in patients with life-threatening ventricular arrhythmias which had proved refractory to other antiarrhythmic medications, response by Holter monitoring was defined as in ESVEM. Response by PES was defined as noninducibility of sustained VT by at least double extrastimuli delivered at a pacing cycle length of 400 msec. Overall survival and arrhythmia recurrence rates in this study were similar to those seen in ESVEM, although there was no comparative group to allow a definitive assessment of outcome.
Antiarrhythmic drugs have not been shown to enhance survival in patients with ventricular arrhythmias.
Sotalol (Sotalol hydrochloride) is also indicated for the maintenance of normal sinus rhythm [delay in time to recurrence of atrial fibrilation/atrial flutter (AFIB/AFL] in patients with symptomatic AFIB/AFL who are currently in sinus rhythm and is marketed under the brand name BETAPACE AF™. Sotalol (Sotalol hydrochloride) is not approved for the AFIB/AFL indication and should not be substituted for BETAPACE AF™ because only BETAPACE AF™ is distributed with a patient package insert that is appropriate for patients with AFIB/AFL.
Sotalol (Sotalol hydrochloride) Contraindications
Sotalol (Sotalol hydrochloride) hydrochloride is contraindicated in patients with bronchial asthma, sinus bradycardia, second and third degree AV block, unless a functioning pacemaker is present, congenital or acquired long QT syndromes, cardiogenic shock, uncontrolled congestive heart failure, and previous evidence of hypersensitivity to Sotalol (Sotalol hydrochloride) .
Sotalol (Sotalol hydrochloride) Warnings
The National Heart, Lung, and Blood Institute's Cardiac Arrhythmia Suppression Trial I (CAST I) was a long-term, multi-center, double-blind study in patients with asymptomatic, non-life-threatening ventricular arrhythmias, 1 to 103 weeks after acute myocardial infarction. Patients in CAST I were randomized to receive placebo or individually optimized doses of encainide, flecainide, or moricizine. The Cardiac Arrhythmia Suppression Trial II (CAST II) was similar, except that the recruited patients had had their index infarction 4 to 90 days before randomization, patients with left ventricular ejection fractions greater than 40% were not admitted, and the randomized regimens were limited to placebo and moricizine.
CAST I was discontinued after an average time-on-treatment of 10 months, and CAST II was discontinued after an average time-on-treatment of 18 months. As compared to placebo treatment, all three active therapies were associated with increases in short term (14-day) mortality, and encainide and flecainide were associated with significant increases in longer-term mortality as well. The longer-term mortality rate associated with moricizine treatment could not be statistically distinguished from that associated with placebo.
The applicability of these results to other populations (e.g., those without recent myocardial infarction) and to other than Class I antiarrhythmic agents is uncertain. Sotalol (Sotalol hydrochloride) hydrochloride is devoid of Class I effects, and in a large (n=1456) controlled trial in patients with a recent myocardial infarction, who did not necessarily have ventricular arrhythmias, Sotalol (Sotalol hydrochloride) did not produce increased mortality at doses up to 320 mg/day (See ). On the other hand, in the large post-infarction study using a non-titrated initial dose of 320 mg once daily and in a second small randomized trial in high-risk post-infarction patients treated with high doses (320 mg BID), there have been suggestions of an excess of early sudden deaths.
Like other antiarrhythmic agents, Sotalol (Sotalol hydrochloride) can provoke new or worsened ventricular arrhythmias in some patients, including sustained ventricular tachycardia or ventricular fibrillation, with potentially fatal consequences. Because of its effect on cardiac repolarization (QT interval prolongation), torsade de pointes, a polymorphic ventricular tachycardia with prolongation of the QT interval and a shifting electrical axis is the most common form of proarrhythmia associated with Sotalol (Sotalol hydrochloride) , occurring in about 4% of high risk (history of sustained VT/VF) patients. The risk of torsade de pointes progressively increases with prolongation of the QT interval, and is worsened also by reduction in heart rate and reduction in serum potassium (See ).
Because of the variable temporal recurrence of arrhythmias, it is not always possible to distinguish between a new or aggravated arrhythmic event and the patients underlying rhythm disorder. (Note, however, that torsade de pointes is usually a drug-induced arrhythmia in people with an initially normal QT.) Thus, the incidence of drug-related events cannot be precisely determined, so that the occurrence rates provided must be considered approximations. Note also that drug-induced arrhythmias may often not be identified, particularly if they occur long after starting the drug, due to less frequent monitoring. It is clear from the NIH-sponsored CAST (see ) that some antiarrhythmic drugs can cause increased sudden death mortality, presumably due to new arrhythmias or asystole, that do not appear early in treatment but that represent a sustained increased risk.
Overall, in clinical trials with Sotalol (Sotalol hydrochloride) , 4.3% of 3257 patients experienced a new or worsened ventricular arrhythmia. Of this 4.3%, there was new or worsened sustained ventricular tachycardia in approximately 1% of patients and torsade de pointes in 2.4%. Additionally, in approximately 1% of patients, deaths were considered possibly drug-related; such cases, although difficult to evaluate, may have been associated with proarrhythmic events. Torsade de pointes arrhythmias were dose related, as in the prolongation of QT (QT) interval, as shown in the table below:
In addition to dose and presence of sustained VT, other risk factors for torsade de pointes were gender (females had a higher incidence), excessive prolongation of the QT interval (see ) and history of cardiomegaly or congestive heart failure. Patients with sustained ventricular tachycardia and a history of congestive heart failure appear to have the highest risk for serious proarrhythmia (7%). Of the patients experiencing torsade de pointes, approximately two-thirds spontaneously reverted to their baseline rhythm. The others were either converted electrically (D/C cardioversion or overdrive pacing) or treated with other drugs (see ). It is not possible to determine whether some sudden deaths represented episodes of torsades de pointes, but in some instances sudden death did follow a documented episode of torsade de pointes. Although Sotalol (Sotalol hydrochloride) therapy was discontinued in most patients experiencing torsade de pointes, 17% were continued on a lower dose.
Nonetheless, Sotalol (Sotalol hydrochloride) should be used with particular caution if the QT is greater than 500 msec on-therapy and serious consideration should be given to reducing the dose or discontinuing therapy when the QT exceeds 550 msec. Due to the multiple risk factors associated with torsade de pointes, however, caution should be exercised regardless of the QT interval. The table below relates the incidence of torsade de pointes to on-therapy QT and change in QT from baseline. It should be noted, however, that the highest on-therapy QT was in many cases the one obtained at the time of the torsade de pointes event, so that the table overstates the predictive value of a high QT.
Sotalol (Sotalol hydrochloride) can be used safely and effectively in the long-term treatment of life-threatening ventricular arrhythmias following a myocardial infarction. However, experience in the use of Sotalol (Sotalol hydrochloride) to treat cardiac arrhythmias in the early phase of recovery from acute MI is limited and at least at high initial doses is not reassuring. (See .) In the first 2 weeks post-MI caution is advised and careful dose titration is especially important, particularly in patients with markedly impaired ventricular function.
The following warnings are related to the beta-blocking activity of Sotalol (Sotalol hydrochloride) .
PATIENTS WITH BRONCHOSPASTIC DISEASE SHOULD IN GENERAL NOT RECEIVE BETA-BLOCKERS.
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Sotalol (Sotalol hydrochloride) Precautions
Sotalol (Sotalol hydrochloride) hydrochloride is mainly eliminated via the kidneys through glomerular filtration and to a small degree by tubular secretion. There is a direct relationship between renal function, as measured by serum creatinine or creatinine clearance, and the elimination rate of Sotalol (Sotalol hydrochloride) . Guidance for dosing in conditions of renal impairment can be found under "DOSAGE AND ADMINISTRATION."
No evidence of carcinogenic potential was observed in rats during a 24-month study at 137 to 275 mg/kg/day (approximately 30 times the maximum recommended human oral dose (MRHD) as mg/kg or 5 times the MRHD as mg/m) or in mice, during a 24-month study at 4141 to 7122 mg/kg/day (approximately 450 – 750 times the MRHD as mg/kg or 36 – 63 times the MRHD as mg/m).
Sotalol (Sotalol hydrochloride) has not been evaluated in any specific assay of mutagenicity or clastogenicity.
No significant reduction in fertility occurred in rats at oral doses of 1000 mg/kg/day (approximately 100 times the MRHD as mg/kg or 9 times the MRHD as mg/m) prior to mating, except for a small reduction in the number of offspring per litter.
Sotalol (Sotalol hydrochloride) Adverse Reactions
During premarketing trials, 3186 patients with cardiac arrhythmias (1363 with sustained ventricular tachycardia) received oral Sotalol (Sotalol hydrochloride) hydrochloride, of whom 2451 received the drug for at least two weeks. The most important adverse effects are torsade de pointes and other serious new ventricular arrhythmias (see ), occurring at rates of almost 4% and 1%, respectively, in the VT/VF population. Overall, discontinuation because of unacceptable side-effects was necessary in 17% of all patients in clinical trials, and in 13% of patients treated for at least two-weeks. The most common adverse reactions leading to discontinuation of Sotalol (Sotalol hydrochloride) are as follows: fatigue 4%, bradycardia (less than 50 bpm) 3%, dyspnea 3%, proarrhythmia 3%, asthenia 2%, and dizziness 2%.
Occasional reports of elevated serum liver enzymes have occurred with Sotalol (Sotalol hydrochloride) therapy but no cause and effect relationship has been established. One case of peripheral neuropathy which resolved on discontinuation of Sotalol (Sotalol hydrochloride) and recurred when the patient was rechallenged with the drug was reported in an early dose tolerance study. Elevated blood glucose levels and increased insulin requirements can occur in diabetic patients.
The following table lists as a function of dosage the most common (incidence of 2% or greater) adverse events, regardless of relationship to therapy and the percent of patients discontinued due to the event, as collected from clinical trials involving 1292 patients with sustained VT/VF.
In an unblinded multicenter trial of 25 patients with SVT and/or VT receiving daily doses of 30, 90 and 210 mg/m with dosing every 8 hours for a total of 9 doses, no torsade de pointes or other serious new arrhythmias were observed. One patient, receiving 30 mg/m daily, was discontinued because of increased frequency of sinus pauses/bradycardia. Additional cardiovascular adverse events were seen at the 90 and 210 mg/m daily dose levels. They included QT flutter and reported chest pain (1 patient). Values for QTC≥ 525 msec were seen in 2 patients at the 210 mg/m daily dose level. Serious adverse events including death, torsades de pointe, other proarrhythmias, high-degree A-V blocks and bradycardia have been reported in infants and/or children.
Sotalol (Sotalol hydrochloride) Overdosage
Intentional or accidental overdosage with Sotalol (Sotalol hydrochloride) hydrochloride has rarely resulted in death.
Sotalol (Sotalol hydrochloride) Dosage And Administration
As with other antiarrhythmic agents, Sotalol (Sotalol hydrochloride) hydrochloride should be initiated and doses increased in a hospital with facilities for cardiac rhythm monitoring and assessment (see ). Sotalol (Sotalol hydrochloride) should be administered only after appropriate clinical assessment (see ), and the dosage of Sotalol (Sotalol hydrochloride) must be individualized for each patient on the basis of therapeutic response and tolerance. Proarrhythmic events can occur not only at initiation of therapy, but also with each upward dosage adjustment.
Sotalol (Sotalol hydrochloride) Dosage In Renal Impairment
Because Sotalol (Sotalol hydrochloride) is excreted predominantly in urine and its terminal elimination half-life is prolonged in conditions of renal impairment, the dosing interval (time between divided doses) of Sotalol (Sotalol hydrochloride) should be modified (when creatinine clearance is lower than 60 mL/min) according to the following table.
Since the terminal elimination half-life of Sotalol (Sotalol hydrochloride) is increased in patients with renal impairment, a longer duration of dosing is required to reach steady-state. Dose escalation in renal impairment should be done after administration of at least 5 – 6 doses at appropriate intervals (see ).
Extreme caution should be exercised in the use of Sotalol (Sotalol hydrochloride) in patients with renal failure undergoing hemodialysis. The half-life of Sotalol (Sotalol hydrochloride) is prolonged (up to 69 hours) in anuric patients. Sotalol (Sotalol hydrochloride) , however, can be partly removed by dialysis with subsequent partial rebound in concentrations when dialysis is completed. Both safety (heart rate, QT interval) and efficacy (arrhythmia control) must be closely monitored.
Sotalol (Sotalol hydrochloride) How Supplied
Sotalol (Sotalol hydrochloride) hydrochloride tablets: Capsule-shaped light-blue scored tablets are available as follows:
Tablets 80 mg—(imprinted "G" on one side and 2711 on the other side)
Tablets 120 mg—(imprinted "G" on one side and 2722 on the other side)
Tablets 160 mg—(imprinted "G" on one side and 2733 on the other side)
Tablets 240 mg—(imprinted "G" on one side and 2744 on the other side)
Sotalol (Sotalol hydrochloride)
Sotalol (Sotalol hydrochloride) Principal Display Panel - Mg Bottle Label
Sotalol (Sotalol hydrochloride) Principal Display Panel - Mg Bottle Label
Sotalol (Sotalol hydrochloride) Principal Display Panel - Mg Bottle Label
Sotalol (Sotalol hydrochloride) Principal Display Panel - Mg Bottle Label
