Medical Care: Treatment of arrhythmia is directed at the underlying cause and the triggers that perpetuate the arrhythmia. The underlying cause includes primary arrhythmias due to an EP abnormality resulting from definable structural heart disease and occurring independently of hemodynamic or metabolic disturbance. Such arrhythmias include coronary heart disease, ischemia, cardiomyopathy, pericarditis, and WPW syndrome. The triggers that perpetuate the arrhythmia include secondary arrhythmias, such as electrolyte imbalance, metabolic defects, and hemodynamic and hypoxemic abnormalities.
Appropriate treatment of WPW syndrome is based on its likely prognosis. Patients with only ECG evidence of preexcitation, without documented episodes of tachyarrhythmias, generally do not require either aggressive workup through EP studies or treatment with antiarrhythmic agents.
The 3 main treatment modalities for WPW syndrome are drug therapy, electrical (ie, RF) ablation, and surgical ablation. Ablation is the first-line treatment for symptomatic WPW syndrome. It has replaced surgical treatment and most drug treatment. However, drug therapy can be useful in some instances, such as in patients who refuse ablation or in patients in whom ablation fails in one or two attempts. For patients treated longitudinally with pharmacotherapy, consideration should be given to a membrane-active antiarrhythmic drug (class IC or III) with an AV nodal blocker, rather than just an AV nodal blocker, because of the potential for extremely rapid rates during preexcited atrial fibrillation or flutter
" Drug therapy (potential antiarrhythmic mechanisms): Antiarrhythmic drugs act on the AV node (ie, AV node blocking agents), myocardial tissue, and/or the accessory pathways. They work by increasing the refractory period or by prolonging the conduction time to prevent perpetuation of an AV reciprocating tachycardia. They may also act to reduce the ventricular response to atrial flutter or atrial fibrillation.
o AV node blocking drugs
" Adenosine, verapamil, metoprolol, and digitalis all prolong conduction time and refractoriness in the AV node.
" Verapamil and metoprolol do not affect conduction in the bypass tract.
" Digitalis exhibits variable effects and may even shorten the refractory period.
" None of these drugs should be given in an acute phase to a patient with ventricular preexcitation who has atrial fibrillation.
" Digoxin is contraindicated in patients with WPW syndrome, although it may play some role in children only. Most deaths from WPW syndrome have been associated with digoxin use.
" Propranolol is almost never administered. Metoprolol or atenolol can be useful in some patients.
o Agents affecting the accessory pathways
" Class IA drugs (eg, procainamide) and class IC drugs (eg, flecainide, propafenone) block conduction in the accessory pathway.
" Amiodarone and sotalol influence both the AV node and the bypass tract. They work in similar fashion but affect only the bypass tract.
" Class IA and IC drugs that prolong the refractory period in the bypass tract are indicated if drug therapy becomes necessary.
" Class IC and IA drugs are best used in conjunction with an AV node blocker, such as metoprolol or verapamil.
" Procainamide and quinidine are relics of the past for long-term treatment.
o Caution when treating WPW syndrome tachycardia
" Digitalis shortens refractoriness in the myocardium and in the bypass tract. Thus, it may accelerate the ventricular response in the setting of atrial fibrillation in a patient with WPW syndrome. Adenosine should not be used in this setting.
" Digitalis should not be used in such patients, except perhaps in pediatric or elderly patients. Instead, medicines that prolong the refractory period in the accessory pathway (eg, class IA and IC agents) should be used.
" Intravenous verapamil can likewise speed up the ventricular response in patients with WPW syndrome who have atrial fibrillation. This does not appear to happen with oral verapamil. Verapamil is not recommended as a sole agent in patients with WPW syndrome.
" Termination of an acute episode
o Narrow-complex AV reentrant tachycardia
" Such tachycardias manifest with normal QRS complexes, a ventricular rate of more than 200 beats per minute, regular R-R intervals, and a retrograde P wave well beyond the end of QRS.
" They should be treated in the same way as AVNRT, by blocking AV node conduction with (1) vagal maneuvers (eg, Valsalva maneuver, carotid sinus massage, splashing cold water or ice water on the face), (2) intravenous adenosine, or (3) intravenous verapamil or diltiazem (ie, if recurrent SVT is present, if adenosine is ineffective, or if the patient is taking theophylline).
" Note that atrial fibrillation can occur after drug administration, particularly adenosine, with a rapid ventricular response. An external cardioverter-defibrillator should be immediately available in case it is necessary.
o Atrial flutter/fibrillation or wide-complex tachycardia
" Atrial flutter/fibrillation can be recognized by the presence of abnormal QRS complexes and irregular R-R intervals. In this setting, drugs that prolong the refractory period of the bypass tract should be used, especially those that also block the AV node (by prolonging refractoriness). Examples of such drugs include procainamide (class IA agent) and propranolol (class II beta-blocker).
" If wide-complex tachycardia is present and the diagnosis of ventricular tachycardia cannot be excluded, the drugs of choice are intravenous procainamide or amiodarone (in lieu of cardioversion if the patient is stable hemodynamically). Ibutilide may also be useful in this setting, although data are lacking.
" Importantly, avoid lidocaine in this setting. It does not prolong refractoriness in the accessory pathway. Lidocaine may increase the ventricular response if atrial fibrillation is present.
o Hemodynamically unstable tachycardia and electrical cardioversion
" In patients with a very fast ventricular rate, hemodynamic instability (eg, hypotension, mental status change) may ensue.
" The initial treatment of choice in such patients is direct-current synchronized electrical cardioversion.
" Electrical cardioversion appears to terminate most effectively the tachycardias due to reentry, such as AVNRT and reciprocating tachycardias associated with WPW syndrome.
" The electrical shock depolarizes all excitable myocardium, lengthens refractoriness, interrupts reentrant circuits, discharges foci, and establishes electrical homogeneity that terminates reentry.
" Because myocardial damage may occur with increases in applied energy, the minimum effective energy should be used and the energy should be titrated. An energy of at least 100 joules (monophasic or lower biphasic) successfully terminates most SVTs and should be tried initially. If that fails, a second shock with higher energy can be delivered.
" Cardioversion can have several adverse effects. It may induce arrhythmias because of inadequate synchronization, with the shock occurring during the ST segment or T wave. Rarely, even a properly synchronized shock can produce ventricular fibrillation. Postcardioversion arrhythmias are generally transient and do not require treatment. Embolic episodes may occur in 1-3% of the patients converted from atrial fibrillation to sinus rhythm if the episodes are longer than 48 hours.
" Long-term maintenance treatment
o Response to long-term antiarrhythmic therapy for the prevention of further episodes of tachycardia in patients with WPW syndrome remains quite variable and unpredictable. Some drugs may paradoxically make the reciprocating tachycardia more frequent. Dual-drug therapy has been used, eg, procainamide and verapamil (class IA and IV), or quinidine and propranolol (class IA and II). Good reasons exist to avoid quinidine and procainamide; newer drugs that are safer and better are available. Class IC drugs (eg, amiodarone, sotalol) are good choices, but class IC drugs should not be given if the patient has structural heart disease. Class IC drugs are typically used with an AV nodal blocking agent.
o The best plan is to not use drugs at all; instead, refer all patients who have symptomatic WPW syndrome for ablation because this cures the tachycardia and eliminates the potential dangerous effects of drugs.
o Patients who have accessory pathways with short refractory periods are poor candidates for medical therapy and are best treated with ablation.
Surgical Care: Ablative procedures are the therapy of choice. Electrode catheters can be advanced intravenously to locate and ablate the accessory tract by delivering electrical or RF energy. Cryothermy, lasers, direct current, and microwave energy sources have also been used in the past, but RF catheter ablation has replaced these modalities because it is much more efficacious, safe, and cost-effective.
" RF ablation is currently the treatment of choice for most adults and many children with symptomatic WPW syndrome (ie, those who have AV reentrant tachycardia or atrial flutter/fibrillation with conduction of the accessory pathway). Success rates for catheter ablation exceed 90%.
o Localization of the bypass tract(s)
" First, perform an EP study to (1) determine that the bypass tract is part of the tachycardia reentrant circuit, and (2) locate the optimal site for ablation. Pathways can be located in the left or right free wall or septum of the heart. Multiple pathways may be present in approximately 5% of patients.
" Pathways at all the sites in the heart and in persons of all age groups can be ablated successfully. The RF ablation creates conduction block that can be seen on intracardiac electrogram findings (ie, during the EP study) between the atrial activation and the bypass tract potential.
o Identification of the ablation site during EP studies
" During the EP studies, direct recordings of the accessory pathway indicate the optimal site for ablation.
" The ventricular insertion site is indicated by the earliest onset of the ventricular electrogram in relation to the delta wave.
" The atrial insertion site is indicated by the region of the shortest VA interval during orthodromic tachycardia (ie, AV reentrant tachycardia) or ventricular pacing.
" Successful ablation sites show stable fluoroscopic and electrical features. During orthodromic AV reentrant tachycardia, the time between the ventricular and atrial potentials is short and a pathway potential may be observed.
" Generally, a thermistor-tipped catheter is used, which shows a stable rise in catheter tip temperature, suggesting catheter stability and optimal catheter-tissue contact. The tip temperature generally rises above 50Β°C.
o Indications for RF ablation
" Patients with symptomatic AV reentrant tachycardia should receive RF ablation.
" Atrial fibrillation or other atrial tachyarrhythmias that have rapid ventricular response via a bypass tract is an indication for RF ablation procedures.
" Patients with AV reentrant tachycardia or atrial fibrillation with rapid ventricular rates found incidentally during EP studies for unrelated arrhythmia should undergo RF ablation.
" Asymptomatic patients with ventricular preexcitation whose livelihood, profession, insurability, or mental well-being may be influenced by unpredictable tachyarrhythmias or in whom such tachyarrhythmias would endanger the public safety should have an RF ablation procedure.
" Patients with atrial fibrillation and a controlled ventricular response via the bypass tract are candidates for RF ablation.
" Patients with a family history of sudden cardiac death should undergo RF ablation.
o Effectiveness of RF ablation: A survey by the North American Society for Pacing and Electrophysiology (NASPE) indicates that ablation is successful. Results are as follows:
" For left free wall accessory pathways, 2312 of 2527 patients (91%) were cured.
" For septal accessory pathways, 1115 of 1279 patients (87%) were cured.
" For right free wall accessory pathways, 585 of 715 patients (82%) were cured.
o Complications of RF ablation
" In the United States, complications have been reported in 94 of 4521 patients (2.1%). Of the 4521 patients, 13 died (0.2%).
" In Europe, the complication rate is reported to be 4.4%. Of 2222 patients, 3 died.
" Surgical ablation
o Surgical open heart procedures were more common before RF ablation was developed.
o Now, RF catheter ablation has virtually eliminated surgical open heart treatments in the vast majority of patients, with the following exceptions:
" Patients in whom RF catheter ablation (with repeated attempts) fails
" Patients undergoing concomitant cardiac surgery (possible exception)
" Patients with other tachycardias with multiple foci who require surgical intervention (very rare)
Diet:
" The majority of patients presenting with WPW syndrome are not elderly.
" Patients presenting with structural heart disease, cardiomyopathy, or heart failure may require a low-salt, low-cholesterol diet.
Activity: Generally, no activity restrictions are recommended in patients with ECG findings of preexcitation but without tachycardias. They should be restricted from high-risk professions (eg, airline pilot) and may be restricted from competitive sports.
" Patients presenting with tachycardias and accessory pathways should avoid participating in competitive sports because catecholamines can decrease the refractoriness of the bypass tract and facilitate tachyarrhythmias.
" Patients with hypertrophic cardiomyopathy or the Ebstein anomaly should also abstain from competitive sports.
" Once a curative procedure (eg, RF ablation of the accessory pathway) has been successfully performed, most patients can return to competitive sports several months later.
DRUG THERAPY :
1. ANTIARRHYTHMICS :
- ADENOSINE
- PROPRANOLOL
-VERAPAMIL
- DIGOXIN : - NOT DESIRABLE DRUG BECAUSE IF ATRIAL FIBRILLATION OCCURS, THERE MAY BE RAPID CONDUCTION OVER THE ACCESSORY PATHWAY AND INDUCTION OF VENTRICULAR FIBRILLATION.
- PROCAINAMIDE
- QUINIDINE
- AMIODARONE
- SOTALOL
- DILTIAZEM
- IBUTILIDE
- DOFETILIDE
- FLECAINIDE
- PROPAFENONE