Wolff parkinson white phenomenon in children treatment. How does WPW syndrome manifest?

Wolff-Parkinson-White syndrome (WPW) is rare, but because of the multifaceted picture, it is considered "tricky" for ECG diagnostics.

The ECG picture of the Wolff-Parkinson-White (WPW) syndrome is characterized by a shortening of the PQ interval (less than 0.12 s), a widening and deformation of the QRS complex, the configuration of which resembles a blockade of the PG stem, the presence of a delta wave, and impaired excitability.

In WPW syndrome, the excitation of the heart occurs in two ways. First, the myocardium of one ventricle is excited partially and ahead of time through an additional pathway, then the excitation is carried out in the normal way through the AV node.

Wolff-Parkinson-White (WPW) syndrome is often seen in young men. For him, attacks of paroxysmal tachycardia (AV nodal tachycardia) are typical.

Wolff-Parkinson-White Syndrome(WPW) is named after the authors who first described it in 1930 (Wolf, Parkinson and White). The frequency of occurrence of this syndrome is small and ranges from 1.6-3.3%o, although among patients with paroxysmal tachycardia, it accounts for 5 to 25% of cases of tachycardia.

Importance diagnosis of Wolff-Parkinson-White syndrome(WPW) is due to the fact that in its ECG manifestations it resembles many other heart diseases and an error in diagnosis is fraught with serious consequences. Therefore, WPW syndrome is considered a "tricky" disease.

Pathophysiology of Wolff-Parkinson-White Syndrome (WPW)

With (WPW), myocardial excitation occurs in two ways. In most cases, the cause of the syndrome is a congenital accessory bundle, namely the accessory muscle bundle, or Kent's bundle, which serves as a short path for the spread of excitation from the atria to the ventricles. This can be represented as follows.

Excitation arises, as usual, in the sinus node, but spreads along an additional conducting path, i.e. the Kent bundle mentioned above, reaching the ventricle faster and earlier than with the usual spread of excitation. The result is premature excitation of part of the ventricle (pre-excitation).

This is followed by the rest part of the ventricles as a result of impulses entering them along the normal path of excitation, i.e. along the path through the AV junction.

Symptoms of Wolff-Parkinson-White Syndrome (WPW)

For Wolff-Parkinson-White syndrome (WPW) are characterized by the following 3 clinical signs:

According to numerous observations, WPW syndrome in men is more common than in women; 60% of cases of WPW syndrome occur in young men.

Patients with Wolff-Parkinson-White (WPW) syndrome often complain of palpitations caused by heart rhythm disturbances. In 60% of cases, patients have arrhythmias, mainly paroxysmal supraventricular tachycardia (reciprocal AV nodal tachycardia). In addition, atrial fibrillation, atrial flutter, atrial and ventricular extrasystole, as well as AV block I and II degree are possible.

In 60% of cases, Wolff-Parkinson-White syndrome (WPW) is detected in people who do not have heart complaints. These are usually people suffering from vegetovascular dystonia. In the remaining 40% of cases, WPW syndrome is diagnosed in patients with cardiac pathology, which is often represented by various heart defects (for example, Ebstein's syndrome, atrial and interventricular septal defects) or coronary artery disease.

WPW syndrome type A.
A 28-year-old patient with a history of paroxysmal tachycardia. The PQ interval is shortened to 0.11 s.
Positive delta wave in leads I, aVL, V, -V6. Small Q wave in lead II, large Q wave in leads III and aVF.
The QRS complex is widened and deformed, as in RBBB, resembling the letter "M" in lead V1. Tall R wave in lead V5.
A clear violation of the excitability of the myocardium.

Diagnosis of Wolff-Parkinson-White Syndrome (WPW)

Diagnose Wolff-Parkinson-White Syndrome(WPW) is possible only with the help of an ECG. Careful reading reveals a peculiar picture: after a normal P wave, an unusually short PQ interval follows, the duration of which is less than 0.12 s. Normally, the duration of the PQ interval, as already mentioned in the chapter on the normal ECG, is 0.12-0.21 s. Prolongation of the PQ interval (for example, in AV block) is observed in various heart diseases, while the shortening of this interval is a rare phenomenon that is observed almost exclusively in WPW and LGL syndromes.

The latter is characterized by shortening of the PQ interval and a normal QRS complex.

Other important ECG sign is a change in the QRS complex. At its beginning, the so-called delta wave is noted, which gives it a peculiar look and makes it broadened (0.12 s or more). As a result, the QRS complex is widened and deformed. It may resemble in shape the changes characteristic of the blockade of RBBB, and in some cases, LBBB.

Because the ventricular depolarization(QRS complex) is clearly changed, then repolarization undergoes secondary changes affecting the ST interval. Thus, in WPW syndrome, there is a distinct depression of the ST segment and a negative T wave in the left chest leads, primarily in leads V5 and V6.

Next, we note that when wolf-parkinson-white syndrome(WPW) often recorded a very wide and deep Q wave in leads II, III and aVF. In such cases, erroneous diagnosis of posterior wall MI is possible. But sometimes a clearly widened and deep Q wave is recorded in the right chest leads, for example, in leads V1 and V2.

An inexperienced specialist in this case may mistakenly diagnose myocardial infarction(IM) of the anterior wall of the left ventricle. But with sufficient experience, as a rule, it is possible to recognize the delta wave characteristic of the WPW syndrome in leads II, III, aVF or V1 and V2. In the left chest leads V5 and V6, a downward delta wave is recorded, so the Q wave does not differentiate.

Treatment of symptomatic WPW syndrome begins with the administration of drugs, such as aymalin or adenosine, after which, if there is no effect, resort to catheter ablation of the additional pathway, which leads to a cure in 94% of cases. In the asymptomatic course of the WPW syndrome, special therapy is not required.

ECG features in Wolff-Parkinson-White syndrome (WPW):
Shortened PQ interval (<0,12 с)
The presence of a delta wave on the ECG (a sign of an additional pathway)
Change in the configuration of the QRS complex, resembling bundle branch block (PH)
Paroxysmal tachycardia (AV nodal tachycardia)
Occurs in young people who often have heart disease

WPW syndrome type B.
The patient is 44 years old. The PQ interval is shortened to 0.10 s. There is a large negative delta wave in lead V1.
The delta wave in leads I, II, aVL, aVF, and V3 is positive. The QRS complex is wide and equal to 0.13 s.
In lead V1, a deep and broadened Q wave is recorded, in leads V4-V6, a high R wave is recorded. Recovery of myocardial excitability is impaired.
Common misdiagnosis: Anterior wall MI (due to large Q wave in lead V1); LDL blockade (due to a widened QRS complex, a large Q wave in lead V1, and impaired recovery of myocardial excitability); LV hypertrophy (due to high R wave and ST segment depression and negative T wave in lead V5).

WPW syndrome (WPW, Wolff-Parkinson-White) - a set of clinical signs that occur in people with congenital cardiac pathology, in which an additional, abnormal, "extra" muscle bundle or atrioventricular pathway appears, located between the atrial and ventricular heart. Pathology is based accelerated conduction of impulses along the heart muscle and premature contraction of the ventricles. The syndrome was discovered in 1930 by Wolf, Parkinson and White, from whom it got its name. SVC syndrome is a fairly rare disease found in children and young people, predominantly male. In mature and elderly persons, the disease is not recorded.

Wolff-Parkinson-White Syndrome is a term that refers to attacks of heart rhythm disturbances. Pathology is manifested by dyspnea, pressure fluctuations, cephalgia, dizziness, cardialgia, fainting. It seems to patients that something freezes in the chest, gurgles, turns over. The heart seems to skip beats, and then its work intensifies. Such uneven activity of the myocardium is the cause of interruptions felt by patients. The syndrome can proceed without a pronounced clinical picture. At the same time, patients do not have signs of the disease, they do not know about the presence of the disorder, they do not visit doctors and are not treated. The problem is discovered by chance during a routine cardiography.

Patients are treated by arrhythmologists and cardiac surgeons. Diagnosis of SVC syndrome consists in performing cardiography, ultrasound and EFI of the heart. The therapeutic tactics of cardiologists is the appointment of antiarrhythmic drugs and radio wave catheter ablation of the heart. The pathology can be completely eliminated only by surgery.

Currently, cardiac pathology occupies a leading place among the diseases leading to death. ERW syndrome is no exception. It has been asymptomatic for a long time. In the body, a persistent violation of the heart rhythm is formed. Often patients, having learned about their illness, find themselves on the operating table. Conservative therapy is unable to cope with complex cardiac dysfunction.

Causal factors

ERW syndrome is a congenital pathology formed as a result of defective intrauterine development of the heart. Additional muscle fibers between the ventricular and atrial parts are present in all embryos. By the twentieth week of embryogenesis, they spontaneously disappear. This is the normal process of organ formation. If it is disturbed, the regression of myocardial fibers stops in the fetus and additional atrioventricular bundles are preserved. The nerve impulse travels along these fibers much faster than the normal path, so the ventricle begins to contract prematurely.

Congenital disorders in the conduction system of the heart lead to the development of dangerous attacks of tachycardia. The pathological pathway leading to SVC syndrome is commonly called Kent's bundle.

conduction system of the heart in a person with SVC syndrome

Factors contributing to the violation of cardiogenesis:

• Heredity - the presence of the syndrome in close relatives,
• Smoking and alcohol intake by the expectant mother,
• Negative emotions and stress during pregnancy,
• fetal hypoxia,
• viral infection,
• The pregnant woman is over 40 years old
• Unfavorable ecological situation.

The syndrome rarely develops on its own. It is usually associated with congenital heart disease, connective tissue disease, or hereditary cardiomyopathy.

Symptoms

The syndrome is asymptomatic for a long time. The appearance of its first clinical signs can be provoked by unfavorable factors: a surge of emotions, stress, physical overstrain, and taking large doses of alcohol. Patients may spontaneously develop an arrhythmia attack. Doctors most often diagnose very dangerous forms of supraventricular tachyarrhythmia, which often lead to disability.

Symptoms of paroxysm are nonspecific. They are practically useless in diagnosing the disease. These include:

1. Violation of the regularity and frequency of contractions of the heart - a feeling that the heart does not work properly, skips beats and freezes, and then its rhythm sharply quickens,
2. Cardialgia and discomfort behind the sternum,
3. suffocation attacks,
4. Violent trembling in the chest, from which the breath is taken away, and there is a cough,
5. Dizziness,
6. sharp weakness,
7. fainting state,
8. Dyspnea is a change in the frequency and depth of breathing,
9. pressure drop,
10. Panic attacks.

Attacks of arrhythmia have different severity and duration - from a few seconds to an hour. Sometimes they go away on their own. Patients with prolonged paroxysms that do not go away and persist for more than an hour are hospitalized in a cardiological hospital for emergency treatment.

Diagnostics

Any diagnostic examination begins with communication between the doctor and the patient. During the conversation, medical specialists find out the general condition of the patient, listen to complaints and analyze the information received. Then they collect anamnestic data: they learn the profession, lifestyle, the presence of cardiac pathologies in relatives and other risk factors that can provoke the manifestations of the syndrome. Physical examination is a very important stage in the diagnosis of almost any disease. Doctors assess the condition of the skin, measure the pulse and pressure, auscultate the heart and lungs.

Electrocardiography is the basis for diagnosing the syndrome. The following pathological changes are found on the ECG:

• relatively short PQ interval,
• extended and altered QRS complex,
• delta waves representing ventricular preexcitation,
• displacement of the RS-T segment relative to the QRS complex,
• inversion of the T wave - a change in its position relative to the isoline.

To find out how the heart rhythm changes during the day, ECG monitoring is performed. Holter monitoring detects attacks of tachycardia.

In addition to electrocardiographic studies, additional instrumental techniques are used that make up a set of diagnostic measures. These include:

1. Transthoracic echocardiography - detection of existing defects in the structure of the heart and large vessels present from birth.
2. Transesophageal stimulation of the heart is a recording of biopotentials from the outer surface of the heart using a special esophageal electrode and a recording device. This technique allows you to study the nature and mechanism of cardiac arrhythmias, diagnose latent coronary insufficiency and stop attacks of tachyarrhythmias.
3. EPS of the heart - determination of the location and number of additional bundles, detection of a latent syndrome, verification of the clinical form of the pathology, evaluation of the effectiveness of the therapy.

Laboratory research methods include: hemogram, blood biochemistry with the determination of the main indicators - cholesterol, glucose, potassium, as well as the determination of the level of hormones in the blood.

Such a comprehensive examination of the patient allows you to make an accurate diagnosis and start treating the pathology.

Healing process

In the absence of attacks of arrhythmia and the asymptomatic course of the syndrome, therapeutic measures are not carried out. In the presence of tachycardia, cardialgia, hypotension and other signs of heart dysfunction, complex therapeutic treatment is indicated.

There are two ways to relieve an arrhythmia attack in a conservative way - vagal and medicinal. The first group includes methods vagus nerve stimulation to normalize the rhythm of the heart. This is washing with ice water, a sharp breath with a closed nose, straining when trying to hold your breath while inhaling with a full chest.

If vagal tests are ineffective, use antiarrhythmic drugs: "Etatsizin", "Ritmonorm", "Propanorm", "Amiodarone". Restoring the rhythm of the heart in advanced cases allows electrocardioversion or electrical stimulation of the heart through the esophagus.

In the interictal period, patients are prescribed medication with antiarrhythmic drugs, which prevents a new arrhythmic paroxysm. Long-term use of such drugs has a negative effect on the body and significantly increases the risk of developing severe complications. Therefore, modern cardiologists are increasingly resorting to surgical intervention.

Radio wave catheter ablation- an operation that destroys an abnormal muscle bundle. It is indicated for persons suffering from frequent paroxysms that disrupt hemocirculatory processes and can lead to the cessation of the effective activity of the heart. Under local anesthesia or general anesthesia, a thin probe with a sensor is inserted through the large blood vessels of the thigh. With the help of EFI, the area of ​​the myocardium from which pathological impulses originate and which requires destruction is determined. After ablation of accessory fibers, an ECG is recorded. The operation is considered successful if a normal heart rhythm begins to register on the cardiogram. The entire course of surgery is monitored by doctors on the monitor of modern medical equipment.

The operation is practically painless and minimally invasive. It gives good results in terms of complete recovery and is not accompanied by postoperative complications. Patients after the intervention feel satisfactory and do not experience symptoms of the disease.

Video: personal experience of surgery for ERW syndrome

Forecasting

Wolff-Parkinson-White syndrome is quite rare. Its etiopathogenetic features and pathomorphological changes occurring in the body are not fully understood. Diagnosis of the disease is difficult, effective therapy is still under development, and the prognosis remains ambiguous.

In persons who have undergone radiofrequency ablation of "extra" muscle bundles, the condition is rapidly improving, relapses do not occur. In the absence of the effect of conservative treatment or refusal of surgery, dangerous complications may develop. Despite this, statistics indicate low mortality rates from pathology.

Since the syndrome is congenital, and the exact causes of it are not determined, it is impossible to prevent the appearance of abnormal muscle fibers. There are measures that reduce the risk of developing pathology, but do not completely protect against it:

1. Annual visit to a cardiologist and electrocardiography,
2. Feasible physical activity - gymnastics, walking, jogging, cardio training,
3. Combating smoking and alcoholism
4. proper nutrition,
5. Pregnant women - protection of the body from the effects of aggressive chemicals, viruses, stress.

Patients with SVC syndrome are registered with a cardiologist and take antiarrhythmic drugs to prevent new attacks of arrhythmia.

ERW syndrome is a chronic pathology. At the slightest complaint about the work of the heart or the appearance of characteristic symptoms, you should consult a doctor. Treatment carried out in full, as well as the implementation of all medical recommendations, will allow the patient to count on a full and long life.

Video: ERW Syndrome Specialist

Fedorov Leonid Grigorievich

Wolff-Parkinson-White Syndrome is a type of cardiac arrhythmias. This condition is manifested by an increase in the speed of contractions of the heart, which is associated with the presence of an additional bundle that conducts an electrical impulse, which is located between the upper and lower parts of the heart. Although the increase in contractions is not directly life-threatening, it can cause life-threatening pathologies.

Description

With the syndrome, there are ways through which the electrical impulse reaches the ventricles without getting into the atrioventricular node. Because of this, it is ahead of the impulse, which moves along the usual path. A person does not notice this process, therefore, to detect it, it is necessary to conduct electrocardiography.

In addition to the syndrome, there is another phenomenon. It differs in that there will be no characteristic changes on the ECG. Otherwise, it is completely the same as the syndrome.

The appearance of additional pathways is associated with the peculiarity of intrauterine development. A person is born with this problem and may not be aware of it for a long time. Symptoms often first appear in old age.

The reasons

The development of the problem is associated with failures in the development of the tissues of the ring of the atrioventricular node.

Studies show that the disease may have a genetic origin. The presence of the syndrome is often detected in people whose immediate family suffered from such a problem.

Due to gene mutation, cardiomyopathy, atrioventricular node block and degenerative processes in the conduction system develop.

Clinical picture

The main manifestation of the syndrome is the presence of episodic. They can occur in people of any age and even early childhood. Such manifestations differ in varying degrees of severity. There may be slight discomfort in the chest area on the left, frequent heartbeat with or without loss of consciousness. But sometimes severe cardiopulmonary disorders develop that can lead to cardiac arrest.

Depending on age, manifestations may have some differences:

If relief does not occur within a few hours, congestive heart failure is suspected.

At an older age, the child may already report disturbing symptoms. In this case, WPW syndrome will be accompanied by chest pain, palpitations, and breathing difficulties.

In adults:

• suddenly the heart starts beating faster;
• there is irregularity, but a high pulse rate;
• physical activity is tolerated with great difficulty.

In most patients, symptoms begin to appear under the influence of physical and emotional stress. In some cases, the deterioration of health is provoked by alcoholic beverages.

An attack often contributes to a decrease in blood pressure and temperature, increased sweating.

In many people at a young age, the syndrome does not affect the quality of life and is manifested by periodic weakness, dizziness, and.

The disease often has an asymptomatic course and is detected during a routine examination.

Diagnostic methods

The examination begins with blood tests. With their help, they confirm or exclude the presence of pathologies not related to the heart, which also contribute to an increase in the rhythm. For this, there is a need to:

• general and biochemical blood tests;
• evaluation of indicators of the liver and pancreas;
• screening for the presence of drugs in the blood.

Usually WPW syndrome on the ECG confirms the diagnosis. In some cases, in addition to standard cardiography, telemetry or Holter monitoring is used.

It is easiest to identify the problem during an attack.

Echocardiography is also used. Thanks to this technique:

• evaluate how the left ventricle works, the thickness of the septum;
• check for the presence of cardiomyopathies and congenital anomalies in the structure of the heart.

Load tests are used as an auxiliary diagnostic method. With their help:

1. Reproducing a transient attack of paroxysmal tachycardia that occurs during exercise.
2. Carry out the fixation of the relationship between the loads and the onset of an attack of frequent heartbeat.
3. Determine how effective antiarrhythmic treatment is.
4. The presence of constant or intermittent excitation is detected when the heart is in different states.

The WPW syndrome of the heart is also determined during the electrophysiological study of the organ. This is necessary for:

Wolff-Parkinson-White Syndrome ( WPW syndrome) is a clinical and electrocardiographic syndrome characterized by preexcitation of the ventricles along additional atrioventricular pathways and the development of paroxysmal tachyarrhythmias. WPW syndrome is accompanied by various arrhythmias: supraventricular tachycardia, atrial fibrillation or flutter, atrial and ventricular extrasystoles with corresponding subjective symptoms (palpitations, shortness of breath, hypotension, dizziness, fainting, chest pain). Diagnosis of WPW syndrome is based on ECG data, 24-hour ECG monitoring, EchoCG, CPEX, EFI. Treatment for WPW syndrome may include antiarrhythmic therapy, transesophageal pacing, catheter RFA.

General information

Wolff-Parkinson-White syndrome (WPW syndrome) is a syndrome of premature ventricular excitation caused by conduction of 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 it manifests at a young age (10-20 years), less often in older people. The clinical significance of the WPW syndrome lies in the fact that when it is present, severe cardiac arrhythmias often develop, which pose a threat to the life of the patient and require special approaches to treatment.

Causes of WPW Syndrome

According to most authors, WPW syndrome is due to the preservation of additional atrioventricular connections 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. In violation of the formation of fibrous atrioventricular rings, muscle fibers are preserved and form the anatomical basis of the WPW syndrome. Despite the congenital nature of accessory AV connections, WPW syndrome may first present at any age. In the familial form of WPW syndrome, multiple accessory atrioventricular connections are more common.

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

Classification of WPW syndrome

According to the WHO recommendation, the phenomenon and syndrome of WPW are distinguished. The WPW phenomenon is characterized by electrocardiographic signs of impulse conduction along accessory connections and ventricular preexcitation, but without clinical manifestations of AV reentry tachycardia (re-entry). The WPW syndrome refers to the combination of ventricular pre-excitation with symptomatic tachycardia.

Taking into account the morphological substrate, several anatomical variants of the WPW syndrome are distinguished.

I. With additional AV muscle fibers:

• through the accessory left or right parietal AV junction
• going through the aorto-mitral fibrous junction
• coming from the auricle of the right or left atrium
• associated with an aneurysm of the sinus of Valsalva or the middle vein of the heart
• septal, paraseptal superior or inferior

II. With specialized muscle AV fibers ("Kent's bundles"), originating from a rudimentary tissue similar to the structure of the atrioventricular node:

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

The pathogenesis of WPW syndrome

The WPW syndrome is caused by the spread of excitation from the atria to the ventricles along additional abnormal conduction pathways. As a result, excitation of part or all of the ventricular myocardium occurs earlier than when the impulse propagates in the usual way - along the AV node, bundle and branches of His. Preexcitation of the ventricles is reflected on the electrocardiogram in the form of an additional wave of depolarization - the delta wave. The P-Q(R) interval is thus 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 confluent QRS complex, which becomes somewhat deformed and broadened. Atypical excitation of the ventricles is accompanied by a violation of the sequence of repolarization processes, which is expressed on the ECG in the form of a shift of the RS-T segment discordant to the QRS complex and a change in the polarity of the T wave.

The occurrence in WPW syndrome of paroxysms of supraventricular tachycardia, atrial fibrillation and flutter is associated with the formation of a circular wave of excitation (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 accessory pathways - in the retrograde direction (from the ventricles to the atria).

Symptoms of WPW Syndrome

The clinical manifestation of WPW syndrome occurs at any age, before that 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 min. Sometimes, with WPW syndrome, less specific arrhythmias develop - atrial and ventricular extrasystole, ventricular tachycardia.

Attacks of arrhythmia can occur under the influence of emotional or physical overstrain, alcohol abuse, or spontaneously, for no apparent reason. During an arrhythmic attack, sensations of palpitations and fading of the heart, cardialgia, a feeling of lack of air appear. Atrial fibrillation and flutter is accompanied by dizziness, fainting, shortness of breath, arterial hypotension; in the transition to ventricular fibrillation, sudden cardiac death can occur.

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

Diagnosis of WPW Syndrome

If WPW syndrome is suspected, complex clinical and instrumental diagnostics is performed: 12-lead ECG, transthoracic echocardiography, Holter ECG monitoring, transesophageal pacing, electrophysiological examination of the heart.

The electrocardiographic criteria for WPW syndrome include: shortening of the PQ interval (less than 0.12 s), a deformed confluent QRS complex, and the presence of a delta wave. 24-hour ECG monitoring is used to detect transient arrhythmias. Cardiac ultrasound reveals concomitant heart defects and requires immediate external electrical cardioversion or transesophageal pacing.

In some cases, reflex vagal maneuvers (massage of the carotid sinus, Valsalva test), intravenous administration of ATP or calcium channel blockers (verapamil), antiarrhythmic drugs (novocainamide, aymalin, propafenone, amiodarone) are effective in stopping paroxysms of arrhythmias in some cases. In the future, patients with WPW syndrome are shown permanent antiarrhythmic therapy.

In case of resistance to antiarrhythmic drugs, the development of atrial fibrillation, catheter radiofrequency ablation of accessory pathways is performed by transaortic (retrograde) or transseptal access. The effectiveness of RFA in WPW syndrome reaches 95%, the risk of recurrence is 5-8%.

Forecast and prevention of WPW syndrome

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

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

Wolff-Parkinson-White syndrome (WPW) is a preexcitation of the ventricles of the heart, passing through an additional pathway and causing various cardiac arrhythmias. In childhood, the manifestation of this pathology is more common than in adults. In most cases, the first manifestation of WPW syndrome occurs at a young age (between 10 and 20 years). It is especially important that the probability of developing sudden cardiac death is from 0.15 to 0.39%, which is higher than the general population risk (less than 0.1%). This disease manifests itself in various forms - from constant clinical and electrophysiological manifestations in the manifest form to the absence of any subjective and objective symptoms in the latent form. The debut of WPW syndrome is also different - from minor tachycardia to life-threatening arrhythmias. That is why early diagnosis and monitoring of these patients is important. Today, scientists are increasingly paying attention to the genetic aspects of various cardiovascular diseases, including the WPW syndrome, which is successfully used in the prediction and diagnosis of latent forms of the disease. The article presents a brief review of the literature on the WPW syndrome: definition, classification, "gold standards" of diagnosis, treatment, as well as genetic aspects.

Keywords: Wolff-Parkinson-White syndrome, WPW, ventricular preexcitation, arrhythmia.
For citation: Chernova A.A., Matyushin G.V., Nikulina S.Yu., Lebedeva I.I. Wolff-Parkinson-White syndrome (literature review) // BC. 2017. No. 4. pp. 269-272

Wolff-Parkinson-White syndrome (literature review)
Chernova A.A., Matyushin G.V., Nikulina S.Yu., Lebedeva I.I.

The Krasnoyarsk State Medical University named after Professor V. F. Voyno-Yasenetsky

Wolff-Parkinsov-White syndrome - pre-excitation of the ventricles of the heart, passing along an additional conducting path, causing various disturbances of the heart rhythm. The manifestation of this pathology is more common in childhood than in the adult. In most cases, the first manifestation of WPW syndrome occurs at a young age (10 to 20 years). Especially important is that the probability of a sudden cardiac death ranges from 0.15 to 0.39%, which is above the general population risk (less than 0.1%). This disease has different forms of manifestation: from persistent clinical and electrophysiological manifestations in the overt form, to the absence of any subjective and objective symptoms in a latent form. The onset of the Wolff-Parkinson-white syndrome also varies from a mild tachycardia, to life-threatening arrhythmias. It makes important the early diagnosis and monitoring of these patients. Today scientists pay more attention to the genetic aspects of various cardiovascular diseases, including WPW syndrome, which has been used successfully in the prediction and diagnostics of latent forms of the disease. The article presents a brief review of literature on Wolff-Parkinson-White syndrome: definition, classification, "gold standards" in diagnosis, treatment, as well as genetic aspects.

key words: Wolff-Parkinson-White syndrome, WPW, ventricular pre-excitation, arrhythmia.
For quote: Chernova A.A., Matyushin G.V., Nikulina S.Yu., Lebedeva I.I. Wolff-Parkinson-White syndrome (literature review) // RMJ. 2017. No. 4. P. 269–272.

The review is dedicated to the Wolf-Parkinson-White syndrome

Definition of Wolff-Parkinson-White Syndrome

Wolff-Parkinson-White syndrome (WPW or WPW) is a combination of an electrocardiographic phenomenon illustrating preexcitation of the heart ventricles by an additional (abnormal) atrioventricular connection (DAVS) and paroxysmal atrioventricular reciprocal (re-entry) tachycardia (AVRT), resulting from the implementation of the mechanism of repeated the input of electrical excitation, the structural components of which are congenital accessory atrioventricular connection, atrioventricular connection, atrial myocardium and ventricular myocardium. The occurrence of reciprocal tachycardia in WPW syndrome is possible if there are at least two different pathways. In the structure of this tachycardia, 2 components must be present: the atrium (atrium) and the ventricle (ventriculum), which is reflected in the name - "atrioventricular" tachycardia. The term "reciprocal" is synonymous with the term "re-entry". The propagation of electrical impulses can be anterograde (from the atria to the ventricles), retrograde (from the ventricles to the atria), or conducted in both directions. According to the recommendations of the World Health Organization (WHO), since 1980, the WPW phenomenon and the WPW syndrome have been distinguished. The WPW phenomenon is spoken of if the patient, against the background of sinus rhythm, on the surface electrocardiogram (ECG) has signs of anterograde (from the atrium to the ventricles) conduction according to DAVS (ventricular preexcitation), but there are no indications of clinical manifestations of AVRT in the anamnesis.

Forms of the WPW syndrome

The following forms of WPW syndrome are clinically distinguished:
1) manifesting form - characterized by the constant presence of a Δ-wave, which is present in 0.15–0.20% of the general population, antegrade and retrograde conduction along accessory pathways (AAC);
2) intermittent form - is detected mainly according to clinical data, and transient signs of pre-excitation are inherent in it;
3) latent form - manifested by signs of pre-excitation only when stimulating the atria (most often the left one) through the coronary sinus during an invasive electrophysiological study (EPS) or slowing down the atrioventricular node (AVN) as a result of massage of the carotid sinus, the introduction of verapamil or propranolol;
4) latent form - characterized only by retrograde atrial pre-excitation. Therefore, paroxysms of antidromic tachycardia or atrial fibrillation with conduction through the DPP do not develop. In sinus rhythm, there are no signs of WPW syndrome on the electrocardiogram.
Much less often, only 5–10% of patients with WPW syndrome have a variant of antidromic re-entry tachycardia. When two or more DAVS are detected, which are involved in re-entry with AVRT, they speak of multiple WPW syndrome. The usual course of WPW syndrome is divided into 3 stages:
- 1st stage - short-term (less than 30 minutes) attacks of orthodromic tachycardia, stopping reflexively;
- Stage 2 - an increase in the frequency and duration (from 30 minutes to 3 hours) of seizures that stop with one antiarrhythmic drug, sometimes in combination with vagal tests. For the prevention of tachycardia, drug treatment is used;
- Stage 3 - frequent and prolonged (more than 3 hours) attacks of orthodromic tachycardia, the appearance of attacks of ventricular tachycardia, atrial fibrillation or ventricular fibrillation, conduction system disorders (sinus node weakness syndrome, bundle branch block, atrioventricular block), tolerance to antiarrhythmic drugs .

Additional pathways

M.S. Arruda et al. (1998), modifying an earlier classification, proposed subdividing DPP according to their localization in 3 main areas into septal, right free wall and left free wall. Septal DPP: anterior septal, anterior paraseptal, mid-septal - along the annulus of the tricuspid valve (TC), posterior septal - along the annulus of the TC and the annulus of the mitral valve (MV). DPP of the right free wall: right anterior, right anterolateral, right lateral, right posterolateral, right posterior. DPP of the left free wall: left anterolateral, left lateral, left posterolateral, left posterior.

WPW syndrome in the population

The WPW syndrome occurs in 0.1-3.1% of 1000 ECGs, and in patients with congenital heart defects - in 0.5%; in all age groups and is detected in 1-30 per 10 thousand people. The ratio between men and women is 3:2. In childhood, WPW syndrome is more common (7–10%) than in adults (3–6%). In most cases, the clinical manifestation of WPW syndrome occurs at a young age (from 10 to 20 years). The probability of developing sudden death (SCD) within 10 years is from 0.15 to 0.39%, which is higher than the general population risk of SCD (less than 0.1%).
In a study of patients with WPW syndrome who underwent cardiac arrest, a number of criteria were retrospectively identified by which patients with an increased risk of SCD can be identified. These include: shortened R–R interval (less than 250 ms) with ventricular preexcitation during spontaneous or induced AF, history of symptomatic tachycardia, multiple accessory pathways, Ebstein anomaly.
Extensive research has been carried out at the Taiwan National University Hospital. Selected cases of WPW syndrome in people younger than 50 years from 2000 to 2010. 6086 patients were identified (61% men, 39% women). The reported prevalence was 0.36 per 1000 and 0.61 per 1000 in the 20–24 age group. The risk of SCD was 0.071% in the general group and 0.02% in the group of people aged 20–24 years. During the study period, 42 SCDs occurred in patients aged 29 years on average. Comorbid CVD was noted in 158 patients (2.6%), including 42 patients with Ebstein anomaly, which increases the risk of SCD. Radiofrequency ablation (RFA) was performed in 2527 patients with a mean age of 25.7 years, in 11 patients at the age of 5 years and in 2231 people over the age of 15 years; of the total - 6% of repeated RFA.
There are descriptions of familial variants of the WPW syndrome in the literature. These forms are rare, but it is with the familial WPW syndrome that they speak of a higher frequency of SCD. In patients with the familial form of WPW syndrome, atrial fibrillation (AF) was observed in 38–44% of cases, in contrast to 15–20% in sporadic forms of the disease.
In studies of ventricular preexcitation syndrome (PVS), the authors conducted genetic counseling and prospective observation of 36 patients with WPW syndrome and 222 of their blood relatives, as well as 40 patients with Clerk-Levy-Critesco syndrome (CLK) and 227 of their relatives. The syndrome or phenomenon of PVH, i.e. the presence of DPP, was first diagnosed in 32% (n=72 out of 222) of the examined relatives of I-IV degrees of kinship: among them, WPW syndrome was observed in 4 (1.8%), CLA syndrome - in 12 (5.4%), CLA phenomenon in 56 (25%) relatives. In the families of patients with CLC syndrome, the syndrome and the phenomenon of long-term survival were detected for the first time in 36% (n=82 out of 227) of the examined relatives of I–IV degrees of kinship; 17 (7%) had CLA syndrome, 60 (26%) had CLA phenomenon, and 5 (2%) had WPW phenomenon.

Structure of arrhythmias

In the structure of all supraventricular tachycardias (SVT), excluding AF, the proportion of arrhythmias reaches 54–75%. Of these, AVRT with manifesting WPW syndrome accounted for 39.4%, AVRT with latent retrograde DAVS - 24.1%. Atrioventricular re-entry tachycardia is the most common tachycardia (70%) among narrow QRS arrhythmias in children and the second most common in adults. It has been noted that in young patients the course of tachyarrhythmias in WPW syndrome is more aggressive than in the elderly. In the context of the WPW syndrome, AF has a different meaning. The presence of AF in a patient with WPW syndrome can lead to ventricular arrhythmia much faster due to the presence of DPP. In patients with WPW syndrome, there are 2 mechanisms for the occurrence of AF: associated with DPP or not associated with DPP. In some cases, when atrial flutter (AF) or AF occurs in patients with WPW syndrome, it becomes possible to develop ventricular tachycardia and ventricular fibrillation (VF). In this case, VF can be the first manifestation of the disease. In one of the foreign studies, VF became the first manifestation in 8 out of 15 patients (53%). Mortality from arrhythmias in WPW syndrome is 1.5%. It is worth mentioning drug-induced atrial flutter (or IC-induced) in patients with "malignant" Kent's bundle. This is a rare form of prognostically unfavorable proarrhythmic effect of antiarrhythmic drugs. Depending on the possibility of ECG recording, the incidence of 1C-induced paroxysm of atrial fibrillation ranges from 3.5% to 20%. R.R. Mamatkazina et al. in their article describe such a rare case.

Diagnostics

According to the standard ECG, it is possible to determine the localization of DPP.
Type A characterized by a positive D-wave in leads V1–V2. DPP between the atrium and the ventricle is located on the left side of the septum, LV is excited earlier.
Type B manifests as a negative D wave in leads V1–V2, but a positive one in leads V4–V6. DPP is located on the right, and, accordingly, the right ventricle is excited earlier.
Type C has a positive D-wave in leads V1–V4 and a negative one in leads V5–V6;
An interesting approach to improve the accuracy of diagnosing ADP localization by ECG was proposed by L.A. Bokeria et al. . With the help of regression analysis, the dependence of the location of the RAP on the amplitude of the D-wave in 12 ECG leads was revealed. The accuracy of localization of AAP in 11 segments of the AV sulcus was 100% in retrospective and 88% in prospective analysis, which is significantly higher than using other algorithms. But to date, intracardiac electrophysiological examination (EPS) remains the "gold standard" and, according to most authors, an obligatory step in the preoperative topical diagnosis of DPP. Recommendations of the All-Russian Scientific Society of Specialists in Clinical Electrophysiology, Arrhythmology and Cardiac Stimulation (VNOA) for EPS in patients with cardiac arrhythmias (2005) have been developed.
It is also worth noting that cases are described when the diagnosis of "WPW syndrome" is made intraoperatively, when performing operations due to another pathology not related to the heart. Foreign authors described a case when a 32-year-old man, who was preparing for a urological operation, was diagnosed with intermittent WPW syndrome. After premedication and spinal anesthesia, WPW syndrome was constantly recorded on the monitor during the operation and in the early postoperative period. The authors write about the need for EPS before surgery and, if WPW syndrome is established, if possible, RFA before a planned operation. The literature describes cases when the WPW syndrome was found already during the operation with spinal anesthesia.

Radiofrequency ablation in the treatment of WPW syndrome

DC catheter ablation and radiofrequency energy have recently been used to treat patients with chronic AV tachycardias, idiopathic ventricular tachycardias, and various types of atrial tachycardias with promising results.
The effectiveness of the RFA procedure in the treatment of atrioventricular re-entry and atrioventricular nodal re-entry tachycardias is more than 95%. On the other hand, researchers note that the risk of recurrent AF after catheter ablation is positively correlated with patient age and increased with other structural heart diseases or left atrial dilatation. In patients under the age of 50, this occurs in 10-12% of cases, over 50 years - in 35-40%, over 60 years - in more than 55%. In such cases, RFA DPP is repeated. Even after effective radiofrequency ablation of the AAP, 25% of patients continue to recur in AF, and experts suggest that AF may occur as a result of concomitant electrophysiological changes in the atria, not associated with the presence of an accessory pathway.
The predisposition to the development of AF in WPW syndrome can be explained by a decrease in the duration of the refractory period of atrial myocardial cells and a violation of intra- and interatrial conduction. There are also suggestions that the occurrence of AF after RFA is also associated with hemodynamic disorders that develop during tachycardia and lead to an increase in the tone of the sympathetic nervous system, atrial myocardial hypoxemia.
In 6-10% of cases, RFA is accompanied by the development of complications: damage to the heart (tamponade) and blood vessels (hematomas), the development of thromboembolism, exudative pericarditis. Therefore, some experts prefer to use the method of open electrical destruction of the DPP.
Currently, complications during endocardial EPS and RFA of DPP can be divided into 4 groups: those caused by radiation exposure; associated with puncture and catheterization of vessels (hematoma, deep vein thrombosis, arterial perforation, arteriovenous fistula, pneumothorax); complications during catheter manipulations (damage to the heart valves, microembolism, perforation of the coronary sinus or myocardial wall, dissection of the coronary arteries, thrombosis); caused by RF exposure (AV blockade, myocardial perforation, spasm or occlusion of the coronary arteries, transient cerebrovascular accident, cerebrovascular complications).
The most common serious complications are complete AV block and cardiac tamponade. The incidence of irreversible complete AV block ranges from 0.17 to 1%. Most often, this complication occurs during RFA of septal DPP located near the AV node and bundle of His. The frequency of cardiac tamponade varies from 0.13 to 1.1%. Mortality associated with the procedure for ablation of the DPP does not exceed 0.2%.
In 2005, VNOA recommendations were developed for the treatment of AF and ventricular preexcitation syndrome. In children, RFA is not the method of choice because it has a very high risk of complications. According to G. Vignati et al. , RFA should be performed in children at least 12 years old, because with increasing age of the patient, there is a possibility of developing fibrosis in the area of ​​​​attachment of the DPP and losing its conductive ability.

Genetics

The familial form of WPW syndrome is inherited in an autosomal dominant manner and is caused by a mutation in the PRAKG2 (7q3) gene. PRKAG2 is a critical enzyme that affects intracellular energy production and mutations in the gene encoding this enzyme can cause hypertrophic cardiomyopathy (HCM), WPW syndrome, conduction disorders, muscular dystrophy, and glycogen storage diseases.
It is worth noting that patients with HCM also have a mutation in the LAMP2 gene. LAMP-2 is an X-linked gene that encodes proteins that regulate the integration and functioning of lysosomes. Mutation of this gene leads to Danon's disease, which includes such manifestations as WPW syndrome, hypertrophic cardiomyopathy, muscular dystrophy, mental retardation.
Returning to the already known PRKAG gene, a predictor of WPW syndrome, it should be noted that its sequencing in patients with WPW reveals missense mutations in 6 positions. Foreign studies have shown that the PRKAG2 gene mutation is characteristic not only of WPW syndrome, but also of sinus bradycardia, right bundle branch block, and short PQ interval. The literature describes cases of isolated familial WPW syndrome (WPW syndrome associated with cardiac hypertrophy and/or AVU damage) with the absence of a mutation in the PRKAG2 gene in all family members. The PRKAG2 gene mutation has also not been found in patients with non-familial WPW syndrome. One of the articles by foreign authors describes a case of WPW syndrome in 3 sisters. Moreover, left-lateral DPP was found in all girls. The girls' parents and other close relatives were healthy. Remarkably, despite the same location of the AAP, only one of the sisters had antegrade conduction, and the disease manifested with persistent tachycardia, while the others noted only rare palpitations in adolescence, which did not bother them. Nevertheless, the authors note that, perhaps, over time, the disease could manifest itself in the other two sisters.
Other foreign researchers observed 2 families (70 people in total): 57 and 13 people. All patients underwent 12-lead ECG and echocardiography. The WPW syndrome predictor gene (PRKAG2) was sequenced in healthy and diseased members of both families. According to the results of the study, 23 people with WPW syndrome were identified in the first family, and 8 in the second. Patients were found to have premature excitation of the ventricles and cardiac hypertrophy.

Conclusion

Considering the world experience in monitoring patients with WPW syndrome, we can conclude that today a standard examination should include a 12-lead ECG, echocardiography, Holter monitoring, and a mandatory genetic test.
If a latent or latent form is suspected, which did not appear on a single-stage and daily ECG, and with a positive genetic test, EFI is performed.
EchoCG at the first stage also makes it possible to suspect latent forms of WPW syndrome by the presence of such pathologies as MV prolapse and additional chords, which often accompany WPW syndrome.
With regard to the treatment of WPW syndrome, RFA is becoming increasingly common today. Although it is worth noting that this technique does not have 100% efficiency and absolute indications. When choosing this method of treatment, it is necessary to take into account many factors: indications and contraindications according to the recommendation of VNOK.

Literature

1. Ardashev V.N., Ardashev A.V., Steklov V.I. Treatment of cardiac arrhythmias. M.: Medpraktika-M, 2005. 240 p. .
2. Kushakovsky M.S. Arrhythmias of the heart. St. Petersburg: Foliant, 1998. 640 p. .
3. Abott J., Eldar M., Seger J. et al. Combined Mahaim and Kent pathways // Circulation. 1985 Vol. 72. P. 269–275.
4. Ward D., Benett O., Camn J. et al. Mechanism of junctional tachycardia showing ventricular preexcitation // Br Heart J. 1984. Vol. 52. P. 369–375.
5. Klein G.J., Gulamhusein S.S. Intermittent preexcitation in the Wolff-Parkinson-White syndrome // Am J. Cardiol. 1983 Vol. 52. P. 292–296.
6. McClelland J.H., Wang X., Beckman K.J et al. Radiofrequency catheter ablation of right atriofascicular (Mahaim) accessory pathways guided by accessory pathway activation potentials // Circulation. 1994 Vol. 89. P. 2655–2666.
7. Ardashev A.V., Rybachenko M.S., Zhelyakov E.G., Shavarov A.A., Voloshko S.V. Wolff-Parkinson-White Syndrome: Classification, Clinical Manifestations, Diagnosis and Treatment // Cardiology. 2009. No. 10. C. 84–94.
8. Bokeria L.A. Tachyarrhythmias. L.: Medicine, 1989. 296 p. .
9. Munger T.M., Packer D.L., Hammill S.C. et al. A population study of the natural history of Wolff-Parkinson-White syndrome in Olmsted County, Minnesota, 1953–1989 // Circulation. 1993 Vol. 87. P. 866–873.
10. Arruda M. S., McClelland J. H., Wang X. et al. Development and validation of an ECG algorithm for identifying accessory pathway ablation site in Wolf-Parkinson-White syndrome // J. Cardiovasc. Electroph. 1998 Vol. 9. P. 212.
11. Timmermans C., Smeets J.L., Rodriguez L.M. et al. Aborted sudden death in the Wolff-Parkinson-White syndrome // Am J Cardiol. 1995. Vol.76. P. 492–494.
12. Miklashevich I.M., Shkolnikova M.A., Syrkin A.L. et al. Natural course of supraventricular tachycardias manifested in childhood. Bulletin of Arrhythmology. 2002. No. 29. S. 60–65.
13. Huttin O., Brembilla-Perrot B. Relationships between age and accessory pathway location in Wolff-Parkinson-White syndrome // Ann. cardiol. Angelol. (Paris). 2008 Vol. 57. R. 225-230.
14. Golitsyn S.P., Malakhov V.I., Bokalov S.A. Diagnosis and possibilities of antiarrhythmic treatment of malignant ventricular arrhythmias // Ter. Arch. 1991. No. 9. C. 38–44.
15. Ardashev A.V., Ardashev V.N., Zhelyakov E.G. et al. Indicators of intracardiac hemodynamics in patients with WPW syndrome before and after RFA surgery. Annals of Arrhythmology. 2007. No. 3. S. 37.
16. Lu C.-W., Wua M.-H., Chen H.-C. et al. Epidemiological profile of Wolff–Parkinson–White syndrome in a general population younger than 50 years of age in an era of radiofrequency catheter ablation // International Journal of Cardiology. 2014. Vol. P. 530–534.
17. Wathen M., Natale A., Wolfe K. et al. Initiation of atrial fibrillation in the Wolff-Parkinson-White syndrome: the importance of the accessory pathway // Am Heart J. 1993. Vol. 125. P. 753–759.
18. Bockeria L. A., Melikulov A. Kh. Wolff-Parkinson-White Syndrome // Annals of Arrhythmology. 2008. No. 2. S. 5–19.
19. Zhang L.P., Hui B., Gao B.R. High risk of sudden death associated with a PRKAG2-related familial Wolff-Parkinson-White syndrome // Journal of Electrocardiology. 2011 Vol. 44. P. 483–486.
20. Fomina I.G., Kuleshov N.P., Logunova L.V., Morgunov N.B., Tarzimanova A.I. The role of genetic counseling in the primary prevention of arrhythmias // Cardiovascular therapy and prevention. 2007. No. 7(7). pp. 74–77.
21. Kugler J.D., Danford D.A., Deal B.J. et al. Radiofrequency catheter ablation for tachyarrhythmias in children and adolescents. The Pediatric Electrophysiology Society // N Engl J Med. 1994 Vol. 330. P. 1481–1487.
22. Calkins H., Sousa J., el-Atassi R. et al. Diagnosis and cure of the Wolff–Parkinson–White syndrome or paroxysmal supraventricular tachycardias during a single electrophysiologic test // N Engl J Med. 1991 Vol. 324. P. 1612-1618.
23. Frolov A.I., Zotov S.Yu., Zinchenko Yu.V. Age differences in electrophysiological parameters in patients with Wolff-Parkinson-White syndrome // Ukr. honey. magazine 2001. No. 2. C. 9–15.
24 Centurion O.A. Atrial Fibrillation in the Wolff-Parkinson-White syndrome // Journal of Atrial Fibrillation. 2011 Vol. 2(5). P. 899–915.
25. Brembilla-Perrot B., Tatar C., C. Suty-Selton. Risk factors of adverse presentation as the first arrhythmia in Wolff-Parkinson-White syndrome // PACE. Wiley Periodicals, Inc. September 2010 Vol. 33. P. 1074–1081.
26 Falk R.H. Proarrhythmic responses to atrial antiarrhythmic therapy. In: Falk RH, Podrid PJ, eds. Atrial fibrillation: mechanisms and management // NY: Raven Press. 1992. P. 283–305.
27. Mamatkazina R.R., Kolos I.P., Serdyuk S.E., Mazygula E.P., Sveshnikov A.V. 1C-induced atrial flutter in a patient with WPW syndrome: a clinical case and literature review // Rational pharmacotherapy in cardiology. 2012. No. 8(2). pp. 196–200.
28. Sumarokov A.V., Moiseev V.S. Clinical Cardiology: A Guide for Physicians. M.: Universum Publishing, 1995. S. 213–214.
29. Bockeria L.A., Revishvili A.Sh., Polyakova I., Kulakova G.V. A new method for topical diagnosis of accessory pathways in patients with Wolff-Parkinson-White syndrome. Kardiologiya. 1989. V. 29. No. 7. S. 49–53.
30. Bokeria L.A. Recommendations of the All-Russian Scientific Society of Specialists in Clinical Electrophysiology, Arrhythmology and Cardiac Stimulation on Conducting Clinical Trials, Catheter Ablation and Implantation of Antiarrhythmic Devices. M.: Golden Apricot, 2005. 238 p. .
31. Nishikawa K., Mizoguchi M., Yukika H. et al. Concealed Wolff-Parkinson white syndrome detected during spinal anaesthesia // Anaesthesia. 2007 Vol. 48. P. 1061.
32. Jackman W.M., Wang X., Friday K.J. et al. Catheter ablation of accessory atrioventricular pathways (Wolff – Parcinson – White syndrome) by radiofrequency current // N. Engl. J. Med. 1991 Vol. 324. P. 1605-1611.
33. Mujovic N., Grujic M., Mrdja S. et al. Recurrence of atrial fibrillation after successful radiofrequency catheter ablation of accessory pathway in patients with Wolff–Parkinson–White syndrome // Srp. Arh. Celok. Lek. 2010 Vol. 138. P. 170–176.
34. Lokshin S.L., Pravosudovich S.A., Dzyak V.G. On the possibility of eliminating atrial fibrillation in patients with WPW syndrome. Bulletin of Arrhythmology. 1998. No. 7. S. 36–41.
35. Shafquat A., Imdad A., Khalid S. et al. Cardiac electrophysiology studies and ablations for treatment of supraventricular arrhythmias-an initial experience from Karachi // J. Pak. Med. Assoc. 2011 Vol. 61. P. 173–175.
36 Cagli K.E., Topaloglu S., Aras D. et al. Evaluation of atrial vulnerability immediately after radiofrequency catheter ablation of accessory pathway in patients with Wolff–Parkinson–White syndrome // J. Interv. card. Electrophysiol. 2009 Vol. 26. R. 217-224.
37. Emkanjoo Z., Ebadi K., Sharifi M. et al. Electrophysiological characteristics of orthodromic reentrant tachycardia in patients with Wolf – Parkinson – White syndrome and atrial fibrillation // Int. J. Cardiol. 2010 Vol. 12. P. 196–198.
38. Zhang Y., Wang L. Atrial vulnerability is a major mechanism of paroxysmal atrial fibrillation in patients with Wolff – Parkinson – White syndrome. Med. hypotheses. 2006 Vol. 7. R. 1345–1347.
39. Kushakovsky M.S. Arrhythmias of the heart. St. Petersburg: Hippocrates, 1998. 544 p. .
40. Brembilla-Perrot B., Chometon F., Groben L. et al. Are the results of electrophysiological study different in patients with a pre-excitation syndrome, with and without syncope? // Europace. 2008 Vol. 10. R. 175-180.
41. Sethi K.K., Dhall A., Chadha D.S. et al. WPW and preexcitation syndromes // J. Assoc. Physicians India. 2007 Vol. 15. P. 10–15.
42 Shapira A.R. Catheter ablation of supraventricular arrhythmias and atrial fibrillation // Am Fam Physician. 2009 Vol. 80. R. 1089-1094.
43. Schaer B.A., Maurer A., ​​Sticherling C. et al. Routine echocardiography after radiofrequency ablation: to flog a dead horse? // Europace. 2009 Vol. 11. R. 155-157.
44. Gusak V.K., Kuznetsov A.S., Komissarov S.I. Surgical treatment of patients with WPW syndrome in combination with atrial fibrillation // Ukr. honey. hour-painting 2001. No. 5(25). pp. 135–138.
45. Guidelines for the management of atrial fibrillation. The Task Force for the Management of Atrial Fibrillation of the European Society of Cardiology // Eur. Heart J. 2010. Vol. 31. P. 2369–2429.
46. ​​Melina G., Codecasa R., Capecchi I. et al. Successful aortic valve repair for severe aortic insufficiency caused by radiofrequency ablation // J. Thorac. Cardiovasc. Surg. 2005 Vol. 130. P. 564–565.
47. Milewicz D.M., Seidman C.E. Genetics of Cardiovascular Disease // Circulation. American Heart Association. November 2000 Vol. 14. P. 102–111.
48. Murphy R.T., Mogensen J., McGarry K. et al. Adenosine monophosphate-activated protein kinase dis-ease mimics hypertrophic cardiomyopathy and Wolff-Parkinson-White syndrome. Natural history // Journal of the American College of Cardiology. 2005 Vol. 45 Vol. 922–930.
49. Yang Z., McMahon C.J., Smith L.R. Danon disease as an underrecognized cause of hypertrophic cardiomyopathy in children // Circulation. 2005 Vol. 112. P. 1612–1617.
50. Gollob M.H., Seger J.J., Gollob T. et al. Novel PRKAG2 mutation responsible for the genetic syndrome of ventricular preexcitation and conduction system disease with childhood onset and absence of cardiac hypertrophy // Circulation. 2001 Vol. 104. P. 3030–3033.
51. Vaughan C.J., Hom Y., Okin D.A. et al. Molecular genetic analysis of PRKAG2 in sporadic Wolff-Parkinson-White syndrome // J Cardiovasc Electrophysiol. 2003 Vol. 14. P. 263–268.
52. Ehtisham J., Watkins H. Is Wolff-Parkinson-White syndrome a genetic disease? // J. Cardiovasc Electrophysiol. 2005 Vol. 16. P. 1258–1262.
53. Bittinger L.D., Tang A.S., Leather R.A. Three Sisters, One Pathway // Canadian Journal of Cardiology. 2011 Vol. 27. P. 870.
54. Gollob M.H., Green M.S., Tang A.S-L. et al. Identification of a gene responsible for familial Wolff–Parkinson–White syndrome // The New England Journal of Medicine. 2001 Vol. 344(24). P. 1823–1831.
55. Vohra J., Skinner J., Semsarian C. Cardiac genetic investigation of young sudden unexplained death and resuscitated out of hospital cardiac arrest // Heart, Lung and Circulation. 2011 Vol. 20. P. 746–750.