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standards of non-Merck sources.
ALERT: U.S. Boxed Warning
The FDA-approved labeling includes a boxed warning. See Warnings/Precautions section for a concise summary of this information. For verbatim wording of the boxed warning, consult the product labeling or www.fda.gov.
Pronunciation
(dye soe PEER a mide)
Generic Available (U.S.)
Yes
Index Terms
Brand Names: U.S.
Brand Names: Canada
Pharmacologic Category
Pharmacologic Category Synonyms
Use: Labeled Indications
Life-threatening ventricular arrhythmias (eg, sustained ventricular tachycardia)
Use: Unlabeled
Alternative agent for the prevention of recurrent symptomatic focal atrial tachycardia (in combination with an AV nodal blocking agent), atrial fibrillation (especially vagally-induced), or atrial flutter (in combination with an AV nodal-blocking agent); obstructive hypertrophic cardiomyopathy (HCM) in combination with ventricular rate-controlling agents (eg, beta blockers or verapamil) to control symptoms of angina or dyspnea who are unresponsive to rate-controlling agents alone; atrial fibrillation in patients with HCM in combination with rate-controlling agents
Pregnancy Risk Factor
C
Pregnancy Considerations
Adverse events have been observed in animal reproduction studies. Disopyramide levels have been reported in human fetal blood. Disopyramide may stimulate contractions in pregnant women. In a case report, disopyramide use in the third trimester resulted in painful uterine contractions after the first dose and hemorrhage after the second dose (Abbi, 1999).
Lactation
Enters breast milk/not recommended
Contraindications
Hypersensitivity to disopyramide or any component of the formulation; cardiogenic shock; pre-existing second- or third-degree heart block (except in patients with a functioning artificial pacemaker); congenital QT syndrome; sick sinus syndrome
Warnings/Precautions
Boxed warnings:
• CAST trial: See “Other warnings/precautions” below.
Concerns related to adverse effects:
• Hypotension: May occur during the initiation of therapy; monitor closely.
• Proarrhythmic effects: Watch for proarrhythmic effects; may cause QTc prolongation and subsequent torsade de pointes; avoid use in patients with diagnosed or suspected congenital long QT syndrome. Monitor and adjust dose to prevent QTc prolongation.
Disease-related concerns:
• Atrial fibrillation/flutter: Appropriate use: In patients with atrial fibrillation or flutter, block the AV node before initiating.
• BPH/urinary retention: Do not use in patients with BPH and/or urinary retention due to significant anticholinergic effects.
• Conduction disturbances: Use with caution in patients with bundle branch block or heart block.
• Electrolyte imbalance: Correct electrolyte disturbances, especially hypokalemia or hypomagnesemia, prior to use and throughout therapy.
• Glaucoma: Do not use in patients with glaucoma due to significant anticholinergic effects.
• Heart failure (HF): Use with caution or avoid in patients with any degree of left ventricular dysfunction or history of HF; may precipitate or exacerbate condition.
• Hepatic impairment: Use with caution in patients with hepatic impairment; reduced dosage recommended.
• Myasthenia gravis: Do not use in patients with myasthenia gravis due to significant anticholinergic effects.
• Renal impairment: Use with caution in renal impairment; reduced dosage recommended. The controlled release form is not recommended for Clcr ≤40 mL/minute.
• Wolff-Parkinson-White syndrome: Use with caution in patients with Wolff-Parkinson-White syndrome.
Concurrent drug therapy issues:
• Drugs with QT prolongation potential: Avoid concurrent use with other drugs known to prolong QTc interval or decrease myocardial contractibility.
Special populations:
• Elderly: Avoid use in this age group due to a risk of developing heart failure (potent negative inotrope) and adverse effects associated with its potent anticholinergic properties; alternative antiarrhythmic agents preferred (Beers Criteria).
Other warnings/precautions:
• CAST trial: [U.S. Boxed Warning]: In the Cardiac Arrhythmia Suppression Trial (CAST), recent (>6 days but <2 years ago) myocardial infarction patients with asymptomatic, non-life-threatening ventricular arrhythmias did not benefit and may have been harmed by attempts to suppress the arrhythmia with flecainide or encainide. An increased mortality or nonfatal cardiac arrest rate (7.7%) was seen in the active treatment group compared with patients in the placebo group (3%). The applicability of the CAST results to other populations is unknown. Antiarrhythmic agents should be reserved for patients with life-threatening ventricular arrhythmias.
Adverse Reactions
The most common adverse effects are related to cholinergic blockade. The most serious adverse effects of disopyramide are hypotension and CHF.
>10%:
Gastrointestinal: Xerostomia (32%), constipation (11%)
Genitourinary: Urinary hesitancy (14% to 23%)
1% to 10%:
Cardiovascular: CHF, hypotension, cardiac conduction disturbance, edema, syncope, chest pain
Central nervous system: Fatigue, headache, malaise, dizziness, nervousness
Dermatologic: Rash, generalized dermatoses, pruritus
Endocrine & metabolic: Cholesterol increased, hypokalemia, triglycerides increased
Gastrointestinal: Dry throat, nausea, abdominal distension, flatulence, abdominal bloating, anorexia, diarrhea, vomiting, weight gain
Genitourinary: Urinary retention, urinary frequency, urinary urgency, impotence (1% to 3%)
Neuromuscular & skeletal: Muscle weakness, muscular pain
Ocular: Blurred vision, dry eyes
Respiratory: Dyspnea
<1% (Limited to important or life-threatening): Agranulocytosis, arrhythmia (new or worsened, proarrhythmic effect); AV block, BUN increased, cholestatic jaundice, creatinine increased, depression, dysuria, fever, gynecomastia, hematocrit decreased, hemoglobin decreased, hepatotoxicity, hypoglycemia, insomnia, numbness, paresthesia, psychotic reaction, respiratory distress, serum creatinine increased, thrombocytopenia, tingling, transaminases increased. Rare cases of lupus have been reported (generally in patients previously receiving procainamide).
Postmarketing and/or case reports: Peripheral neuropathy, psychosis, pupillary dilation, toxic cutaneous blisters
Metabolism/Transport Effects
Substrate of CYP3A4 (major); Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential
Drug Interactions
AbobotulinumtoxinA: Anticholinergic Agents may enhance the anticholinergic effect of AbobotulinumtoxinA. Risk C: Monitor therapy
Acetylcholinesterase Inhibitors (Central): Anticholinergics may diminish the therapeutic effect of Acetylcholinesterase Inhibitors (Central). Acetylcholinesterase Inhibitors (Central) may diminish the therapeutic effect of Anticholinergics. If the anticholinergic action is a side effect of the agent, the result may be beneficial. Risk C: Monitor therapy
Alfuzosin: May enhance the QTc-prolonging effect of QTc-Prolonging Agents. Risk C: Monitor therapy
Amiodarone: May enhance the QTc-prolonging effect of Antiarrhythmic Agents (Class Ia). Amiodarone may increase the serum concentration of Antiarrhythmic Agents (Class Ia). Management: Risk of QTc prolongation and Torsades de Pointes may be increased; consider alternative therapy when possible. Risk D: Consider therapy modification
Anticholinergics: May enhance the adverse/toxic effect of other Anticholinergics. Exceptions: Levocabastine (Nasal); Paliperidone. Risk C: Monitor therapy
Artemether: May enhance the QTc-prolonging effect of QTc-Prolonging Agents. Risk X: Avoid combination
Barbiturates: May increase the metabolism of Disopyramide. Risk C: Monitor therapy
Beta-Blockers: Disopyramide may enhance the bradycardic effect of Beta-Blockers. Exceptions: Levobunolol; Metipranolol. Risk C: Monitor therapy
Cannabinoids: Anticholinergic Agents may enhance the tachycardic effect of Cannabinoids. Risk C: Monitor therapy
Chloroquine: May enhance the QTc-prolonging effect of QTc-Prolonging Agents. Risk C: Monitor therapy
Ciprofloxacin: May enhance the QTc-prolonging effect of QTc-Prolonging Agents. Risk C: Monitor therapy
Ciprofloxacin (Systemic): May enhance the QTc-prolonging effect of QTc-Prolonging Agents. Risk C: Monitor therapy
Conivaptan: May increase the serum concentration of CYP3A4 Substrates. Risk X: Avoid combination
CYP3A4 Inducers (Strong): May increase the metabolism of CYP3A4 Substrates. Risk C: Monitor therapy
CYP3A4 Inhibitors (Moderate): May decrease the metabolism of CYP3A4 Substrates. Risk C: Monitor therapy
CYP3A4 Inhibitors (Strong): May decrease the metabolism of CYP3A4 Substrates. Risk D: Consider therapy modification
Deferasirox: May decrease the serum concentration of CYP3A4 Substrates. Risk C: Monitor therapy
Dronedarone: QTc-Prolonging Agents may enhance the QTc-prolonging effect of Dronedarone. Risk X: Avoid combination
Eribulin: May enhance the QTc-prolonging effect of Antiarrhythmic Agents (Class Ia). Risk C: Monitor therapy
Etravirine: May decrease the serum concentration of Disopyramide. Risk C: Monitor therapy
Fingolimod: May enhance the arrhythmogenic effect of Antiarrhythmic Agents (Class Ia). Management: Obtain baseline ECG (if not recently available) if initiating fingolimod during treatment with class Ia antiarrhythmic agents. Monitor for bradycardia and AV block. The Canadian labeling recommends avoiding concomitant use of these agents. Risk C: Monitor therapy
Fosphenytoin: May decrease the serum concentration of Disopyramide. Risk C: Monitor therapy
Gadobutrol: May enhance the QTc-prolonging effect of QTc-Prolonging Agents. Risk D: Consider therapy modification
Herbs (CYP3A4 Inducers): May increase the metabolism of CYP3A4 Substrates. Risk C: Monitor therapy
Indacaterol: May enhance the QTc-prolonging effect of QTc-Prolonging Agents. Risk C: Monitor therapy
Ivacaftor: May increase the serum concentration of CYP3A4 Substrates. Risk C: Monitor therapy
Lidocaine: Disopyramide may enhance the arrhythmogenic effect of Lidocaine. Disopyramide may increase the serum concentration of Lidocaine. Specifically, the unbound/free fraction of lidocaine. Risk C: Monitor therapy
Lidocaine (Systemic): Disopyramide may enhance the arrhythmogenic effect of Lidocaine (Systemic). Disopyramide may increase the serum concentration of Lidocaine (Systemic). Specifically, the unbound/free fraction of lidocaine. Risk C: Monitor therapy
Lumefantrine: May enhance the QTc-prolonging effect of QTc-Prolonging Agents. Risk X: Avoid combination
Lurasidone: May enhance the QTc-prolonging effect of Disopyramide. Management: Consider alternatives to disopyramide in patients with acute lurasidone overdose. If disopyramide treatment cannot be avoided, monitor for excessive QTc interval prolongation. Risk D: Consider therapy modification
Macrolide Antibiotics: May enhance the QTc-prolonging effect of Disopyramide. Macrolide Antibiotics may decrease the metabolism of Disopyramide. Exceptions: Azithromycin; Azithromycin (Systemic); Fidaxomicin; Spiramycin. Risk X: Avoid combination
Mifepristone: May enhance the QTc-prolonging effect of QTc-Prolonging Agents. Management: Avoid use of mifepristone for treatment of hyperglycemia in Cushing's syndrome in patients receiving QT interval prolonging agents. Avoid initiation of QT prolonging agents for 2 weeks following mifepristone discontinuation. Risk X: Avoid combination
Nilotinib: May enhance the QTc-prolonging effect of QTc-Prolonging Agents. Risk X: Avoid combination
OnabotulinumtoxinA: Anticholinergic Agents may enhance the anticholinergic effect of OnabotulinumtoxinA. Risk C: Monitor therapy
Phenytoin: May decrease the serum concentration of Disopyramide. Risk C: Monitor therapy
Pimozide: QTc-Prolonging Agents may enhance the QTc-prolonging effect of Pimozide. Risk X: Avoid combination
Potassium Chloride: Anticholinergic Agents may enhance the ulcerogenic effect of Potassium Chloride. Risk D: Consider therapy modification
Pramlintide: May enhance the anticholinergic effect of Anticholinergics. These effects are specific to the GI tract. Risk D: Consider therapy modification
QTc-Prolonging Agents: May enhance the adverse/toxic effect of other QTc-Prolonging Agents. Their effects can be additive, causing life-threatening ventricular arrhythmias. Risk D: Consider therapy modification
QUEtiapine: May enhance the QTc-prolonging effect of QTc-Prolonging Agents. Risk X: Avoid combination
QuiNINE: QTc-Prolonging Agents may enhance the QTc-prolonging effect of QuiNINE. QuiNINE may enhance the QTc-prolonging effect of QTc-Prolonging Agents. Risk X: Avoid combination
Rifamycin Derivatives: May decrease the serum concentration of Disopyramide. Risk C: Monitor therapy
RimabotulinumtoxinB: Anticholinergic Agents may enhance the anticholinergic effect of RimabotulinumtoxinB. Risk C: Monitor therapy
Secretin: Anticholinergic Agents may diminish the therapeutic effect of Secretin. Risk D: Consider therapy modification
Tetrabenazine: QTc-Prolonging Agents may enhance the QTc-prolonging effect of Tetrabenazine. Risk X: Avoid combination
Thioridazine: QTc-Prolonging Agents may enhance the QTc-prolonging effect of Thioridazine. Risk X: Avoid combination
Tocilizumab: May decrease the serum concentration of CYP3A4 Substrates. Risk C: Monitor therapy
Toremifene: QTc-Prolonging Agents may enhance the QTc-prolonging effect of Toremifene. The risk for potentially dangerous arrhythmias may be increased. Risk X: Avoid combination
Vandetanib: QTc-Prolonging Agents may enhance the arrhythmogenic effect of Vandetanib. Risk X: Avoid combination
Vemurafenib: QTc-Prolonging Agents may enhance the QTc-prolonging effect of Vemurafenib. Risk X: Avoid combination
Verapamil: May enhance the adverse/toxic effect of Disopyramide. Of particular concern is the potential for profound depression of myocardial contractility. Risk X: Avoid combination
Ziprasidone: QTc-Prolonging Agents may enhance the QTc-prolonging effect of Ziprasidone. The risk of a severe arrhythmia may be increased. Risk X: Avoid combination
Ethanol/Nutrition/Herb Interactions
Ethanol: Ethanol may increase CNS depression. Management: Avoid ethanol.
Food: Management: Administer at the same time around-the-clock on an empty stomach.
Herb/Nutraceutical: St John's wort may decrease disopyramide levels. Ephedra may worsen arrhythmia. Management: Avoid St John's wort and ephedra.
Storage
Extemporaneously prepared suspension is stable for 4 weeks refrigerated.
Mechanism of Action
Class Ia antiarrhythmic: Decreases myocardial excitability and conduction velocity; reduces disparity in refractory between normal and infarcted myocardium; possesses anticholinergic, peripheral vasoconstrictive, and negative inotropic effects
Pharmacodynamics/Kinetics
Onset of action: 0.5-3.5 hours
Duration: Immediate release: 1.5-8.5 hours
Absorption: 60% to 83%
Distribution: Vd: 0.8-2 L/kg
Protein binding (concentration dependent): 20% to 60%
Metabolism: Hepatic; N-dealkylation to the active metabolite N-despropyldisopyramide (or mono-N-dealkylated [MND] metabolite) and other inactive metabolites
Half-life elimination: Adults: 4-10 hours; prolonged with hepatic or renal impairment
Time to peak, serum: Immediate release: Within 2 hours; Controlled release: 4-7 hours
Excretion: Urine (~50% as unchanged drug; ~20% as MND; 10% other metabolites); feces (10% to 15%)
Dosage
Oral:
Children: Arrhythmias: Immediate release:
<1 year: 10-30 mg/kg/24 hours in 4 divided doses
1-4 years: 10-20 mg/kg/24 hours in 4 divided doses
4-12 years: 10-15 mg/kg/24 hours in 4 divided doses
12-18 years: 6-15 mg/kg/24 hours in 4 divided doses
Adults:
Ventricular arrhythmias: Note: Since newer agents with less toxicity are available, the use of disopyramide for this indication has fallen out of favor. Controlled release formulation not to be used when rapid achievement of disopyramide plasma concentrations is desired. A maximum dose up to 400 mg every 6 hours (immediate release) may be required for patients with severe refractory ventricular tachycardia.
<50 kg:
Immediate release: An initial loading dose of 200 mg may be administered if rapid onset is required. Maintenance dose: 100 mg every 6 hours
Controlled release: Maintenance dose: 200 mg every 12 hours
≥50 kg:
Immediate release: An initial loading dose of 300 mg may be administered if rapid onset is required. Maintenance dose: 150 mg every 6 hours. If rapid control is necessary and no response seen within 6 hours of loading dose, may increase maintenance dose to 200 mg every 6 hours.
Controlled release: Maintenance dose: 300 mg every 12 hours
Hypertrophic cardiomyopathy (obstructive physiology) with or without atrial fibrillation (unlabeled use): Initial: Controlled release: 200-250 mg twice daily. If symptoms do not improve, increase by 100 mg/day at 2-week intervals to a maximum daily dose of 600 mg (Gersh, 2011; Sherrid, 2005).
Elderly: Dose with caution, starting at the lower end of dosing range
Dosing adjustment in renal impairment:
Manufacturer recommendations:
Immediate release:
Clcr >40 mL/minute: 100 mg every 6 hours
Clcr 30-40 mL/minute: 100 mg every 8 hours
Clcr 15-30 mL/minute: 100 mg every 12 hours
Clcr <15 mL/minute: 100 mg every 24 hours
Controlled release:
Clcr >40 mL/minute: 200 mg every 12 hours
Clcr ≤40 mL/minute: Not recommended for use
Alternative recommendations (Aronoff, 2007): Immediate release:
Clcr >50 mL/minute: 100-200 mg every 8 hours
Clcr 10-50 mL/minute: 100-200 mg every 12-24 hours
Clcr <10 mL/minute: 100-200 mg every 24-48 hours
Dialysis: Not dialyzable (0% to 5%) by hemo- or peritoneal methods; supplemental dose is not necessary.
Dosing interval in hepatic impairment: Manufacturer's recommendations:
Immediate release: 100 mg every 6 hours
Controlled release: 200 mg every 12 hours
Administration: Oral
Do not break or chew controlled release capsules. Administer around-the-clock to promote less variation in peak and trough serum levels. Should be taken on an empty stomach.
Monitoring Parameters
ECG, blood pressure, urinary retention, CNS anticholinergic effects (confusion, agitation, hallucinations, etc); disopyramide drug level (if available)
Reference Range
Therapeutic concentration:
Atrial arrhythmias: 2.8-3.2 mcg/mL
Ventricular arrhythmias 3.3-7.5 mcg/mL
Toxic concentration: >7 mcg/mL
Dietary Considerations
Should be taken on an empty stomach.
Patient Education
Take at regular intervals around-the-clock on an empty stomach. Do not crush or chew controlled release form. Avoid (or limit) alcohol. You may experience dizziness, blurred vision, or dry mouth. Report any change in urinary pattern or difficulty urinating, chest pain, palpitations, irregular heartbeat, unusual cough, respiratory difficulty, swelling of extremities, muscle tremors or weakness, confusion or acute lethargy, or skin rash.
Geriatric Considerations
Due to changes in total clearance (decreased) in the elderly, monitor closely; the anticholinergic action may be intolerable and require discontinuation; monitor for CNS anticholinergic effects (confusion, agitation, hallucinations, etc). Note: Dose needs to be altered with Clcr <40 mL/minute which may be found frequently in older adults.
Clinical studies of Norpace®/Norpace® CR did not include sufficient numbers of subjects ≥65 years of age to determine whether they respond differently from younger subjects. Other reported clinical experience has not identified differences in responses between elderly and younger patients. In general, dose selection for an elderly patient should be cautious, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy.
Because of its anticholinergic activity, disopyramide phosphate should not be used in patients with glaucoma, urinary retention, or benign prostatic hyperplasia (medical conditions commonly associated with the elderly) unless adequate overriding measures are taken. In the event of increased anticholinergic side effects, plasma levels of disopyramide should be monitored and the dose of the drug adjusted accordingly. A reduction of the dose by one third, from the recommended 600 mg/day to 400 mg/day, would be reasonable, without changing the dosing interval. This drug is known to be substantially excreted by the kidney, and the risk of toxic reactions to this drug may be greater in patients with impaired renal function. Because elderly patients are more likely to have decreased renal function, care should be taken in dose selection, and it may be useful to monitor renal function.
This medication is considered to be potentially inappropriate in this patient population (Beers Criteria: Quality of evidence - low; Strength of recommendation - strong).
Cardiovascular Considerations
Disopyramide has limited antiarrhythmic effects and has a very narrow therapeutic index. Close monitoring of ECG, particularly of the QT interval, should be conducted when initiating therapy. Increases in QT >25% over baseline should result in cessation or reduction in disopyramide dosing. Because of the risk of QT prolongation and arrhythmias, disopyramide should be initiated within the hospital with cardiac monitoring. In patients with pre-existing cardiovascular disease, the incidence of proarrhythmic effects and mortality may be increased with Class Ia antiarrhythmic agents.
Disopyramide has significant anticholinergic effects which also limits its role in patients with cardiovascular disease. Disopyramide is being used experimentally for the treatment of vasovagal syncope.
Disopyramide may be used in the treatment of symptoms associated with obstructive HCM in combination with rate controlling agents (eg, beta blockers, verapamil) as it significantly reduces the left ventricular outflow gradient and improves symptoms. Some patients may not tolerate the anticholinergic effects such as dry mouth or urinary retention, frequency, and urgency. Up to 1/3 may not improve and will require other nonpharmacologic interventions. When treating atrial fibrillation (AF) in patients with HCM, it is important to use disopyramide with either a beta blocker or verapamil since disopyramide enhances AV conduction during episodes of AF. Disopyramide is a potent negative inotrope that should be avoided in patients with any degree of left ventricular dysfunction or history of heart failure. Consideration should be given to discontinuing disopyramide when the HCM patient develops systolic dysfunction (Gersh, 2011).
Dental Health: Effects on Dental Treatment
Key adverse event(s) related to dental treatment: Xerostomia (normal salivary flow resumes upon discontinuation).
Dental Health: Vasoconstrictor/Local Anesthetic Precautions
Disopyramide is one of the drugs confirmed to prolong the QT interval and is accepted as having a risk of causing torsade de pointes. The risk of drug-induced torsade de pointes is extremely low when a single QT interval prolonging drug is prescribed. In terms of epinephrine, it is not known what effect vasoconstrictors in the local anesthetic regimen will have in patients with a known history of congenital prolonged QT interval or in patients taking any medication that prolongs the QT interval. Until more information is obtained, it is suggested that the clinician consult with the physician prior to the use of a vasoconstrictor in suspected patients, and that the vasoconstrictor (epinephrine, mepivacaine and levonordefrin [Carbocaine® 2% with Neo-Cobefrin®]) be used with caution.
Dental Comment
Disopyramide is known to prolong the QT interval. The QT interval is measured as the time and distance between the Q point of the QRS complex and the end of the T wave in the ECG tracing. After adjustment for heart rate, the QT interval is defined as prolonged if it is more than 450 msec in men and 460 msec in women. A long QT syndrome was first described in the 1950s and 60s as a congenital syndrome involving QT interval prolongation and syncope and sudden death. Some of the congenital long QT syndromes were characterized by a peculiar electrocardiographic appearance of the QRS complex involving a premature atria beat followed by a pause, then a subsequent sinus beat showing marked QT prolongation and deformity. This type of cardiac arrhythmia was originally termed “torsade de pointes” (translated from the French as “twisting of the points”). Disopyramide is considered as having a risk of causing torsade de pointes. Since it is not known what effect vasoconstrictors in the local anesthetic regimen will have in patients with a known history of congenital prolonged QT interval or in patients taking any medication that prolongs the QT interval, a medical consult is suggested.
Mental Health: Effects on Mental Status
May cause drowsiness or nervousness; rare reports of depression and psychosis
Mental Health: Effects on Psychiatric Treatment
Contraindicated with ziprasidone; use cautiously with TCAs; may cause AV block or QT prolongation; phenobarbital and carbamazepine may decrease the effects of disopyramide via enzyme induction
Nursing: Physical Assessment/Monitoring
Monitor QTc with initiation and during therapy.
Dosage Forms
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Capsule, oral: 100 mg, 150 mg
Norpace®: 100 mg, 150 mg
Capsule, controlled release, oral:
Norpace® CR: 100 mg, 150 mg
Pricing: U.S. (www.drugstore.com)
Capsule, 12-hour (Norpace CR)
100 mg (60): $129.99
150 mg (60): $153.67
Capsules (Disopyramide Phosphate)
100 mg (90): $46.99
150 mg (30): $28.79
Capsules (Norpace)
100 mg (90): $163.48
150 mg (30): $65.39
Extemporaneously Prepared
A 1 mg/mL oral suspension may be made with a tablet and Simple Syrup, NF. Crush one 100 mg tablet in a mortar and reduce to a fine powder. Add small portions of the vehicle and mix to a uniform paste; mix while adding the vehicle in incremental proportions to almost 100 mL; transfer to a calibrated bottle, rinse mortar with vehicle, and add quantity of vehicle sufficient to make 100 mL. Label “shake well” and “refrigerate”. Stable for 28 days.
A 10 mg/mL oral suspension may be made with tablets and Simple Syrup, NF. Crush ten 100 mg tablets in a mortar and reduce to a fine powder. Add small portions of the vehicle and mix to a uniform paste; mix while adding the vehicle in incremental proportions to almost 100 mL; transfer to a calibrated bottle, rinse mortar with vehicle, and add quantity of vehicle sufficient to make 100 mL. Label “shake well” and “refrigerate”. Stable for 28 days.
Nahata MC, Pai VB, and Hipple TF, Pediatric Drug Formulations, 5th ed, Cincinnati, OH: Harvey Whitney Books Co, 2004.
References
"American Geriatrics Society Updated Beers Criteria for Potentially Inappropriate Medication Use in Older Adults," J Am Geriatr Soc, 2012 [epub ahead of print].
Blomström-Lundqvist C, Scheinman MM, Aliot EM, et al, “ACC/AHA/ESC Guidelines for the Management of Patients With Supraventricular Arrhythmias--Executive Summary. A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias),” Circulation, 2003, 108(15):1871-909.
Coplen SE, Antman EM, Berlin JA, et al, “Efficacy and Safety of Quinidine Therapy for Maintenance of Sinus Rhythm After Cardioversion. A Meta-analysis of Randomized Control Trials,” Circulation, 1990, 82(4):1106-16.
Crijns HJ, Gosselink AT, and Lie KI, “Propafenone versus Disopyramide for Maintenance of Sinus Rhythm After Electrical Cardioversion of Chronic Atrial Fibrillation: A Randomized, Double-blind Study,” Cardiovasc Drugs Ther, 1996, 10(2):145-52.
Echt DS, Liebson PR, Mitchell LB, et al, “Mortality and Morbidity in Patients Receiving Encainide, Flecainide, or Placebo: The Cardiac Arrhythmia Suppression Trial,” N Engl J Med, 1991, 324(12):781-8.
Flaker GC, Blackshear JL, McBride R, et al, “Antiarrhythmic Drug Therapy and Cardiac Mortality in Atrial Fibrillation. The Stroke Prevention in Atrial Fibrillation Investigators,” J Am Coll Cardiol, 1992, 20(3):527-32.
Fuster V, Ryden LE, Cannom DS, et al, “ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation-Executive Summary. A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation). Developed in Collaboration With the European Heart Rhythm Association and the Heart Rhythm Society,” J Am Coll Cardiol, 2006, 48(4):854-906.
Gersh BJ, Maron BJ, Bonow RO, et al, “2011 ACCF/AHA Guideline for the Diagnosis and Treatment of Hypertrophic Cardiomyopathy: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines,” Circulation, 2011, 124(24):e783-831.
Maron BJ, "Hypertrophic Cardiomyopathy: A Systematic Review," JAMA, 2002, 287(10):1308-20.
Morganroth J and Goin JE, “Quinidine-Related Mortality in the Short-to-Medium Term Treatment of Ventricular Arrhythmias," Circulation, 1991, 84(5):1977-83.
Sherrid MV, Barac I, McKenna WJ, et al, "Multicenter Study of the Efficacy and Safety of Disopyramide in Obstructive Hypertrophic Cardiomyopathy," J Am Coll Cardiol, 2005, 45(8):1251-8.
Wann SL, Curtis AB, January CT, et al, “2011 ACCF/AHA/HRS Focused Update on the Management of Patients With Atrial Fibrillation (Updating the 2006 Guideline): A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines,” Circulation, 2011, 123 (1):104-23.
International Brand Names
Lexi-Comp.com
Last full review/revision April 2012
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