Off Label. Only Generics. Pregnancy Category A Adequate and well-controlled studies have failed to demonstrate a risk to the fetus in the first trimester of pregnancy and there is no evidence of risk in later trimesters. B Animal reproduction studies have failed to demonstrate a risk to the fetus and there are no adequate and well-controlled studies in pregnant women.
C Animal reproduction studies have shown an adverse effect on the fetus and there are no adequate and well-controlled studies in humans, but potential benefits may warrant use in pregnant women despite potential risks. D There is positive evidence of human fetal risk based on adverse reaction data from investigational or marketing experience or studies in humans, but potential benefits may warrant use in pregnant women despite potential risks.
N FDA has not classified the drug. Has no currently accepted medical use in treatment in the United States. There is a lack of accepted safety for use under medical supervision. Has a currently accepted medical use in treatment in the United States or a currently accepted medical use with severe restrictions.
Drugs for acute coronary syndrome
Abuse may lead to severe psychological or physical dependence. Has a currently accepted medical use in treatment in the United States. Abuse may lead to moderate or low physical dependence or high psychological dependence. It has a currently accepted medical use in treatment in the United States. Abuse may lead to limited physical dependence or psychological dependence relative to those in schedule 3.
In a recent European survey, beta-blockers, flecainide, propafenone, and amiodarone were most frequently used first-line AAD for rhythm control. Limited data are available on the best type of rate control therapy and optimal heart rate during AF. Pharmacological rate control strategies rely on agents prolonging AV node refractoriness including beta-blockers, non-dihydropyridine calcium channel antagonists, digitalis, and amiodarone alone or in combination.
Non-dihydropyridine calcium channel antagonists are not recommended in patients with significant left ventricular systolic dysfunction because of their negative inotropic effect. Amiodarone may slow the ventricular rate in haemodynamically unstable patients, especially in the acute setting. It may be also used for chronic treatment, but its side effects limit long-term tolerability.
Dronedarone should not be used for rate control in patients with permanent AF because of safety concerns. Medication for rate control inf atrial fibrillation adapted from Algorithm for management of the proarrhythmic risk. In patients with pre-excited AF, agents acting primarily on the AV node e. The acute management of VT includes the use of beta-blocker therapy and typically the use of AADs such as amiodarone, lidocaine and procainamide intravenously.
The amiodarone i. Antiarrhythmic drugs therapy for the prevention of SCD due to ventricular tachyarrhythmias has not been shown to be effective in randomized controlled clinical trials, and therefore should be considered as adjunct therapy to ICD or catheter ablation. Most patients with ventricular arrhythmias have structural heart disease, and therefore pharmacologic treatment is limited to amiodarone, sotalol, or other AAD in conjunction with ICD.
In patients with monomorphic VT, catheter ablation has evolved as alternative treatment and results in a significant reduction of VT recurrences. Patients suffering from VT arising from the right ventricular outflow tract, the left ventricular fascicular system or the mitral annulus, may respond to beta-blockade and or non-dihydropyridine-calcium channel blockers i.
In patients not responding to conventional beta-blocker therapy, sotalol, flecainide, mexiletine, propafenone, or amiodarone may be used as alternative treatments. As idiopathic VT can be successfully treated by catheter ablation in the majority of cases, usually patients will undergo the procedure having failed beta-blockade. Although beta-blockers are considered the mainstay of AAD therapy, their efficacy is low in preventing monomorphic sustained VT. Amiodarone has been shown to reduce ICD interventions when used for secondary prevention. The PVT which occurs in the setting of normal QT interval is distinct from that which occurs in the setting of QT prolongation; the last, called TdP, is characterized by QRS morphology which is twisting around the isoelectric line.
Not only the ECG appearance but also the management is different between the two forms. Deep sedation, neuraxial modulation, mechanical ventilation, and catheter ablation are recommended in unstable patients non-responding to pharmacological therapy. Immediate coronary angiography is indicated when ischaemia is the cause. In all patients, the search for and correction of reversible causes hypokalaemia, hypomagnesaemia, acute decompensated heart failure, and proarrhythmic drugs are indicated. Hypomagnesaemia is typically associated with PVT and responds to intravenous magnesium.
The addition of flecainide should be considered in patients who experience recurrent PVT or syncope while on beta-blocker, or in patients non-suitable for ICD implantation. Torsadogenic drugs differ significantly in their arrhythmic risk profile. The anti-torsadogenic mechanism of magnesium is poorly understood. Increasing heart rate with isoproterenol or repletion of potassium to serotherapeutic levels 4. One unique situation in which prophylactic treatment with lidocaine might have a role is its use after cardiac arrest and successful resuscitation, where it has led to suppression of recurrent ventricular arrhythmias and improved survival.
Early use of beta-blockers in the setting of ACS reduces mortality, and the incidence of ventricular arrhythmias and is therefore recommended. Correction of hypomagnesaemia and hypokalaemia may help in selected patients. Amiodarone may have the most balanced efficacy-to-risk profile, and should be considered only if episodes of VT or VF are frequent, and can no longer be controlled by successive electrical cardioversion or defibrillation. However, the effect on global mortality is neutral.
Lidocaine may reduce the incidence of ventricular arrhythmias related to myocardial ischaemia, although no beneficial effect on early mortality has been demonstrated. Statin therapy reduces mortality in patients with coronary artery disease, mostly through prevention of recurrent coronary events, and is therefore part of the recommended routine medication. Evidence does not support the use of AADs for overall mortality reduction in patients with ventricular arrhythmias post-myocardial infarction and neither as prophylactic treatment in patients without demonstrable ventricular arrhythmias.
Beta-blockers improve survival in patients who have had myocardial infarction in part by reducing the incidence of SCD. A substantial part of the survival benefit seen with beta-blockers in patients with heart failure is due to a significant reduction in SCD. Amiodarone may be considered for prevention of SCD, particularly in patients who cannot receive or do not have access to ICD therapy. Angiotensin-converting enzyme ACE inhibitors improve survival in all stages of heart failure.
Antiarrhythmic drugs play a major role in the treatment of both arrhythmogenic diseases such as arrhythmogenic right ventricular cardiomyopathy ARVC , hypertrophic cardiomyopathy as well as in ion channel diseases, since catheter ablation is associated with little or no success, and because electrical storm in these patients can only be controlled by AADs.
Patients with ARVC are often well controlled with amiodarone or sotalol, since they suffer most frequently from recurrent monomorphic VT. In LQTS, there are reports on many different beta-blockers. The most frequently used drugs are propranolol, metoprolol, and bisoprolol. Nadolol, which is very efficient, is used infrequently because of its limited availability in many countries. In Brugada syndrome, quinidine is the therapy of choice as adjunct to an ICD or if a patient refuses an ICD, with reported favourable outcome. There is a large series of patients reported from Belhassen et al.
In catecholaminergic PVT, beta-blockade is first line therapy and flecainide can be added with considerable success if beta-blockade does not suppress arrhythmias effectively. In the setting of an electrical storm accompanying early repolarization syndrome, short-QT syndrome, and Brugada syndrome, quinidine can be used.
Additionally, isoproterenol infusion is recommended in Brugada syndrome. Pacemakers PM are usually indicated for patients with symptomatic or high-risk bradyarrhythmia. They may also be indicated when a mandatory antiarrhythmic or other medication causes significant chronotropic or dromotropic side effects. Antiarrhythmic drugs blocking sodium channel currents may increase pacing thresholds and lead to loss of capture. Specifically, some type IA agents quinidine, procainamide and most type IC agents encainide, flecainide, propafenone increase the pacing threshold, especially at higher doses.
Caution is advised in PM-dependent patients, when using these drugs, either a higher safety margin or automatic output regulation is recommended. These drugs may also slow down atrial tachyarrhythmia below the mode switch rate and may lead to inadvertent rapid ventricular pacing or affect device statistics.
Propranolol, a Class II agent, also has some sodium channel-blocking effect and can increase the stimulation threshold when administered intravenously. Table 15 Effect of antiarrhythmic medications on the pacing threshold. Among AAD therapies, amiodarone plus beta-blocker is effective for reducing ICD therapy, 52 though amiodarone adverse effects need to be appreciated. Sotalol is also effective, but less than amiodarone plus a beta-blocker.
Table 16 Antiarrhythmic drugs for implantable cardioverter-defibrillator patients. In the first randomized study which evaluated the effects of AAD after radiofrequency catheter ablation of AF, after month follow-up, no significant difference was observed in the rates of AF recurrences, either in patients with paroxysmal or persistent AF, but AAD increased the proportion of patients with asymptomatic AF episodes. Antiarrhythmic drugs were discontinued in Table 17 Randomized trials of empirical antiarrhythmic drug therapy after ablation of atrial fibrillation on the recurrence rate.
Randomized trials of empirical antiarrhythmic drug therapy after ablation of atrial fibrillation on the recurrence rate. However, not all studies demonstrated a benefit of AAD therapy in patients who underwent catheter ablation. For instance, a retrospective, non-randomized, single-centre study of ablation patients demonstrated no difference in the rates of early AF recurrence among those treated with an AAD or an AV nodal blocking agent alone.
With the exception of beta-blockers, AADs have not been demonstrated to prevent life-threatening ventricular arrhythmias and SCD. However, most AAD might cause proarrhythmia. Mexiletine and disopyramide should also be avoided in post-myocardial infarction patients. Dofetilide may provoke TdP in patients with severe heart failure. Amiodarone may also cause TdP although this is a very rare effect of the drug.
Digitalis may cause diverse arrhythmias [e. In addition, several drugs e. Since polypharmacy is very often necessary, drug-drug interactions and their pharmacological consequences especially QT interval modification might become crucial Table However, other forms of drug induced rhythm disturbances, as bradycardia, may occur. The list is very long, including almost all classes of drugs other than AAD: antianginal e. There is an individual genetic predisposition to proarrhythmia to a specific drug, the PD sensitivity, and vulnerability due to abnormal high plasma concentration of a drug given in therapeutical dosage.
The PK sensitivity, is explained by the interference of a single metabolizing pathway e. Table 18 Mechanisms promoting proarrhythmia. This monitoring is appropriate in hospital settings. Important are also the identification and modification whenever possible of risk factors potentially associated with arrhythmia onset or worsening e. In the case of drug-related proarrhythmia, the first-line of management is to stop the offending drug; however, in selected cases, the implantation of ICD needs to be considered based on the individual characteristics of the patient and the future risk of life-threatening ventricular tachyarrhythmias.
Sodium channel blocker-related proarrhythmia, generally secondary to slowing of conduction, include atrial flutter with AV conduction and incessant slow VT. Besides discontinuation of the offending drug, management is based on control of the ventricular response by intravenous beta-blocker or calcium antagonist whereas incessant slow VT can be reversed by intravenous administration of sodium or sodium bicarbonate.
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Beta-blockers have been reported to be effective in treating ventricular arrhythmias related to flecainide. In milder cases, arrhythmias due to digitalis toxicity can be managed by discontinuation of the drug, potassium supplementation, and observation. For digitalis-induced life threatening arrhythmias, several AAD have been proposed in the past e. More recently, digitalis-specific antibodies have proven effective in reversing digitalis toxicity by rapidly binding to and acutely lowering serum digitalis. The pharmacological management of AF and other arrhythmias requires careful consideration from a safety perspective Table The full profile of potential cardiac effects should therefore be considered for each AAD and carefully tailored to the individual patient history before treatment is initiated.
Table 19 Cardiac effects, extracardiac toxicities, and contraindications for antiarrhythmic drugs. Not only thyroid tests can be modified, but, also, hyopthyroidism or hyperthyroidism can be induced. Amiodarone-induced hypothyroidism usually develop in patients with underlying thyroid abnormalities. Stopping amiodarone or adding hormone replacement, are acceptable strategies in AIHT. Amiodarone-induced thyrotoxicosis is encountered mainly in the regions with insufficient iodine intake and it is more prevalent in men.
Type 1 amiodarone-induced thyrotoxicosis occurs in patients with abnormal thyroid function, whereas Type 2 is a direct consequence of amiodarone. Inflammatory markers IL-6 are markedly elevated in Type 2 amiodarone-induced thyrotoxicosis and thyroid autoantibodies are typically present in Type 1. Amiodarone should be stopped in amiodarone-induced thyrotoxicosis.
In Type 1 amiodarone-induced thyrotoxicosis, prophylactic thyroid ablation thyroidectomy or radioactive iodine following the restoration of the normal thyroid function is recommended. However, Dronedarone is less effective than amiodarone and has itself adverse effects discussed in previous sections.
Periodic monitoring of lung function is required, and amiodarone should be avoided in patients with impaired pulmonary function. Supplementary material is available at Europace online. Gregory Lip Chair , Prof. Bulent Gorenek Co-chair , Prof. Christian Sticherling, Prof. Laurent Fauchier, Prof. Andreas Goette, Prof. Werner Jung, Prof. Sign In. Advanced Search. Article Navigation. Close mobile search navigation Article Navigation.
Volume Article Contents. Table of Contents. Decisions to initiate antiarrhythmic drug therapy and follow-up. Classification of antiarrhythmic drugs and overview of clinical pharmacology. Monitoring of antiarrhythmic drugs. Individualizing recommendations for pharmacological therapy of arrhythmias. Antiarrhythmic drug therapy to prevent sudden cardiac death in high-risk patients.
Antiarrhythmic drugs as adjuvant to devices and arrhythmia interventions. Safety issues for patients treated with antiarrhythmic drugs. Supplementary material. Corresponding author. Oxford Academic. Google Scholar. Antoni Martinez-Rubio. Stefan Agewall. Giuseppe Boriani. Martin Borggrefe. Fiorenzo Gaita. Isabelle van Gelder. Bulent Gorenek. Juan Carlos Kaski. Keld Kjeldsen. Gregory Y H Lip. Bela Merkely. Ken Okumura. Saiseikai Akumamoto Hospital, Kumamoto, Japan. Jonathan P Piccini. Tatjana Potpara. Birgitte Klindt Poulsen. Magdi Saba. Irina Savelieva.
Juan L Tamargo. Christian Wolpert. Article history. Cite Citation. Permissions Icon Permissions. Table 1. Table 2. Figure 1. View large Download slide. Table 3. Figure 2. Figure 3. Table 4. Table 5. GI, gastrointestinal; PK, pharmacokinetics; Vd, distribution volume. Table 6. Table 7. Effect of antiarrhythmic drugs on heart rate, conduction, and repolarization. Table 8. Table 9. Drugs recommended for acute management of haemodynamically stable and regular tachycardia.
Table Figure 4. Figure 5. Antiarrhythmic drugs currently used for cardioversion of atrial fibrillation. Figure 6. Antiarrhythmic drugs currently used for rhythm control in atrial fibrillation. Figure 7. Figure 8. Antiarrhythmic drugs for implantable cardioverter-defibrillator patients. Cardiac effects, extracardiac toxicities, and contraindications for antiarrhythmic drugs. Allen LaPointe. Search ADS. Adherence to guideline recommendations for antiarrhythmic drugs in atrial fibrillation.
Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction. Google Preview. Cost-benefit and cost-savings analyses of antiarrhythmic medication monitoring. Vaughan Williams. A classification of antiarrhythmic actions reassessed after a decade of new drugs.
Antiarrhythmic therapy: a pathophysiologic approach by Members of the Sicilian Gambit. A new approach to the classification of antiarrhythmic drugs based on their actions on arrhythmogenic mechanisms. New approaches to antiarrhythmic therapy, Part I: emerging therapeutic applications of the cell biology of cardiac arrhythmias. Upstream therapies for management of atrial fibrillation: review of clinical evidence and implications for European Society of Cardiology guidelines. Part I: primary prevention. Upstream therapies for management f atrial fibrillation: review of clinical evidence and implications for European Society of Cardiology guidelines.
Part II: secondary prevention. Novel pharmacological targets for the rhythm control management of atrial fibrillation.
Drugs Causing QT Prolongation
Anti-arrhythmic drug therapy for atrial fibrillation: current anti-arrhythmic drugs, investigational agents, and innovative approaches. Investigational antiarrhythmic agents: promising drugs in early clinical development. Cellular and molecular electrophysiology of atrial fibrillation initiation, maintenance, and progression. Relationship between plasma levels of procainamide, suppression of premature ventricular complexes and prevention of recurrent ventricular tachycardia.
Updated European Heart Rhythm Association Practical Guide on the use of non-vitamin K antagonist anticoagulants in patients with non-valvular atrial fibrillation. Drug-induced proarrhythmia: risk factors and electrophysiological mechanisms. Impact of interferences including metabolite crossreactivity on therapeutic drug monitoring results. Twenty-five years in the making: flecainide is safe and effective for the management of atrial fibrillation.
Benefit-risk assessment of dronedarone in the treatment of atrial fibrillation. Efficacy and safety of sustained-release propafenone propafenone SR for patients with atrial fibrillation. Risk factors and predictors of torsade de pointes ventricular tachycardia in patients with left ventricular systolic dysfunction receiving Dofetilide. Age- and sex-related differences in clinical manifestations in patients with congenital long-QT syndrome: findings from the International LQTS Registry.
Risk of proarrhythmia with class III antiarrhythmic agents: sex-based differences and other issues. Comparison of beta-blockers, amiodarone plus beta-blockers, or sotalol for prevention of shocks from implantable cardioverter defibrillators: the OPTIC Study: a randomized trial. Antiarrhythmics for maintaining sinus rhythm after cardioversion of atrial fibrillation. The European Society of Cardiology Guidelines on the management of atrial fibrillation: an evolution or revolution? Dispersion of ventricular repolarization in left ventricular hypertrophy: influence of afterload and dofetilide.
antiarrhythmics a quick reference guide Manual
Left ventricular hypertrophy and antiarrhythmic drugs in atrial fibrillation: impact on mortality. Chronic kidney disease in patients with cardiac rhythm disturbances or implantable electrical devices: clinical significance and implications for decision making-a position paper of the European Heart Rhythm Association endorsed by the Heart Rhythm Society.
Myocardial stimulation threshold in patients with cardiac pacemakers: effect of physiologic variables, pharmacologic agents, and lead electrodes. Effectiveness of sotalol as first-line therapy for fetal supraventricular tachyarrhythmias. ESC Guidelines on the management of cardiovascular diseases during pregnancy. Rate control versus rhythm control for atrial fibrillation after cardiac surgery. Disappointing success of electrical cardioversion for new-onset atrial fibrillation in cardiosurgical ICU patients. A randomized, double-blind comparison of intravenous diltiazem and digoxin for atrial fibrillation after coronary artery bypass surgery.
Interventions for preventing post-operative atrial fibrillation in patients undergoing heart surgery. Preoperative amiodarone as prophylaxis against atrial fibrillation after heart surgery. Oral amiodarone for prevention of atrial fibrillation after open heart surgery, the Atrial Fibrillation Suppression Trial AFIST : a randomised placebo-controlled trial. Prophylactic amiodarone for prevention of atrial fibrillation after cardiac surgery: a meta-analysis. Amiodarone vs. Effects of magnesium on atrial fibrillation after cardiac surgery: a meta-analysis. Vernakalant hydrochloride for the rapid conversion of atrial fibrillation after cardiac surgery: a randomized, double-blind, placebo-controlled trial.
Pharmacological cardioversion of atrial fibrillation with vernakalant: evidence in support of the ESC Guidelines. Efficacy and safety of ibutilide fumarate for the conversion of atrial arrhythmias after cardiac surgery. Effectiveness of oral propafenone for the prevention of atrial fibrillation after coronary artery bypass grafting. Hemodynamic effects of intravenous amiodarone in patients with depressed left ventricular function and recurrent ventricular tachycardia. Drug-induced QT-interval prolongation and proarrhythmic risk in the treatment of atrial arrhythmias.
Inpatient versus outpatient antiarrhythmic drug initiation: safety and cost-effectiveness issues. Oral propafenone to convert recent-onset atrial fibrillation in patients with and without underlying heart disease. A randomized, controlled trial. Oral loading with propafenone for conversion of recent-onset atrial fibrillation: a review on in-hospital treatment.
Conversion of recent-onset atrial fibrillation to sinus rhythm: effects of different drug protocols. Pharmacological cardioversion of atrial fibrillation: current management and treatment options. Effect of acetylator phenotype on the rate at which procainamide induces antinuclear antibodies and the lupus syndrome. Novel rare variants in congenital cardiac arrhythmia genes are frequent in drug-induced torsades de pointes.
Outpatient evaluation and management of patients with ventricular premature beats or non-sustained ventricular tachycardia. Radiofrequency ablation versus antiarrhythmic medication for treatment of ventricular premature beats from the right ventricular outflow tract: prospective randomized study. Arrhythmia-induced cardiomyopathies: the riddle of the chicken and the egg still unanswered? Asymptomatic ventricular premature depolarizations are not necessarily benign.
Relationship between burden of premature ventricular complexes and left ventricular function. The conundrum of ventricular arrhythmia and cardiomyopathy: which abnormality came first? Mortality and morbidity in patients receiving encainide, flecainide, or placebo. The Cardiac Arrhythmia Suppression Trial.
Arrhythmia-induced cardiomyopathies mechanisms, recognition, and management. Excessive supraventricular ectopic activity and increased risk of atrial fibrillation and stroke. Excessive atrial ectopy and short atrial runs increase the risk of stroke beyond incident atrial fibrillation. Premature atrial contractions in the general population: frequency and risk factors.
Effectiveness of loading oral flecainide for converting recent-onset atrial fibrillation to sinus rhythm in patients without organic heart disease or with only systemic hypertension. Oral loading with propafenone: a placebo-controlled study in elderly and nonelderly patients with recent onset atrial fibrillation. Amiodarone versus placebo and class Ic drugs for cardioversion of recent-onset atrial fibrillation: a meta-analysis.
Meta-analysis of randomised controlled trials of the effectiveness of antiarrhythmic agents at promoting sinus rhythm in patients with atrial fibrillation. Conversion of recent-onset atrial fibrillation with intravenous amiodarone: a meta-analysis of randomized controlled trials. Conversion efficacy and safety of repeated doses of ibutilide in patients with atrial flutter and atrial fibrillation.
Study Investigators. A prospective, randomized controlled trial comparing the efficacy and safety of sotalol, amiodarone, and digoxin for the reversion of new-onset atrial fibrillation. Prospective comparison of flecainide versus sotalol for immediate cardioversion of atrial fibrillation. Canadian Cardiovascular Society Atrial fibrillation guidelines rate and rhythm management. Rate vs rhythm control in patients with atrial fibrillation: a meta-analysis. Improving outcomes in patients with atrial fibrillation: rationale and design of the Early treatment of Atrial fibrillation for Stroke prevention Trial.
Developed with the special contribution of the European Heart Rhythm Association. Likelihood of spontaneous conversion of atrial fibrillation to sinus rhythm. Practical management guide for clinicians who treat patients with amiodarone. A randomized placebo-controlled trial of pre-treatment and short- or long-term maintenance therapy with amiodarone supporting DC cardioversion for persistent atrial fibrillation. Systematic electrocardioversion for atrial fibrillation and role of antiarrhythmic drugs: a substudy of the SAFE-T trial.
Facilitating transthoracic cardioversion of atrial fibrillation with ibutilide pretreatment. Meta-analysis of ablation of atrial flutter and supraventricular tachycardia. Safety and efficacy of ibutilide in cardioversion of atrial flutter and fibrillation. Efficacy and safety of vernakalant in patients with atrial flutter: a randomized, double-blind, placebo-controlled trial. Low-dose amiodarone versus sotalol for suppression of recurrent symptomatic atrial fibrillation. Low dose amiodarone and sotalol in the treatment of recurrent, symptomatic atrial fibrillation: a comparative, placebo controlled study.
Efficacy of amiodarone for the termination of chronic atrial fibrillation and maintenance of normal sinus rhythm: a prospective, multicenter, randomized, controlled, double blind trial. Comparison of sotalol versus amiodarone in maintaining stability of sinus rhythm in patients with atrial fibrillation Sotalol-Amiodarone Fibrillation Efficacy Trial [Safe-T].
Long-term maintenance of normal sinus rhythm in patients with current symptomatic atrial fibrillation: amiodarone vs propafenone, both in low doses. A randomized trial of prophylactic antiarrhythmic agents amiodarone and sotalol in patients with atrial fibrillation for whom direct current cardioversion is planned. Prevention of symptomatic recurrences of paroxysmal atrial fibrillation in patients initially tolerating antiarrhythmic therapy. A multicenter, double-blind, crossover study of flecainide and placebo with transtelephonic monitoring. Flecainide Supraventricular Tachycardia Study Group.
Van Gelder. Efficacy and safety of flecainide acetate in the maintenance of sinus rhythm after electrical cardioversion of chronic atrial fibrillation or atrial flutter. A comparison between flecainide and sotalol in the prevention of recurrences of paroxysmal atrial fibrillation. Safety of long-term flecainide and propafenone in the management of patients with symptomatic paroxysmal atrial fibrillation: report from the Flecainide and Propafenone Italian Study Investigators.
Maintenance of sinus rhythm after electrical cardioversion of persistent atrial fibrillation; sotalol vs bisoprolol. Short-term versus long-term antiarrhythmic drug treatment after cardioversion of atrial fibrillation Flec-SL : a prospective, randomised, open-label, blinded endpoint assessment trial. Propafenone versus hydroquinidine in long-term pharmacological prophylaxis of atrial fibrillation. Propafenone versus sotalol for suppression of recurrent symptomatic atrial fibrillation. Long-term efficacy and safety of propafenone and sotalol for the maintenance of sinus rhythm after conversion of recurrent symptomatic atrial fibrillation.
Sotalol versus propafenone for long-term maintenance of normal sinus rhythm in patients with recurrent symptomatic atrial fibrillation. Efficacy of propafenone for maintaining sinus rhythm in patients with recent onset or persistent atrial fibrillation after conversion: a randomized, placebo-controlled study. Dronedarone for maintenance of sinus rhythm in atrial fibrillation or flutter. Le Heuzey.
A short-term, randomized, double-blind, parallel-group study to evaluate the efficacy and safety of dronedarone versus amiodarone in patients with persistent atrial fibrillation: the DIONYSOS study. Sotalol versus quinidine for the maintenance of sinus rhythm after direct current conversion of atrial fibrillation. Efficacy and safety of sotalol in digitalized patients with chronic atrial fibrillation. The Sotalol Study Group. Efficacy and safety of sotalol versus quinidine for the maintenance of sinus rhythm after conversion of atrial fibrillation.
The Drug And Pace Health cliNical Evaluation DAPHNE study: a randomized trial comparing sotalol versus beta-blockers to treat symptomatic atrial fibrillation in patients with brady-tachycardia syndrome implanted with an antitachycardia pacemaker. Multicenter study of the efficacy and safety of disopyramide in obstructive hypertrophic cardiomyopathy. Propafenone versus disopyramide for maintenance of sinus rhythm after electrical cardioversion of chronic atrial fibrillation: a randomized, double-blind study. The efficacy of quinidine and disopyramide in the maintenance of sinus rhythm after electroconversion from atrial fibrillation.
A double-blind study comparing quinidine, disopyramide and placebo. Disopyramide in the maintenance of sinus rhythm after electroconversion of atrial fibrillation. A placebo-controlled one-year follow-up study. A practical guide for clinicians who treat patients with amiodarone: Disopyramide a.
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Procainamide a. Quinidine a. Lidocaine a. Propafenone a. Amiodarone a. Verapamil a. Reduced tablet dissolution Reduced solubility for basic drugs Decreased absorption of acid drugs Less drug absorption. Decreased body mass Increased body fat Decreased proportion of body water Decreased plasma albumin.
Increased Vd of lipid soluble drugs Decrease Vd of water-soluble drugs Changed proportion of free drug. Reduced glomerular filtration Reduced renal tubular function Reduced renal blood flow. SAN, AV, or conduction disease. Renal disease Liver disease Asthma. SAN, AV node, or conduction disease. Moderate renal disease Asthma. Concomitant QT prolonging drugs Pre-existing liver disease. SAN, AV node or conduction disease. Flecainide a. Ibutilide a. Sotalol a. Adenosine b. Beta-blockers c. Verapamil d.
Digoxin b. Recurrent, unresponsive to beta-blockers or calcium channel blockers and patients refusing catheter ablation.