Wolff parkinson white syndrome heredity. Life-threatening Wolff-Parkinson-White syndrome and methods to combat it. Additional pathways

Wolff-Parkinson-White syndrome (WPW) is pre-excitation of the ventricles of the heart, passing along an accessory pathway and causing various heart rhythm disturbances. The manifestation of this pathology occurs more often in childhood than in adults. In most cases, the first manifestation of WPW syndrome occurs at a young age (10 to 20 years). It is especially important that the probability of developing sudden cardiac death ranges from 0.15 to 0.39%, which is higher than the general population risk (less than 0.1%). This disease manifests itself in different 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 onset 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 WPW syndrome, which is successfully used in predicting and diagnosing latent forms of the disease. The article presents short review literature on WPW syndrome: definition, classification, “gold standards” of diagnosis, treatment, as well as genetic aspects.

Keywords: Wolff–Parkinson–White syndrome, WPW, ventricular preexcitation, arrhythmia.
For quotation: Chernova A.A., Matyushin G.V., Nikulina S.Yu., Lebedeva I.I. Wolff–Parkinson–White syndrome (literature review) // Breast cancer. 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, that 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 citation: 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 Wolff–Parkinson–White syndrome

Definition of Wolff–Parkinson–White syndrome

Wolff–Parkinson–White syndrome (WPU or WPW) is a combination of an electrocardiographic phenomenon illustrating preexcitation of the ventricles of the heart through an additional (abnormal) atrioventricular connection (DAVC) and paroxysmal atrioventricular reentry tachycardia (AVRT), resulting from the implementation of the mechanism of repeated input of electrical excitation, the structural components of which are the 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 conduction pathways. The structure of this tachycardia must contain 2 components: 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 WPW syndrome have been distinguished. The WPW phenomenon is said to occur if the patient, against the background of sinus rhythm, has signs of anterograde (from the atrium to the ventricles) conduction along the DAVS (ventricular pre-excitation) on the surface electrocardiogram (ECG), but there is no history of clinical manifestations of AVRT.

Forms of WPW syndrome

Clinically, the following forms of WPW syndrome are distinguished:
1) manifesting form – characterized by the constant presence of a Δ wave, present in 0.15–0.20% of the general population, antegrade and retrograde conduction along accessory pathways (APP);
2) intermittent form - detected mainly by clinical data, and it is characterized by transient signs of pre-excitation;
3) latent form - manifests itself with signs of pre-excitation only when the atria are stimulated (most often the left) through the coronary sinus during an invasive electrophysiological study (EPS) or when conduction through the atrioventricular node (AVN) slows down as a result of massage of the carotid sinus, administration of verapamil or propranolol;
4) latent form - characterized only by retrograde preexcitation of the atria. Therefore, paroxysms of antidromic tachycardia or atrial fibrillation with conduction through the AP do not develop. In sinus rhythm, no signs of WPW syndrome are detected on the electrocardiogram.
Much less often - only in 5-10% of patients with WPW syndrome a variant of antidromic re-entry tachycardia is observed. When two or more DAVS are detected that are involved in re-entry during AVRT, they speak of multiple WPW syndrome. The usual course of WPW syndrome is divided into 3 stages:
– Stage 1 – short-term (less than 30 minutes) attacks of orthodromic tachycardia, which are stopped reflexively;
– Stage 2 – increased frequency and duration (from 30 minutes to 3 hours) of attacks, which can be controlled with one antiarrhythmic drug, sometimes in combination with vagal tests. To prevent 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 or ventricular fibrillation, conduction system disorders (sick sinus syndrome, bundle branch block, atrioventricular block), tolerance to antiarrhythmic drugs .

Additional pathways

M.S. Arruda et al. (1998), modifying an earlier classification, proposed dividing the DPP according to their localization in 3 main areas into septal, right free wall and left free wall. Septal APPs: anteroseptal, anterior paraseptal, mid-septal - along the tricuspid valve (TV) ring, posteroseptal - along the TC ring and the mitral valve (MV) ring. 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

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. WPW syndrome occurs more often in childhood (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 ranges 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 suffered cardiac arrest, a number of criteria were retrospectively identified that can be used to identify patients at increased risk of SCD. These include: a shortened R-R interval (less than 250 ms) with ventricular preexcitation during spontaneous or induced AF, a history of symptomatic tachycardia, multiple additional conduction pathways, and Ebstein's anomaly.
Extensive research has been conducted at National Taiwan University Hospital. Cases of WPW syndrome in people under 50 years of age from 2000 to 2010 were selected. 6086 patients were identified (61% men, 39% women). According to the data obtained, the prevalence was 0.36 per 1000 and 0.61 per 1000 in the group of people aged 20–24 years. The risk of SCD was 0.071% in general group and 0.02% in the group of people 20–24 years old. During the study period, 42 SCDs occurred in patients with an average age of 29 years. Concomitant CVD was noted in 158 patients (2.6%), including 42 patients with Ebstein's anomaly, which increases the risk of SCD. Radiofrequency ablation (RFA) was performed in 2527 patients with an average age of 25.7 years, in 11 patients aged 5 years and in 2231 people aged over 15 years; from total number– 6% repeat RFA.
In the literature there are descriptions of familial variants of WPW syndrome. These forms are rare, but it is with familial WPW syndrome that they speak of a higher incidence of SCD. In patients with familial 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 premature ventricular excitation syndrome (PVS), the authors conducted medical genetic counseling and prospective observation of 36 patients with WPW syndrome and 222 of their blood relatives, as well as 40 patients with Clerk-Lewy-Critesco syndrome (CLS) and 227 of their relatives. The syndrome or phenomenon of PPV, 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%), KL syndrome - in 12 (5.4%), the phenomenon of KLK – in 56 (25%) relatives. In families of patients with CLC syndrome, the syndrome and the phenomenon of PVH were identified for the first time in 36% (n = 82 out of 227) of the examined relatives of I–IV degrees of kinship; 17 (7%) had the KL syndrome, 60 (26%) had the KL phenomenon, and 5 (2%) had the 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 hidden 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 with WPW syndrome is more aggressive than in older patients. In the context of WPW syndrome, AF has a different meaning. The presence of AF in a patient with WPW syndrome can lead to ventricular arrhythmia much more quickly due to the presence of atrial fibrillation. In patients with WPW syndrome, there are 2 mechanisms for the occurrence of AF: associated with APP or not associated with APP. In some cases, when atrial flutter (AF) or AF occurs in patients with WPW syndrome, there is a possibility of developing ventricular tachycardia and ventricular fibrillation (VF). In this case, VF may become 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 arrhythmia in WPW syndrome is 1.5%. It is worth mentioning drug-induced atrial flutter (or 1C-induced) in patients with a “malignant” bundle of Kent. This is a rare form of prognostically unfavorable proarrhythmic effect of antiarrhythmic drugs. Depending on the possibility of recording an ECG, the incidence of 1C-induced paroxysm of atrial fibrillation ranges from 3.5% to 20%. R.R. Mamatkazina et al. in their article they describe such a rare case.

Diagnostics

Using a standard ECG, it is possible to determine the localization of the AP.
Type A characterized by a positive D-wave in leads V1–V2. The APP between the atrium and the ventricle is located on the left side of the septum; the LV is excited earlier.
Type B manifests itself as a negative D-wave in leads V1–V2, but a positive one in leads V4–V6. The AP 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 negative in V5–V6, the AP is located in the lateral wall of the LV and connects the subepicardial portion of the left atrium with the lateral wall of the LV.
An interesting approach to improve the accuracy of diagnosing the localization of the AP by ECG was proposed by L.A. Bockeria et al. . By using regression analysis the dependence of the location of the AP on the amplitude of the D-wave in 12 ECG leads was revealed. The accuracy of APP localization in 11 segments of the AV sulcus was 100% in retrospective analysis and 88% in prospective analysis, which is significantly higher than using other algorithms. But today, intracardiac electrophysiological study (EPS) remains the “gold standard” and, according to most authors, a mandatory stage in the preoperative topical diagnosis of DPP. Recommendations from the All-Russian Scientific Society of Specialists in Clinical Electrophysiology, Arrhythmology and Cardiac Stimulation (VNOA) for conducting EPS in patients with cardiac arrhythmias have been developed (2005).
It is also worth noting that cases have been 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 in which an intermittent WPW syndrome was identified in a 32-year-old man preparing for urological surgery. After premedication and spinal anesthesia, WPW syndrome was constantly recorded on the monitor during surgery and in the early postoperative period. The authors write about the need to perform EFI before surgery and, if WPW syndrome is established, if possible, perform RFA before a planned operation. The literature describes cases where WPW syndrome was found already during surgery during spinal anesthesia.

Radiofrequency ablation in the treatment of WPW syndrome

Direct current catheter ablation and radiofrequency energy have recently been used to treat patients with chronic AV tachycardias, idiopathic ventricular tachycardias, and various types 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, the researchers note that the risk of recurrent AF after catheter ablation correlates positively with patient age and is increased with other structural heart disease or left atrial dilatation. In patients under 50 years of age this occurs in 10–12% of cases, over 50 years of age – in 35–40%, over 60 years of age – in more than 55%. In such cases, RFA of the DPP is repeated. Even after effective radiofrequency ablation of the accessory tract, 25% of patients continue to experience recurrent AF, and experts suggest that AF may result from concomitant electrophysiological changes in the atria that are not related to the presence of the accessory pathway.
The predisposition to the development of AF in WPW syndrome may be explained by a decrease in the duration of the refractory period of atrial myocardial cells and impaired intra- and interatrial conduction. There are also suggestions that the occurrence of AF after RFA is associated with hemodynamic disorders that develop during tachycardia and lead to an increase in sympathetic tone nervous system, hypoxemia of the atrial myocardium.
In 6–10% of cases, RFA is accompanied by the development of complications: damage to the heart (tamponade) and blood vessels (hematoma), the development of thromboembolism, and exudative pericarditis. Therefore, some experts prefer to use the method of open electrical destruction of DPP.
Currently, complications during endocardial EPI and RFA of DPP can be divided into 4 groups: 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 heart valves, microembolism, perforation of the coronary sinus or myocardial wall, dissection of the coronary arteries, thrombosis); caused by RF exposure (AV block, 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 APs located near the AV node and the His bundle. The incidence of cardiac tamponade varies from 0.13 to 1.1%. Mortality associated with the DPP ablation procedure does not exceed 0.2%.
In 2005, VNOA recommendations for the treatment of AF and ventricular preexcitation syndrome were developed. In children, RFA is not the method of choice, as it has a very high risk of complications. According to G. Vignati et al. , RFA should be performed on children no younger than 12 years of age, since as the patient’s age increases, there is a possibility of fibrosis developing in the area of ​​the accessory tract and loss of its conductive capacity.

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 lysosome integration and function. Mutation of this gene leads to Danon disease, which includes such manifestations as WPW syndrome, hypertrophic cardiomyopathy, muscular dystrophy, and 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 mutation of the PRKAG2 gene 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 lesions) 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 the non-familial form of WPW syndrome. One of the articles by foreign authors describes a case of WPW syndrome in 3 siblings. Moreover, all girls had a left-lateral APP. The girls' parents and other close relatives were healthy. What is noteworthy is that, despite the same location of the APP, only one of the sisters had antegrade conduction, and the disease manifested itself with persistent tachycardia, while others noted only rare heartbeats in adolescence, which did not bother them. However, the authors note that it is possible that over time the disease could have manifested 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 predictor gene for WPW syndrome (PRKAG2) was sequenced in healthy and affected 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. The patients were found to have premature excitation of the ventricles and cardiac hypertrophy.

Conclusion

Taking into account the global experience of 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 or 24-hour ECG, and if the genetic test is positive, an EPI is performed.
EchoCG at the first stage also allows one to suspect latent forms of WPW syndrome by the presence of pathologies such as MV prolapse and additional chordae, which often accompany WPW syndrome.
As for the treatment of WPW syndrome, RFA is becoming increasingly common today. Although it is worth noting that this technique is not 100% effective and does not have absolute indications. When choosing this method treatment, it is necessary to take into account many factors: indications and contraindications according to the recommendations of the VNOK.

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WPW syndrome, Wolf-Parkinson-White syndrome (Wolff, Parkinson, White), LGL syndrome (Laun-Ganong-Levine), CLC syndrome (Clerk-Levy-Cristesco)

Version: MedElement Disease Directory

Premature excitation syndrome (I45.6)

general information

Short description

I45.6 Premature excitation syndrome. Anomalies of atrioventricular excitation
Atrioventricular conduction:
. accelerated
. via additional routes
. with premature excitation
Lown-Ganong-Levine syndrome
Wolff-Parkinson-White syndrome

Syndromes of preexcitation (premature excitation) of the ventricles are the result of congenital disorders in the conduction system of the heart, associated with the presence of additional abnormal conduction pathways between the myocardium of the atria and ventricles, often accompanied by the development of paroxysmal tachycardias.

In clinical practice, the most common 2 syndromes (phenomena) of pre-excitation are:

Wolff-Parkinson-White syndrome (Wolff-Parkinson-White or WPW syndrome).
- Clerk-Levy-Christesco syndrome (CLC syndrome), or short PQ interval syndrome. In the English-language literature, this syndrome is also called LGL (Lown-Ganong-Levine) syndrome.

The clinical significance of pre-excitation syndromes is determined by the fact that when they are present, cardiac arrhythmias (paroxysmal tachycardias) develop frequently, are severe, sometimes life-threatening, requiring special approaches to therapy.

Diagnosis of ventricular preexcitation syndromes is based on identifying characteristic ECG signs.

Wolf-Parkinson-White syndrome (Wolff, Parkinson, White)- due to the presence of an additional abnormal conduction pathway between the atria and ventricles. Other names for the syndrome are WPW syndrome, premature ventricular excitation syndrome.

CLC (Clerk-Levy-Cristesco) syndrome is caused by the presence of an additional abnormal path of electrical impulse conduction (James bundle) between the atria and the His bundle.

Classification

There are two types of WPW syndrome:

Type A (rare)- an additional pathway for impulse conduction is located to the left of the atrioventricular node between the left atrium and the left ventricle, which contributes to premature excitation of the left ventricle;

Type B- the accessory pathway of impulses is located on the right between the right atrium and the right ventricle, which contributes to premature excitation of the right ventricle.

Etiology and pathogenesis

• Etiology of ventricular preexcitation syndromes

  Ventricular preexcitation syndromes are caused by the preservation of additional impulse pathways as a result of incomplete cardiac restructuring during embryogenesis.

  The presence of additional abnormal pathways in WPW syndrome (bundles, or paths, of Kent) is a hereditary disorder. The association of the syndrome with a genetic defect in the PRKAG2 gene, located on the long arm of chromosome 7 at the q36 locus, has been described. Among the patient's blood relatives, the prevalence of the anomaly is increased by 4-10 times.

  WPW syndrome is often (up to 30% of cases) combined with congenital heart defects and other cardiac anomalies such as Ebstein's anomaly (represents a displacement of the tricuspid valve towards the right ventricle with valve deformation; the genetic defect is presumably localized on the long arm of chromosome 11), as well as stigmas of embryogenesis (dyspolasia syndrome connective tissue). There are familial cases in which multiple additional pathways are more common and the risk of sudden death is increased. Combinations of WPW syndrome with genetically determined hypertrophic cardiomyopathy are possible.

  Neurocirculatory dystonia and hyperthyroidism contribute to the manifestation of WPW syndrome. Wolff-Parkinson-White syndrome can also manifest itself against the background of ischemic heart disease, myocardial infarction, myocarditis of various etiologies, rheumatism and rheumatic heart defects.

  CLC syndrome is also a congenital abnormality. Isolated shortening of the PQ interval without paroxysmal supraventricular tachycardia can develop with ischemic heart disease, hyperthyroidism, active rheumatism and is benign in nature.

Pathogenesis of ventricular preexcitation syndromes

The essence of the syndrome (phenomenon) of premature excitation of the ventricles is the abnormal spread of excitation from the atria to the ventricles along the so-called accessory pathways, which in most cases partially or completely “shunt” the AV node.

As a result of the abnormal spread of excitation, part of the ventricular myocardium or the entire myocardium begins to be excited earlier than is observed with the normal spread of excitation along the AV node, the His bundle and its branches.

Several additional (abnormal) AV conduction pathways are currently known:

Kent's bundles connecting the atria and ventricular myocardium, including hidden retrograde ones.
- Macheim's fibers connecting the AV node to the right side of the interventricular septum or the branches of the right bundle branch, less often - the trunk of the His bundle to the right ventricle.
- Bundles of James, connecting the sinus node to the inferior part of the AV node.
- Tract of Breschenmanche, connecting the right atrium with the common trunk of the His bundle.

The presence of additional (abnormal) pathways leads to disruption of the sequence of ventricular depolarization.

Having formed in the sinus node and causing depolarization of the atria, excitation impulses propagate to the ventricles simultaneously through the atrioventricular node and the accessory pathway.

Due to the absence of the physiological delay of conduction characteristic of the AV node, in the fibers of the accessory tract, the impulse propagated through them reaches the ventricles earlier than the one conducted through the AV node. This causes a shortening of the PQ interval and deformation of the QRS complex.

Since the impulse is conducted through the cells of the contractile myocardium at a lower speed than through the specialized fibers of the cardiac conduction system, the duration of ventricular depolarization and the width of the ORS complex increase. However, a significant part of the ventricular myocardium is covered by excitation, which manages to spread in the normal way, through the His-Purkinje system. As a result of excitation of the ventricles from two sources, confluent QRS complexes are formed. The initial part of these complexes, the so-called delta wave, reflects the premature excitation of the ventricles, the source of which is the accessory pathway, and its final part is caused by joining their depolarization with an impulse that is conducted through the atrioventricular node. In this case, the widening of the QRS complex neutralizes the shortening of the PQ interval, so that their total duration does not change.

However, the main clinical significance of additional conduction pathways is that they are often included in the loop of circular motion of the excitation wave (re-entry) and thus contribute to the occurrence of supraventricular paroxysmal tachycardias.

Currently, it is proposed that premature excitation of the ventricles, not accompanied by the occurrence of paroxysmal tachycardia, be called “ “pre-excitation phenomenon”, and cases when there are not only ECG signs of pre-excitation, but also paroxysms of supraventricular tachycardia develop - “ pre-excitation syndrome”, however, a number of authors do not agree with this division.

As mentioned above, with WPW syndrome, an abnormal excitation impulse propagates along the Kent bundle, which can be located to the right or left of the atrioventricular node and the His bundle. In more rare cases, the abnormal excitation impulse may propagate through the James bundle (connects the atrium to the terminal part of the AV node or the beginning of the His bundle), or the Mahaim bundle (passes from the beginning of the His bundle to the ventricles). In this case, the ECG has a number of characteristic features:

• The propagation of the impulse along the Kent bundle leads to the appearance of a shortened PQ interval, the presence of a delta wave, and widening of the QRS complex.
• The propagation of the impulse along the James bundle leads to the appearance of a shortened PQ interval and an unchanged QRS complex.
• When the impulse propagates along the Mahaim beam, a normal (less often elongated) PQ interval, a delta wave and a widened QRS complex are recorded.

Epidemiology

Sign of prevalence: Extremely rare

The prevalence of WPW syndrome, according to various sources, ranges from 0.15 to 2%; CLC syndrome is detected in approximately 0.5% of the adult population.

The presence of additional conduction pathways is found in 30% of patients with supraventricular tachycardia.

Ventricular preexcitation syndromes are more common among men. Ventricular preexcitation syndromes can occur at any age.

Clinical picture

Clinical diagnostic criteria

Various heart rhythm disturbances, subjectively - palpitations, dizziness, pain in the heart area

Symptoms, course

Clinically, ventricular preexcitation syndromes do not have specific manifestations and do not themselves affect hemodynamics.

Clinical manifestations of pre-excitation syndromes can be observed at different ages, spontaneously or after any disease; up to this point the patient may be asymptomatic.

Wolff-Parkinson-White syndrome is often accompanied by various heart rhythm disorders:

In approximately 75% of patients, WPW syndrome is accompanied by paroxysmal tachyarrhythmias.

In 80% of cases with WPW syndrome, reciprocal supraventricular tachycardia occurs (with age it can degenerate into atrial fibrillation).

In 15-30% of cases of Wolff-Parkinson-White syndrome, fibrillation develops, in 5% of cases - atrial flutter, and a high frequency of fibrillation or flutter is characteristic (up to 280-320 beats per minute, with flutter with 1:1 conduction) with a corresponding pronounced symptoms (palpitations, dizziness, fainting, shortness of breath, chest pain, hypotension or other hemodynamic disturbances) and an immediate threat of progression to ventricular fibrillation and death.

With WPW syndrome, it is also possible to develop less specific arrhythmias - atrial and ventricular extrasystoles, ventricular tachycardias.

Patients with CLC syndrome also have an increased tendency to develop paroxysmal tachycardias.

Diagnostics

• Characteristic features of the ECG in WPW syndrome

  The PQ interval is usually shortened to 0.08-0.11 s;

  The P wave is normal in shape;

  The shortened PQ interval is accompanied by a widened QRS complex up to 0.12-0.15 s, while it has a large amplitude and is similar in shape to the QRS complex with bundle branch block;

  At the beginning of the QRS complex, an additional delta wave is recorded, shaped like a ladder, located at an obtuse angle to the main tooth of the QRS complex;

  If the initial part of the QRS complex is directed upward (R wave), then the delta wave is also directed upward;

  If the initial part of the QRS complex is directed downward (Q wave), then the delta wave also points downward;

  The longer the duration of the delta wave, the more pronounced the deformation of the QRS complex;

  In most cases, the ST segment and T wave are shifted in the direction opposite to the direction of the main wave of the QRS complex;

  In leads I and III, the QRS complexes are often directed in opposite directions.

  ECG for WPW syndrome (type A):

  The ECG resembles the ECG for right bundle branch block;

  The alpha angle lies within +90°;

  In the precordial leads (or right precordial leads), the QRS complex is directed upward;

  In lead V1, the ECG looks like an R wave of large amplitude with a steep rise, or Rs, RS, RSr", Rsr";

  In lead V6, as a rule, the ECG looks like Rs or R.

  ECG for WPW syndrome (type B):

  The ECG resembles the ECG for left bundle branch block;

  In the right chest leads, the negative S wave predominates;

  In the left chest leads there is a positive R wave;

  The Eos of the heart is deviated to the left.

• ECG signs of CLC syndrome

  Shortening the PQ(R) interval, the duration of which does not exceed 0.11 s.
  - The absence of an additional excitation wave in the QRS complex - delta waves.
  - The presence of unchanged (narrow) and undeformed QRS complexes (except for cases of concomitant blockade of the legs and branches of the His bundle).
  

  ECG Holter monitoring is used to detect periodic rhythm disturbances.

  Echocardiography necessary to identify concomitant cardiomyopathies, heart defects and signs of Ebstein's anomaly.

  Exercise testing - bicycle ergometry or treadmill test. The use of these techniques in the diagnosis of pre-excitation syndromes is limited, since the presence of a history of paroxysmal tachycardias is a relative contraindication to stress testing, which is especially important in the case of pre-excitation syndromes, when tachycardias are especially dangerous.

  CLC and WPW syndromes often cause false-positive results during exercise testing.

  Transesophageal cardiac pacing (TEC), carried out in case of overt WPW syndrome makes it possible to prove, and in case of latent syndrome, to suggest the presence of additional conduction pathways (characterized by a refractory period of less than 100 ms), induce supraventricular paroxysmal tachycardia, atrial fibrillation and flutter. Transesophageal cardiac stimulation does not allow for accurate topical diagnosis of additional pathways, assessment of the nature of retrograde conduction, or identification of multiple additional pathways.

  Electrophysiological study of the heart (EPS)

  Due to the spread in last years Surgical methods for treating patients with WPW syndrome (destruction of an abnormal beam) are constantly improving methods for accurately determining its localization. The most effective methods are intracardiac EPI, in particular endocardial (preoperative) and epicardial (intraoperative) mapping.

  At the same time, with the help complex technique determine the area of ​​the earliest activation (pre-excitation) of the ventricular myocardium, which corresponds to the localization of the additional (abnormal) bundle.

  Cardiac electrophysiology (EPS) is used in patients with WPW syndrome for the following purposes:

  To evaluate the electrophysiological properties (conduction capacity and refractory periods) of additional abnormal pathways and normal pathways.
  - In order to determine the number and localization of additional pathways, which is necessary for further high-frequency ablation.
  - In order to clarify the mechanism of development of concomitant arrhythmias.
  - To evaluate the effectiveness of drug or ablative therapy.

  Surface multipolar ECG mapping

  In recent years, in order to accurately determine the localization of the abnormal bundle, the method of surface multipolar ECG mapping of the heart has been used, which in 70-80% of cases also allows the approximate location of the Kent bundles to be determined. This significantly reduces the time for intraoperative detection of additional (abnormal) beams.

Differential diagnosis

Differential diagnosis of manifest syndrome of premature excitation of the ventricles in sinus rhythm is carried out with bundle branch blocks with similar graphics of the QRS complex. In this case, it is important to search for the delta wave through careful analysis of the ECG in all 12 leads.

Complications

Complications of ventricular preexcitation syndromes

Tachyarrhythmia.
- Sudden cardiac death.

Risk factors for sudden death in WPW syndrome include:

The duration of the minimum RR interval for atrial fibrillation is less than 250 ms.
- The duration of the effective refractory period of additional pathways is less than 270 ms.
- Left-handed additional paths or several additional paths.
- History of symptomatic tachycardia.
- Presence of Ebstein's anomaly.
- Familial nature of the syndrome.
- Recurrent course of ventricular preexcitation syndromes.

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Treatment

Ventricular preexcitation syndromes do not require treatment in the absence of paroxysms. However, observation is necessary, since cardiac arrhythmias can occur at any age.

Relief of paroxysms of orthodromic (with narrow complexes) reciprocal supraventricular tachycardia in patients with WPW syndrome is carried out in the same way as other supraventricular reciprocal tachycardias.

Antidromic (wide complex) tachycardias treated with ajmaline 50 mg (1.0 ml of 5% solution); The effectiveness of ajmaline in paroxysmal supraventricular tachycardias of unspecified etiology makes it highly likely to suspect WPW. Administration of amiodarone 300 mg, rhythmylene 100 mg, procainamide 1000 mg may also be effective.

In cases where paroxysm occurs without pronounced hemodynamic disorders and does not require emergency relief, regardless of the width of the complexes, amidarone is especially indicated for pre-excitation syndromes.

Class IC drugs and “pure” class III antiarrhythmics are not used for WPW tachycardias due to the high risk of their inherent proarrhythmic effect. ATP can successfully stop tachycardia, but should be used with caution as it can provoke atrial fibrillation with a high heart rate. Verapamil should also be used with extreme caution (the danger of an increase in heart rate and transformation of arrhythmia into atrial fibrillation!) - only in patients with a history of successful experience with its use.

In case of antidromic (wide complex) paroxysmal supraventricular tachycardia in cases where the presence of pre-excitation syndrome has not been proven and the diagnosis of ventricular paroxysmal tachycardia cannot be excluded, if the attack is well tolerated and there are no indications for emergency electrical pulse therapy, it is advisable to conduct transesophageal cardiac stimulation (TEC) during the paroxysm in order to clarification of its genesis and relief. If this is not possible, drugs that are effective for both types of tachycardia should be used: procainamide, amiodarone; if they are ineffective, they are stopped as with ventricular tachycardia.

After testing 1-2 drugs, if they are ineffective, you should move on to transesophageal cardiac stimulation or electrical pulse therapy.

Atrial fibrillation with the participation of additional conduction pathways poses a real danger to life due to the likelihood of a sharp increase in ventricular contractions and the development of sudden death. To relieve atrial fibrillation in this extreme situation use amiodarone (300 mg), procainamide (1000 mg), ajmaline (50 mg) or rhythmylene (150 mg). Often, atrial fibrillation with a high heart rate is accompanied by severe hemodynamic disturbances, which necessitates the need for emergency electrical cardioversion.

Cardiac glycosides, calcium antagonists of the verapamil group and beta-blockers are absolutely contraindicated in atrial fibrillation in patients with WPW syndrome, since these drugs can improve conduction along the accessory pathway, which causes an increase in heart rate and possible development ventricular fibrillation! When using ATP (or adenosine), a similar development of events is possible, however, a number of authors still recommend its use - if you are ready for immediate pacemaker.

Radiofrequency catheter ablation accessory pathways is currently the main method of radical treatment of premature ventricular excitation syndrome. Before performing ablation, an electrophysiological study (EPS) is performed to accurately determine the location of the accessory pathway. It should be borne in mind that there may be several such paths.

The right-sided accessory pathways are accessed through the right jugular or femoral vein, and the left-sided accessory pathways are accessed through the femoral artery or transseptal vein.

Treatment success, even with multiple accessory pathways, is achieved in approximately 95% of cases, and the complication rate and mortality are less than 1%. One of the most severe complications is the occurrence of high-degree atrioventricular block when attempting to ablate the accessory pathway located near the atrioventricular node and the His bundle. The risk of relapse does not exceed 5-8%. It should be noted that catheter ablation is more cost-effective than long-term drug prophylaxis and open-heart surgery.

Indications for high-frequency ablation:

Patients with symptomatic tachyarrhythmia are poorly tolerated or refractory to medical therapy.

Patients with contraindications to the administration of antiarrhythmics or the impossibility of their administration due to conduction disturbances that manifest themselves at the time of relief of paroxysmal tachycardia.

Young patients - to avoid long-term use of medications.

Patients with atrial fibrillation, as this is at risk of developing ventricular fibrillation.

Patients with antidromic (wide complex) reentrant tachycardia.

Patients with the presence of several abnormal conduction pathways (according to EPI) and various variants of paroxysmal supraventricular tachycardia.

Patients with other cardiac anomalies requiring surgical treatment.

Patients whose professional performance may be affected by recurrent unexpected episodes of tachyarrhythmias.

Patients with a family history of sudden cardiac death.

In the presence of arrhythmias against the background of WPW syndrome, “wait-and-see” tactics (refusal of preventive antiarrhythmic therapy) are practically not used.

Forecast

In patients with signs of premature excitation of the ventricles in the absence of complaints, the prognosis is good, since the likelihood of rapid impulse conduction through the accessory pathway is low.

According to most experts, such patients do not require electrophysiological examination of the heart (EPS) or special treatment. Exceptions include patients with a family history of sudden death, as well as those with social indications, such as professional athletes or pilots.

However, it is important to remember that approximately 80% of patients with WPW experience paroxysmal reentrant tachycardia, 15-30% experience atrial fibrillation, and 5% experience atrial flutter. Ventricular tachycardia develops quite rarely. Patients with WPW syndrome have a small risk of sudden cardiac death (0.1% of cases). The use of digoxin and verapamil in treatment may increase the likelihood of sudden cardiac death.

If there are complaints, especially in patients with a history of attacks of atrial fibrillation, the risk of rapid atrioventricular impulse conduction during atrial fibrillation and the development of ventricular fibrillation is higher.

To indirectly assess the risk of rapid atrioventricular impulse conduction, three simple signs can be used. A fairly long (more than 280-300 ms) effective refractory period of antegrade impulse conduction along the accessory pathway and therefore a low risk of sudden death is evidenced by:

1. Detection of intermittent premature excitation, that is, alternation of wide QRS complexes with a delta wave and narrow complexes without it, when recording a 12-lead ECG or ECG monitoring.

2. Sudden disappearance of signs of premature excitation of the ventricles during stress tests, when hypercatecholaminemia contributes to shortening the effective refractory period of the accessory pathway. This sign has a very high negative predictive value, but is observed in no more than 10% of patients.

3. The occurrence of complete blockade of conduction along the accessory atrioventricular pathway after intravenous administration of procainamide at a dose of 10 mg/kg for 5 minutes. It is determined by the disappearance of the delta wave and prolongation of the PQ interval against the background of sinus rhythm.

High-frequency ablation in most cases significantly improves the prognosis.

Prevention

Prevention for WPW syndrome is secondary and includes appropriate antiarrhythmic therapy to prevent recurrent episodes of arrhythmias.

Prevention of supraventricular tachycardia is carried out by general rules treatment of paroxysmal supraventricular tachycardias. However, therapy with verapamil, diltiazem, and digoxin is contraindicated, since they can lead to severe tachyarrhythmia during a possible paroxysm of atrial fibrillation.

For drug prevention of paroxysms of atrial fibrillation in the presence of premature ventricular excitation syndrome, it is most advisable to use drugs that can suppress ectopic activity in the atria and ventricles and thereby prevent the formation of extrasystoles, as well as lengthen the effective refractory period simultaneously in the atrioventricular node and the accessory pathway, so as not to allow a significant ventricular rate in cases of atrial fibrillation. These requirements are best met by class 1C antiarrhythmic drugs (ethacizine 75-200 mg/day, propafenone (preferably retard forms) 600-900 mg/day). An alternative is class IA drugs (disopyramide 300-600 mg/day, quinidine-durules 0.6 mg/day), which, however, are less effective and more toxic. In case of ineffectiveness or intolerance of drugs of classes 1C and IA and in cases of impossibility of ablation of the accessory pathway, long-term administration of amiodarone is resorted to.

Patients with ventricular preexcitation syndromes should be periodically observed by their attending physician to assess the frequency of recurrence of arrhythmias, the effectiveness of antiarrhythmic therapy, and the presence of side effects from pharmacotherapy. Periodic Holter monitoring is necessary. Monitoring of patients after high-frequency ablation is also necessary.

Information

Information

1. Ardashev V.N., Steklov V.I. Treatment of heart rhythm disorders. M., 1998., 165 p.
2. Fomina I.G. Heart rhythm disturbances. M., “Russian Doctor”, 2003. - 192 p.
3. Bunin Yu.A. Treatment of cardiac tachyarrhythmias. M. 2003.- 114 p.
4. Prokhorovich E.A., Talibov O.B., Topolyansky A.V. Treatment of rhythm and conduction disorders at the prehospital stage. Attending physician, 2002, No. 3, p. 56-60
5. ACC/AHA/ESC guidelines for management of patients with atrial fibrillation. European Heart J., 2001, 22, 1852-1923
6. Doshchicin V.L. Practical electrocardiography. — 2nd ed., revised. and additional - M.: Medicine, 1987. - 336 p.
7. Isakov I. I., Kushakovsky M. S., Zhuravleva N. B. Clinical electrocardiography (heart rhythm and conduction disorders): A guide for doctors. — Ed. 2nd revision and additional - L.: Medicine, 1984. - 272 p.
8. A.B. de Luna. Clinical ECG Guide. - M., Medicine, 1993
9. Diseases of the heart and blood vessels. Guide for doctors in 4 volumes. Ed. Chazova E.I. - M., Medicine, 1992
10. Internal illnesses. Ed. E. Braunwald, K. Isselbacher, R. Petersdorf and others - M., Medicine, 1994.
11. Mazur N.A. Paroxysmal tachycardia. - M., Medicine, 1984.
12. Murashko V.V., Strutynsky A.V. Electrocardiography. - M., Medicine, 1991.
13. Orlov V.N. Guide to electrocardiography. - M., Medicine, 1984.
14. Smetnev P.S., Grosu A.A., Shevchenko N.M. Diagnosis and treatment of cardiac arrhythmias. - “Shtiintsa”, 1990.
15. Yanushkevicius Z.I. and others. Disturbances of rhythm and conduction of the heart. - M., Medicine, 1984.
16. Kushakovsky M.S. Cardiac arrhythmias. -1992,1999. -Folio. -639 pp.

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Symptoms and course of the disease

Wolff-Parkinson-White syndrome can be asymptomatic if the heart rate does not exceed 200 beats per minute and is detected only by cardiac examination. If tachycardia exceeds 200 heartbeats, clinical manifestations occur in the form of a feeling of the heart “jumping out”, dizziness, and loss of consciousness often occurs.

According to statistics, in 70% of patients, VPU syndrome occurs in a mild form, without causing circulatory disorders and disability due to adaptive mechanisms.

The main manifestations of WPW syndrome:

1. Sudden onset of palpitations.
2. Interruptions in the functioning of the heart.
3. Throbbing in the head or throat.
4. General weakness, dizziness, decreased tolerance to physical activity, increased fatigue during an attack.
5. Possible loss of consciousness.
6. Dyspnea.
7. During an attack, dizziness or loss of consciousness may develop.
8. Decreased blood pressure (hypotension or unstable blood pressure).

Wolff-Parkinson-White syndrome can be accompanied by sudden episodes of very fast heartbeats and a palpitating sensation.

Already in children of the first year of life, with a prolonged attack, heart failure can develop. Sometimes the child seems to be suffocating; sometimes he sleeps all the time, stops eating well; rapid visible pulsations of the chest wall appear.

The first episodes usually occur in the teens or early 20s. Typical attacks begin suddenly, often during physical activity. They last from a few seconds to several hours, but rarely longer than 12 hours. In a young and otherwise physically healthy person, attacks of tachycardia usually cause few symptoms, but very fast heartbeats are unpleasant and distressing to the person. Sometimes they can lead to fainting or heart failure.

The tachycardia typical of Wolff-Parkinson-White syndrome sometimes develops into atrial fibrillation. The latter is especially dangerous for about 1% of patients with Wolff-Parkinson-White syndrome, because in them the additional conduction pathway can very quickly conduct many more impulses to the ventricles than the normal pathway. The result is an extremely fast ventricular rate, which is potentially life-threatening. Not only does the heart work very inefficiently when the ventricles contract at this rate, it can progress to life-threatening ventricular fibrillation.

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Treatment of the disease

There are two treatment methods for WPW syndrome: conservative and surgical.

1. Conservative method. Prevention of attacks of tachycardia (rapid heartbeat). For this purpose, prophylactic antiarrhythmic drugs are used (drugs that prevent the development of rhythm disturbances (any rhythm other than normal - rhythm healthy person). Some antiarrhythmic drugs are contraindicated in WPW syndrome because they may worsen its course. These are: blockers of slow calcium channels (drugs that act on the cells of the heart and blood vessels, causing a decrease in heart rate, reducing vascular tone); β-blockers (drugs that interfere with the stimulation of receptors for adrenaline and norepinephrine (stress hormones)); cardiac glycosides (drugs that increase the force of heart contractions). Termination of an attack of tachycardia. For this purpose, intravenous administration of antiarrhythmic drugs is used.
2. Surgical method. Indications for surgical treatment are:

• frequent attacks of atrial fibrillation (more than 1 time per week);
• attacks of tachycardia with impaired general circulation (loss of consciousness, weakness, decreased blood pressure);
• persistence of tachycardia attacks when taking antiarrhythmic drugs;
• situations where long-term drug therapy is undesirable (young age).

If conservative treatment is ineffective, as well as with tachycardia of more than 200 beats per minute, surgical treatment is used - an artificial pacemaker is implanted into the heart or destruction of the additional nerve bundle of Kent.

A popular treatment method for this disease is radiofrequency ablation of the Kent beam. The method has significant advantages over implantation of a pacemaker, since it does not require opening chest, implantation of equipment and care for it, constant monitoring by a doctor and taking anticoagulants. The essence of the procedure is that a conductor (thin tube) is inserted into the heart through the femoral vessels. An impulse is sent through the conductor, destroying (cauterizing) the beam. After the manipulation, testing is carried out to monitor its effectiveness. If necessary, repeat ablation is performed immediately until the full effect is achieved.

Diagnosis of the disease

Any diagnosis begins with a visual examination by a specialist who, while listening to the work of the myocardium, observes pathogenic noises. In addition, abnormal heart rate also causes a certain amount of alarm, forcing a full clinical examination.

Diagnosis of Wolff-Parkinson-White syndrome is not limited to just a conventional electrocardiographic study. Modern methods are used:

• daily (Holter) and fragmentary ECG monitoring;
• electrophysiological study of the heart (EPS);
• endocardial mapping;
• computed tomography of the heart;
• ultrasound scanning;
• echocardiography;
• Magnetic resonance imaging;
• esophageal cardiography, which gives more accurate results compared to a conventional ECG;
• Holter cardiography, which allows you to constantly record the patient’s heart rhythm throughout the day in his usual mode of life, both during wakefulness and during sleep, using a special portable electronic sensor.

Typically, a full range of diagnostic measures takes no more than two days.

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Since the pathologies are very different, their treatment methods also differ significantly from each other. Vascular surgery in Israel carries out a variety of operations by type, level of complexity, etc. which effectively help eliminate the problem and save a person’s life.

Wolff-Parkinson-White syndrome (WPW) is a syndrome of abnormal excitation of the ventricles of the heart along the accessory duct between the ventricle and the atrium. Many people with WPW syndrome do not experience significant health problems until a certain point. And although WPW syndrome cannot always be detected on an ECG, approximately 0.15 to 0.30% of the total population of the planet suffers from this pathology. Men are more susceptible to this disease than women.

general information

WPW syndrome was first isolated and described by three doctors independently in 1930, but it was not named until ten years later.

Essentially, WPW syndrome is a heart rhythm disorder caused by the formation of an additional channel between the atrium and ventricle, bypassing the normal structure of the cardiac conduction system.

Cardiac impulses travel faster along the accessory connection, which leads to overexcitability of the ventricles. This sometimes appears on the ECG as a delta wave.

WPW syndrome is a heart rhythm disorder caused by the formation of an additional channel between the atrium and ventricle

Etiology

The disease is a congenital pathology of the structure of the heart, the cause of which is currently unknown. In some cases of the disease, a connection with the development of the syndrome and a mutation in the PRKAG2 gene, which is inherited in an autosomal dominant manner, has been identified.

Manifestations of the disease

The onset of WPW syndrome will vary depending on the age at which the disease appears. All age categories are susceptible to this pathology, however, most often the disease is detected in the patient’s childhood or adolescence (from 10 to 20 years).

The syndrome is not associated with structural abnormalities of the heart, but may be a concomitant pathology of congenital defects.

In clinical practice, it is customary to distinguish forms of the disease:

• latent – ​​absence of signs of ventricular overexcitation during sinus rhythm;
• manifesting - a combination of ventricular overexcitation and tachyarrhythmia;
• intermittent – ​​transient signs of ventricular excitation, sinus rhythm with confirmed AVRT;
• multiple – the presence of two or more additional channels;
• WPW phenomenon - the absence of rhythm disturbance in the presence of a delta wave on the ECG.

Depending on the age of the patient during the period of manifestation (manifestations of the disease after a latent course), symptoms may vary.

WPW phenomenon – absence of rhythm disturbance in the presence of a delta wave on the ECG

WPW syndrome in newborns has the following symptoms:

• tachypnea (rapid breathing);
• pallor;
• anxiety;
• refusal to feed;
• sometimes fever may occur.

SVC syndrome in older children usually has the following symptoms:

• feeling of heartbeat;
• chest pain;
• labored breathing.

Mature and elderly patients may describe the following:

• sudden stabbing pain in the heart;
• throbbing sensation in the head or throat;
• dyspnea;
• rapid pulse (usually the pulse is so fast that it is almost impossible to count);

Increased heart rate, usually the pulse is so fast that it is almost impossible to count

• weakness;
• unstable blood pressure levels;
• dizziness;
• decreased activity;
• rarely – loss of consciousness.

In this case, during inspections and examinations the following may be observed:

• In the vast majority of cases normal result cardiograms.
• During episodes of tachycardia, the patient experiences increased sweating, decreased blood pressure, and “coolness” of the skin.

Diagnostics

If a patient is suspected of having WPW syndrome, a comprehensive diagnosis is necessary, including a number of clinical, laboratory and instrumental examinations:

• daily ECG monitoring (electrocardiogram using the Holter method);
• electro-physiological study of the cavities of the heart;
• EchoCG;

Ultrasound of the heart, one of the types of diagnosis of the disease

• TEES (transesophageal cardiac conduction system test);
• extended blood test;
• liver tests;
• kidney function analysis;
• hormonal panel (in this case, the thyroid gland is examined);
• drug screening.

Treatment and prevention

Provided there is no deterioration, SVC syndrome does not require specific treatment. Therapy will be aimed at preventing attacks.

The main method of preventing recurrence of SVC syndrome is catheter ablation. This is a surgical operation to destroy the source of arrhythmia.

For pharmacological prevention of episodes of tachycardia, antiarrhythmic and antihypertensive drugs are used (if the patient does not have a decrease in blood pressure):

• "Amiodarone";
• "Cordaron";
• "Sotalol";

Cordarone tablets 200 mg No. 30

• "Rotaritmil";
• "Disopyramide".

However, one should be careful with antiarrhythmic drugs, which can improve impulse conduction and increase the refractory period of the AB junction. In this case, drugs from the following groups will be contraindicated:

• calcium channel blockers;
• cardiac glycosides;
• B-blockers.

If supraventricular tachycardia develops against the background of SVC, ATP (adenosine triphosphoric acid) is used.

If atrial fibrillation occurs, defibrillation is performed.

Forecasts

SVC syndrome with timely treatment and compliance with preventive measures has a favorable prognosis. The course of the disease, after its detection, depends on the duration and frequency of tachycardia attacks. Attacks of arrhythmia rarely lead to circulatory problems. In 4% of cases, death is possible due to sudden cardiac arrest.

Patients diagnosed with SVC syndrome are advised to undergo systematic examinations and consultations with a cardiologist. Patients need to undergo an ECG examination at least once a year.

Even if the disease occurs in a latent or mild form, there is a risk of negative dynamics in the future.

Excessive physical and emotional stress is contraindicated for patients. If you have WPW syndrome, you should be careful with any type of physical activity, including therapeutic exercise. physical culture and sports. The decision to start classes should not be made independently; in such a situation, consultation with a specialist is required.

Normally, an electrical impulse is generated in the sinus node of the heart, passes through the atrial pathways to the atrioventricular junction, and from there it is sent to the ventricles. This arrangement allows the chambers of the heart to contract sequentially, ensuring its pumping function.

Wolff-Parkinson-White syndrome is characterized by the fact that in this disease, an additional conduction pathway bypasses the A-V node, directly connecting the atria and ventricles. Often it does not cause any complaints. But this condition can cause a serious heart rhythm disorder - paroxysmal tachycardia.

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General information

Wolff-Parkinson-White (WPW) syndrome is the second most common cause of attacks of supraventricular tachycardia. It was described in 1930 as ECG changes in young healthy patients accompanied by episodes of rapid heartbeat.

The disease occurs in 1 - 3 people out of 10 thousand. With congenital heart defects, its prevalence is 5 cases per 10 thousand. Many newborns have additional pathways, but as the child grows, they disappear on their own. If this does not happen, the WPW phenomenon occurs. The transmission of the disease by inheritance has not been proven, although there is evidence of its genetic nature.

Mechanism of development of WPW syndrome

Patients with WPW usually do not have any heart disease. Sometimes the disease occurs against the background of Marfan syndrome or with ventricular or septal defects.

The pathology first manifests itself in the prenatal period or in children of the first years of life with attacks of palpitations. But most often the disease is asymptomatic. There are also difficulties in ECG diagnosis, so some cases of WPW syndrome remain unrecognized.

Development mechanism

Wolff-Parkinson-White syndrome in children is caused by the presence of “muscle bridges”. They connect the myocardium of the atria and ventricles, bypassing A-B node. Their thickness does not exceed 7 mm. Externally, they do not differ from ordinary myocardium.

Additional pathways can be located in the septum between the atria (septal), in the right or left wall of the heart. Previously, they were called by the names of the scientists who described them - Maheim fibers, Kent bundles, Brechenmacher and James tracts. Nowadays, precise anatomical classification prevails in medical practice.

Excitation from the conduction pathways of the atria enters the ventricular myocardium, causing its premature excitation. In some cases, the electrical impulse seems to close into a ring formed by normal and additional beams. It begins to rapidly circulate along a closed path, causing a sudden attack of heartbeat - atrioventricular tachycardia.

Depending on the direction of impulse movement, orthodromic and antidromic A-V tachycardias in WPW syndrome are distinguished. In the orthodromic form, which is recorded in 90% of patients, the excitation first passes along the normal path through the A-V node, and then returns to the atria along additional bundles. Antidromic tachycardia is caused by a signal entering the myocardium along an accessory pathway and returning in the opposite direction through A-B connection. The symptoms of these types of arrhythmia are the same.

Antidromic tachycardia in WPW syndrome

The disease may be accompanied by the development of atrial flutter or fibrillation. These arrhythmias are complicated by ventricular tachycardia and ventricular fibrillation, which increases the risk of sudden death compared with healthy people.

Classification

Doctors identify the WPW phenomenon (in English literature - a pattern). This is a condition when only ECG signs of pathology are detected, and palpitations do not occur.

WPW syndrome has the following forms:

• manifesting: there are persistent signs of WPW syndrome on the ECG;

• intermittent: ECG signs are inconsistent, the disease is detected with the development of tachycardia;

• latent: occurs only with stimulation of the atria during an electrophysiological study (EPS) or with the administration of verapamil or propranolol, as well as with massage of the coronary sinus area in the neck;

• hidden: There are no signs of WPW on the ECG, the patient is worried about attacks of tachyarrhythmia.

ECG normal and with WPW syndrome

Clinical manifestations

With a disease such as WPW syndrome, symptoms first appear in childhood or adolescence. It manifests itself extremely rarely in adults. Boys get sick 1.5 times more often than girls.

In the case of normal sinus rhythm, the patient does not have any complaints. Attacks of arrhythmia sometimes occur after emotional and physical stress. In adults, they can be triggered by alcohol consumption. In most patients, episodes of tachyarrhythmia occur suddenly.

Main complaints during an attack of arrhythmia:

• paroxysmal rhythmic accelerated heartbeat;

• “fading” of the heart;

• chest pain;

• feeling of lack of air;

• dizziness, sometimes fainting.

Many patients experience episodes of arrhythmias every month. They develop and stop suddenly. Their duration ranges from several seconds to several hours. They pass on their own or with the help of vagal tests. Prolonged attacks occur in 90% of patients and require medical attention.

Diagnostics

The basis of diagnosis is a resting ECG.

Wolf-Parkinson-White syndrome has the following ECG signs:

• shortened less than 0.12 s P-Q interval, reflecting the absence of normal conduction delay in the A-V node;

• delta wave, which occurs when an impulse passes along an additional path, bypassing the AB node;

• expansion and change in the shape of the ventricular QRS complex associated with improper propagation of excitation in the myocardium;

• the displacement of the ST segment and T wave is discordant, that is, in the opposite direction from the isoline, compared to the QRS complex.

Depending on the direction of the delta wave, there are three types of WPW syndrome:

• Type A: the delta wave is positive in the right precordial leads (V1 – V2); an additional path lies along the left side of the septum, the signal arrives earlier in the left ventricle.

• Type B: in the right chest leads the delta wave is negative, the right ventricle is excited earlier.

• Type C: the delta wave is positive in leads V1 - V4 and negative in V5 - V6, an additional path lies in the lateral wall of the left ventricle.

By analyzing the polarity of the delta wave in all 12 leads, the location of the additional beam can be determined quite accurately.

To learn how WPW syndrome occurs and what it looks like on an ECG, watch this video:

Surface ECG mapping resembles a regular ECG, with the difference that it is recorded a large number of leads. This makes it possible to more accurately determine the location of the additional excitation path. The method is used in large arrhythmology medical centers.

The method for diagnosing WPW syndrome, which is carried out in institutions at the regional level, is transesophageal electrophysiological study (). Based on its results, the diagnosis is confirmed, the characteristics of an attack of tachycardia are studied, and latent and latent forms of the disease are identified.

The study is based on stimulating heart contractions using an electrode inserted into the esophagus. It may be accompanied by unpleasant sensations, but in most cases patients easily tolerate them. To identify structural changes in the heart (prolapse, septal defects), echocardiography or ultrasound of the heart is performed.

Endocardial electrophysiological research is carried out in specialized arrhythmology departments and clinics. It is prescribed in the following cases:

• before surgery to destroy the accessory pathway;

• a history of fainting or an episode of sudden death in a patient with WPW syndrome;

• difficulties in choosing medication therapy A-B junctional tachycardia caused by this disease.

Treatment

For a pathology such as WPW syndrome, treatment can be medication or surgery.

If an attack of tachycardia occurs, accompanied by fainting, chest pain, decreased blood pressure, or acute heart failure, immediate external electrical cardioversion is indicated. Transesophageal pacing can also be used.

If the paroxysm of orthodromic tachycardia is tolerated relatively well by the patient, the following methods are used to stop it:

• Valsalva maneuver(straining after a deep breath) or lowering your face into cold water while holding your breath;

• intravenous administration of ATP, verapamil or beta blockers.

For antidromic tachycardia, the use of beta blockers, verapamil and cardiac glycosides is prohibited. One of the following drugs is administered intravenously:

• procainamide;

• propafenone;

• cordarone;

• nibentan.

Continuous therapy is prescribed when the frequency of attacks is more than 2 times a year. Propafenone or flecainide are commonly used. Their efficiency is 35%. Within 5 years, drug resistance occurs in 60–70% of patients. The use of verapamil and beta blockers for chronic therapy is contraindicated. Constant use of medications is indicated only for those patients who refuse surgery.

If tachycardia occurs only 1-2 times a year, the “pill in the pocket” strategy is recommended - the attack is stopped by the patient himself after taking propafenone or by a medical professional.

Surgical treatment of WPW syndrome is carried out by. The additional conductive path is “cauterized” with a special electrode. The effectiveness of the intervention reaches 95%.

Radiofrequency ablation

Indications:

• attacks of A-B junctional tachycardia, resistant to medications, or the patient’s refusal to take medications on a regular basis;

• attacks of atrial fibrillation or atrial tachycardia with WPW syndrome and the ineffectiveness of drugs or the patient's reluctance to continue drug therapy.

• the appearance of A-V junctional tachycardia or atrial fibrillation diagnosed during TEE;

• absence of episodes of palpitations in persons with WPW who have socially significant professions (pilots, machinists, drivers);

• a combination of signs of WPW on the ECG and indications of a previous paroxysm of atrial fibrillation or an episode of sudden cardiac death.

RFA surgery is not performed if there are no attacks of arrhythmia, they are easily tolerated, quickly relieved with medications, and also if the patient refuses surgical intervention.

Forecast

The disease occurs in young people, often reducing their ability to work. In addition, individuals with WPW syndrome have an increased risk of sudden cardiac death.

A-B tachycardia rarely causes cardiac arrest, but it is usually poorly tolerated by patients and is a common reason for calling an ambulance. Over time, attacks become protracted and difficult to treat with medications. This reduces the quality of life of such patients.

Therefore, safe and effective RFA surgery throughout the world is the “gold standard” for treating this disease, allowing it to be completely eliminated.

Wolff-Parkinson-White syndrome is asymptomatic or accompanied by attacks of rapid heartbeat, which can be life-threatening. Therefore, most patients are recommended radiofrequency ablation, a virtually safe surgical procedure that results in a cure.

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