The Second Edition of this valuable reference responds to changes in the available medications as well as in the way they are currently used. About the Author Richard N.
Table of contents Preface. Part 1 Basic Principles. Chapter 1 Mechanisms of Cardiac Tachyarrhythmias. Chapter 2 Introduction to Antiarrhythmic Drugs. Part 2 Clinical Features of Antiarrhythmic Drugs. Chapter 3 Class I Antiarrhythmic Drugs. Heart failure and sudden death Cha, Y-M. Sudden Death. Heart Diseases. Heart failure and Sudden death Cha, Y-M. Springer-Verlag London Ltd , Vol. Sudden Cardiac Death. Ventricular Tachycardia. Myocardial Infarction. Senescence and arrhythmogenesis Mirza, M.
Cardiovascular Diseases. Practice Guidelines. Elsevier Inc.
Diastolic Heart Failure. Springer London , p. Invasive electrophysiologic testing: Role in sudden death prediction Nemec, J. The same principles apply to management of patients with NSVT. Patients with frequent idiopathic runs of NSVT should be evaluated for the inherited cardiac conditions predisposing to sudden death.
In those without significant heart disease, NSVT may respond to beta-blockers or calcium antagonists; however, if AAD therapy is required the choice of the drugs is limited to amiodarone and less preferable sotalol. The latter is suitable for symptomatic patients with moderate structural heart disease 51 including coronary artery disease, preferably in patients with ICD 7 because of the proarrhythmic risk of sotalol.
Class IC agents may be used in patients without myocardial infarction or evidence of ischaemia and without other significant myocardial structural diseases.
AAD, antiarrhythmic drugs; VT, ventricular tachycardia. Atrial premature beats APBs and non-sustained atrial tachycardia NSAT are a common finding in older individuals and frequent APBs are considered a marker of atrial electrical vulnerability and predictors of incident AF. The efficacy of sotalol, flecainide, and propafenone has been demonstrated for suppression of sustained atrial tachycardia and can be extrapolated to frequent APBs and NSAT. Amiodarone and beta-blockers are the preferred option in the presence of left ventricular systolic dysfunction if AAD treatment is indicated.
When frequent APBs and NSAT occur in the presence of structural heart disease, optimization of medical therapy for the underlying condition may reduce the arrhythmia burden and deter the development of arrhythmia-induced cardiomyopathy. Supraventricular tachyarrhythmias SVT represent a spectrum of tachycardias with a mechanism that involves tissue from the His bundle or above. Although formally AF and atrial flutter are also from supraventricular origin, they are presented separately. Echocardiographic or other image explorations e.
Exercise testing might be useful for detection of arrhythmias related to exertion. Ambulatory Holter, wearable event monitoring and hand-held ECG event-recorders are advisable for patients complaining of frequent transient not documented tachyarrhythmias. Implantable loop recorders are helpful for those patients with rare and severe symptoms e. Thereafter, the best strategy for the person can be decided based on the confirmed individual characteristics.
Figure 4 shows the algorithm for evaluation of patients presenting with palpitations. The correct diagnostic of arrhythmia, including differential diagnostic of narrow and wide QRS tachycardia, is crucial for appropriate treatment and is presented elsewhere. Table 9 Drugs recommended for acute management of haemodynamically stable and regular tachycardia.
- Table of Contents.
- Energy Recovery!
- Antiarrhythmic agent - Wikipedia.
- Business Systems and Organizational Capabilities: The Institutional Structuring of Competitive Competences.
- Handbook of Pediatric Cardiovascular Drugs.
- Self-ligating Brackets in Orthodontics: Current Concepts and Techniques.
All drugs should be administered intravenously. Adenosine should be used with caution in patients with severe coronary artery disease because it may cause vasodilatation of normal coronary arteries causing ischaemia in stenotic territories. It should only be used with full CPR equipment available. Beta-blockers may be used as first-line therapy for catecholamine-sensitive tachycardia e. Therapies recommended for long-term treatment of patients with atrioventricular nodal re-entrant tachycardia.
Contraindicated for patients with coronary artery disease, left ventricular dysfunction, or other significant heart disease. Evaluation of patients presenting with palpitations. Acute management of haemodynamically stable and regular tachycardia. Reproduced from reference. The sinus node may be involved in several arrhythmias. The sinus node re-entry tachycardia may respond to vagal manoeuvres, adenosine, beta-blockers, non-dihydropyridine calcium-channel blockers, amiodarone, and digoxin. In very rare cases, catheter ablation may be required.
Supplementary material online, Table S5 strategies for management of patients with inappropriate sinus tachycardia and postural orthostatic tachycardia syndrome. Adenosine should be used with caution because it may provoke AF with a rapid ventricular response in the presence of pre-excitation, and it can also induce or worsen myocardial ischaemia due to the vasodilator-induced coronary steal phenomenon in the presence of severe coronary stenosis. Importantly, drugs that mainly slow the conduction through the AV node e.
Class IC AADs flecainide, propafenone are contraindicated in the presence of structural heart disease especially after myocardial infarction. Furthermore, Class III drugs are discouraged for the treatment of SVT although they might be effective because of their toxicity and the potential of proarrhythmias e. However, for the latter, amiodarone may be used if other AADs are ineffective. Therapies recommended for long-term treatment of patients with atrioventricular re-entrant tachycardia. Supplementary material online, Table S6 presents the therapeutic options for focal and non-paroxysmal junctional tachycardia, and Table 12 shows recommendations for the treatment of patients with focal AT.
Focal AT may be induced by digitalis excess usually with AV block and exacerbated by hypokalaemia. It may rarely be terminated by vagal manoeuvres but is adenosine-sensitive. In patients with automatic AT, pacing, adenosine, and electrical cardioversion seldom terminate the arrhythmia, unless the mechanism is micro-re-entry or triggered automaticity. Multifocal atrial tachycardia is usually associated to severe pulmonary disease and often requires treatment with calcium-channel blockers without any definitive role for other antiarrhythmic drugs, DC cardioversion or ablation.
Table 12 Recommendations for treatment of focal atrial tachycardias. All drugs for acute treatment are to be given intravenously. Excluded are patients with multifocal atrial tachycardia in whom beta-blockers and sotalol are often contraindicated due to severe pulmonary disease. Current evidence suggests that rhythm control has no morbidity or mortality benefit compared with ventricular rate control in elderly AF patients with established cardiac co-morbidity and moderately symptomatic AF.enter site
Cardiac Rhythm Device Reading List
Severely haemodynamically compromised AF patients i. In haemodynamically stable AF patients, elective cardioversion either electrical or pharmacological is performed to improve symptoms, and the choice of cardioversion mode should be based on the clinical setting. Intravenous flecainide and propafenone are restricted to patients without altered cardiac substrate. Ibutilide is an alternative to intravenous flecainide and propafenone; however, it is torsadogenic and should be avoided in patients with long QT and the QTc interval should be carefully monitored during and immediately after the infusion.
Table 13 Antiarrhythmic drugs currently used for cardioversion of atrial fibrillation. The use of dofetilide for AF cardioversion is recommended by the US guidelines, but not by the Canadian AF guidelines, and the drug is not available in Europe. AV, atrioventricular; HF, heart failure; i. Rarely used for cardioversion of AF not indicated in reference 8. Pharmacological restoration and maintenance of sinus rhythm in AF patients.
Colour code: yellow indicates minimal structural heart disease; violet indicates significant structural heart disease including moderate HFrEF and HFpEF ; grey indicates significant heart failure rEF and significant aortic stenosis. Acute pharmacological AF cardioversion is generally performed in the hospital setting and requires continuous medical supervision and ECG monitoring during the drug infusion and afterwards for at least half of the drug half-life.
Most AADs are given intravenously, with the exception of flecainide and propafenone which could be administered orally with similar efficacy Table Oral bolus of flecainide or propafenone can also be self-administered by selected outpatients with infrequent symptomatic paroxysmal AF, provided that their safety has been previously established in the hospital setting.
Typical atrial flutter is best treated by catheter ablation, which is comparably safe and more effective than AAD. Flecainide and propafenone may slow the flutter cycle thus facilitating AV conduction with increased ventricular rates. Ibutilide is more effective in conversion of flutter than AF, whereas vernakalant is ineffective for typical atrial flutter. However, quinidine and disopyramide [OR 2. AV, atrioventricular; b. Caution is needed when using any AAD in patients with conduction system disease e.
Amiodarone is more effective in rhythm control than other AADs, but extracardiac adverse effects may limit its long-term use. 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.
Hinari - Найти материалы по категории тем
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. 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.