Wolf Parkinson White Syndrome Causes Symptoms and Treatment

An electrical impulse causes the ventricles to contract and expel blood. In the heart of a healthy person, it enters the ventricles through the pathways from the right atrium. Between the ventricles is a cluster of cells called the atrioventricular node. In this node, the impulse is delayed, allowing the ventricles to fill with blood.

WPW syndrome is the second name for Wolf-Parkinson-White syndrome. This disease develops in utero and is characterized by the formation of additional muscle fibers or the so-called Kent bundle in the fetal heart.

That is, with this disease, the impulse does not linger in the atrioventricular node, but through additional muscle fibers or the Kent bundle enters immediately into the ventricles, causing them to contract (be excited) prematurely. As a result, the ventricles cannot be fully filled with blood.

Of all cardiac pathologies, this disease accounts for only 0,15-2%. In this case, it occurs most often in men. In young children, the disease is detected very rarely. Most often, the first signs begin to appear at the age of 10 to 20 years. In adulthood, the disease manifests itself quite rarely, which is caused by a deterioration in the conductivity of the additional pathway, leading to the disappearance of the symptoms of the disease.

The greatest danger of WPW syndrome is that it provokes various cardiac arrhythmias, which in severe cases threaten the patient’s life. In half the cases, the disease is accompanied by the following pathological conditions:

  • reciprocal arrhythmias;
  • flutter and atrial fibrillation.

This disease, as a rule, is independent. However, in some cases, the development of WPW syndrome may occur against the background of other diseases. These include:

  • hypertrophic cardiomyopathy;
  • Ebstein anomaly;
  • mitral valve prolapse.

145.6. Premature Arousal Syndrome.

Wolff-Parkinson-White Syndrome (WPW syndrome) is a syndrome of premature ventricular excitation caused by impulses along additional abnormal conductive bundles connecting the atria and ventricles. The prevalence of WPW syndrome, according to cardiology, is 0,15-2%. WPW syndrome is more common among men;

in most cases, manifests at a young age (10-20 years), less often in older people. The clinical significance of WPW syndrome is that if it is present, severe heart rhythm disturbances often develop that pose a threat to the patient’s life and require special treatment approaches.

Causes

According to most authors, WPW syndrome is due to the preservation of additional atrioventricular compounds as a result of incomplete cardiogenesis. In this case, incomplete regression of muscle fibers occurs at the stage of formation of fibrous rings of the tricuspid and mitral valves.

Normally, additional muscle pathways connecting the atria and ventricles exist in all embryos in the early stages of development, but gradually they become thinner, contract and completely disappear after the 20th week of development. If the formation of fibrous atrioventricular rings is impaired, muscle fibers are preserved and constitute the anatomical basis of WPW syndrome. Despite the innate nature of the additional AV compounds, WPW syndrome can first manifest itself at any age. In the familial form of WPW syndrome, multiple supplementary atrioventricular connections are more likely to occur.

In 30% of cases, WPW syndrome is combined with congenital heart defects (Ebstein’s anomaly, mitral valve prolapse, atrial and interventricular septal defects, Fallot’s tetrad), dysembryogenetic stigma (connective tissue dysplasia), hereditary hypertrophic cardiomyopathy.

WPW syndrome develops due to genetic disorders of the Kent bundle. In fact, this is the only reason leading to the onset of the disease. Various factors can provoke a violation of the heart rhythm, including the following:

  • taking certain medications;
  • physical overstrain;
  • high consumption of caffeine, alcohol, tobacco;
  • stress, emotional exhaustion.

Since the syndrome of ERW is a congenital pathology, this disease is detected in children, starting from the first days of life. According to experts, this ailment tends to be inherited.

The Kent bundle is an additional muscle pathway that forms in the embryo in the early stages of development. Normally, they disappear by the 20th week of pregnancy. However, in some cases, the structural structure of the heart is violated, which leads to the preservation of additional muscle pathways, and subsequently to the development of the child’s ERW syndrome.

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It should be noted that in addition to WPW syndrome, there is a WPW phenomenon. These two states differ from each other in that the symptoms of the disease, which are most often expressed in attacks of tachycardia, are disturbed by the patient’s ERW syndrome. With the phenomenon of ERW, there are no such manifestations. However, when conducting an ECG, it can be found that electrical impulses are conducted along additional paths, and the ventricles are excited prematurely.

Classification of the disease

Depending on the structure of the detours, two types of disease are distinguished:

  • with additional muscle fibers;
  • with specialized muscle fibers (Kent bundle).

Depending on the clinical manifestations, the following forms of ERW syndrome are distinguished:

  • manifest;
  • intermittent or transient WPW syndrome;
  • transient or hidden.

The manifest form is characterized by the presence of a delta wave on the ECG, as well as sinus rhythm and episodes of supraventricular tachycardia.

Intermittent WPW syndrome is characterized by periodic premature excitation of the ventricles, as well as the presence of sinus rhythm and confirmed supraventricular tachycardia.

A feature of hidden WPW syndrome is that it is impossible to see signs of the disease on the ECG. However, this pathology is characterized by retrograde conduction of impulses along additional muscle fibers, and a person is periodically disturbed by manifestations of the disease in the form of supraventricular tachycardia.

Several species may have WPW syndrome. Treatment, however, depends on the particular species. Depending on the symptoms, the features of the Kent beam work out syndromes:

    Manifesting – it is diagnosed if, along with overexcitation of the ventricles, tachyarrhythmia, arrhythmia, atrioventricular reciprocal (by the type of re-entri) tachycardia or AVRT is manifested.

Separately, the phenomenon (and not the syndrome) of WPW is highlighted. Its peculiarity lies in the fact that during the examination the patient has a delta wave, but there is no arrhythmia. About two-thirds of people with this phenomenon begin to complain of symptoms after 40 years.

On the recommendation of WHO, distinguish between the phenomenon and syndrome of WPW. The WPW phenomenon is characterized by electrocardiographic signs of impulse conduction through additional connections and ventricular pre-excitation, but without the clinical manifestations of AV reciprocal tachycardia (re-entry). WPW syndrome refers to a combination of ventricular pre-excitation with symptomatic tachycardia.

Given the morphological substrate, several anatomical variants of WPW syndrome are distinguished.

I. With additional muscle AV fibers:

  • going through additional left or right parietal AV connection
  • going through the aortic-mitral fibrous connection
  • coming from the ear of the right or left atrium
  • associated with aneurysm of the Valsalva sinus or middle heart vein
  • septal, paraseptal upper or lower
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II. With specialized muscle AV fibers (“Kent bundles”) originating from a vestigial tissue similar to the structure of the atrioventricular node:

  • atrio-fascicular – entering the right leg of the bundle of His
  • entering the myocardium of the right ventricle.

There are several clinical forms of WPW syndrome:

  • a) manifesting – with a constant presence of a delta wave, sinus rhythm and episodes of atrioventricular reciprocal tachycardia.
  • b) intermittent – with transient pre-excitation of the ventricles, sinus rhythm and verified atrioventricular reciprocal tachycardia.
  • c) covert – with retrograde conduction through an additional atrioventricular connection. Electrocardiographic signs of WPW syndrome are not detected, there are episodes of atrioventricular reciprocal tachycardia.

Symptoms of WPW Syndrome

Although WPW syndrome is congenital, and therefore, it can be recognized even in the hospital, the first symptoms appear in adolescence. A sudden attack of frequent palpitations is the main symptom of the disease. This condition can last from a few seconds to several hours. Attacks can occur daily, or maybe only 2 times a year. With the onset of tachycardia, the patient feels:

  • strong and fast heartbeats;
  • dizziness;
  • fainting condition;
  • fatigue during any physical exertion (even when walking).

WPW syndrome is extremely rarely combined with structural pathologies of the heart, but if this happens, then the symptoms become even more severe and pronounced. Shortness of breath and chest pain appear. Sudden death is possible.

The clinical manifestation of WPW syndrome occurs at any age, before which its course may be asymptomatic. WPW syndrome is accompanied by various cardiac arrhythmias: reciprocal supraventricular tachycardia (80%), atrial fibrillation (15-30%), atrial flutter (5%) with a frequency of 280-320 beats. in minutes Sometimes with WPW syndrome, less specific arrhythmias develop – atrial and ventricular extrasystoles, ventricular tachycardia.

Arrhythmias can occur under the influence of emotional or physical stress, alcohol abuse or spontaneously, for no apparent reason. During an arrhythmic attack, there are sensations of a heartbeat and a sinking heart, cardialgia, a feeling of lack of air. Atrial fibrillation and flutter is accompanied by dizziness, fainting, shortness of breath, arterial hypotension; upon transition to ventricular fibrillation, sudden cardiac death may occur.

Paroxysms of arrhythmias in WPW syndrome can last from a few seconds to several hours; sometimes they stop on their own or after performing reflex receptions. Long paroxysms require hospitalization of the patient and the intervention of a cardiologist.

Pathogenesis of WPW Syndrome

WPW syndrome is caused by the spread of excitement from the atria to the ventricles through additional abnormal routes. As a result of this, the excitation of part or all of the ventricular myocardium occurs earlier than during the propagation of the impulse in the usual way – along the AV node, bundle and branches of His. The ventricular preexcitation is reflected on the electrocardiogram in the form of an additional wave of depolarization – a delta wave. The PQ (R) interval is shortened, and the duration of the QRS is increased.

When the main wave of depolarization arrives in the ventricles, their collision in the heart muscle is recorded in the form of the so-called QRS confluent complex, which becomes somewhat deformed and broadened. The atypical ventricular excitation is accompanied by a violation of the sequence of repolarization processes, which finds expression on the ECG in the form of displacement of the RS-T segment and change in polarity of the T wave discordant to the QRS complex.

The occurrence of paroxysms of supraventricular tachycardia, atrial fibrillation and flutter in WPW syndrome is associated with the formation of a circular excitation wave (re-entry). In this case, the impulse along the AB node moves in the anterograde direction (from the atria to the ventricles), and along the additional paths – in the retrograde direction (from the ventricles to the atria).

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Seizure treatment

When an attack occurs, vagal tests are often used. As first aid you need:

  • apply ice to the patient’s face or sprinkle cold water on it;
  • cause a gag or cough reflex;
  • massage the carot >

The effectiveness of such techniques is 50%. Among the drugs that help relieve the attack, procainamide, propafenone are isolated. True, they need to be administered intravenously. Adenosine is less commonly used. In hospital conditions, an external electric cardioversion is performed, which provides for the supply of a strong electric pulse using a defibrillator. The patient is under anesthesia.

Prediction and prevention of WPW syndrome

In patients with asymptomatic course of WPW syndrome, the prognosis is favorable. Treatment and observation is only required for persons with a family history of sudden death and professional indications (athletes, pilots, etc.). In the presence of complaints or life-threatening arrhythmias, a full range of diagnostic tests is necessary to select the optimal treatment method.

Patients with WPW syndrome (including those who underwent RFA) need to be monitored by a cardiologist-arrhythmologist and cardiac surgeon. Prevention of WPW syndrome is secondary and consists of antiarrhythmic therapy to prevent recurring episodes of arrhythmias.

Surgical treatment method

Surgical intervention is used when drug treatment no longer helps, and WPW syndrome can lead to sudden death. The operation in this case can be effective. The most popular in cardiology and surgery today is radiofrequency ablation. The procedure is quite unpleasant, but extremely important.

As mentioned above, in men, WPW syndrome is more common. Do they take in the army with this diagnosis? Of course, it is definitely impossible to answer, because the draft board takes into account various aspects, in particular, the type of disease, its duration, the presence of symptoms, success in treatment. After the operation, the probability of recovery is almost 100%.

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Svetlana Borszavich

General practitioner, cardiologist, with active work in therapy, gastroenterology, cardiology, rheumatology, immunology with allergology.
Fluent in general clinical methods for the diagnosis and treatment of heart disease, as well as electrocardiography, echocardiography, monitoring of cholera on an ECG and daily monitoring of blood pressure.
The treatment complex developed by the author significantly helps with cerebrovascular injuries and metabolic disorders in the brain and vascular diseases: hypertension and complications caused by diabetes.
The author is a member of the European Society of Therapists, a regular participant in scientific conferences and congresses in the field of cardiology and general medicine. She has repeatedly participated in a research program at a private university in Japan in the field of reconstructive medicine.

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