DOCSLIB.ORG

Therapeutic Alternatives in Atrial Fibrillation

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Therapeutic Alternatives in Atrial Fibrillation Le Journal canadien de la pharmacie hospitaliere Volume 48, N° 6, decembre 1995 360 PHARMACY PRACTICE Therapeutic Alternatives in Atrial Fibrillation William John Perks, Carmine Stumpo, Brian Jurewitsch and Christian Klem INTRODUCTION verting to normal sinus rhythm in equipotent doses to control the Atrial Fibrillation (AF) is the most (NSR); and, VRR. Esmolol was considered the common sustained dysrhythmia. It is maintaining NSR after initial prototype because of its short half­ more prevalent in the elderly and is a conversion; life, and ease of titration. Use of common complication of cardiac sur­ b) onset of effect; esmolol can demonstrate how a patient gery. Treatment of AF is often based c) usual dosing regimens; will respond to a beta-blocker in terms on previous experience and the most d) pharmacoki netics; of causing hypotension or brady­ appropriate therapeutic regimen for e) toxicity; cardia. The short half-life of esmolol each patient may not be selected. f) drug interactions; and should ensure a short duration of the Therefore, this Therapeutic Alterna­ g) availability/cost. adverse effect. Other less expensive tive Chart for AF was developed to These agents were also classified beta-blockers such as metoprolol, help both medical and pharmacy clin­ into groups by their pharmacologic propranolol, atenolol, and others may icians choose and utilize the most effects which: be substituted for longer-term control appropriate therapy for the treatment i) only control VRR (i.e., beta­ of VRR once response to a beta­ of AF in a specific patient. Currently blockers, calcium channel blocker has been demonstrated. For the chart is used by practicing phar­ blockers, digoxin); the post-operative patient, the macists at St. Michael's Hospital as a ii) only convert to NSR (i.e., pro­ intravenous forms of these drugs arc tool in providing pharmaceutical care. cainamide, quinidine, disopyra­ used initially because of their more Additionally, it is used as an educa­ mide); rapid onset; the parenteral forms can tional tool for pharmacists, residents, iii) control both VRR and convert be substituted with oral agents once students, and other health profes­ to NSR (i.e., sotalol, amio­ the patient is stabilized and is sionals. darone, flecainide, propa­ absorbing enterally. Similar oral fenone). conversions for other anti-arrhyth­ METHODS Disopyramide was not included in mic drugs can also be made. A thorough review of the current the chart as the authors felt that its use Although no column in the chart biomedical literature was undertaken is quite infrequent secondary to its was set aside specifically for the using a Medline search of the primary negative inotropic and anticholinergic duration of action, the overall duration literature back to 1984. All effective effects. of action of a drug is a function of the agents captured in this literature pharmacokinetic half-life (listed on search were then reviewed specif­ DISCUSSION the chart under kinetics), pharma­ ically for: While the therapeutic chart only codynamic half-life, and receptor includes esmolol under the beta­ response (i.e., up or down regulated). a) efficacy in: controlling ventri­ blocker row, other beta-blockers The duration of effect may, therefore, cular response rate (VRR); con- would be equally effective when used differ depending on the patient, the William John Perks, B.Sc.Phm. is a Staff Pharmacist, Department of Pharmacy, St. Michael's Hospital, Toronto, Ontario. Carmine Stumpo, B.Sc.Phm, at time of writing, Mr. Stumpo was a Pharmacy Resident, St. Michael's Hospital, Toronto, Ontario. Currently Mr. Stumpo is a Pharm.D. candidate at the College of Pharmacy, Wayne State University, Detroit, Michigan. Brian Jurewitsch, B.Sc.Phm., is a Staff Pharmacist, Department of Pharmacy, St. Michael's Hospital. Christian Klem, Pharm.D. at time of writing, Dr. Klem was Clinical Coordinator, Critical Care at St. Michael's Hospital. Currently Dr. Klem is a Pharmacotherapy Specialist, Tampa General HealthCare and Assistant Professor, University of South Florida, Tampa, Florida. Address Correspondence to: Mr. Wm. Perks, B.Sc.Phm., Department of Pharmacy, St. Michael's Hospital, 30 Bond Street, Toronto, Ontario M5B IWS. Acknowledgements: The authors would like to thank Dr. Al Rasymas, Pharm.D., Clinical Coordinator, St. Michael's Hospital for his guidance and coordination in the preparation of this paper. U.,) Table I: Therapeutic Alternatives in Atrial Fibrillation °'._ Drug Efficacy Onset Dose Kinetics Toxicity Drug Interactions Comments Availability/Cost 8-Blockers VRR = excellent (similar to PO= l-2hrs Complex (multiple bolus infusions) Ester hydrolysis by RBC bradycardia, symptomatic calcium channel blockers, -little risk of proarrhythmic effects / IV: IOOmg/JOml = $9.48 verapamil)1 500 mcg/kg over I min then 300 esterases. hypotension (10%) 1· 4· 34 digoxin, disopyramide torsades des pointes 2.5G/10ml = $134.10 2 E~molol CONY = similar to placebo IV= 2-5 min (may mcg/kg/min x 3 min then 50-300 tl/2=9min .J. contractility, .J. conduction, -may aggravate asthma, AV block, 11 (Brevibloc®l -may be higher than placebo take longer to mcg/kg/min bronchospasm, .J. glycogenesis diabetes, CHF Metoprolol if hyperadrenergic state 1 titrate)30 (quick offset with esmolol) -benefit in hyperadrenergic post-op Others patients 4 30 Diltiazem VRR = 94% bolus3• IV= 2-5 min3 0.25 mg/kg over 2 min. Hepatic elimination symt hypotension 3%3. B-blockers, digoxin - .J. HR is dose-related IV: 25mg/5ml = $13.00 (Cardizem®l = 76% infusion3· 4 (duration 3 hours)30 If no response in 15 min tl/2=3-5h bradycardia, less -ve inotropic - Calcium infusion may decrease 50mg/10ml = $24.00 CONY= similar to placebo5 PO= 1-2 hrs then O.35 mg/kg over 2 Active metabolites:4 effects vs. verapamiJ 35·38 hypotension PO: 60mg = $0.33 min then 5-15mg/hr11 desacetyl/N-desmethyldiltiazem -Use dependent effects46 120mg SR= $0.58 Verdpamil* VRR = excellent IV= 2-5 min 2.5-10 mg IV (0.0375-0.15mglkg) Hepatic elimination symt hypotension (10%)1.30.39, 8-blockers - Calcium infusion may decrease IV: 5mg/2ml = $17.80 7 (lsoptin®) (similar to diltiazem)4 (30-90 min duration over 2 min then 2.5-10 mg/hr bradycardia. diltiazem hypotension39.4 PO: 80mg = $0.20 2 11 CONY = similar to placebo post bolus) .J. contractility, .J. conduction warfarin 120mg=$0.33 PO= l-2hrs 80-120 mg PO Q6-8h 11 constipation. digoxin 240mg SR= $1.33 Digoxin* VRR = moderate (loss of effect IV= 3-4 hrs IV loading = I 0-15 mcg/kg (7-11 Renal elimination bradycardia, nausea, GI effects, quinidine, verapamil, -beneficial effect~ in LV dysfunction IV: 0.5mg/2ml = $3.27 (Lanoxin®J with i adrenergic states)6-7 PO =4-6 hrs mcg/kg if renal dysfunction) in (May require dose adjustment arrhythmias, i PR interval, diltiazem, amiodarone, -may require higher plasma level PO: 0.125mg = $0.09 26 CONY = similar to placebo - ,8 divided doses over 24 hours and/or closer monitoring with .J. AV block, CNS effects cholestyramine, antacids, for effect 1-2.6 nmol/L 0.25mg = $0.09 then 0.0625-0.25 mg/day 11 renal function interactions)32 propafenone32 (0.8-2 ng/ml)32,48 40 Procainamide t VRR=poor IV= 10-30 min 10-15 mg/kg IV (max 50 mg/min) Hepatic & renal (50%) proarrhythmia (9%) digoxin, amiodamne, -requires prior VRR control IV: lg/lOml = $10.15 ~ (Pronestyl®J CONY= 38-80%2·9·13 PO= 2-4 hrs then 2-4 mg/min elimination. cimetidine, lrimethoprim -levels: 4-8 mcg/ml (17-34 µmol/L) PO: 250mg = $0. I 8 (1:, MAINT=? tl/2 = 2.5-5 hrs nausea/vomiting, tremors, -NAPA-toxic/activemet(l4-29µmol/L) 375mg = $0.23 ~ 250-750 mg PO Q3-4h hypotension (IV), ANA (SLE- (may require dose adjustment/ 500mg SR= $0.48 ;:::: 1 500-1000 mg SR PO Q6h I NAPA is primarily renally like symptoms) (20-30%), monitoring of levels with .J. renal ~ eliminated. blood dyscrasia.~ (0.5% )11 function) ~ ;:::: Quinidinet VRR=poor IV= 1-2 hrs 5-10 mg/kg IV over 30 min Hepatic elimination proarrhythmia (15% )40 digoxin, amiodarone, -requires prior VRR control IV: 190mg/lml=$4.98(sulfate) (Quinate®, CONY= 60-80%2·12·14 PO= 4-24 hrs (infuse 0.9% NaCl concomitantly to tl/2 = 5-9 hrs Torsades des JX>intes ()-8%)41 warfarin, verapamil -3% mortality with use 15 800mg/10ml (gluconate) ~ :::: Cardioquin®) MAINT = 50% 15 maintain preload).May repeat 400mg F=0.7 pain with IV admin./phlebitis -levels: 2-6 mcg/ml (6-18 µmo1!L)48 ~ iv q2h to max 3g daily. Vo=3L/kg nausea/vomiting, diarrhea, cinchonism PO: sulfate 200mg = $0.05 dizziness, tinnitus, nystagmus (22%) gluconate 375mg = $0.26 :2.. 200-300 mg PO Q6-8h 11 blood dyscrasia, 19 ~ 17 16 40 ~ Propafenone1 VRR = moderate to good 16- IV = 10-30 min 18 2 mg/kg JV then 2mg/min Hepatic elimination (saturnble) proarrhythmia (4-8%) - 8-blockers, calcium -<lose-related 8-blockade (genetic IV: 70mg/20ml =? 'ij (Rhythmol®l CONY= 5J-9J<)15,12.13.16.18 PO=l-3hrs tl/2 = 2-10 hrs (fa~l) (90%) channel blockers, disposition) (emergency relea~e) MAINT = 30-78% 16-19 150-300mg POQ8h 11 12-32 hrs (slow) (10'1) .!.contrnctility, AV block, digoxin, warfarin, -active metabolite 5-0H propafenone [ hypotension. dil.Ziness(l0%), nausea cimetidine PO: 300mg = $1 .26 (efficacy may be dose dependent) 16 F = 0.1- 0.2 (non-linear) (9%), constipation, tremor, 150mg=$0.71 ""Cl parnsthesia, taste changes, (15% )42 ~ 40 43 ~ Aecainide'JI VRR = modc·rate20 IV = 10-60 min 2 mg/kg JV over IO min. Renal (25%) & hepatic proarrhythmia (4-12% ) - procainamide. sotalol, -use-<lependent effects IV:') ~ CONY= _92%5.9.12-14.19 48 (Tambocor®J 52 PO=l-3hrs 100-200 mg PO Q12h elimination.
Load more

Recommended publications
  • Table 2. 2012 AGS Beers Criteria for Potentially
    Table 2. 2012 AGS Beers Criteria for Potentially Inappropriate Medication Use in Older Adults Strength of Organ System/ Recommendat Quality of Recomm Therapeutic Category/Drug(s) Rationale ion Evidence endation References Anticholinergics (excludes TCAs) First-generation antihistamines Highly anticholinergic; Avoid Hydroxyzin Strong Agostini 2001 (as single agent or as part of clearance reduced with e and Boustani 2007 combination products) advanced age, and promethazi Guaiana 2010 Brompheniramine tolerance develops ne: high; Han 2001 Carbinoxamine when used as hypnotic; All others: Rudolph 2008 Chlorpheniramine increased risk of moderate Clemastine confusion, dry mouth, Cyproheptadine constipation, and other Dexbrompheniramine anticholinergic Dexchlorpheniramine effects/toxicity. Diphenhydramine (oral) Doxylamine Use of diphenhydramine in Hydroxyzine special situations such Promethazine as acute treatment of Triprolidine severe allergic reaction may be appropriate. Antiparkinson agents Not recommended for Avoid Moderate Strong Rudolph 2008 Benztropine (oral) prevention of Trihexyphenidyl extrapyramidal symptoms with antipsychotics; more effective agents available for treatment of Parkinson disease. Antispasmodics Highly anticholinergic, Avoid Moderate Strong Lechevallier- Belladonna alkaloids uncertain except in Michel 2005 Clidinium-chlordiazepoxide effectiveness. short-term Rudolph 2008 Dicyclomine palliative Hyoscyamine care to Propantheline decrease Scopolamine oral secretions. Antithrombotics Dipyridamole, oral short-acting* May
    [Show full text]
  • Drugs and Life-Threatening Ventricular Arrhythmia Risk: Results from the DARE Study Cohort
    Open Access Research BMJ Open: first published as 10.1136/bmjopen-2017-016627 on 16 October 2017. Downloaded from Drugs and life-threatening ventricular arrhythmia risk: results from the DARE study cohort Abigail L Coughtrie,1,2 Elijah R Behr,3,4 Deborah Layton,1,2 Vanessa Marshall,1 A John Camm,3,4,5 Saad A W Shakir1,2 To cite: Coughtrie AL, Behr ER, ABSTRACT Strengths and limitations of this study Layton D, et al. Drugs and Objectives To establish a unique sample of proarrhythmia life-threatening ventricular cases, determine the characteristics of cases and estimate ► The Drug-induced Arrhythmia Risk Evaluation study arrhythmia risk: results from the the contribution of individual drugs to the incidence of DARE study cohort. BMJ Open has allowed the development of a cohort of cases of proarrhythmia within these cases. 2017;7:e016627. doi:10.1136/ proarrhythmia. Setting Suspected proarrhythmia cases were referred bmjopen-2017-016627 ► These cases have provided crucial safety by cardiologists across England between 2003 and 2011. information, as well as underlying clinical and ► Prepublication history for Information on demography, symptoms, prior medical and genetic data. this paper is available online. drug histories and data from hospital notes were collected. ► Only patients who did not die as a result of the To view these files please visit Participants Two expert cardiologists reviewed data the journal online (http:// dx. doi. proarrhythmia could be included. for 293 referred cases: 130 were included. Inclusion org/ 10. 1136/ bmjopen- 2017- ► Referral of cases by cardiologists alone may have criteria were new onset or exacerbation of pre-existing 016627).
    [Show full text]
  • Flecainide Considerations For
    Flecainide (Tambocor) Considerations for Use* US/FDA Approved Indications: Heart Rhythm Control for Atrial Fibrillation Black Box Warning* Proarrhythmic. Increased mortality in patients with non-life-threatening ventricular arrhythmias, structural heart disease (ie, MI, LV dysfunction); not recommended for use with chronic atrial fibrillation. Mechanism of Action Depresses phase 0 depolarization significantly, slows cardiac conduction significantly (Class 1C). Dosing† Cardioversion: 200 to 300 mg PO‡1 Maintenance: 50 to 150 mg PO every 12 hrs Hepatic Impairment: Reduce initial dosage. Monitor serum level frequently. Allow at least 4 days after dose changes to reach steady state level before adjusting dosage. Renal Impairment: CrCl > 35 ml/min: No dosage adjustment is required. CrCl <= 35 ml/min: Initially, 100 mg PO once daily or 50 mg PO twice daily. Adjust dosage at intervals > 4 days, since steady-state conditions may take longer to achieve in these patient Contraindications cardiogenic shock sick sinus syndrome or significant conduction delay 2nd/3rd degree heart block or bundle brand block without pacemaker acquired/congenital QT prolongation patients with history of torsade de pointes Major Side Effects hypotension, atrial flutter with high ventricular rate, ventricular tachycardia, HF Dosage forms and Strengths PO: 50, 100, 150mg tablets Special Notes Close monitoring of this drug is required. When starting a patient on flecainide, it is prudent to do a treadmill stress test after the patient is fully loaded.4 Do not use in patients with ischemic heart disease or LV dysfunction; increases risk of arrhythmias. Additional AV nodal blocking agent may be required to maintain rate control when AF recurs.
    [Show full text]
  • A Proposal for the Clinical Use of Flecainide
    A Proposal for the Clinical Use of Flecainide JEFFREY L. ANDERSON, MD, JAMES R. STEWART, MD, and BARRY J. CREVEY, MD Effective antiarrhythmic therapy requires a carefully sponse rate is observed in preventing induction of considered approach, including an understanding sustained ventricular tachycardia, and these pa- of the arrhythmia, the underlying cardiac disease tients should be carefully selected. Flecainide is and the drug’s pharmacokinetics. Flecainide is a promising in the treatment of supraventricular new antiarrhythmic drug that may soon be released tachycardias using atrioventricular nodal or extra- for general use. Flecainide demonstrates unsur- nodal reentrant pathways, although this use is still passed efficacy in chronic ventricular arrhythmias investigational in the United States. The drug’s use in stable patients and may become a first-choice for arrhythmias during acute myocardial infarction drug because of its ease of administration, efficacy requires further study. Flecainide possesses modest and favorable tolerance. Twice-daily dosing with negative inotropic potential. Proarrhythmic or other 100 to 200 mg usually provides effective therapy. adverse reactions have occurred primarily in set- Clinical experience suggests flecainide to be indi- tings of high drug level, poor ventricular function cated in the treatment of uniform and multiform or refractory, malignant arrhythmias, suggesting ventricular premature complexes, coupled ven- caution in these groups. tricular premature complexes, and episodes of nonsustained
    [Show full text]
  • Guideline for Preoperative Medication Management
    Guideline: Preoperative Medication Management Guideline for Preoperative Medication Management Purpose of Guideline: To provide guidance to physicians, advanced practice providers (APPs), pharmacists, and nurses regarding medication management in the preoperative setting. Background: Appropriate perioperative medication management is essential to ensure positive surgical outcomes and prevent medication misadventures.1 Results from a prospective analysis of 1,025 patients admitted to a general surgical unit concluded that patients on at least one medication for a chronic disease are 2.7 times more likely to experience surgical complications compared with those not taking any medications. As the aging population requires more medication use and the availability of various nonprescription medications continues to increase, so does the risk of polypharmacy and the need for perioperative medication guidance.2 There are no well-designed trials to support evidence-based recommendations for perioperative medication management; however, general principles and best practice approaches are available. General considerations for perioperative medication management include a thorough medication history, understanding of the medication pharmacokinetics and potential for withdrawal symptoms, understanding the risks associated with the surgical procedure and the risks of medication discontinuation based on the intended indication. Clinical judgement must be exercised, especially if medication pharmacokinetics are not predictable or there are significant risks associated with inappropriate medication withdrawal (eg, tolerance) or continuation (eg, postsurgical infection).2 Clinical Assessment: Prior to instructing the patient on preoperative medication management, completion of a thorough medication history is recommended – including all information on prescription medications, over-the-counter medications, “as needed” medications, vitamins, supplements, and herbal medications. Allergies should also be verified and documented.
    [Show full text]
  • An Electrocardiographic Series of Flecainide Toxicity
    Indian Pacing and Electrophysiology Journal xxx (xxxx) xxx Contents lists available at ScienceDirect Indian Pacing and Electrophysiology Journal journal homepage: www.elsevier.com/locate/IPEJ An electrocardiographic series of flecainide toxicity * Alexandra Smith , Gregg Gerasimon San Antonio Military Medical Center, Electrophysiology Division, Cardiology Section, 3551 Roger Brooke Drive, San Antonio, TX, 78234, USA article info abstract Article history: Anti-arrhythmic drugs (AADs) uniquely affect the various electrolyte channels in the heart and can slow Received 16 October 2018 conduction, increase refractoriness, and/or decrease automaticity with the goal of preventing tachyar- Received in revised form rhythmias. Due to these properties, these same drugs are by nature pro-arrhythmic. Vaughan-Williams 8 November 2018 classification Ic AADs belong to a class of medications that inhibit sodium channels, leading to decreased Accepted 27 November 2018 conduction velocity of myocytes and Purkinje fibers as well as to decreased automaticity of pacemaker Available online xxx cells. When present in toxic amounts, this leads to classic changes on the electrocardiogram (ECG) that are harbingers of potentially lethal arrhythmias. Presented is a clinical series of ECGs that occurred in a Keywords: fl Flecainide patient who presented with ecainide toxicity. © Antiarrhythmic drugs Copyright 2018, Indian Heart Rhythm Society. Production and hosting by Elsevier B.V. This is an open Toxicity access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). Atrial fibrillation Flecainide toxicity can lead to bradycardia, sinoatrial block, and Abbreviations asystole, as well as to first and second degree atrioventricular block. Sinus bradycardia is more common in patients with pre-existing AAD Antiarrhythmic drug sinus node dysfunction [2].
    [Show full text]
  • Drug Interaction of Amiodarone, Flecainide, Metoprolol and Diltiazem Leading to Heart Block Vijay Kahajuria, Sanjeev Gupta, Roshi, Neelam Rani
    JK SCIENCE CASE REPORT Drug Interaction of Amiodarone, Flecainide, Metoprolol and Diltiazem leading to Heart Block Vijay Kahajuria, Sanjeev Gupta, Roshi, Neelam Rani Abstract Amiodarone, flecainide, metoprolol and diltiazem individually are known to cause heart blocks due to their cardiac depressant property but the current case report is worth reporting because it resulted because of drug interaction of multiple drugs due to possible medication error. Key Words Amiodarone, Flecainide, Metoprolol, Diltiazem, Heart Blocks Introduction Adverse Drug Reactions (ADRs) in cardiology are thyroid dysfunction. His hemoglobin levels were 13g/dl, common. There are numerous reports of drug induced total leucocyte count 6000/UL, neutrophils 56.5%, bradycardia and heart block (1). Co-morbid conditions lymphocytes 30.5%, eosinophils 5.2%, monocytes often coexist with cardiac ailments and results in 7.6%,basophils 0.2%, platelet count 1.5 lacs, serum urea- polypharmacy which enhance the chances of drug 33mg/dl, serum creatinine 0.90mg/dl, prothrombin time interactions culminating to adverse events. In the current 10.9 sec ,INR 1.04,hepatitis serology was non reactive, study report patient was prescribed multiple drugs for blood sugar random 182 mg/dl, TSH 1.4uIU/ml, serum cardiac arrhythmia and he presented with heart block sodium 142 mmol/L,serum potassium 5 mmol/L. and bradycardia. Though amiodarone, flecainide, He was prescribed tab.atenolol 20mg and metoprolol and diltiazem individually are known to cause tab.procainamide 20mg which did not bring any relief. heart blocks due to their cardiac depressant property but So radiofrequency ablation was done which was the current case report is worth reporting because it uneventful.
    [Show full text]
  • Flecainide in Ventricular Arrhythmias: from Old Myths to New Perspectives
    Journal of Clinical Medicine Review Flecainide in Ventricular Arrhythmias: From Old Myths to New Perspectives Carlo Lavalle 1,*, Sara Trivigno 1 , Giampaolo Vetta 1 , Michele Magnocavallo 1 , Marco Valerio Mariani 1 , Luca Santini 2, Giovanni Battista Forleo 3 , Massimo Grimaldi 4, Roberto Badagliacca 1, Luigi Lanata 5 and Renato Pietro Ricci 6 1 Department of Cardiovascular, Respiratory, Nephrological, Anesthesiological and Geriatric Sciences, Sapienza University of Rome, Policlinico Umberto I, 00161 Rome, Italy; [email protected] (S.T.); [email protected] (G.V.); [email protected] (M.M.); [email protected] (M.V.M.); [email protected] (R.B.) 2 Department of Cardiology, Ospedale GB Grassi, 00121 Ostia, Italy; [email protected] 3 Department of Cardiology, Azienda Ospedaliera-Universitaria “Luigi Sacco”, 20057 Milan, Italy; [email protected] 4 Department of Cardiology, Ospedale Generale Regionale F. Miulli, Acquaviva delle Fonti, 70021 Bari, Italy; fi[email protected] 5 Medical Affairs Department, Dompé Farmaceutici SpA, 20057 Milan, Italy; [email protected] 6 Centro Cardio-Aritmologico, 00152 Rome, Italy; [email protected] * Correspondence: [email protected]; Tel.: +39-335376901 Abstract: Flecainide is an IC antiarrhythmic drug (AAD) that received in 1984 Food and Drug Administration approval for the treatment of sustained ventricular tachycardia (VT) and subsequently Citation: Lavalle, C.; Trivigno, S.; for rhythm control of atrial fibrillation (AF). Currently, flecainide is mainly employed for sinus Vetta, G.; Magnocavallo, M.; Mariani, rhythm maintenance in AF and the treatment of idiopathic ventricular arrhythmias (IVA) in absence M.V.; Santini, L.; Forleo, G.B.; Grimaldi, M.; Badagliacca, R.; Lanata, of ischaemic and structural heart disease on the basis of CAST data.
    [Show full text]
  • FLECAINIDE ACETATE Tablets, USP Rx Only DESCRIPTION CLINICAL PHARMACOLOGY
    FLECAINIDE ACETATE Tablets, USP Rx only DESCRIPTION Flecainide is an antiarrhythmic drug available in tablets of 50, 100, or 150 mg for oral administration. Flecainide acetate is benzamide, N-(2-piperidinylmethyl)-2,5-bis (2,2,2-trifluoroethoxy)- monoacetate. The structural formula is given below. Flecainide acetate is a white crystalline substance with a pKa of 9.3. It has an aqueous solubility of 48.4 mg/mL at 37°C. Flecainide Acetate Tablets, USP also contain: croscarmellose sodium, hydrogenated vegetable oil, magnesium stearate, microcrystalline cellulose, and pregelatinized starch. CLINICAL PHARMACOLOGY Flecainide has local anesthetic activity and belongs to the membrane stabilizing (Class 1) group of antiarrhythmic agents; it has electrophysiologic effects characteristic of the IC class of antiarrhythmics. Electrophysiology In man, flecainide produces a dose-related decrease in intracardiac conduction in all parts of the heart with the greatest effect on the His-Purkinje system (H-V conduction). Effects upon atrioventricular (AV) nodal conduction time and intra-atrial conduction times, although present, are less pronounced than those on ventricular conduction velocity. Significant effects on refractory periods were observed only in the ventricle. Sinus node recovery times (corrected) following pacing and spontaneous cycle lengths are somewhat increased. This latter effect may become significant in patients with sinus node dysfunction. (See WARNINGS.) Flecainide causes a dose-related and plasma-level related decrease in single and multiple PVCs and can suppress recurrence of ventricular tachycardia. In limited studies of patients with a history of ventricular tachycardia, flecainide has been successful 30 to 40% of the time in fully suppressing the inducibility of arrhythmias by programmed electrical stimulation.
    [Show full text]
  • Oral Antiarrhythmic Drugs in Converting Recent Onset Atrial Fibrillation
    Review article Oral antiarrhythmic drugs in converting recent onset atrial fibrillation • Vera H.M. Deneer, Marieke B.I. Borgh, J. Herre Kingma, Loraine Lie-A-Huen and Jacobus R.B.J. Brouwers Introduction Pharm World Sci 2004; 26: 66–78. © 2004 Kluwer Academic Publishers. Printed in the Netherlands. Atrial fibrillation is the most common arrhythmia. The incidence of atrial fibrillation depends on the age of V.H.M. Deneer (correspondence, e-mail: the study population. The incidence varies between 2 [email protected]), M.B.I. Borgh, L. Lie-A-Huen: Department of Clinical Pharmacy or 3 new cases per 1,000 population per year between J.H. Kingma: Department of Cardiology, St Antonius Hospital, the ages of 55 and 64 years to 35 new cases per 1,000 Koekoekslaan 1, 3435 CM Nieuwegein, The Netherlands population per year between the ages of 85 and 94 J.R.B.J. Brouwers: Groningen University Institute for Drug 1 Exploration (GUIDE), Section of Pharmacotherapy, University years . Treatment of an episode of paroxysmal atrial fi- of Groningen, Antonius Deusinglaan 1, 9713 AV Groningen, brillation consists of restoring sinus rhythm by DC- The Netherlands electrical cardioversion or by the intravenous adminis- Key words tration of an antiarrhythmic drug, but frequently the Atrial fibrillation arrhythmia spontaneously terminates1–3. After one or Amiodarone more episodes of atrial fibrillation chronic prophylac- Antiarrhythmic drugs Digoxin tic treatment with an antiarrhythmic drug is often Episodic treatment started for maintenance of sinus rhythm4–8. Another Flecainide treatment strategy consists of allowing the arrhythmia Propafenone Quinidine to exist in combination with pharmacological ven- Sotalol tricular rate control.
    [Show full text]
  • Prevention of Pazopanib-Induced Prolonged Cardiac Repolarization and Proarrhythmic Effects Tulay Akman1,2, Oytun Erbas3, Levent Akman4,5, Ahmet U
    Original Article Prevention of Pazopanib-Induced Prolonged Cardiac Repolarization and Proarrhythmic Effects Tulay Akman1,2, Oytun Erbas3, Levent Akman4,5, Ahmet U. Yilmaz6 Tepecik Education and Research Hospital, Department of Medical Oncology1; Dokuz Eylul University, Institute of Oncology, Department of Basic Oncology2; Ege University Medical School, Department of Physiology3; Ege University Medical School, Department of Obstetrics and Gynecology4; Ege University, Institute of Health Sciences, Department of Stem Cell5; Izmir University, Medical Park Hospital, Department of Medical Oncology6 Abstract Background: Pazopanib (PZP) may induce prolonged cardiac repolarization and proarrhythmic effects, similarly to other tyrosine kinase inhibitors. Objectives: To demonstrate PZP-induced prolonged cardiac repolarization and proarrhythmic electrophysiological effects and to investigate possible preventive effects of metoprolol and diltiazem on ECG changes (prolonged QT) in an experimental rat model. Methods: Twenty-four Sprague-Dawley adult male rats were randomly assigned to 4 groups (n = 6). The first group (normal group) received 4 mL of tap water and the other groups received 100 mg/kg of PZP (Votrient® tablet) perorally, via orogastric tubes. After 3 hours, the following solutions were intraperitoneally administered to the animals: physiological saline solution (SP), to the normal group and to the second group (control-PZP+SP group); 1 mg/kg metoprolol (Beloc, Ampule, AstraZeneca), to the third group (PZP+metoprolol group); and 1mg/kg diltiazem (Diltiazem, Mustafa Nevzat), to the fourth group (PZP+diltiazem group). One hour after, and under anesthesia, QTc was calculated by recording ECG on lead I. Results: The mean QTc interval values were as follows: normal group, 99.93 ± 3.62 ms; control-PZP+SP group, 131.23 ± 12.21 ms; PZP+metoprolol group, 89.36 ± 3.61 ms; and PZP+diltiazem group, 88.86 ± 4.04 ms.
    [Show full text]
  • 2020 Aetna Standard Plan
    Plan for your best health Aetna Standard Plan Aetna.com Aetna is the brand name used for products and services provided by one or more of the Aetna group of subsidiary companies, including Aetna Life Insurance Company and its affiliates (Aetna). Aetna Pharmacy Management refers to an internal business unit of Aetna Health Management, LLC. Aetna Pharmacy Management administers, but does not offer, insure or otherwise underwrite the prescription drug benefits portion of your health plan and has no financial responsibility therefor. 2020 Pharmacy Drug Guide - Aetna Standard Plan Table of Contents INFORMATIONAL SECTION..................................................................................................................6 *ADHD/ANTI-NARCOLEPSY/ANTI-OBESITY/ANOREXIANTS* - DRUGS FOR THE NERVOUS SYSTEM.................................................................................................................................16 *ALLERGENIC EXTRACTS/BIOLOGICALS MISC* - BIOLOGICAL AGENTS...............................18 *ALTERNATIVE MEDICINES* - VITAMINS AND MINERALS....................................................... 19 *AMEBICIDES* - DRUGS FOR INFECTIONS.....................................................................................19 *AMINOGLYCOSIDES* - DRUGS FOR INFECTIONS.......................................................................19 *ANALGESICS - ANTI-INFLAMMATORY* - DRUGS FOR PAIN AND FEVER............................19 *ANALGESICS - NONNARCOTIC* - DRUGS FOR PAIN AND FEVER.........................................
    [Show full text]