Pathogenesis and treatment of premature ventricular excitation syndrome. Premature excitation syndrome (I45.6) Right posteroseptal DP

This means that the processes of disturbance of conductivity and excitability are “involved” in the origin.

Preexcitation leads to earlier “unscheduled” ventricular contraction. Among the population, the syndrome is rare - in 0.15% of cases. But, if we look at combinations with other arrhythmias, we get more alarming statistics:

• in patients with paroxysmal tachycardia - up to 85%;
• with atrial fibrillation - up to 30%;
• with atrial flutter - in almost every tenth person.

In 30–35% of cases, the syndrome occurs secretly.

A little history

Typical signs were first described in 1913. For a long period of time, the cause of the pathology was considered to be a type of blockade of the His bundle and its branches.

The joint report of L. Wolf, D. Parkinson and P. White in 1930 laid the foundation for research into the pathogenesis of conditions with increased excitability and conductivity of the nerve impulse.

After 2 years, the theory of additional vascular bundles was presented, which were found on histological sections only in 1942 by F. Wood.

Active research on the electrophysiology of the heart muscle has made it possible to finally establish the localization of additional tracts and discover their diversity.

If you go the other way

The origin of pre-excitation syndrome is caused by the abnormal passage of impulses through atypical pathways.

From the sinus node, located in the right atrium, excitation is directed through several bundles to the atrioventricular node, diverging along the way to the atrial myofibrils. Having passed the atrioventricular junction, it moves to the area of ​​the trunk of His, to its legs. Further along the Purkinje fibers it reaches the apices of both ventricles of the heart.

The study of the conduction system has shown the presence of additional shorter tracts through which excitation can reach the ventricles in a roundabout way. These include:

• Kent's bundle (runs from the atria to both ventricles);
• James bundle (from the atria to the lower part of the atrioventricular node and the trunk of His);
• Maheim fibers (extend deep into the myocardium of the ventricles of the heart from the trunk of His);
• the Breschenmache bundle (atriofascicular) directly connects the right atrium and the trunk of His.

Physiologists have identified other pathways. Until a certain time, they can hide in the general conduction system. But if activated, they are able to conduct nerve impulses in the opposite direction (retrograde) from the ventricles to the atria. It has also been established that up to 10% of patients with arrhythmias have several abnormal conduction pathways.

Causes

Most cardiologists treat the syndrome as a congenital anomaly. It can appear at any age. More often in young people with mitral valve prolapse and cardiomyopathies.

Premature arousal is combined with a rare congenital defect - Ebstein's anomaly

• valve insufficiency between the right cavities of the heart;
• non-closed foramen ovale (between the atria);
• reduced cavity of the right ventricle.

The opinion is expressed that the embryonic stage of the formation of abnormal excitation pathways is associated with a general disorder of the development of connective tissue in the fetus.

Types of Premature Arousal

Depending on which path the impulse takes, it is customary to distinguish 3 ECG variants of pre-excitation syndrome.

Kent type or Wolff-Parkinson-White (WPW) syndrome

Associated with the passage of an excitation wave from the atria to the ventricles along the bundle of Kent. Found in 1% of the population. It is typical to have all three signs. Normal arousal is possible at the same time. Based on the shape of the ventricular complexes, three types of WPW are distinguished:

• A - The delta wave is positive in the chest lead V1, where the highest R wave is simultaneously located.
• B - The delta wave in V1 is negative, R is low or absent, and the complex assumes a QS pattern. This type is thought to be caused by premature activation of the right ventricle.
• AB - characterized by mixed manifestations.

Often this variant of the syndrome is combined with an abnormal heart rhythm

A larger number of observations concern paroxysmal tachycardia (up to 80% of cases). The heart rate reaches 150–250 per minute.

Atrial fibrillation has a high frequency (up to 300 per minute), arrhythmogenic collapse is possible.

James type or Lown-Genong-Levine syndrome (LGL)

The impulse travels along the James bundle, which connects the atria to the main trunk of the His bundle. It is characterized only by a shortened PQ interval with an unchanged ventricular complex.

Sometimes the ECG shows an alternation of LGL and WPW syndromes, which confirms the possibility of excitation spreading through both bundles at once. The same rhythm disturbances are characteristic. It is observed in patients with myocardial infarction and thyrotoxicosis.

Maheim type

The impulse bypasses the normal tract along fibers arising from the His bundle after the atrioventricular node. ECG signs exclude a shortened PQ interval. The ventricular complex is the same as in the WPW type.

Dependence of the syndrome on the degree of pre-excitation

ECG signs in severity depend on the strength of the resulting pre-excitation and the constancy of the altered impulse pathways. It is customary to distinguish the following types of syndrome:

• manifest - signs on the ECG remain constant and do not disappear over time;
• intermittent - manifestations of pre-excitation are transient (non-permanent) in nature;
• latent - a normal ECG pattern is replaced by signs of pre-excitation during provocative tests (with physical activity, irritation of the vagus nerve zones) and during the period of paroxysmal rhythm disturbance;
• hidden - a standard ECG study does not reveal changes.

Relation of the syndrome to sudden death

Retrospective studies of ECG signs in patients who suffered sudden cardiac arrest showed an interesting relationship:

• in half of the patients, accelerated ventricular excitability appeared after restoration of heart contractions;
• among all patients with preexcitability syndrome, the incidence of sudden death is up to 0.6% annually.

The highest risk of death includes cases of combination with:

• history of tachycardia;
• Ebstein's vice;
• established multiple variants of abnormal impulse transmission pathways;
• shortening of the R-R interval on the ECG.

The patients' complaints are not caused by the presence of pre-excitation syndrome, but by a combination with rhythm disturbances. Up to 60% of patients note:

• palpitations;
• shortness of breath;
• feeling of fear amid chest discomfort;
• dizziness.

Such factors are not associated with the manifestation of the syndrome:

What are the criteria for the syndrome?

The syndrome does not cause any typical manifestations in the form of complaints or poor health. The World Health Organization, in its recommendations, even suggests calling the syndrome without other manifestations the “pre-excitation phenomenon,” and in the presence of clinical symptoms and ECG changes, “pre-excitation syndrome.”

It is important that the electrophysiological early appearance of the impulse precedes or accompanies complex tachyarrhythmias (atrial fibrillation, group extrasystoles, supraventricular forms).

The diagnosis is made only on the basis of studying the electrocardiogram

The main criteria for the ECG picture in diagnosis are:

• shortened PQ interval (less than 0.12 sec.);
• a peculiar change in the shape of the initial part of the QRS complex in the form of a “step” called Δ (delta wave);
• expansion of the ventricular QRS complex – more than 0.12 seconds.

ECG signs do not always include all elements of the syndrome.

Examination methods

To determine the presence or absence of additional bundles in the heart muscle, the most accessible method is electrocardiography. For an unstable type of syndrome, Holter monitoring is used, followed by interpretation.

In cardiac centers and specialized departments, the method of spatial vector electrocardiography is used. It allows you to identify additional pathways with high accuracy.

Magnetocardiography records in detail electrical impulses from different parts of the myocardium, helping to establish the exact localization of abnormal impulses and tracts.

Treatment measures

An asymptomatic course does not require any measures. However, if a person knows about unfavorable heredity in the family and works in particularly difficult conditions, or plays sports professionally, then the risk of sudden death and the effect of the syndrome on arrhythmia attacks should be taken into account.

Supraventricular rhythm disturbances begin to be stopped by massaging the carotid sinus area (on the neck), performing a test with breath holding and straining (Valsalva).

If there is no effect, Verapamil and drugs from the β-blocker group are used. The drugs of choice are: Novocainamide, Disopyramide, Cordarone, Etatsizin, Amiodarone.

Heart medications can only be taken as prescribed by a doctor.

Verapamil, Diltiazem, Lidocaine and cardiac glycosides are contraindicated in patients with a wide QRS complex. They are able to increase the speed of the impulse in the accessory tract with the subsequent transfer of fibrillation from the atria to the ventricles.

Non-drug methods include:

• transesophageal or endocardial temporary pacing;
• radiofrequency ablation (cutting) of additional pathways;
• installation of a permanent pacemaker if it is impossible to block pathological foci, the development of heart failure, or a high risk of sudden death.

The effectiveness of destruction of additional bundles by surgical methods ensures up to 95% of arrhythmia cessation. Relapses were recorded in 8% of cases. As a rule, repeated ablation achieves its goal.

In cardiology, they are wary of any manifestations of premature ventricular excitability. The patient should carefully consider the doctor's suggestions for examination and treatment.

Partial ventricular preexcitation syndrome

Ventricular preexcitation syndromes are the result of congenital disorders in the conduction system of the heart associated with the presence of additional abnormal pathways between the myocardium of the atria and ventricles.

Ventricular preexcitation syndromes are 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.

WPW syndrome, in accordance with the ECG picture, which reflects the characteristics of the pathomorphological substrate, is divided into a number of types - types A, B, C, as well as atypical WPW syndrome. Some authors identify up to 10 subtypes of Wolff-Parkinson-White syndrome. There are also intermittent (intermittent) and transient (transient) WPW syndrome.

• Epidemiology of ventricular preexcitation syndromes

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.

I45.6 – premature excitation syndrome.

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 (connective tissue dyspolasia syndrome). 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.

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, 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 commonly, the trunk of the His bundle to the right ventricle.
• James bundles connecting the sinus node to the inferior part of the AV node.
• The Breschenmanche tract connects 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.

The severity of premature excitation and, accordingly, the duration of the delta wave and the PQ interval may vary. The greater the conduction velocity along the accessory pathway and the less through the atrioventricular node, the larger part of the ventricular myocardium is covered by premature excitation. In the same patient, it can fluctuate depending on a number of factors, the main one of which is the tone of the sympathetic and parasympathetic parts of the autonomic nervous system, which has a significant impact on atrioventricular conduction.

The functioning of the internodal James tract is manifested only by the acceleration of atrioventricular conduction with unchanged ventricular excitation, which spreads through the His-Purkinje system, which is manifested by a shortening of the PO interval in the absence of a delta wave and aberrance of the QRS complex (CLC syndrome). The opposite picture is observed with the functioning of the accessory fasciculoventricular tract of Macheim in the distal parts of the His-Purkinje systems. Premature excitation of a small part of the myocardium of one of the ventricles causes the formation of a vaguely defined delta wave on the ECG and a moderate widening of the QRS complex (about 0.12 s) with unchanged atrioventricular conduction time. This type of premature excitation of the ventricles is sometimes called an atypical variant of Wolff-Parkinson-White syndrome.

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.

It is currently proposed that premature excitation of the ventricles, not accompanied by the occurrence of paroxysmal tachycardia, be called the “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 such a division.

Clinic and complications

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 is characterized by a high frequency of fibrillation or flutter (beats per minute, with flutter with 1: 1 conduction) with corresponding severe 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 extrasystole, ventricular tachycardia.

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

• 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 multiple additional paths.
  • History of symptomatic tachycardia.
  • Presence of Ebstein's anomaly.
  • Familial nature of the syndrome.
• Recurrent course of ventricular preexcitation syndromes.

Diagnostics

Diagnosis of ventricular preexcitation syndromes is based on identifying characteristic ECG signs. Hereditary history data (hereditary disorder) are of great importance.

It is necessary to obtain a detailed hereditary history in order to identify relatives who died as a result of sudden cardiac death or who had episodes of severe tachyarrhythmias and cardiac arrest.

• ECG signs of WPW syndrome
  • ECG triad of WPW syndrome
    • Shortening of the PQ(R) interval (less than 120 ms).
    • The presence of an additional δ (delta) wave on the ascending limb of the QRS complex, which reflects accelerated conduction of the impulse from the atria to the ventricle along additional pathways. To determine the localization of additional pathways, the polarity of the delta wave in various leads is assessed, as well as the polarity of the QRS complex in leads V1-V3, which is important in preparation for surgical treatment. Accordingly, morphological types of WPW syndrome are distinguished (types A, B, C, atypical variants).
    • Wide (confluent, deformed) QRS complex (more than 120 ms). Secondary changes in the ST segment and T wave are possible (discordance).
  • This triad is not always observed in its entirety. A temporary disappearance of the pre-excitation wave is possible as a result of changes in vegetative status, bradycardia, physical activity and other reasons (a transient form of the syndrome).
  • Intermittent (intermittent) WPW syndrome is determined by the alternation of complexes characteristic of the syndrome with normal sinus cycles on the same ECG.
  • The development of a pedicle block on the side of the accessory pathway localization masks the delta wave. Discordance of the terminal part of the ventricular complex in WPW syndrome can mimic manifestations of ischemic heart disease.

  ECG for CLC syndrome.

  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.

  ECG signs of the most relevant arrhythmias in pre-excitation syndromes:

  • Electrocardiographic signs of supraventricular tachycardia of the re-entry type with the participation of accessory pathways in the syndrome of premature excitation of the ventricles:
    • Correct heart rhythm with a frequency within (250) beats per minute.
    • QRS complexes are often unchanged or (less commonly) widened, in some cases with the presence of a delta wave in the initial part.
      • In the presence of arrhythmia with a wide QRS complex, it must be differentiated from supraventricular tachycardia with transient bundle branch block and ventricular tachycardia. This requires an assessment of previously taken ECGs (presence of pre-excitation syndrome).
      • In doubtful cases, wide complex tachycardias should be regarded as ventricular.
    • P waves follow the ORS complexes. Their polarity may vary depending on the location of the accessory pathway.
  • Features of the ECG for atrial fibrillation in patients with premature excitation of the ventricles:
    • Severe tachycardia. Heart rate is usually more than 180-200 beats per minute.
    • QRS complexes are often wide, with signs of premature ventricular excitation (delta wave). Wide QRS complexes can alternate with narrow and confluent ones.
  • See also: Paroxysmal supraventricular tachycardia, Atrial fibrillation and flutter.

ECG Holter monitoring is used to detect periodic rhythm disturbances.

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

Physical exercise tests - 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) performed in cases of overt WPW syndrome allows one to prove, and in case of hidden ones, 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.

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

In this case, using a complex technique, the area of ​​the earliest activation (pre-excitation) of the ventricular myocardium is determined, 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.

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.

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 can be stopped 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, amiodarone (300 mg), procainamide (1000 mg), ajmaline (50 mg) or rhythmylene (150 mg) are used. 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 the possible development of ventricular fibrillation! When using ATP (or adenosine) A similar development of events is possible, but a number of authors still recommend its use - if you are ready for immediate ECS.

Radiofrequency catheter ablation of accessory tracts 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 data) 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.

Prevention of supraventricular tachycardias is carried out according to the general rules for the 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 (etacizin mg/day, propafenone (preferably retard forms) mg/day). An alternative is class IA drugs (disopyramide 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.

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 preexcitation, 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.

A more reliable method of assessing risk, however, is to directly determine the duration of the effective refractory period of the accessory pathway when inducing atrial fibrillation with signs of premature ventricular excitation using programmed atrial or transesophageal pacing.

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.

High-frequency ablation can be highly effective and can avoid further tachyarrhythmias.

This is premature excitation of the ventricles, which is associated with the pathology of the development of the conduction system of the heart. This is not a disease, but a clinical manifestation of a congenital pathology associated with the formation, even in intrauterine development, of additional pathways conducting impulses from the atria to the ventricles. It should not be confused with extrasystole, which is characterized by an extraordinary contraction of the ventricle associated with the formation of an extraordinary impulse in any part of the conduction system outside the sinus node. Ventricular preexcitation syndrome can cause the development of extrasystole, atrial fibrillation, ventricular flutter, and so on.

In the medical literature there are two opinions regarding this syndrome. Some believe that the presence of additional pathways, regardless of the manifestation, is already a syndrome of ventricular preexcitation. Another part of the authors are inclined to believe that if the development of paroxysmal tachycardia is not observed, then the pathology should only be called a “pre-excitation phenomenon.” And accordingly, a syndrome can be considered only if paroxysms of supraventricular tachycardia occur.

Pathogenesis of ventricular preexcitation syndromes

The cause of the syndrome is the abnormal propagation of an excitation impulse throughout the myocardium due to the presence of additional pathological pathways that completely or partially “shunt” the AV node. This leads to the fact that part or all of the myocardium begins to excite earlier, weeks with the usual spread from the AV node to the His bundle and further along its legs.

The following pathological AV pathways are known today:
- Kent beams, including hidden retrograde ones. They connect the atrium and ventricles.
- James's buns. They connect the sinus node and the inferior region of the AV node.
- Maheim fibers. They connect the AV node either to the interventricular septum in its right region or to the right bundle branch. Sometimes Macheim's fibers connect the trunk of the His bundle and the right ventricle.
- Breschenmanche tract. It connects the right atrium and the trunk of the His bundle.
Types of ventricular preexcitation syndrome

In clinical cardiology today, two types of syndrome are distinguished:

• Wolff-Parkinson-White syndrome (WPW syndrome or Wolff-Parkinson-White syndrome). It is characterized by a shortened interval in P-Q(R), slight deformation and widening of the QRS and the formation of an additional delta wave, as well as changes in the T wave and ST segment. More often occurs with abnormal AV conduction of the Kent bundle. There are a number of types of this type of syndrome, as well as intermittent (intermittent) and transient (transient). Some authors even distinguish up to ten subtypes of WPW syndrome.
• Clerk-Levy-Christesco syndrome (short PQ interval syndrome or CLC syndrome). In English sources it is referred to as Lown-Ganong-Levine syndrome (LGL syndrome). It is also characterized by a shortened P-Q(R) interval, but without changes in the QRS complex. Usually occurs due to abnormal AV conduction of the James bundle.

Symptoms

The syndrome itself does not manifest itself in any way. A person can live happily ever after without even suspecting that he has a pathological accessory pathway in the heart muscle. The first signs can occur at any age, usually against the background of another disease, not necessarily of the myocardium. This could be, for example, any infectious disease.

In patients with CLC syndrome, the first manifestations often begin with paroxysmal tachycardias.
WPW syndrome is manifested by the following rhythm disturbances:

Supraventricular reciprocal tachycardia, which develops into atrial fibrillation with age. This manifestation of WPW syndrome occurs in 80% of patients.
- Paroxysmal tachyarrhythmias occur in 75% of patients with WPW syndrome.
- Fibrillation occurs in 15-30% of people with WPW syndrome.
- Atrial flutter or fibrillation occurs in 5% of patients.

Diagnosis of ventricular preexcitation syndromes

The main diagnostic method is ECG. Typically, characteristic signs are clearly visible on the ECG. To determine the type and type of syndrome, the following is prescribed:
- ECG with stress,
- Holter monitoring,
- Monopolar surface ECG mapping,
- Echocardiography,
- EPI (electrophysiological study of the myocardium),
- TEPS (transesophageal myocardial stimulation).

Treatment

If there are no paroxysms, then no treatment is carried out. In other cases, drug treatment is used, which should be prescribed by a specialist depending on the situation. Drugs are always selected individually, taking into account pathology, concomitant diseases and other individual characteristics of the body.
If drug therapy does not bring the desired effect, electrical pulse therapy is prescribed, that is, electrical cardiac stimulation.
Radical treatment methods include radiofrequency catheter ablation to destroy pathological pathways. Today this is the only method that has a positive result in 95% of cases. Of course, there are complications, and the mortality rate is 1% of all cases. Before ablation, the patient must undergo an EPI.

Forecast

Highly depends on the severity of the syndrome, the presence of complications and side diseases. But even in the most severe cases, high-quality high-frequency ablation greatly improves the prognosis. Much also depends on the patient: a healthy lifestyle, following all doctor’s recommendations, timely contact with a specialist.

Ventricular preexcitation is an ECG phenomenon manifested by a shortening of the P-Q interval to 0.11 s or less.

Isolated shortening of the P-Q interval is called the LCL (Lown-Cannong-Levine) phenomenon. In cases where P-Q shortening is combined with QRS widening and an A-wave, partially superimposed on the ventricular complex, it is called the WPW (Wolf-Parkinson-White) phenomenon.

The frequency of pre-excitation phenomena in athletes and non-athletes is the same and amounts to 0.2-0.6%. According to other authors, the WPW phenomenon occurs more often among athletes. It becomes clinically significant when paroxysms appear [Kushakovsky M. S., 1974].

The phenomena of ventricular preexcitation are most often associated with the existence of accessory pathways between the atria and ventricles. In some cases, these additional pathways are highly refractory and do not reveal themselves. Adverse external influences, including excessive physical activity, can change the state of atrioventricular conduction and contribute to the appearance of the phenomenon of pre-excitation.

Let us give an example of the occurrence of the WPW phenomenon during excessive physical exertion.

At baseline, athlete V., 17 years old, class I speed skater (Fig. 9), recorded sinus rhythm (a) P - Q - 0.17 s. During a repeated examination during a period of extremely intense daily training, the phenomenon of WPW, type A (b) appeared, which disappeared 1 month after the complete cessation of sports training (c).

The appearance and disappearance of the pre-excitation phenomenon in this case was not accompanied by any clinical symptoms. It can be assumed that the reason contributing to the inclusion of the abnormal conduction pathway is the deterioration of atrioventricular conduction or a decrease in the refractoriness of the accessory pathway.

The phenomena of pre-excitation in athletes always require close attention. The fact is that the athlete may not feel short tachycardias, and often hide the facts of the sudden occurrence of palpitations. At the same time, preexcitation syndromes are dangerous not only because of the development of paroxysms of tachycardia, but also because in 20-30% of cases preexcitation of the ventricles is accompanied by other anomalies of heart development, among which we should first of all mention defects of the interatrial or interventricular septum, prolapse of the mitral valve leaflets [Kushakovsky M. S., Zhuravleva N. B., 1981]. It is obvious that the identification of combined defects in heart development is necessary, first of all, at the stage of selection for physical education and sports. In the case of such combined cardiac malformations, as well as in the presence of the pre-excitation phenomenon, sports are contraindicated.

The situation is more complicated when resolving expert questions about the possibility of playing sports in cases where pre-excitation phenomena are detected in active athletes. Attempts to use tests with atropine and physical exercise to assess the clinical significance of pre-excitation phenomena are unpromising.

It should be remembered that preexcitation syndrome may underlie paroxysm of atrial flutter and atrial fibrillation. As is known, these conditions account for about 1/10 of all tachyarrhythmias in WPW syndrome and, according to Chung (1977), Wallens (1983), more often develop with the left-sided location of the Kent bundle. 2 cases of atrial flutter occurring against the background of WPW syndrome in athletes were described by G.I. Perov and S.E. Svetlichnaya (1986), therefore, if a paroxysm of atrial flutter or atrial fibrillation is detected, after eliminating the attack, one should search for additional conduction pathways, and, if necessary, carry out such athletes undergo electrophysiological studies and, what is very important, exclude organic changes in the heart (for example, undiagnosed left venous orifice, etc.).

Heart rhythm disturbances are considered an important cardiac problem, since they often complicate the course and worsen the prognosis of many diseases and are one of the most common causes of sudden death.

Of particular interest to both clinicians and electrophysiologists is premature ventricular excitation syndrome (PVS), which in some cases, in the absence of clinical manifestations, can be an electrocardiographic finding, and in others it can be accompanied by life-threatening tachyarrhythmias.

Despite the successes achieved in the study of PPV, the issues of its diagnosis, patient management and treatment remain relevant today.

Definition. Classification

PPV (preexcitation syndrome, preexcitation syndrome) is an accelerated conduction of the excitation impulse from the atria to the ventricles along additional abnormal conduction pathways. As a result, part of the myocardium or all of the ventricular myocardium begins to be excited earlier than with the usual spread of excitation through the atrioventricular node, the His bundle and its branches.

According to the recommendations of the WHO expert group (1980), premature excitation of the ventricles, not accompanied by clinical symptoms, is called the “pre-excitation phenomenon”, and in the case when there are not only electrocardiographic signs of pre-excitation, but also paroxysms of tachyarrhythmia develop - “pre-excitation syndrome”.

The anatomical substrate of PVS are bundles of specialized muscle fibers outside the conduction system of the heart, capable of conducting electrical impulses to different parts of the myocardium, causing their premature excitation and contraction.

Accessory atrioventricular connections are classified according to their location relative to the annulus fibrosus of the mitral or tricuspid valves, type of conduction (decremental type - increasing slowing of conduction along the accessory pathway in response to an increase in the frequency of stimulation - or non-decremental), and also according to their ability to antegrade, retrograde or combined implementation. Typically, accessory pathways have rapid, nondecremental conduction similar to that of normal tissue of the His–Purkinje conduction system and atrial and ventricular myocardium.

Currently, several types of abnormal pathways (tracts) are known:

• atrioventricular (Kenta), connecting the myocardium of the atria and ventricles, bypassing the atrioventricular node;
• atrionodal (James), located between the sinoatrial node and the lower part of the atrioventricular node;
• nodoventricular (Maheima), connecting the atrioventricular node (or the beginning of the His bundle) with the right side of the interventricular septum or the branches of the right bundle branch;
• atriofascicular (Breschenmash), connecting the right atrium with the common trunk of the His bundle.

There are also other additional conduction pathways, including “hidden” ones, capable of conducting an electrical impulse retrogradely from the ventricles to the atria. A small (5–10%) proportion of patients have multiple abnormal conduction pathways.

In clinical practice there are:

• Wolff–Parkinson–White syndrome (WPW syndrome), caused by the presence of bundles of Kent;
• Clerk-Levy-Christesco syndrome (CLC syndrome, shortened P-Q (R) interval syndrome), caused by the presence of the James bundle.

Electrocardiographic manifestations of PPV depend on the degree of preexcitation and the persistence of conduction along additional pathways. In this regard, the following variants of the syndrome are distinguished:

• manifest PPV (the ECG constantly shows signs of pre-excitation);
• intermittent (transient) PPV (on the ECG, signs of pre-excitation are transient);
• latent PPV (the ECG is normal under normal conditions, signs of pre-excitation appear only during a paroxysm of tachycardia or during provocation - physical activity, electrophysiological study (EPI), vagal or drug tests);
• hidden (changes are not detected on a standard ECG due to the conduction of excitation along additional pathways only in a retrograde manner).

Prevalence

According to various sources, the prevalence of PPV in the general population is approximately 0.15%. At the same time, paroxysms of tachyarrhythmias occur in every second patient (in 80–85% of cases – orthodromic tachycardia, 20–30% – atrial fibrillation (AF), 5–10% – atrial flutter and antidromic tachycardia). Hidden PPV is detected in 30–35% of patients.

PPV is a congenital anomaly, but can clinically manifest at any age, spontaneously or after any disease. Typically, this syndrome manifests itself at a young age. In most cases, patients do not have any other heart pathology. However, combinations of PPV with Ebstein's anomaly, cardiomyopathies, and mitral valve prolapse are described. There is an assumption that there is a relationship between PVS and connective tissue dysplasia.

In families of patients suffering from this syndrome, an autosomal dominant type of inheritance of additional pathways was identified in relatives of the 1st, 2nd, and 3rd degrees of kinship with various clinical and electrocardiographic manifestations.

The incidence of sudden death in patients with PPV is 0.15–0.6% per year. In almost half of the cases, cardiac arrest in persons with PPV is its first manifestation.

Studies of patients with PPV who have suffered cardiac arrest have retrospectively identified a number of criteria that can be used to identify individuals at increased risk of sudden death. These include the presence of the following signs:

• shortened R-R interval - less than 250 ms during spontaneous or induced AF;
• history of symptomatic (hemodynamically significant) tachycardia;
• multiple additional paths;
• Ebstein's anomalies.

Story

An ECG with a shortened P-Q interval and at the same time a widened QRS complex was first described by A. Cohn and F. Fraser in 1913. Isolated similar cases were subsequently described by some other authors, but for many years the cause of this ECG pattern was considered to be blockade of the branches of the His bundle.

In 1930, L. Wolff, J. Parkinson and P. White presented a report in which electrocardiographic changes of this type were considered as the cause of paroxysmal cardiac arrhythmias. This work provided the basis for conducting comprehensive studies aimed at elucidating the pathogenesis of these changes on the ECG, which were subsequently named Wolff-Parkinson-White syndrome.

Two years later, M. Holzman and D. Scherf suggested that the basis of WPW syndrome is the spread of the excitation impulse along additional atrioventricular pathways. In 1942, F. Wood provided the first histological confirmation of the presence of a muscular connection between the right atrium and the right ventricle, identified during autopsy of a 16-year-old patient with a history of episodes of paroxysmal tachycardia.

Despite these data, an active search for alternative mechanisms for the development of the syndrome continued until the 1970s, when EPI and surgical treatments confirmed the theory of accessory pathways.

Pathogenesis

The conduction of impulses from the atria to the ventricles during PPV occurs simultaneously along the normal conduction system of the heart and along the accessory pathway. In the conduction system at the level of the atrioventricular node, there is always some slowdown in the conduction of impulses, which is not typical for the anomalous tract. As a result, depolarization of a certain area of ​​the ventricular myocardium begins prematurely even before the impulse propagates through the normal conduction system.

The degree of preexcitation depends on the ratio of conduction velocities in the normal conduction system of the heart, primarily in the atrioventricular node, and in the accessory conduction pathway. An increase in the conduction velocity along the accessory pathway or a slowdown in the conduction velocity through the atrioventricular node leads to an increase in the degree of ventricular preexcitation. In some cases, ventricular depolarization may be entirely due to the conduction of impulses along the accessory pathway. At the same time, when the conduction of impulses through the atrioventricular node accelerates or the conduction through the accessory pathway slows down, the degree of abnormal ventricular depolarization decreases.

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 tachyarrhythmias.

With PPV, orthodromic reciprocal supraventricular tachycardia most often occurs, in which the impulse is conducted antegrade through the atrioventricular node, and retrograde through the accessory pathway. Paroxysm of orthodromic supraventricular tachycardia is characterized by frequent (140–250 per 1 min), devoid of signs of preexcitation, normal (narrow) QRS complexes. In some cases, inverted P waves are observed after the QRS complex, indicating retrograde activation of the atria.

With antidromic supraventricular tachycardia, the impulse circulates in the opposite direction: antegrade - along the abnormal conduction pathway, retrograde - along the atrioventricular node. Paroxysm of antidromic supraventricular tachycardia in patients with PPV is manifested on the ECG by a frequent regular rhythm (150–200 per 1 min) with ventricular complexes of the type of maximally pronounced preexcitation (QRS = 0.11 s), after which inverted P waves are sometimes detected.

In 20–30% of patients with PPV, paroxysms of AF occur, in which, as a result of antegrade conduction of a large number of atrial impulses along the accessory pathway, the ventricular contraction frequency (VFR) can exceed 300 per minute.

Clinic

In many cases, PPV is asymptomatic and is detected only by electrocardiography. 50–60% of patients complain of palpitations, shortness of breath, chest pain or discomfort, fear and fainting. Paroxysms of AF become particularly dangerous in the case of PPV, since they are accompanied by a large heart rate, hemodynamic disturbances, and can often transform into ventricular fibrillation. In such cases, patients not only experience syncope, but also have a high risk of sudden death.

Independent risk factors for the development of AF in patients with PPV are age, male gender, and a history of syncope.

Diagnostics

The main method for diagnosing PPV is ECG.

In case of WPW syndrome against the background of sinus rhythm, a shortening of the P-Q interval is detected (<0,12 с) и D-волну (пологий наклон в первые 30–50 мс) на восходящей части зубца R или нисходящей части зубца Q, комплекс QRS обычно расширен (і0,11 с). Характерно также отклонение сегмента SТ и зубца Т в сторону, противоположную D-волне и основному направлению комплекса QRS.

Electrocardiographic signs of CLC syndrome are shortening of the P-Q (R) interval, the duration of which does not exceed 0.11 s, the absence of an additional excitation wave - D-wave - in the QRS complex, the presence of unchanged (narrow) and undeformed QRS complexes (except in cases of concomitant blockade of the legs or branches of the His bundle).

With PPV, caused by the functioning of the Maheim beam, a normal P-Q interval is determined in the presence of a D wave.

The simultaneous functioning of the James and Maheim beams leads to the appearance on the ECG of signs characteristic of WPW syndrome (shortening of the P-Q (R) interval and the presence of a D-wave).

In connection with the spread in recent years of surgical methods for the treatment of patients with PPV (destruction of an abnormal bundle), methods for accurately determining its localization are constantly being improved.

On the ECG, the location of the Kent beam is usually determined by the direction of the initial moment vector of ventricular depolarization (the first 0.02–0.04 s), which corresponds to the time of formation of the abnormal D-wave. In those leads whose active electrodes are located directly above the area of ​​the myocardium that is abnormally excited by the Kent beam, a negative D-wave is recorded. This indicates the spread of early abnormal excitation away from the active electrode of this lead.

Of particular practical interest are the capabilities of the spatial vector electrocardiography method, which makes it possible to accurately determine the localization of additional conduction pathways.

More detailed, compared to ECG data, information about the location of additional conduction pathways can be obtained using magnetocardiography.

However, the most reliable and accurate methods are intracardiac EPI, in particular endocardial (preoperative) and epicardial (intraoperative) mapping. In this case, using a complex technique, the area of ​​the earliest activation (pre-excitation) of the ventricular myocardium is determined, which corresponds to the localization of the additional abnormal bundle.

Treatment

In patients with asymptomatic PPV, treatment is usually not required. Exceptions include individuals with a family history of sudden death, athletes, and those whose work involves danger to themselves and others (for example, divers and pilots).

In the presence of paroxysms of supraventricular tachycardia, treatment consists of stopping attacks and preventing them using various medicinal and non-medicinal methods. In this case, the nature of the arrhythmia (ortho-, antidromic tachycardia, AF), its subjective and objective tolerability, heart rate, as well as the presence of concomitant organic heart diseases are important.

With orthodromic reciprocal supraventricular tachycardia, the excitation impulse is conducted antegrade in the normal way, so its treatment should be aimed at suppressing conduction and blocking impulses in the atrioventricular node. For this purpose, reflex vagal tests are used, which are most effective when applied as early as possible.

The first-line drug for stopping orthodromic reciprocal supraventricular tachycardia is considered to be adenosine, the potential disadvantage of which is a transient increase in atrial excitability, which can provoke their extrasystole and fibrillation immediately after stopping the paroxysm of such tachycardia. Verapamil is considered to be another drug of choice for stopping orthodromic tachycardia in the absence of severe arterial hypotension and severe systolic heart failure. β-blockers are usually used as second-line drugs.

If these drugs are ineffective, procainamide is used to block conduction through the accessory atrioventricular pathway. Due to its safety and effectiveness, novocainamide is the drug of choice in the treatment of tachycardia with wide QRS complexes, when the diagnosis of orthodromic reciprocal supraventricular tachycardia is in doubt.

Reserve drugs are amiodarone, sotalol and class 1C antiarrhythmic drugs (AAPs): propafenone or flecainide.

In case of antidromic reciprocal supraventricular tachycardia, the impulse is conducted retrogradely through the atrioventricular node, therefore the use of verapamil, diltiazem, lidocaine and cardiac glycosides for its relief is contraindicated due to the ability of these drugs to accelerate antegrade conduction along the accessory pathway and thereby increase heart rate. The use of these drugs, as well as adenosine, can provoke the transition of antidromic supraventricular tachycardia to AF. The drug of choice for stopping such tachycardia is procainamide; if it is ineffective, amiodarone or class 1C AAP are used.

When paroxysmal AF occurs, the main goal of drug therapy is to control the ventricular rate and slow down conduction simultaneously along the accessory tract and the AV node. The drug of choice in such cases is also novocainamide. Intravenous administration of amiodarone and class 1C AAP is also highly effective.

It should be noted that the use of verapamil, digoxin and beta-blockers in AF for the purpose of controlling heart rate in individuals with PPV is contraindicated due to their ability to increase conduction velocity along the accessory pathway. This can transfer fibrillation from the atria to the ventricles.

To prevent paroxysms of supraventricular tachyarrhythmias caused by the presence of additional conduction pathways, class IA, IC and III AAPs are used, which have the property of slowing down conduction along abnormal pathways.

Non-drug methods for stopping attacks of supraventricular tachyarrhythmias include transthoracic depolarization and atrial (transesophageal or endocardial) pacing, and for their prevention - catheter or surgical ablation of accessory pathways.

In patients with PPV, electrical cardioversion is used for all forms of tachycardia, which are accompanied by severe hemodynamic disturbances, as well as when drug therapy is ineffective and in cases where it causes a deterioration in the patient's condition.

Radiofrequency catheter ablation of accessory tracts is currently the main method of radical treatment of PPV. Indications for its implementation are a high risk of sudden death (primarily the presence of AF paroxysms), ineffectiveness or poor tolerability of drug therapy and prevention of attacks of supraventricular tachycardia, as well as the patient’s reluctance to take AAP. If a short effective refractory period of the abnormal tract is detected in individuals with rare and mild paroxysms of arrhythmia, the question of the advisability of ablation in order to prevent sudden death is decided individually.

Before catheter ablation, EPI is performed, the purpose of which is to confirm the presence of an additional conduction pathway, determine its electrophysiological characteristics and role in the formation of tachyarrhythmia.

The effectiveness of radiofrequency catheter ablation is high (reaches 95%), and the mortality associated with the procedure does not exceed 0.2%. The most common serious complications of this treatment method are complete atrioventricular block and cardiac tamponade. Recurrences of conduction along the accessory pathway occur in approximately 5–8% of cases. Repeated radiofrequency ablation usually completely eliminates conduction along additional pathways.

Currently, the scope of surgical destruction of accessory tracts has significantly narrowed. For the same indications as catheter ablation, surgical treatment is resorted to in cases where the latter is impossible to perform for technical reasons or is unsuccessful, as well as when open-heart surgery is necessary due to concomitant pathology.

Literature

1. Sychev O.S. Heart rhythm disturbances // Guide to cardiology / Ed. V.N. Kovalenko. – K.: Morion, 2008. – P. 1059-1248, 1215-1218.
2. ACC/AHA/ESC 2006 Guidelines for the management of patients with atrial fibrillation // Circulation. – 2006. – No. 114. – P. 257-354.
3. ACC/AHA/ESC Guidelines for the management of patients with supraventricular arrhythmias – executive summary // JACC. – 2003. – No. 8. – R. 1493-1531.
4. Griffin B., Topol E. Manual of Cardiovascular Medicine. – The Lippincott Williams & Wilkins, 2004. – P. 1248.
5. Hanon S., Shapiro M., Schweitzer P. Early history of the preexcitation syndrome // Europace. – 2005. – No. 7. – P. 28-33.
6. Keating L., Morris A., Brady W.O. Electocardiographic Features of Wolff–Parkinson–White syndrome // Emerg. Med. J. – 2003. – No. 20. – R.491-493.

N.T. Vatutin, N.V. Kalinkina, E.V. Yeshchenko.

Donetsk State Medical University. M. Gorky;

Institute of Emergency and Reconstructive Surgery named after. VC. Gusak of the Academy of Medical Sciences of Ukraine.

Ukrkardio

Cardiac diseases are diverse. A special place among such pathologies is occupied by heart rhythm disturbances. In most cases, they are associated with dysfunctions and anomalies of the conduction system, which must ensure the correct sequence of myocardial function. Such diseases include premature ventricular excitation syndrome. It is accompanied by unpleasant sensations in the chest, shortness of breath, tachycardia, and in some cases it does not manifest itself at all, being an accidental finding on the electrocardiogram (ECG).

This disease is associated with the formation of abnormal pathways of nerve impulses. This ensures a violation of the sequence of work of the atria and ventricles. As a rule, the pathology is congenital and manifests itself in adolescence. If the syndrome is asymptomatic, it does not require treatment. To combat severe manifestations of the disease, both medicinal and surgical methods are used.

Classification of pathology

The division of the disease into types is based on the nature of the changes recorded on the cardiogram. They are associated with the characteristics of the transformation of the conduction system of the heart. It is customary to distinguish three main types of partial ventricular preexcitation syndrome on the ECG:

1. The bundle of Kent is one of the most common anomalies in cardiac innervation. It is detected in 1% of the population and causes the development of Wolff-Parkinson-White disease (WPW). This syndrome is caused by a pathology in the transmission of nerve impulses from the atria to the ventricles. A normal sequence of excitation is also possible. The heart rate in Kent type reaches 250 beats per minute. There are high risks of atrial fibrillation and the development of collapse against the background of arrhythmia. The problem has three manifestations on the ECG, and its characteristic features are changes in the delta wave in the V1 precordial lead and the configuration of the R wave.
2. The presence of the James bundle causes the development of Lown-Ganong-Levine (LGL) syndrome. Accompanied by a shortening of the PQ interval on the cardiogram, while the complex of ventricular contractions remains unchanged. It is often diagnosed in patients with a history of myocardial infarction, as well as thyroid dysfunction. May alternate with Wolff-Parkinson-White syndrome. This confirms the possibility of pulse propagation along both beams simultaneously.
3. The formation of Mechane fibers allows excitation to bypass the normal conduction tract through structures arising from the His bundle, below the atrioventricular node. On the cardiogram, this type of pathology is characterized by the same changes in the ventricular complex as WPW. In this case, the shortening of the PQ interval is not recorded.

Causes

Anomalies of the cardiac conduction system are among congenital pathologies. This is precisely why the possibility of their manifestation in childhood and adolescence is connected. The disease can remain latent for a long time. However, it is often associated with cardiomyopathies. The main etiological factors of the problem include:

1. The presence of additional pathways for nerve impulses is defined as a hereditary developmental disorder. There is evidence of the presence of a specific defective gene in patients with identified premature excitation of the ventricles.
2. The manifestation of Wolff-Parkinson-White syndrome is facilitated by hyperfunction of the thyroid gland, which leads to the formation of thyrotoxicosis.
3. A patient’s history of vegetative-vascular dystonia also indicates an increased risk of developing this heart pathology.

Many scientists are inclined to believe that defects in embryonic development, in particular abnormalities in the formation of connective tissue, play a decisive role in the fetus. In some cases, symptoms require a trigger, such as an infectious disease, injury, or severe stress.

Syndrome and sudden death

Cardiac pathologies are considered so dangerous because they can lead to death. Premature excitation of the ventricles of the heart, although rare, is a dangerous disease. A retrospective analysis of electrocardiograms taken from patients who suffered cardiac arrest proves that in half of the victims an increased rate of impulse transmission to the cardiac chambers was recorded after restoration of normal rhythm.

People who suffer from tachyarrhythmias and Ebstein's disease are at greatest risk of complications. The chances of sudden cardiac arrest are also high in patients whose ECG revealed a shortening of the R-R interval.

The opinion regarding the dependence of the prognosis on gender and age is erroneous. Blood cholesterol levels also do not affect the risk of developing unpleasant consequences of the disease.

Diagnostics

Since in many cases the disease does not have characteristic clinical manifestations, examination is required to confirm it. The most informative method is an ECG. It allows you not only to suspect a problem, but also to determine its form by the presence of characteristic changes. Holter monitoring is also actively used in cardiology to diagnose rhythm disturbances. Early ventricular excitation syndrome requires not only confirmation with an ECG, but also identification of the exact localization of the pathological focus. Magnetocardiography is used for this. It allows you to record pulses with high accuracy. This helps doctors differentiate between birth defects.

Treatment of pathology

If ventricular preexcitation syndrome is an incidental diagnostic finding, no therapy is required. The disease may not bother the patient for a long time and may not need correction. However, if a person’s work activity is associated with increased physical and emotional stress, as well as in the presence of a predisposition or pronounced symptoms, it is necessary to take into account the possible risks of developing premature excitation of the ventricles. Both conservative methods based on the use of medications and surgical techniques are used.

Drugs

To restore normal impulse transmission through the myocardium, various groups of drugs are used. All of them are aimed at suppressing the pathological activity of foci located outside the natural conduction system of the heart. First-line drugs in the treatment of premature ventricular excitation include adenosine-based drugs. The substance has a pronounced antiarrhythmic effect. Medicines that block calcium channels, such as Verapamil, are also used. Selective adrenergic blockers are used as second-line agents.

Pharmacological therapy is usually prescribed for mild symptoms. It has a temporary effect, therefore it is used as a supporting stage, as well as in the presence of contraindications to surgical intervention.

Operation

Pathological excitability of the ventricles is caused by the formation of abnormal impulse transmission pathways. The most effective method of combating the disease is to remove defective structures. Surgical interventions have a number of contraindications, since they are classified as radical methods of combating pre-excitation syndrome. At the same time, radiofrequency ablation allows you to get rid of the symptoms of the problem in 90% of cases without relapses.

The surgical technique is based on the use of special equipment. A catheter is used that is capable of creating special electrical currents. No special access is required: the device is inserted into the heart through a blood vessel. It is first necessary to accurately determine the location of the abnormal pathway, which requires specific diagnostics. Radiofrequency pulses generated by the guidewire are capable of causing limited necrosis. In this way, pathological tissue areas are removed minimally invasively. When treating tachyarrhythmias of various origins, in 85% of cases, a single ablation is sufficient. If a relapse develops, repeated intervention is 100% effective. It has been established that the greatest success is achieved by removing lesions located on the left side of the heart.

The first publications on the effectiveness of radiofrequency ablation in the treatment of premature excitation of the ventricles date back to 1991. Even then, doctors were inclined to believe that surgery should be the means of choice when dealing with such pathologies. Subsequently, the effectiveness of this operational technique was repeatedly proven in several countries around the world.

Other treatments

Doctors' recommendations include cardiac stimulation. There are transesophageal and endocardial techniques. They allow you to achieve normalization of the process of transmission of nerve impulses. The installation of special devices that allow blocking pathological excitation also shows good results. In this case, it is advisable to begin treatment with vagal tests. They are a set of unique breathing exercises aimed at stimulating the activity of the vagus nerve, which has an inhibitory effect on the heart.

Prognosis and prevention

The course and outcome of the disease depend both on the main cause of its formation and on the severity of hemodynamic disorders that occur against the background of myocardial dysfunction.

Preventing the development of the syndrome comes down to regular medical examinations. Patients whose family history is burdened with cases of detection of a similar problem are recommended to visit a cardiologist at least once a year. Significant physical and emotional overload should also be avoided, as they can provoke the development of the clinical picture.