Image: Classic delta wave in WPW
Pictured: The bundle of Kent is an abnormal extra or accessory conduction pathway between the atria and ventricles. This pathway may communicate between the left atrium and the left ventricle, in which case it is termed a “type A pre-excitation”, or between the right atrium and the right ventricle, in which case it is termed a “type B pre-excitation”.
Wolff–Parkinson–White syndrome (WPW) is a disorder of the conduction system of the heart that is commonly referred to as pre-excitation syndromes. WPW is caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles (the bundle of Kent). Electrical signals traveling down this abnormal pathway (known as the bundle of Kent) may stimulate the ventricles to contract prematurely, resulting in a unique type of supraventricular tachycardia referred to as an atrioventricular reciprocating tachycardia.
Signs and symptoms
People with WPW are usually asymptomatic. However, the individual may experience
- Shortness of breath
- Syncope (fainting or near fainting) during episodes of supraventricular tachycardia. The telltale “delta wave” may sometimes—but not always—be seen on an electrocardiogram.
Transmission of a cardiac action potential through the conduction system of the normal human heart
Electrical activity in the normal human heart is initiated when a cardiac action potential arises in the sinoatrial (SA) node, in the right atrium. From there, the electrical stimulus is transmitted via internodal pathways to the atrioventricular (AV) node. After a brief delay at the AV node, the stimulus is conducted through the bundle of His to the left and right bundle branches and then to the Purkinje fibers and the endocardium at the apex of the heart.
The AV node serves an important function as a “gatekeeper”, limiting the electrical activity that reaches the ventricles. In situations where the atria generate excessively rapid electrical activity (such as atrial fibrillation or atrial flutter), the AV node limits the number of signals conducted to the ventricles. For example, if the atria are electrically activated at 300 beats per minute, half those electrical impulses may be blocked by the AV node, so that the ventricles are stimulated at only 150 beats per minute—resulting in a pulse of 150 beats per minute. Another important property of the AV node is that it slows down individual electrical impulses. This is manifested on the electrocardiogram as the PR interval (the time from electrical activation of the atria to electrical activation of the ventricles), which is usually shortened to less than 120 milliseconds in duration.
Individuals with WPW have an accessory pathway that communicates between the atria and the ventricles, in addition to the AV node. This accessory pathway is known as the bundle of Kent (see below). This accessory pathway does not share the rate-slowing properties of the AV node, and may conduct electrical activity at a significantly higher rate than the AV node. For instance, in the example above, if an individual had an atrial rate of 300 beats per minute, the accessory bundle may conduct all the electrical impulses from the atria to the ventricles, causing the ventricles to contract at 300 beats per minute. Extremely rapid heart rates such as this may result in hemodynamic instability or cardiogenic shock. In some cases, the combination of an accessory pathway and cardiac dysrhythmias can trigger ventricular fibrillation, a leading cause of sudden cardiac death.
One beat from a rhythm strip in V2 demonstrating characteristic findings in Wolff–Parkinson–White syndrome. Note the characteristic delta wave (above the blue bar), the short PR interval (red bar) of 80 ms, and the long QRS complex (blue bar plus green bar) at 120 ms.
WPW is commonly diagnosed on the basis of the electrocardiogram in an asymptomatic individual. In this case it is manifested as a delta wave, which is a slurred upstroke in the QRS complex that is associated with a short PR interval. The short PR interval and slurring of the QRS complex is actually the impulse making it through to the ventricles prematurely (across the accessory pathway) without the usual delay experienced in the AV node.
When an individual is in normal sinus rhythm, the ECG characteristics of WPW are a short PR interval (less than 120 milliseconds in duration), widened QRS complex (greater than 120 milliseconds in duration) with slurred upstroke of the QRS complex, and secondary repolarization changes (reflected in ST segment-T wave changes).
In case of type A pre-excitation (left atrioventricular connections), a positive R wave will be seen in V1 (“positive delta”) on the precordial leads of the electrocardiogram, while in type B pre-excitation (right atrioventricular connections), a predominantly negative delta wave will be seen in lead V1 (“negative delta”)
The definitive treatment of WPW is a destruction of the abnormal electrical pathway by radiofrequency catheter ablation. This procedure is performed by cardiac electrophysiologists. Radiofrequency catheter ablation is not performed in all individuals with WPW because there are inherent risks involved in the procedure. When performed by an experienced electrophysiologist, radiofrequency ablation has a high success rate. Findings from 1994 indicate success rates of as high as 95% in people treated with radiofrequency catheter ablation for WPW.
However, people with WPW who are experiencing tachydysrhythmias may require synchronized electrical cardioversion if they are demonstrating severe signs or symptoms (for example, low blood pressure or lethargy with altered mental status). If they are relatively stable, pharmacologic treatment may be used.
People with atrial fibrillation and rapid ventricular response are often treated with amiodarone or procainamide to stabilize their heart rate. Procainamide, amiodarone, and cardioversion are now accepted treatments for conversion of tachycardia found with WPW.