Ventricular preexcitation syndromes 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.

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.

• ICD-10 code

  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.

• 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, 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 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 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.

• Methods for diagnosing ventricular preexcitation syndromes

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) 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 (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.

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

Wolff-Parkinson-White syndrome (WPW syndrome) is a syndrome of premature excitation of the ventricles, caused by the conduction of impulses along additional abnormal conduction bundles connecting the atria and ventricles. The prevalence of WPW syndrome, according to cardiology, is 0.15-2%. WPW syndrome is more common among men; in most cases it manifests at a young age (10-20 years), less often in older people. The clinical significance of WPW syndrome is that in its presence, severe heart rhythm disturbances often develop, which pose a threat to the patient’s life and require special treatment approaches.

Causes of WPW syndrome

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

Normally, additional muscular tracts connecting the atria and ventricles exist in all embryos in the early stages of development, but they gradually become thinner, shorten and completely disappear after the 20th week of development. When the formation of fibrous atrioventricular rings is disrupted, muscle fibers are preserved and form the anatomical basis of WPW syndrome. Despite the congenital nature of accessory AV connections, WPW syndrome may first appear at any age. In the familial form of WPW syndrome, multiple accessory atrioventricular connections are more likely to occur.

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

Classification of WPW syndrome

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

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

I. With accessory muscle AV fibers:

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

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

• atrio-fascicular - entering the right bundle branch
• entering the myocardium of the right ventricle.

There are several clinical forms of WPW syndrome:

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

Pathogenesis of WPW syndrome

WPW syndrome is caused by the spread of excitation from the atria to the ventricles along additional abnormal conduction pathways. As a result of this, excitation of part or all of the ventricular myocardium occurs earlier than when the impulse propagates in the usual way - along the AV node, bundle and branches of His. Pre-excitation of the ventricles is reflected on the electrocardiogram in the form of an additional wave of depolarization - a delta wave. In this case, the P-Q(R) interval is shortened, and the QRS duration increases.

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

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

Symptoms of WPW syndrome

Clinical manifestation of WPW syndrome occurs at any age; before this, its course can be asymptomatic. WPW syndrome is accompanied by various heart rhythm disturbances: reciprocal supraventricular tachycardia (80%), atrial fibrillation (15-30%), atrial flutter (5%) with a frequency of 280-320 beats. per minute Sometimes, with WPW syndrome, less specific arrhythmias develop - atrial and ventricular extrasystole, ventricular tachycardia.

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

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

Diagnosis of WPW syndrome

If WPW syndrome is suspected, a comprehensive clinical and instrumental diagnosis is carried out: 12-lead ECG, transthoracic echocardiography, Holter ECG monitoring, transesophageal pacing, electrophysiological study of the heart.

Electrocardiographic criteria for WPW syndrome include: shortening of the PQ interval (less than 0.12 s), deformed QRS complex, and the presence of a delta wave. Daily ECG monitoring is used to detect transient rhythm disturbances. An ultrasound of the heart reveals concomitant heart defects and cardiomyopathy.

Carrying out transesophageal cardiac pacing in WPW syndrome makes it possible to prove the presence of additional conduction pathways and induce arrhythmia paroxysms. Endocardial EPI allows you to accurately determine the location and number of additional pathways, verify the clinical form of WPW syndrome, select and evaluate the effectiveness of drug therapy or RFA. Differential diagnosis of WPW syndrome is carried out with bundle branch blocks.

Treatment of WPW syndrome

In the absence of arrhythmia paroxysms, WPW syndrome does not require special treatment. In case of hemodynamically significant attacks accompanied by syncope, angina pectoris, hypotension, and increasing signs of heart failure, immediate external electrical cardioversion or transesophageal pacing is required.

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

In case of resistance to antiarrhythmic drugs and development of atrial fibrillation, catheter radiofrequency ablation of additional conduction pathways is performed using transaortic (retrograde) or transseptal access. The effectiveness of RFA for WPW syndrome reaches 95%, the risk of relapse is 5-8%.

Forecast and prevention of WPW syndrome

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

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

DEFINITION OF THE CONCEPT AND ANATOMICAL CLASSIFICATION OF ACCESSORY PATHWAYS

In the period from 1913 to 1929, isolated descriptions of ECGs appeared in the literature, usually considered as electrocardiographic curiosities, which can be retrospectively defined as cases of ventricular preexcitation. Only in 1930 did L. Wolff, J Parkinson and P. White come to the conclusion that we were talking about a special clinical-electrocardiographic syndrome,

named after them as WPW syndrome. These authors observed 11 young people who periodically suffered attacks of tachycardia, and outside of tachycardia, had a short P-R interval and a QRS complex similar to leg block on the ECG. Even earlier, A. Kent (1893, 1913, 1914) in a series of works reported the discovery in the heart of mammals of lateral “nodes” connecting the right atrium with the wall of the right ventricle. True, he considered

val them as a substrate of the normal atrioventricular connection. Soon followed by the amazing vision of G. Mines (1914) that the structures described by A. Kent could be the basis of the circular rhythm in the human heart. The same hypothesis was put forward by S. de Boer (1921).

In 1932, M. Holzman and D. Scherf indicated that the peculiarity of the ECG in WPW syndrome can be associated with the partial spread of sinus impulses along the Kent bundle. Regardless of them, S. Wolferth and F. Wood (1933) came to a similar conclusion, who also suggested that the PT characteristic of this syndrome is a consequence of re-entry and retrograde movement of the impulse through the Kent's node. After 10 years, F. Wood et al. (1943) confirmed their assumption by discovering an additional muscular atrioventricular junction in the heart of a boy who died from an attack of tachycardia, complicating WPW syndrome. A year later, R. Oehnell (1944) reported the death of a patient in whose heart an additional muscular connection was also found between the left atrium and the left ventricle. R. Oehnell proposed the term “pre-excitation” (pre-excitation). According to R Anderson et al. (1981), it is these researchers (F. Wood, R Oehnell), and not A. Kenty, who are the real credit for the discovery of abnormal atrioventricular muscular connections in individuals with electrocardiographic signs of WPW syndrome

It should be noted that the myogenic theory of the congenital origin of WPW syndrome gained recognition slowly and with great difficulty. To explain the genesis of this syndrome, other interesting hypotheses were proposed, in particular: about the electrotonic propagation of excitation from the atria to the ventricles without the participation of additional anatomical pathways, about the longitudinal division of the AV node and (or) the His-Purkinje system into two channels with accelerated conduction through one of them and with earlier excitation of any part of the ventricular myocardium, a violation of synchrony in synoventricular conduction and uneven movement of the excitation front in the trunk of the His bundle, etc. [Isakov I. I., 1953, 1961; Salmanovich V.S., Udelnov M.G., 1955; Lirman A.V., 1956; Soddi-Pallares D. et al., 1948; Prinzmetal M., 1961; Sherf L., James T, 1969].

The discussion about the mechanisms of ECG formation in WPW syndrome has noticeably declined after N. Burchell et al. (1967) showed that as a result of surgical transection of the myocardial area where the AP was supposed to pass, the characteristic electrocardiographic signs of pre-excitation disappeared and the attacks of tachycardia stopped. This fact, repeatedly confirmed by various cardiac surgeons, is now beyond doubt (see Chapter 6).

So the term "pre-exitation"(pre-excitation) means that part of the ventricular myocardium or the entire ventricular myocardium is excited by sinus (atrial) impulses through the AP ahead of what happens under normal conditions, when the same impulses are conducted to the ventricles only through the AV node and the His-Purkinje system. Nowadays, the concept of pre-excitation includes a number of previously unknown phenomena, in particular the presence of: a) hidden APs that selectively conduct impulses in the retrograde direction from the ventricle to the atrium (the so-called hidden retrograde “bundles of Kent”); b) muscle connections between the AV node or the trunk of the His bundle and the ventricle; c) multiple DP, etc.

The WHO Expert Working Group (1980) rightly proposed to distinguish two concepts: WPW phenomenon and WPW syndrome; only in the second case do patients experience attacks of AV reciprocal tachycardia. In our presentation, for the sake of brevity, we will use the single name “WPW syndrome.”

The variety of abnormal, circuitous pathways and connections made it necessary to classify them. This work was carried out by the European research group on the study of ventricular preexcitation. It is recommended that the term “connection” denote abnormal conductive

paths penetrating the contractile myocardium, the term “tract” is an abnormal path ending in specialized conducting tissue.

Anatomical classification of accessory tracts (provided with some explanations):

1. Atrium-ventricular (AV) connections (“bundles of Kent”).

2. Nodoventricular connection between the AV node and the right side of the interventricular septum (Maheim fibers).

3. Nodofascicular tract between the AV node and the branches of the right bundle branch (Maheim's fibers).

4. Fasciculoventricular connection between the common trunk of the His bundle and the myocardium of the right ventricle (Maheim fibers); function in very rare cases.

5. Atriofascicular tract connecting the right atrium with the common trunk of the His bundle (Breschenmache tract); is rare.

6. Atrionodal tract between the SA node and the lower part of the AV node (posterior internodal tract of James); is present, apparently, in all people, but usually does not function.

The latter 2 tracts are also called AV nodal shunts because they allow sinus or atrial impulses to reach the common trunk of the His bundle without AV delay. This category also includes the so-called short paths in the AV node itself, as well as the “small”, “underdeveloped” AV node, etc. The above classification does not mention hidden retrograde “bundles of Kent”, multiple DPs.

Abnormal muscle bundles (remnants of embryonic AV junctions) can be located anywhere in the atrioventricular groove, except for the area between the aorta and the mitral valve annulus. They are usually divided into parietal,septal and paraseptal. The first join the free walls of the left and right ventricles, the rest connect the interventricular septum with the interventricular

kova, ending anteriorly or posteriorly in its membranous part, in the right triangle of the central fibrous body of the heart, often under the endocardium in close proximity to the normal AV conduction system. G. Guiraudon et al. (1986) showed that the posteroseptal DP can connect the posterior part of the left ventricle with the adjacent part of the right atrium. It should be mentioned that the possibility of the existence of septal connections was pointed out by G. Paladino (1896).

W. Untereker et al. (1980) summarized the anatomical data available in the literature on the hearts of 35 deceased patients in whom signs of WPW syndrome were recorded on the ECG during their lifetime. In 30 cases, short (from 1 to 10 mm) and narrow (average diameter - 1.3 mm) muscle bundles were found, starting in the lower parts of the atria and penetrating into the ventricular muscle. Left-sided AF in most cases are located outside the compact, well-formed fibrous mitral annulus and in the immediate vicinity of it cross the fatty layer of the epicardial groove. Right-sided DP often penetrates the ventricle through congenital defects (“holes”) of the tricupidal fibrous ring, which is less well formed, not as compact, and has “ruptures,” as A. Kent put it (1914). There are also superficial DPs that lie away from the fibrous rings in the fatty tissue of the coronary sulcus. The general layout of the DP is shown in Fig. 131 Most histologically studied DPs consisted of normal muscle fibers. However, atrioventricular connections have been described that included specialized, in particular automatic, fibers [Bo-se E. et al., 1979] (see p. 362).

Information provided by

Fig. 131 Diagram of anatomical accessory connections (according to R Anderson and A Decker). 1) Accessory atrioventricular connections, 2) accessory nodoventricular tracts; 3) accessory fasciculovenous-tricular connections, 4) accessory atriofascicular tract, 5) intranodular shunts

personal research groups regarding the distribution of DP, basically coincide. An illustration can be found in the data obtained by the group of J. Gallagher. In 111 patients, DP were located as follows: in the free wall of the left ventricle - in 52%, in the free wall of the right ventricle - in 19%, in the interventricular septum - in 29% of cases Among these patients there were 74 men and 37 women aged from 7 to 62 years (on average - 31.4 years).In all 111 patients, the DP could conduct impulses in the anterograde and retrograde directions. In the other 25 people (17.4%) AP conducted impulses only in the retrograde direction (the place of unidirectional blockade is often located at the ventricular end of AP - Kuck K-H. et al., 1990). Finally, in 7 cases (4.9%) selective anterograde conduction was noted DP (total 143 patients).

ELECTROCARDIOGRAM FOR SYNDROMEW.P.W.

The existence of two independent atrioventricular tracts in the heart creates the basis for “competition”

ration" between them. The greater and lesser participation of the AP in the conduction of the impulse to the ventricles depends on the duration of the ERP in the AP and in the AV node and the speed of the impulse in these structures. Pre-excitation of the ventricle occurs because the time of propagation of the impulse from the SA node to the ventricle through the AP is shorter than the time movement of the impulse through the AV node - the His-Purkinje system. These features are reflected on the ECG, which is characterized by such signs as a short PR interval; wave A, or delta wave; expansion of the QRS complex The short interval Р-R, more precisely Р-А, is calculated from the beginning of the P wave to the beginning of wave A, which is a thickening or notch (“ladder”) that deforms the beginning of the QRS complex. It is the result of early, premature excitation of a section of the myocardium of one of the ventricles through the AP. In most adults, the P-A interval is 0.12 s; in children<0,09 с Длительность волны А составляет 0,02-0,07 с, ее высота в период си­нусового ритма редко превышает 5 мм Обычно волна А направлена вверх, если комплекс QRS имеет на­правление кверху; при направлении основного зубца QRS книзу волна А тоже обращена книзу. Во фронталь­ной плоскости вектор волны А может располагаться в пределах от +120° до -75°, большей частью он откло­няется влево. У ряда больных реги­стрируется «горизонтальная, или изоэлектрическая», волна А на сег­менте Р-R как бы до начала QRS (вектор волны А оказывается пер­пендикулярным к оси отведения) На внутрисердечных ЭГ видно, что такая волна А является самой ран­ней частью комплекса QRS. Волна А может быть двухфазной; иногда она выявляется четко лишь в 1-2 из 12 электрокардиографических отведе­ний.

The QRS complex in WPW syndrome has a confluent character -

it is expanded to 0.11-0.12 s in adults and to 0.10 s and more in children by adding wave A to its initial part. The final part of the QRS complex does not change, since in WPW syndrome the bulk of the ventricular myocardium is activated in a normal manner through the AV node - the His-Pourquinier system. The P-J interval (P-S), from the beginning of the P wave to the junction of the QRS with the ST segment, remains the same as normal (usually = £; 0.25 s). The degree of QRS expansion, therefore, depends on what proportion of the ventricular myocardium is excited through AP, i.e., on the magnitude of wave A. With complete AV nodal anterograde block, the QRS complex is a continuous wave A. On the contrary, in the case of complete anterograde blockade -grade blockade of DP disappears signs of ventricular preexcitation, i.e. the QRS complex loses wave A and the PR interval lengthens accordingly. Between these two extremes there are many intermediate ones. So, the “degree of pre-excitation” on the ECG (wave A) depends primarily on the relationship between the conduction velocity through the AV node and the AP. In addition, the magnitude of wave A is influenced by: a) the distance from the place of AP attachment to the atrium wall to the SA node; b) intraatrial conduction velocity.

In WPW syndrome, expansion of the QRS complex is accompanied by secondary changes in the ST segment and T wave, which often acquire a direction discordant with respect to the QRS. Early asynchronous excitation of part of the ventricular myocardium leads to disturbances in the repolarization sequence. For the same reason, exercise testing gives false-positive results in patients with WPW syndrome. T wave abnormalities may be preserved and after the disappearance of pre-excitation: these teeth are inverted in those leads in which

A negative wave A is recorded during the period of pre-excitation. Such changes are associated with electrotonic influences on the process of ventricular repolarization (“memory of the heart”). For example, in right lateral DP, the A wave axis is directed upward and to the left, and T waves (outside the preexcitation period) may be inverted in leads II, III, aVF, and possibly in Vi and Va. Similarly, T waves are sometimes inverted in leads II, III, aVF in patients with posterior non-septal DP (outside the pre-excitation period). In the case of left lateral DP, the T waves are inverted in leads I and aVL, and in the case of anteroseptal DP - in leads V] and V2. All these ECG deviations can be observed when the QRS complexes are formed normally (without wave A), and they are erroneous are considered as a manifestation of myocardial ischemia.

DETERMINATION BY ECGLOCALIZATION OF ABNORMALATRIO-VENTRICULARCONNECTIONS

From a practical point of view, the question of the possibility of determining the location of ventricular preexcitation using ECG is of constant interest. After F. Rosenbaum et al. in 1945. identified two electrocardiographic types of WPW syndrome (A and B), followed by a description of a number of other types, including: type AB, types C and D. All of them were correlated with certain DPs.

Type A syndromeW.P.W.. The spatial vector of wave A is oriented forward, down and slightly to the right. This direction of the vector reflects premature excitation of the posterobasal or basal-septal region of the left ventricle. In right and left

In the chest leads, the A wave and the QRS complex are directed upward due to the downward direction of the A vectors. In leads vsr and Vi, the QRS complex can look like R, RS, Rs, RSr, Rsr. The electrical QRS axis deviates to the right. In lead I, wave A is often negative, simulating an enlarged Q wave (Qr complex); Positive A (RS complex) is less common; in lead III, wave A is usually positive. With this type of WPW syndrome, the P-R interval sometimes exceeds 0.12 s (up to 0.14 s).

Type B syndromeW.P.W.. Here the spatial vector of wave A is oriented to the left, down and somewhat posteriorly. According to AP, part of the base of the right ventricle is prematurely excited near the atrioventricular groove. In the right precordial leads, the A wave and the QRS complex are directed downward. In leads vsr and Vi, the QRS complex looks like QS, Qs, rS. In the left precordial leads, the A wave and the QRS complex are directed upward. The electrical axis of the heart deviates to the left. In lead I, the QRS complex is represented by a high R wave, wave A is positive, in lead III - the QS complex, wave A is often negative and can enhance the Q wave. In this case, a wide and deep Q sometimes imitates signs of lower (diaphragmatic) myocardial infarction.

Type AB. The spatial vector of wave A is directed to the left, anteriorly, reflecting the premature excitation of the posterobasal part of the right ventricle. In leads vsr and Vi, wave A is directed upward, as in type A. The electrical QRS axis deviates to the left (as in type B): in lead I, wave A and the QRS complex have a positive polarity, in lead III they are discordant.

Type C. The AP connects the subepicardial portion of the left atrium with the lateral wall of the left ventricle. In the area of

Vj-4 complexes R, Rs, wave A is positive; in leads Vs-e there are complexes rS, RS, wave A is negative or isoelectric. The electrical QRS axis deviates to the right; in leads I, aVL wave A is negative, in leads III, aVF wave A is positive.

It should be emphasized that such traditional typing of WPW syndrome allows only a rough estimate of the location of the DP. Therefore, other electrocardiographic classifications have been proposed. One of them is the proposal of T. Iwa (1978) to distinguish: 1) left type of WPW syndrome: in lead Vi the QRS is directed upward, wave A is positive; 2) right type: in lead V] the QRS is directed downward, wave A is positive; 3) septal type: in lead V] the QRS is directed downward, wave A is negative. This classification also does not bring satisfaction, since with pre-excitation of the right ventricle, wave A in lead V] is often negative, and septal APs cause significant fluctuations in the direction of excitation, therefore, in lead V t QRS can be negative, equiphasic (R = S) or completely positive.

A significant step forward in the development of electrocardiographic criteria for the location of the AP was made by J. Gallagher et al. (1978), who compared the polarity of wave A in the QRS complexes with maximum signs of preexcitation in 12 ECG leads with the results of epi- and endocardial mapping in a large group of patients with WPW syndrome. Subsequently, the same work was carried out by A. A. Kirkutis (1983), who obtained similar data.

According to J. Gallagher et al. (1978) should be distinguished 10 plotsventricular preexcitation and, accordingly, 10 localizations of DP: 1) right anterior paraseptal; 2) right front; 3) right bo-

Table 14 Wave polarity D depending on the location of ventricular preexcitation

Note. (±) means that the initial 40 ms of wave A are isoelectric, (+) - positive; (-) - negative.

forged; 4) right rear; 5) right paraseptal; 6) left posterior paraseptal; 7) left rear; 8) left side; 9) left front; 10) left anterior paraseptal (Fig. 132). Below, in the table. 14, the polarity of wave A is indicated for these 10 options for ventricular pre-excitation. As the experience of our clinic shows [Butaev T.D., 1986], this method allows 65-70%

cases to judge the location of the DP (Fig. 133, 134, 135). However, there are ECGs on which it is difficult to give a final conclusion, since wave A is not always clearly visible. In addition, its shape and size can change in patients with various congenital or acquired changes in the ventricular myocardium, as well as in the presence of several DP, etc. Regulations ongets better thanks to more

pup. 133. WPW syndrome On the left - type 1 with intraventricular block, interval P - S = 0.32 s) On the right - type 2.

90% of DPs are in 4-5 main positions. According to G. Reddy and L. Schamroth (1987), these positions are as follows: left lateral, right lateral, posterior nonseptal, anteroseptal (left and right). V. Lindsay et al. (1987) add a left posterior position.

To recognize DP, these authors use only 3 signs: a) direction of the average axis of wave A in the frontal plane; b) polarity (axis direction) of the main oscillation (wave) of the QRS complexes in the frontal plane; c) polarity (direction) of the main oscillation (wave) of the QRS complexes in the horizontal plane.

Left side DP. The most common abnormal atrioventricular connection (46% of all APs). In the frontal plane, the axis of wave A is located between +90° and +120°, i.e. wave A has negative polarity in leads I and aVL. In cases where this wave is negative only in lead aVL, and in lead I it is low-amplitude or equiphase, an increasing frequency is carried out

stimulation of the atrium, which enhances preexcitation and reveals a negative wave A in lead I. In leads II, III, aVF, wave D is positive. The axis of the main oscillation of the QRS complex in the frontal plane is directed between + 60° and + 90°. In all chest leads - from Vi to Ve, the main oscillation of the QRS complexes is directed upward, it is maximum in lead Va. The PR interval may be close to normal, since the atrial end of the AP is located at a distance from the SA node. If, with electrocardiographic signs of left lateral AP, there is no negative wave D in leads aVL and I, this means that the AP is located anteriorly on the left - left anterior AP .

Left posteroseptal DP. Together with the right posteroseptal DP it makes up 26-33% of all DP. In the frontal plane, the axis of wave A is directed to the sector - 60° and even to the left: wave D is negative in leads II, III, aVF and often in aVR. The axis of the main QRS oscillation in the frontal plane is also shifted to the left (-70°).

Fig. 134. WPW A syndrome - type 10; B - type 10 with a large wave D; B - type 10 together with intraventricular block; G - type 9

QRS lation in V] is positive, it increases towards the leads V 2 and V 3 ; in all other chest leads, the QRS complexes are also directed upward. Wave A is always positive in lead Vi.

Right side DP. Occurs in 18% of all DPs. The axis of wave A in the frontal plane is directed towards the region from -30° to -60°; this wave is negative in the leads

III, II, aVF, positive in leads I and aVL. The axis of the main QRS oscillation in the frontal plane is directed towards -60°. Ebstein's anomaly is usually combined with pre-excitation through the right lateral

Right posteroseptal DP.

The axis of wave A in the frontal plane is from -30° to -50°, which gives the negative polarity of wave A

Fig. 135. \\PVV syndrome, type 6.

Table 15

Differential diagnostic signs of five localizations of DP in the syndrome

in leads III, aVF and often in lead II. It is positive in leads I and aVL. The average QRS axis in the frontal plane is directed towards -30°. In lead Vi, the main QRS oscillation is directed downwards (rS), in leads V2 and knots - the Rs or R complexes. Wave A in lead Vi is usually isoelectric, less often - negative.

Anteroseptal DP. These paraseptal DPs occur in 10% of WPW syndrome: the right DP is perhaps more common than the left, although their distinction is difficult. The D wave axis in the frontal plane ranges from 0 to +60°; this wave has a positive polarity in leads I, II, III, aVL, aVF. Sometimes, with the left anterior paraseptal AP, the axis of wave A shifts to the right more than +60°; as a result, it becomes negative in lead aVL. The average QRS axis in the frontal plane is directed in the region from 0 to + 30° - with the right anterior paraseptal DP and more vertically (from +60° to +90°) - with the left anterior paraseptal DP. The main QRS oscillation deviates downward in leads Vi-Uz in both the right and left anterior paraseptal DP. If we remember that the left-sided AP has a positive QRS complex in these leads, it will become obvious that the left anterior paraseptal AP is in this

I mean, it's an exception. Recently J. Gallagher et al. (1988) identified a subtype of septal DP lying in close proximity to the His bundle (para-His DP, or intermediate DP). There is a high risk of complete AV block when this AP is destroyed.

In table 15 summarizes the main features of the 5 DPs indicated by G. Reddy and L. Schamroth (1987).

Noteworthy is the absence in the table. 15 indications of the polarity of QRS complexes in leads V4-Ve. These leads are not critical for determining the location of the AP joining the ventricles, since regardless of their location, the QRS complexes are directed upward or predominantly upward. Only when the electrical QRS axis deviates to the left in the frontal plane can the R or Rs complex in leads Vs-e transform into the Rs or rS complex. The polarity of the main QRS oscillation in the V]-knot leads, on the contrary, provides the most important diagnostic data. We have already mentioned that if it is directed upward, especially in lead Ua (Rs or R), then, with rare exceptions, this indicates left-sided AP. If the main QRS oscillation in these leads, especially in V2 (rS), is directed downward, then it is possible to diagnose right-sided DP with a high degree of probability. Only occasionally in patients with left-sided

A negative or equiphase QRS complex is recorded in lead Vi of the posterior septal and left lateral AP. The correct conclusion is facilitated by electrical stimulation of the atria, which increases the degree of pre-excitation and returns the QRS complex in lead Vi to a positive polarity.

Wave A with negative polarity in leads II, III, aVF (right lateral and posteroseptal DP) can imitate the pathological Q wave characteristic of infarction of the inferior wall of the left ventricle. A negative A wave in leads I, aVL, often combined with a negative A wave in Vs-e (left lateral AP), can imitate a pathological Q wave, characteristic of a lateral wall infarction. Cases of erroneous diagnosis of myocardial infarction are not so rare: 10 patients with WPW syndrome, observed by our staff at different times, were first placed in infarction departments.

T. D. Butaev together with N. B. Zhuravleva and G. V. Myslitskaya (1985) conducted vector analysis A waves, T waves in the frontal plane in patients with WPW syndrome who had a negative A wave in leads II, III, aVF, on the one hand, and the average QRS axes (initial 0.04 s), T waves in a group of patients who underwent lower myocardial infarction, on the other hand. In WPW syndrome, A waves and T waves had a discordant direction with their axes diverging by an average of 125° (from 95 to 175°). In patients with inferior myocardial infarction, the direction of the mean QRS axes (initial 0.04 s) and T waves was concordant with a slight divergence of these axes by an average of 27° (from 10 to 40°). These differences can certainly be used in differential diagnosis in unclear cases.

In conclusion, it should be mentioned that in recent years vectorcardiographic

Chinese and electrotopocardiographic methods (registration of potentials on the body surface) to determine the localization of the DP, as well as recording the Kent bundle potential, echocardiography, radionuclide ventriculography are used [Ostroumov E. N. et al., 1990; Revishvili A. Sh. et al., 1990].

ELECTROPHYSIOLOGICAL STUDIES IN WPW SYNDROME

EFI goals in patients with WPW syndrome, extensive: confirmation of the diagnosis; localization of DP; their electrophysiological, pharmacological properties, especially the identification of patients with short anterograde ERP in the DP (see pp. 358-359); involvement of the DP in the circle of reciprocal tachycardia; reactions to antiarrhythmic drugs (choice of treatment).

During the period of sinus rhythm in patients with WPW syndrome, the A-H interval on the EPG (Fig. 136) is not changed, the H-V interval is shortened (in the observations of S. P. Golitsyn, on average up to 7.2 ms); Often the H potential plunges into the ventricular complex, appearing simultaneously with wave A (H-V = 0), or the H potential is recorded after the onset of the ventricular complex (in 12 observations by S. P. Golitsyn, the H-V interval had a negative value). During atrial stimulation with increasing frequency or when single atrial extrastimuli are applied with increasing prematurity, conduction in the AV node slows down with a prolongation of the A-H interval. The time of conduction of the impulse to the ventricles through the AP does not change, and accordingly the P-R (A-V) interval remains constant. This seems to lead to a shift of the H potential towards the ventricular complex, to their

Rice. 136 EPI for WPW syndrome. Interval P -A = 0.12 s, A -H = 100 ms,

“fusion” and even the appearance of H after V. At the same time, the zone of the ventricular myocardium, excited in an abnormal way (wave A), expands. When the stimulation of the atria reaches a high frequency, anterograde blockade of the AV node occurs, and the ventricles are completely activated by impulses coming through the AP. The QRS complex, sharply expanding, turns into a solid wave A, but the RA interval does not change (!). A further increase in the frequency of artificial atrial stimulation can lead to complete blockade of AP, which is immediately reflected in the complexes conducted through the AV node by a sudden lengthening of the PR interval, disappearance of the A wave and narrowing of the QRS [Bredikis Yu Yu, 1979, 1986, 1987; Golitsyn S. P, 1981; Kirkutis A. A, 1983; Zhdanov A M., 1985; Butaev T. D, 1985; Grishkin Yu N., 1987; Mellens H., 1976, Prystowsky E. et al., 1984].

The presence of an additional atrioventricular bundle can also be established by stimulating the ventricles with increasing frequency or by applying single ventricles.

daughter extrastimuli with increasing prematurity. In persons with WPW syndrome or in those who have hidden retrograde DP, constancy of intervalV-A, i.e., the time of impulse conduction through the AP. Only with the earliest extrastimuli does a slight prolongation of the retrograde conduction time occur, which depends on the intraventricular delay of the impulse in the area between the stimulating electrode and the end of the AP in the ventricular wall [Golitsyn S P, 1981; Kirkutis A A, 1983; Svenson R. et al., 1975; Galla-gher J. et al., 1978; Wellens H., 1970] In rare cases, the V-A interval remains stable during increasing frequency of ventricular stimulation, despite the fact that impulses propagate to the atria through the normal conduction system. This simulates retrograde conduction through the AP. To clarify, it is proposed to repeat the study after administration of verapamil , which has little effect on the electrophysiological properties of LTP, but slows down VA nodal conduction. If verapamil prolongs the V-A interval, then this in most cases indicates retrograde movement of the impulse through the AV node. A test with propranolol gives similar results. The absence of conduction through the AP during ventricular stimulation does not exclude the possibility of hidden, i.e., partial penetration of ventricular impulses into the AP. The observation of our employees G.V. Myslitskaya and Yu.M. Kharchenko (1986) illustrates this fact (Fig. 137).

Retrograde conduction of ventricular stimuli to the atria occurs in an unusual, eccentric sequence, which is detected primarily at the site where the AP joins the atrium wall. With left-sided DP, the average axis of the retrograde P wave in the frontal plane is directed upward and to the right (the “northwest” region), therefore the P wave has a negative polarity in lead I, sometimes in aVL; in addition, the P waves are negative in leads II, III, aVF. In some patients, these waves are negative in leads Vs and Ve and the formation of a P wave of the “dome and spire” type in lead V]. When conducting ventricular stimuli through the right-sided AP, the average axis of the retrograde P wave in the frontal plane is directed upward; the P waves have a negative polarity in leads II, III, aVF; in lead I, the P wave is equiphasic or weakly positive.

The presence of an atrioventricular junction is confirmed by EPI by the fact of normalization of the QRS complex (disappearance of wave A) during electrical stimulation of the His bundle branch, as well as in spontaneous His extrasystoles propagating along the His-Purkinje system.

An integral part of EPI is the determination of refractoriness and conductivity in the DP. ERP is measured by endocardial or

transesophageal methods of programmed electrical stimulation of the atria and ventricles according to known rules. Anterograde ERP of AP is the longest interval ai-A 2 (recorded near the atrial end of AP), in which wave A2 is conducted to the ventricles without signs of pre-excitation (QRS without wave A). On the EPG there is a sudden prolongation of the Hi-H2 interval (Vi-V 2). If the ERP of the AV node is shorter than the ERP of the DP, anterograde blockade of the DP may be manifested by the absence of H 2 and V 2 potentials in response to the A 2 stimulus. Retrograde ERP AP - longest interval Vi - Vz (recorded near the ventricular end of the AP), in which wave V 2 is not conducted along the AP to the atria. On the EPG there is a sudden and distinct prolongation of the ai - A 2 interval. If the retrograde ERP of the AV node exceeds the retrograde ERP of the AP node, the latter cannot be determined. The level of conduction in the AP is assessed by the largest number of impulses passing through the AP from the atrium to the ventricle (anterograde conduction) and from the ventricle to the atrium (retrograde conduction). The preservation of conductivity along the DP type 1: 1 is taken into account when stimulating the corresponding chamber of the heart with increasing frequency up to a stimulation cycle length of 250 ms (240 pulses per 1 min).

A. Tonkin et al. (1985) noted that with increasing stimulation rhythm, the anterograde ERP of the DP shortened in 12 of 20 patients, lengthened in 6, and did not change in 2. The retrograde ERP shortened in 13 of 15 patients, lengthened in 1, and did not change in 1 sick. With the transesophageal method of measuring ERP in the AP, a correction is required for the time it takes the extrastimulus to travel the distance from the esophagus to the place where the AP joins the atrium. In approximately 30% of cases, the determination of anterograde ERP in the AP is hampered by atrial refractoriness. During

sinus rhythm, i.e., during a long cardiac cycle, the AP conducts more quickly than the AV node, but the anterograde ERP in the AP is longer, i.e., excitability here is restored more slowly. This is directly related to the onset of AV reciprocal AT, the electrocardiographic features that are indicated.

ELECTROCARDIOGRAM WITH PRE-EXCITATION VIA MAHEIM FIBERS

During sinus rhythm, the ECG is mostly normal. The P-R interval is not shortened (>0.12 s) because there is a delay in the sinus impulse crossing the AV node before it reaches the origin of the Macheim fibers. In some patients, a fuzzy A wave is visible, which is also sometimes isoelectric. In these cases, the right ventricle (right bundle branch), to which the Macheim fibers approach, is activated earlier than the left ventricle, which leads to a moderate widening of the QRS complex (up to 0.12 s), which takes on the appearance of a left bundle branch block. The septal q waves disappear in leads oriented to the left, since the excitation of the septum goes from right to left.

On EPG with sinus rhythm, the A-H interval remains normal, the H-V interval may shorten (<30 мс). Стимуляция предсердий с нарастающей частотой или програм­мированная предсердная стимуляция вызывает увеличение интервалов А- Н (Р-R), правда, они редко удлиня­ются больше, чем на 50 мс. Появляет­ся (увеличивается) волна А в тех случаях, когда волокна Махейма за­канчиваются в мышце правого желу­дочка либо возникает (усиливается) блокада левой ножки с отклонением электрической оси QRS влево. По­тенциал Н смещается к желудочко­вой ЭГ с укорочением интервала H-V.

To distinguish between similar nodes

and fasciculoventricular variants of preexcitation use artificial electrical stimulation of the common trunk of the His bundle: a) normalization of the QRS complex indicates that the Macheim fibers are located above the site of stimulation (probably in the AV node); b) preservation of the QRS complex (wave A) in the same form as at the moment of atrial stimulation is evidence that the Macheim fibers begin in the common trunk of the His bundle.

Pre-excitation of the ventricles during the functioning of the James and Maheim pathways. The P-R and A-H intervals are short, wave A is recorded, and the H-V interval is also shortened. For example: P-A = 35 ms, A-N = 45 ms, H-V = 10 ms, P-R = 0.09 s, QRS = 0.14 s (wave A). During atrial stimulation, the P-R and A-H intervals lengthen only slightly, the H-V interval does not change, as does the QRS complex. When the His bundle is stimulated, wave D remains. The ECG resembles type A of the classic WPW syndrome or type D is formed: in leads II, III, aVF, V b V 4 -e - QS complexes; wave A is negative in leads II, III, aVF and Vi; isoelectric - in leads We- In leads I, aVL, Va-3, the QRS complexes and waves A are directed upward.

CLINICAL DATA ABOUT WPW SYNDROME

WPW syndrome, along with other rarer variants of pre-excitation, occurs in all age groups, from newborns to the elderly, in 1-30 cases per 10,000 ECG, or in 0.04-0.31% in children and 0.15% -In adults. Cases predominate in young people and are much less common in people over 50 years of age. When recording an ECG in 22,500 healthy pilots, signs of preexcitation

ventricular pins were detected in 0.25%. These digital data cannot be considered as exhaustive, if only because latent, transient, intermittent forms of WPW syndrome are not always taken into account. There is no doubt that WPW syndrome is observed more often in men than in women: the former account for 60-70% of observations.

Most of these young people do not have any acquired heart disease (although they may develop later). However, combinations of WPW syndrome with other cardiac anomalies are not uncommon: atrial and ventricular septal defects, tetralogy of Fallot, Marfaia, Ehlers-Danlos, MVP syndromes, early ventricular repolarization syndrome [Bockeria L.A., 1984; Vorobyov L.P. et al., 1988]. According to calculations by E. Chung (1977), congenital (hereditary) heart defects can be detected in 30% of patients with ECG signs of WPW syndrome. In the materials from our clinic, the combination of WPW syndrome with MVP was observed in 17% of patients, mainly with left-sided DP. N. Wellens et al. (1980) found manifestations of WPW syndrome in 25% of cases of Ebstein's anomaly. We have already mentioned that patients with this anomaly often (in 50% of cases) have several APs located on the right and joining the posterior part of the interventricular septum or the posterolateral wall of the right ventricle; preexcitation occurs in the atrialized ventricle. It is possible that the hyperplasia and elongation of the artery of the SA node discovered by T. D. Butaev together with E. V. Ryzhov and V. A Minko (1986) in more than half of patients with left-sided DP also belong to the category of anomalous phenomena. There are also indications of a more frequent development of SA node dysfunction in WPW syndrome

[Shulman V.A. et al., 1986; Zipes D., 1984]. Known and family optionsYou WPW syndrome. P. Zetterqvist et al. (1978) noted its electrocardiographic signs in 5 members of the same family in four generations. D. Bennett et al. (1978) observed WPW syndrome in twins (autosomal dominant type of inheritance, according to N. Vidaillet et al., 1987). Recently, V. S. Smolensky et al. (1988) once again drew attention to the phenotypic features inherent in individuals with WPW syndrome (“funnel chest,” “straight” back, flat feet, excessive joint mobility, high, “Gothic” palate, malocclusion, etc.). This symptom complex is considered as a manifestation of connective tissue dysplasia - mild generalized diseases (anomalies) of connective tissue [Fomina I.G. et al., 1988; Child A., 1986].

Worth considering transient, intermittent forms WPW syndrome, occurring, according to Yu. Yu. Bredikis, in 11.4% of cases (Fig. 138). Clinical experience shows that such instability of pre-excitation is often associated with fluctuations in the tone of the autonomic nervous system. For example, ventricular pre-excitation can resume when a patient massages the sinocarotid region, which increases vagal inhibition of the AV node and accordingly stimulates the passage of the sinus impulse through the AP. Isoproterenol helps to identify and increase wave A by improving the conditions in the AP. A number of other pharmacological drugs are also used for the same diagnostic purposes. Isoptin, administered intravenously over 2 minutes at a dose of 15 mg, causes an increase in wave A in 2/3 patients while maintaining its shape and polarity. It is obvious that inhibition of AV nodal conduction under the influence of isoptin creates more favorable conditions for

Rice. 138. Transient syndrome of WPW and extrasystoles from DP.

Above, in the first complex on the left, P - Q = 0.15 s (wave D is absent), in the second complex the interval P - d = 0.08 s, etc. In the middle: the third complex-extrasystole from the accessory pathway (wave D; P wave behind the QRS, post-extrasystolic pause, then normal sinus complex). Below are two consecutive ectopic complexes from the accessory tract (parasystole of the accessory tract?). PECG - transesophageal ECG.

movement of the impulse along the DP. With intravenous administration of 50 mg of ajmaline (ptlurythmal) per L min, wave A disappears in 4/5 patients with WPW syndrome, which reflects the development of complete anterograde blockade or a sharp prolongation of the ERP in the AP. Pharmacological tests of this type were successfully used by S. P. Golitsyn (1981), A. I. Lukosevichiute, D. I. Reingardene (1981), T. D. Butaev (1986), D. Krikler, E. Rowland (1975) , Singh V. et al. (1980).

Ventricular preexcitation in itself does not have a noticeable effect on cardiohemodynamics, i.e., on the values ​​of EF, SV, and MO. Most individuals with WPW syndrome have normal heart sizes and high exercise tolerance. It can be pointed out that in patients with type 6 WPW syndrome, echocardiographic examination reveals an unusual movement of the posterior wall of the left ventricle: systolic “two-hump”, reflecting the uneven excitation and contraction of the posterior wall, to which the AP approaches. This “two-humpedness” is more pronounced, the more pronounced wave A [Buta-rv T.D., 1986]. Let us recall that the fi-ro type of WPW syndrome is characterized by a negative A wave in leads II, III, aVF, simulating an infarction Q wave. However, in patients who have suffered an inferior myocardial infarction, hypo-, akinesia of the posterior wall without systolic “double hump” is noted.

ARRHYTHMIAS AND BLOCKS IN WPW SYNDROME

If we exclude some diagnostic problems, then the clinical significance of WPW syndrome is determined by tachyarrhythmias, complicating its otherwise benign, asymptomatic course. These rhythm disturbances were recorded, depending on the selection, in 12-80% of those examined [Lirman A.V.

et al., 1971; Bredshs Yu. Yu., 1985; Shevchenko N. M., Grosu A. A., 1988; Wollens. Reciprocal (circular) AV paroxysmal tachycardias account for (according to various sources) about 80% of these tachyarrhythmias, AF - from 10 to 32%, AFL - about 5%. For example, in 183 patients with WPW syndrome, H. Wellens et al. (1980) managed to register on an ECG or reproduce with EPI various tachycardias, which were distributed as follows: atrial tachycardia - in 1.6%, AV nodal reciprocal AT - in 4.4%, AV reciprocal AT with the participation of AP - in 70.3 %, ventricular tachycardia - in 1.1%, AF - in 17.1%, AF and AV reciprocal AT - in 5.5% of cases. In total, AV reciprocal PT occurred in almost 76% of patients, and AF occurred in more than 22% of patients. Finally, atrial and ventricular extracontractions are detected in 18-63% of cases of WPW syndrome, the former 2 times more often than the latter. Since the electrocardiographic (electrophysiological) characteristics of the AV reciprocal (circular) AT were given in Chap. 11, we will focus on describing AF (AF) in patients with WPW syndrome. The occurrence of AF paroxysms(TP). Patients with WPW syndrome have an increased incidence of AF compared with the general population (see Chapter 12); AV reciprocal (ortho- and antidromic) tachycardia often degenerates into AF. All this should be seen as very unfavorable turn during the course of the disease, in particular, as the addition of atrial arrhythmic disease to the WPW syndrome (impaired intra- and interatrial conduction, shortening of refractoriness in the atria and an increase in its dispersion, which usually increases the vulnerability of the atria). Recently A. Michelucchi et al. (1988) confirmed that in patients with WPW syndrome, ERP in the upper and lower parts of the right atrium

days are shorter than in healthy people. The dispersion of ERP and FRP in WPW syndrome was 46 ± 22 and 45 + 26 ms, respectively, versus 24 ± 16 and 19 ± 13 ms in healthy individuals. In most patients, AF occurred when 1-2 atrial extrastimuli were applied in the lower part of the right atrium, where refractoriness was shorter. Such electrical instability of the atria may be predisposed by the abnormal DP itself and especially by the frequently repeated retrograde, eccentric excitation of the atrium during attacks of AV reciprocal tachycardia. Obviously, AF (AF) is observed more often in patients with left-sided DP. According to L. Sherf, N. Neufeld (1978), a retrogradely arriving impulse causes AF if it enters the vulnerable (vulnerable) phase of the atrial cycle.

The relationship between attacks of AV reciprocal (circular) tachycardia and paroxysms of AF (AF) develops differently in patients. In some patients, these arrhythmias occur independently, at different times. R. Bauernfeind et al. (1981) caused AV reciprocal tachycardia during EPI in 51 patients, 23 of whom had a history of AF paroxysms. In other patients, supraventricular (AV reciprocating) tachycardia directly turns into AF, which was first noted by T. Lewis (1910). R. Sung et al. (1977) recorded spontaneous transitions of AT to AF in 7 of 36 patients with WPW syndrome who underwent EPI. According to S. Roark et al. (1986), in one year, in every 5th patient with WPW syndrome and attacks of AV reciprocal tachycardia, the disease is complicated by paroxysms of AF. According to our observations, this happens less frequently.

The entry of a large number of waves of AF or AFL into the AV node causes, as usual, an extension of its ERP and functional AV nodal block; The ERP in the DP, on the contrary, is shortened [Golitsyn S.P. et al., 1983;

Tonkin A. et al., 1975]. As a result, an intense flow of irregular impulses penetrates the ventricles through the AP without significant delay. The ECG during AF records a frequent (220-360 per minute), irregular ventricular rhythm with QRS complexes of different shape, width and amplitude (“false ventricular tachycardia”). When atrial impulses reach the ventricles only through the AP, the QRS complexes are a continuous wave D. If the impulses propagate through the AV node, which has temporarily left the refractory state, the QRS complexes remain narrow (Fig. 139a). Between these extreme options, there are many intermediate QRS complexes in shape with a larger or smaller wave D. With a relatively rare rhythm, you can see several narrow QRS complexes following each other, which is apparently associated with hidden conduction of impulses in the AP (anterograde from the atria or retrograde from the ventricles), temporarily interrupting its functioning.

During AFL, the ECG may show a frequent regular ventricular rhythm with wide QRS complexes (large D waves). This painting imitates attack of ventricular tachycardia (!). If anterograde blockade occurs in type 2:1 AP, then the number of ventricular complexes is reduced to 140-160 per minute (Fig. 1396). Conduction of each flutter wave (1:1) through the AP increases the number of ventricular contractions to 280-320 per minute. In AFL in individuals who do not have DP, 1:1 AV nodal conduction is extremely rare (see Chapter 17).

The duration of the anterograde ERP accessory pathway is a factor that determines the maximum ventricular rate that can be achieved in AF (AF). Korotcue ERP leads, as we have already mentioned,

This led to frequent ventricular excitations with even shorter R-R intervals, which was noted by N. Wellens et al. (1982), who associated this phenomenon with the effect of sympathetic nerve stimuli on LTP after the onset of AF. Frequent and irregular activation of the ventricles Ti of an unusual sequence is the path to the occurrence of VF. Long anterograde ERP the accessory pathway prevents the occurrence of these life-threatening ventricular arrhythmias. Yu. Yu. Bredikis (1985) recorded the transition of AF to VF in 8 patients with WPW syndrome. J. Gallagher and W. Sealy (1981) resuscitated 34 patients who developed VF over a 10-year observation period. G. Klein et al. (1979) noted that in 6 patients with WPW syndrome, ventricular fibrillation developed a few minutes after a single intravenous injection of digitalis prescribed for the treatment of paroxysms of AF. Cardiac glycosides, slowing down AV nodal conduction, can simultaneously shorten the antero-padded ERP of the accessory pathway (!). There is agreement among clinicians that there are a number of signs that indicate the threat of transition from AF to VF in WPW syndrome (“risk factors”): a) duration of anteropadal ERP of the accessory pathway<270 мс; б) длительность самого ко­роткого интервала R-R в период ФП <220 мс (комплексы QRS ши­рокие с волной А)- очевидный риск: при кратчайшем интервале R-R >220-<250 мс - вероятный риск; при кратчайшем интервале R-R >250-<300 мс - возможный риск; при кратчайшем интервале R-R >300 ms - slight risk of VF FKlein G. et al., 1990]; c) the presence of several DP: d) left-sided location of the DP [Brady-Gotts Yu. Yu.. 1985. 1987; Bockeria L.A., 1986, 1987; Gallapher J. et a!., 1978; Wellens P. et al., 1980; Prystowsky E. et al., 1984; R/aho T. et al!, 19891."Co-

according to G. Klein et al. (1990), over 10 years of prospective observation, from 1 to 5.6% of patients with WPW syndrome died, in whom the shortest R-R interval during AF was ^250 ms. In total, therefore, among individuals with WPW syndrome, sudden death from VF occurs extremely rarely.

As a person ages, the tendency for rapid ventricular responses through AP (in AF) decreases markedly.

It should be taken into account that the degree of pre-excitation of the ventricle during sinus rhythm has no relation to the likelihood of frequent ventricular responses in AF (AF). Developed pharmacological tests, allowing to identify a group of high-risk patients, i.e. those whose anterograde ERP of the accessory pathway is shorter than 270 ms. One of them is the already mentioned test with ajmaline; during sinus rhythm, 50 mg of the drug is administered intravenously to the patient over 3 minutes. The disappearance of the L wave indicates blockade of the AP, the ERP of which is >270 ms. In patients with ERP <270 ms, ajmaline rarely blocks anterograde conduction along the AP. In a modified version, ajmaline is administered intravenously at a rate of 10 mg/min up to a maximum dose of 100 mg. According to L. Fananapazir et al. (1988), the procainamide test is of limited value for identifying patients with WPW syndrome who have a potential risk of sudden death. The absence of a short anterograde ERP in the AP is also indicated by such signs as the intermittent nature of preexcitation and the disappearance of ventricular preexcitation during exercise.

WPW syndrome and anterograde blockade of the AV node and (or) AP. The transient, intermittent WPW syndrome, which was already discussed above, occurs approximately in \ \ % of cases The appearance at different times (or on the same ECG) of QRS complexes with and without wave A, sometimes the correct alternation of such complexes, indicates the transcursor nature of ventricular preexcitation, which in turn depends from instability of AP block (“intermittent WPW syndrome”, “alternating WPW syndrome”) The results of recent radionuclide studies with technetium 99 t should be taken into account, showing that there may not be an A wave on the ECG, although a small degree of pre-excitation (pre-excitation) contraction) of the ventricle is preserved, i.e., there is no complete anterograde blockade of AP

The disappearance of wave A in the QRS complex after a long pause in sinus rhythm or during sinus bradycardia should be considered

Rice. 139. a - paroxysm of AF in a patient with WPW syndrome (explanation in the text); b - VVPW syndrome; TP with PV blockade 2:1 with transition to complete blockade of the AV node and AP (pause lasting 5.5 s during the continuation of the ECG).

rush as a consequence Brady-dependent blockade of DP(phase 4 blockade of AP). This fact, in turn, serves as an indirect indication of the presence of spontaneous diastolic depolarization (automatism) in some cells of the DP, which, in general, rarely occurs. The automatic activity of such cells is also associated with the formation of escape QRS complexes without a P wave. They have the same shape (wave A) as sinus complexes with signs of preexcitation. The automaticity of LTP can be enhanced by atropine, i.e. some of its cells are sensitive to vagal influences like the cells of the AV junction. The disappearance of preexcitation in complexes after a short sinus pause and during AF is evidence ta.gizavisimy blockade of DP(block and phase 3 PD). There are cases when the signs of ventricular pre-excitation clearly recorded on the ECG disappeared irrevocably the following day. PTU transformation was observed both in children in the first year of life and in older people. In some of them, fibrous degeneration of the DP was found post mortem. The opposite phenomenon is lengthbody latency syndrome WPW, when its manifestations occur in patients only in old age. It is still unclear what reasons contribute to such a late-onset improvement in conductivity along the AP, which has been blocked for many decades. It is possible that the deterioration of conduction in the AV node that progresses as a person ages is important. The increase in wave A from complex to complex and its subsequent gradual decrease vMem-is associated with acceleration or deceleration of conduction in the AV node (changes in the A-H intervals on the EPG). This phenomenon, called the “concertina effect”, or “accordion effect”, is encountered

occurs infrequently. Its causes are: a) fluctuations in the tone of the vagus nerve; b) displacement of the atrial pacemaker; c) the occurrence of additional A waves due to preexcitation of the ventricle along several APs; d) ischemia of the AV node in acute inferior myocardial infarction or Prinzmetl’s angina (spasm of the right coronary artery).

The transition of the classic WPW syndrome to a form with an extended PR interval while maintaining wave A indicates a combined first-degree anterograde blockade of the AP and AV node: the impulse through the AP moves faster than through the AV node. Prolongation of the PR interval with a simultaneous increase in wave A and widening of the QRS means that pronounced anterograde T-degree blockade in the AV node is combined with moderate anterograde blockade of the first degree of AP. In patients with AV nodal shunts (James, Bretpenmapte tracts), normalization of the PR interval may be associated with slowing of conduction in the His-Purkinje system (extension of the H-V interval of the His electrogram without widening of the QRS) or with interatrial blockade (widening and splitting of P waves).

WPW syndrome and bundle branch block. If the bundle branch block occurs on the same side as the AP, it may mask signs of preexcitation. This usually happens when the right leg is blocked and the AP is located on the right side (Fig. 140). True, in such cases, attention is drawn to the very late activation of part of the right ventricle (lead Vi-a). The addition of left bundle branch block to type A WPW syndrome is accompanied by a noticeable expansion of the QRS complex and its splitting in leads Vs-e. It is easier to recognize those combinations in which the bundle branch block and the preexcitation zone are localized in different ventricles. A number of authors have observed

Rice. 140 Combinations sin[)o\1с1 WPW

d-tina 9th with complete blockade of the right leg, b - (left-sided anterior paraseital DP)

with expansion and hypertrophy of the left ventricle (diasgolic diameter - L.2 cm, thickness

posterior wall and interventricular septum - 1.8 cm), c - AFL with AV block 4 1

type A of WPW syndrome is the appearance of right leg block during catheterization of the right ventricular cavity (typical QRS complexes in Vi-2 in combination with wave A and a short PR interval). People with AV node shunts tend to have narrow QRS complexes. If these

If individuals develop coronary artery disease or other myocardial disease with bundle branch blocks, they do not affect the duration of the P-R and A-H intervals.

Prognosis and treatment for the syndromeW.P.W.. Quite favorable prognosis for patients with WPW syndrome

sharply worsens, as already emphasized, when paroxysms of AF (AF) occur. Congenital or acquired heart diseases also have a negative effect when combined with ventricular pre-excitation. Deaths directly related to WPW syndrome are rare. The literature provides mortality rates ranging from 0 to 2%. The main mechanism of death is VF, caused by frequent arrival of AF waves (AF) to the ventricles. We have already mentioned the danger of prescribing cardiac glycosides to patients with WPW syndrome. Caution is also required when using other drugs that can prolong the ERP in the AV node and

complicate the selection of drug therapy.

SYNDROMES OF PREMATURE VENTRICULAR EXCITATION

These syndromes are caused by the presence of congenital abnormal impulse pathways in the heart.

The atrioventricular pathways - the bundles of Kent - left- and/or right-sided - directly conduct excitation from the atria to the ventricles, bypassing the atrioventricular junction. In this case, part of the ventricular myocardium, excited through the Kent bundle, depolarizes earlier than the bulk of the ventricular myocardium, which receives an impulse in the usual way.

Obviously, this process must be accompanied by the following changes (Fig. 52):

shortening the interval P-Q (less than 120 ms);

the beginning of the ventricular complex with the manifestation of excitation passing through the bundle of Kent - delta wave;

expansion of the deformed QRS complex over 0.10 s; in this case, the T wave is often discordant with the QRS complex.

This syndrome is called WPW (Wolf-Parkinson-White) syndrome. WPW syndrome can be a permanent or transient (if the Kent bundle is blocked for some reason) electrocardiographic phenomenon of no practical significance. However, approximately half of people with WPW syndrome develop paroxysms of supraventricular tachycardia (less commonly, atrial fibrillation). Arrhythmias are caused by the macro-re-entry mechanism: excitation passes through the atrioventricular junction and returns through the bundle of Kent, or (less often) is carried out antegrade through the bundle of Kent and then retrograde through the atrioventricular junction.

Paroxysms of supraventricular tachycardia can be either mild or severe, and sometimes develop into ventricular fibrillation.

IN Depending on the location of the Kent beam, type A or type A is recorded on the ECG

IN WPW syndrome. In type A, a high R wave with The D-wave is present in the right precordial leads (the basal parts of the myocardium of the right ventricle are prematurely excited), in leads II, III and aVF. In type B, the R wave with a delta wave is recorded in the left chest leads, leads I, aVL; at the same time, in the right chest leads, leads II, III, aVF, the QRS complex is recorded in the form of rS or QS, which sometimes leads to erroneous diagnosis of a previous myocardial infarction.

The atrionodal tract - the James bundle, connecting the atria with the lower part of the atrioventricular junction, again eliminates the delay of the impulse when passing from the atria to the ventricles, but unlike WPW syndrome, all parts of the latter are excited in the usual manner. Accordingly, the ECG shows a shortening of the P-Q interval of less than 0.12 s, but the ventricular complex does not change. Arrhythmias may occur, similar to what occurs with WPW syndrome. This type of premature excitation of the ventricles is called LGL (Laun-Genong-Levine) syndrome in the presence of supraventricular arrhythmias or CLC (Clerk-Levy-Christesco) syndrome in their absence.

Nodoventricular tract - Macheim fibers between the distal part of the atrioventricular junction and the ventricular myocardium. On the ECG, the P-Q interval has a normal duration, but the ventricular complex begins with a D wave.

Various combinations of abnormal pathways are possible.

ELECTROCARDIOGRAM FOR ISCHEMIA AND MYOCARDIAL INFARCTION

The experiment showed that myocardial necrosis is accompanied by changes in the QRS complex, “damage” by changes in the ST segment, and ischemia by changes in the T wave. In the clinic, these electrophysiological relationships are not absolute. The most common and specific sign of myocardial ischemia is

horizontal (less often oblique) depression of the ST segment with flattening or inversion of the T wave (Fig. 53). In chronic ischemic heart disease, these ECG changes can be permanent and are often combined with disturbances in heart rhythm and conduction (usually blockades in the atrioventricular bundle system). Less commonly, myocardial ischemia is accompanied by transient disturbances in conduction and heart rhythm (mainly blockade of the legs of the atrioventricular bundle, extrasystole). However, in many patients with coronary artery disease who have not suffered a myocardial infarction in the past, the ECG outside an attack of angina may remain normal, and ischemic changes will be detected only if an attack of angina occurs at the time of recording the ECG - independently or during stress tests (see below). In special cases, with the so-called variant angina, or Prinzmetal angina (angina at rest, caused by spasm of the epicardial parts of the coronary arteries), there is an elevation of the ST segment, indistinguishable in pattern from the beginning of myocardial infarction (see below), but disappearing after the cessation of the attack of angina. .

Electrocardiographic criteria for the severity of ischemia are the depth of ST segment depression (at least 1 mm) and the depth of the inverted T wave, as well as the number of leads in which these changes are recorded and their duration. Of course, the level of load at which the angina attack and/or ECG changes occurred is of utmost importance.

During myocardial infarction, ischemia, “damage,” necrosis, and scarring successively develop in the heart muscle; post-infarction cardiosclerosis - scar

usually persists for the rest of your life. Each of these stages has its own electrocardiographic display. It should be borne in mind that in the cardiac muscle around the focus of necrosis, a peri-infarction (perinecrotic) zone of ischemia and “damage” persists for some time, so that all these conditions can simultaneously affect the ECG picture.

Depending on the depth of necrosis, transmural and non-transmural (usually subendocardial) myocardial infarctions are distinguished. However, in the clinic such detail is not always possible, especially if only an electrocardiographic research method is available.

Today, the international classification of myocardial infarction according to electrocardiographic characteristics provides only two options: myocardial infarction with a Q wave and myocardial infarction without a Q wave. Myocardial infarction with a Q wave (QS) is called transmural.

As a rule, the presence of a QS wave indicates a larger extent of myocardial necrosis than in the presence of a Q wave.

The picture and dynamics of the ECG in transmural myocardial infarction are diagnostically most convincing.

During such a myocardial infarction the following stages can be distinguished (Fig. 54).

1. Stage of damage. It is characterized by a short-term rise in the ST segment with the formation of a high, pointed T wave. These changes are so short-lived that, as a rule, they do not have time to be recorded even on an ECG taken shortly after the onset of the attack. Then, over the course of several hours, the rise of the concave upward ST segment continues to increase, forming a single arc with the T wave (“monophasic curve” in acute myocardial infarction).

This stage of myocardial infarction can be called the most acute; it is fundamentally reversible provided that blood flow in the infarct-related coronary artery is immediately restored.

2. Acute stage, the beginning of which occurs within the next few hours from the beginning

myocardial infarction, and the duration usually ranges from several days to 1-2 weeks7. At this stage, a focus of necrosis is formed, a pathological Q wave (QS) is formed, the ST segment begins to decrease slightly and a negative T wave appears.

3. Subacute stage characterized by gradual replacement of the necrosis focus with connective tissue and at the same time stabilization of the myocardium in the peri-infarction zone. The degree of ST segment elevation continues to decrease until it returns to the isoelectric line, and a deep, pointed, symmetrical T wave (“coronary T”) is formed. The duration of this stage is measured in several weeks.

7 ECG dynamics can be much faster, especially when

restoration of blood flow in the corresponding artery.

4. Stage of scar changes- a “calling card” of a transmural myocardial infarction that persists for many years, usually for the rest of one’s life. This ECG picture is described as post-infarction (large focal) cardiosclerosis. On the ECG, the Q wave (QS) and the “coronary” T wave are preserved; the ST segment is on the isoelectric line. Accordingly, this stage is also called the “Q-T stage.” Slow (years!) positive dynamics are possible: the pathological Q wave decreases (and even disappears), the amplitude of the negative T wave decreases, it can become smoothed and even weakly positive (Fig. 55, 56).

When assessing the ECG at this stage, especially if there is no ECG of previous stages of myocardial infarction, it is extremely important to assess whether the Q wave is pathological, i.e., caused by a previous myocardial infarction, and not by any other reasons (ventricular myocardial hypertrophy, etc.).

The main criteria for a pathological Q wave are the following:

In case of myocardial infarction of the anterior wall of the left ventricle (for topical diagnosis of myocardial infarction, see below), the Q wave in leads I, aVL and chest leads is considered pathological if its width exceeds 0.03 s, and the amplitude is at least 25% of the R wave in the same abduction or exceeds 4 mm. (It should be noted that such “pathological” Q waves can also occur with blockades of the atrioventricular bundle branches, severe ventricular hypertrophy, and in a number of other cases.)

In case of myocardial infarction of the posterior phrenic wall of the left ventricle, the main sign of a pathological Q wave in leads II, III, aVF is its amplitude over 1/4 of the R wave.

A special variant of the ECG during myocardial infarction is a “frozen” ECG, when the pattern of the subacute stage does not undergo further dynamics and a more or less significant rise in the ST segment remains stable almost for life. More often this happens in the presence of a QS wave. This picture reflects a significant amount of necrosis (scar) and is considered an electrocardiographic sign of chronic post-infarction

left ventricular aneurysm. However, the latter can also occur in the absence of a “frozen” ECG.

An important additional factor in the ECG picture during myocardial infarction is the appearance of oppositely directed (discordant, reciprocal) changes in the ST segment in leads characterizing “electrically opposite” areas of necrosis of the myocardium. So, if during an anterior myocardial infarction of the left ventricle, along with elevation of the ST segment in leads I, aVL, its depression will be recorded in leads II, III, aVF, then with a posterior myocardial infarction the picture will be the opposite (Fig. 57). This is discussed in more detail when discussing the topical diagnosis of myocardial infarction.

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.