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Wolff Parkinson White Syndrome (WPW) is considered to be a congenital abnormality that involves the presence of abnormal electrical conductive circuits between the atria and ventricles. The disorder includes accessory electrical pathways that bypass the AV node. This activity reviews the evaluation and treatment of WPW by an interprofessional healthcare team.
Objectives:
- Identify the etiology of Wolff Parkinson White syndrome.Outline the evaluation of Wolff Parkinson White syndrome.Review the management options available for Wolff Parkinson White syndrome.Describe the interprofessional team strategies for improving care coordination and improve patient outcomes in patients with Wolff Parkinson White syndrome.
The normal heart consists of two electrically insulated units, the atria and the ventricles. These units are connected by a conduction system that allows for normal cardiac synchrony and function. The cardiac electrical potential originates from the sinoatrial node of the right atrium and propagates through the atria to the atrioventricular (AV) node. The action potential is delayed in the AV node and is then quickly transmitted through the His-Purkinje system to the ventricular myocytes allowing for rapid ventricular depolarization and synchronized contraction.[1] Patients with WPW syndrome have an accessory pathway that violates the electrical isolation of the atria and ventricles, which can allow electrical impulses to bypass the AV node. In some settings, this pathway can result in the transmission of abnormal electrical impulses leading to malignant tachyarrhythmias. The ECG findings of the WPW pattern are caused by the fusion of ventricular preexcitation through the accessory pathway and normal electrical conduction. Most patients with WPW pattern will never develop arrhythmia and will remain asymptomatic. Some accessory pathways will not manifest the described typical ECG findings, and as a result, some patients can develop a tachyarrhythmia with no prior ECG evidence that the pathway exists. These are referred to as concealed bypass tracts.[2][3][4]
In the early 1900s, Frank Wilson and Alfred Wedd are thought to have first described ECG patterns that would later be recognized as a WPW pattern. In 1930, Louis Wolff, Sir John Parkinson, and Dr. Paul Dudley White published a case series consisting of 11 patients who experienced paroxysmal tachycardia associated with an underlying ECG pattern of sinus rhythm with short PR and bundle branch block/wide QRS. This phenomenon was subsequently named as Wolff-Parkinson-White (WPW) syndrome. The electrocardiographic features of preexcitation were first correlated with anatomic evidence of anomalous conducting tissue or bypass tracts in 1943.[5][6]
WPW pattern arises from the fusion of ventricular preexcitation through the accessory pathway and normal electrical conduction through the AV node. This accessory pathway is thought to arise from chamber myocardium during improper early atrial and ventricular folding in cardiac embryogenesis. As a result, electrically conductive myocardial bundles violate the normal electrical insulation of the atrium and ventricle, forming the accessory pathway.[1][7] This pathway usually has non-decremental or non-delayed conduction, which is in contrast to the properties of the normal AV node. The electrical conducting characteristics of the accessory pathway can vary and depend upon factors such as the speed of conduction, direction of conduction, and refractory period. These characteristics, along with location and number of pathways, will determine how the pathway may be involved in the initiation or transmission of an arrhythmia leading to WPW syndrome.[8][9]
The natural history of asymptomatic WPW patients has been speculated from the available data on symptomatic WPW patients and from those who have been incidentally discovered to have a WPW ECG pattern. In large-scale population-based studies involving pediatric and adult populations, the general prevalence of WPW has been estimated between 1 to 3 per 1000 individuals (0.1 to 0.3 %). Identification of the truly asymptomatic patients with WPW pattern is difficult, as these individuals by definition are those who have no clinical symptoms. A general estimate by experts suggests that about 65% of adolescents and 40% of individuals over 30 years with a WPW pattern on a resting ECG are asymptomatic. The incidence of patients with the WPW pattern progressing to arrhythmia is thought to be around 1% to 2% per year, and WPW syndrome prevalence peaks from age 20 to 24.[10][11][2]
Familial studies have shown a slightly higher incidence of WPW, about 0.55% among first-degree relatives of an index patient with WPW. A familial form of WPW syndrome has been observed with a missense mutation in the PRAKAG2 gene leading to an increase in prevalence to 3.4% in first-degree relatives, and the condition is associated with congenital structural heart disease including Ebstein anomaly and hypertrophic cardiomyopathy.[12][13]
There are two ways in which an accessory pathway can lead to WPW syndrome. The pathway can either initiate and maintain an arrhythmia or allow conduction of an arrhythmia generated elsewhere. The first type occurs when a circuit is formed between the normal conduction system of the heart and the accessory pathway (or two or more accessory pathways), allowing for atrioventricular reentrant tachycardia (AVRT). An incorrectly timed extra electrical impulse can lead to a recurring cycle between the atria, AV node, ventricles, and the accessory pathway. Orthodromic AVRT occurs when conduction progresses from the atria with antegrade conduction through the AV node to the ventricle and retrograde conduction through the accessory pathway. This will usually result in a narrow complex QRS as the His-Purkinje system is used unless aberrant conduction is present. Antidromic AVRT is the opposite with antegrade conduction passing from the atria through the accessory pathway to the ventricle and retrograde conduction back up the AV node and is usually associated with a wide complex QRS.
The other way an accessory pathway can lead to arrhythmia is by allowing conduction of an arrhythmia that is generated elsewhere to propagate to a portion of the heart that would normally be electrically insulated from this arrhythmia. The accessory pathway is typically comprised of myocardial tissue and usually has non-decremental or non-delayed conduction allowing immediate ventricular activation. This non-decremental conduction property predisposes patients with WPW syndrome to sudden cardiac death. This occurs due to rapid ventricular rates in conditions with rapid atrial depolarization, such as atrial fibrillation (AF) or atrial flutter. These fast ventricular rates can degenerate into ventricular fibrillation (VF) and cardiac arrest.[7][14][15][16][17]
Patients with a WPW pattern who have never developed an arrhythmia will be asymptomatic, and therefore, their history and physical exam will be mostly unremarkable. Prior ECG may have diagnosed the pattern, and the patient may be aware of their condition, but some accessory pathway conduction is transient or concealed, which may lead to prior normal or intermittently normal ECGs. Patients with WPW pattern may have a family history of WPW pattern or syndrome.
Patients with WPW pattern who develop a tachyarrhythmia will often experience symptoms associated with the arrhythmia including palpitations, chest pain, dyspnea, dizziness, lightheadedness, presyncope, syncope, collapse, and/or sudden death. The history will be notable for these symptoms, which may be episodic and resolved, or ongoing at presentation if the arrhythmia persists. Physical exam should be focused on the patient's cardiovascular, pulmonary perfusion status, and neurological exam and may be completely normal if the arrhythmia has resolved. A persisting arrhythmia will usually be symptomatic, and vitals signs will be notable for tachycardia. Blood pressure may range from normal or elevated to hypotension depending on the severity of the tachyarrhythmia, comorbidities, and the patient's ability to compensate for the arrhythmia. Respiratory rate will vary based on the patient's level of distress and the ability to maintain perfusing blood pressure. The physical exam will again vary depending on the severity of the arrhythmia. The cardiac exam will demonstrate a regular or irregular tachycardia. The remainder of the physical exam may be normal or show signs of discomfort, distress, hypoperfusion, cardiogenic shock, and unresponsiveness depending on the severity of the arrhythmia.[16][14][18][19]
WPW pattern is a constellation of electrocardiographic findings, so initial evaluation relies on a surface electrocardiogram. The ECG will show a short PR interval (120 ms), and a QRS morphology consisting of a slurred delta wave. The preexcitation of the ventricle causes this morphology through the accessory pathway that forms a fusion complex with the normal QRS complex arising from normal cardiac conduction. The absence of this pattern does not rule out the presence of an accessory pathway since some pathways are only capable of conducting impulses under certain conditions or in a retrograde direction. Such a pathway could only conduct from the ventricle to the atrium and would not cause ventricular preexcitation during normal sinus beats. This concealed accessory pathway will only be evident on ECG during an electrical impulse generated in the ventricle, such as a premature ventricular contraction or ventricular pacing.
Recommendations for further evaluation, risk stratification, electrophysiologic study, and accessory pathway ablation for asymptomatic patients with WPW pattern vary depending on age, risk factors, history of symptoms, comorbidities, baseline ECG pattern, as well as a personal and expert opinion. In general, young, healthy patients without comorbid conditions or significant risk factors who have the WPW pattern on ECG but are asymptomatic and without a history of suspected tachyarrhythmia are likely safe for watchful waiting with primary care and or cardiology follow up. Patients who are at higher risk for arrhythmia should be referred for close cardiology follow up for the discussion of risk stratification testing and/or electrophysiologic study with accessory pathway mapping and possible ablation.[15][8][16] It is also important to note that since the WPW pattern changes the baseline morphology of the ECG, the diagnosis of conditions that rely on ECG criteria may be altered in patients with the WPW pattern. Further testing, an adaptation of ECG diagnostic criteria, or expert consultation may be needed in these cases.[20]
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