Normally, the heartbeat begins at the sinoatrial (SA) node, located in your right atrium. When the SA node fires, electrical activity spreads through the right and left atria, causing them to contract. The impulses travel to the atrioventricular (AV) node, which is the bridge that allows the impulses to go from the atria to the ventricles. The impulse then travels through the walls of the ventricles, causing them to contract. The heart’s regular pattern of electrical impulses causes the heart to fill with blood and contract in a normal fashion.
When you have WPW, along with your normal conduction pathway, you have an extra pathway called an accessory pathway. They are normal heart muscle, not specialized electric tissue, and they may:
The impulses travel through the extra pathway (short cut) as well as the normal AV-HIS Purkinje system. The impulses can travel around the heart very quickly, in a circular pattern, causing the heart to beat unusually fast. This is called re-entry tachycardia.
HistoryRe-entry arrhythmias occur in about 50 percent of people with WPW; some patients may also have atrial fibrillation(a common irregular heart rhythm distinguished by disorganized, rapid, and irregular heart rhythm). Although rare, the greatest concern for people with WPW is the possibility of having atrial fibrillation with a fast ventricular response that worsens to ventricular fibrillation, a life-threatening arrhythmia.
In 1930, Wolff, Parkinson and White described a distinct electrocardiograph (ECG) pattern in healthy young people with short bursts of tachycardia. In 1933, other doctors noted the reason for this irregular rhythm was a faster passage of impulses traveling through the ventricles. In 1944, doctors confirmed the presence of extra pathways.
WPW is a congenital heart abnormality. It is the most common type of ventricular preexcitation (preexcitation: the impulses travel to the ventricle earlier than what you would expect them to if they traveled down the normal pathway through the AV node).
WPW occurs randomly in the general population, occurring in about 1 to 3 per 1,000 persons. In the general population, men have a higher incidence of WPW than women do, and there is a higher incidence of multiple accessory pathways in men.
Some cases of WPW are inherited. Parents who have accessory pathways may pass them on to their children. One paper suggested the incidence of preexcitation in first-degree relatives could be as high as 5.5 per 1,000 persons. About 7 to 20 percent of patients with WPW also have congenital defects within the heart.
People may first experience symptoms at any age, from infancy through adult years.
Symptoms of WPW may include one or more of the following:
Some people have WPW without any symptoms at all.
WPW can only be diagnosed by reviewing an ECG (electrocardiogram), A holter or ambulatory monitor and exercise testing are also helpful in evaluating patients known to have WPW.
In the past, patients with WPW but without symptoms had been observed by a cardiologist for many years. Recently, new guidelines have been published for this group of patients. Your cardiologist may order a holter monitor or stress test to look for a persistent patter of WPW. If the WPW pattern persists, invasive electrophysiology testing is now recommended.
The results of your diagnostic tests and the answers to these questions will help guide your therapy.
Treatment depends on the type and frequency of arrhythmias, associated symptoms such as syncope, and presence of structural heart disease. Patients with symptoms or tachycardias can be treated with medications or with an ablation procedure.
In people with WPW, whose heart rate can not be controlled with medications, ablation can improve symptoms and cure the abnormal arrhythmias. During ablation, either heart (thermal) or cryoenergy (freeze) is delivered through a catheter to “destroy” the abnormal pathways