WPW (Wolff-Parkinson-White) syndrome.

WPW (Wolff-Parkinson-White) syndrome is a condition characterized by the existence of an additional pathway through which impulses are conducted.

In the absence of any abnormalities, when the heart is functioning normally, the ventricles and atria contract one after the other. The heart contracts as a result of impulses coming from the sinus node. The sinus node, also called the pacemaker, is the main generator of impulses, which is why its role in the cardiac conduction system is dominant. The impulse produced in the sinus node reaches the atria, causes them to contract, and then goes to the atrioventricular node (AV), located between the ventricles and atria. This is the only possible path by which the impulse can reach the ventricles. For several fractions of a second, there is a delay in the impulse in this AV node, which is caused by the need to give some time for the blood to completely move from the atria to the ventricles. Then the impulse goes in the direction of the His bundle branches, and the ventricles contract.

In the case of the WPW syndrome, there are other ways for the impulse to reach the ventricles without passing through the atrioventricular node, bypassing the latter. For this reason, this bypass path contributes to some extent to the faster conduction of the impulse along it compared to the one that follows the appropriate normal channels. Such a phenomenon may not affect the condition of a person with this cardiac syndrome in any way, and be practically imperceptible. It is often possible to detect it only in the heart activity indicators displayed in the electrocardiogram.

It should be noted separately that in addition to WPW syndrome, there is also the phenomenon of CLC, which in essence is almost completely identical to it, with the only exception being that characteristic changes are not observed on the ECG.

To sum up, we note that WPW syndrome as a phenomenon of the emergence of additional impulse conduction pathways has predominantly the character of a congenital cardiac anomaly and its actual prevalence is greater than the number of recorded cases. At a young age, its existence in humans is not accompanied by any pronounced symptoms. But over time, certain factors can arise that provoke the development of such a syndrome. This happens mainly if the conductivity of the impulse in the main path of its passage worsens.

Causes of WPW syndrome

The causes of WPW syndrome, as most scientists in the field of medical science claim, are based mainly on congenital factors. Namely, the fact that additional atrioventricular connections are preserved during the process of incomplete formation of the heart. This is accompanied by the fact that during the period when fibrous rings are formed in the mitral and tricuspid valves, muscle fibers do not regress completely.

The normal course of development is gradual thinning and subsequently (upon reaching the 20-week period) complete disappearance of all additional muscle pathways existing at early stages in all embryos. Anomalies with which fibrous atrioventricular rings can form contribute to the preservation of muscle fibers, which becomes the main anatomical prerequisite for WPW syndrome.

The familial form of WPW syndrome is significantly more often characterized by the presence of a large number of additional atrioventricular connections.

In approximately one third of all clinical cases, the syndrome is associated with congenital heart defects - mitral valve prolapse, Ebstein's anomaly. In addition, the cause may be a deformed interventricular, interatrial septum, tetralogy of Fallot, dysplasia of connective tissue - dysembryogenetic stigmas. An important role is also played by the heredity factor, in particular, hereditary hypertrophic cardiomyopathy.

The causes of WPW syndrome, as we see, mainly consist of a disruption in the formation of such an important organ as the human heart during embryonic development. However, although this syndrome is largely caused by unfavorable congenital anatomical features, its first manifestations can be detected both in childhood and in adulthood.

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Wolff-Parkinson-White syndrome

Statistical data show that Wolff-Parkinson-White syndrome is observed in 0.1 to 0.3% of the entire population. It is characterized by the greatest number of cases due to the fact that there is such a cardiac anomaly as an additional bundle of Kent, located between one of the ventricles and the left atrium. The existence of the bundle of Kent is one of the fundamental pathogenic factors in the occurrence of such a syndrome. Among people who have been diagnosed with Wolff-Parkinson-White syndrome, men generally prevail over women.

The clinical picture of this syndrome in some patients may be completely unobvious. The main detectable consequence of the faster passage of the impulse along the additional conduction pathway is, first of all, that the rhythms of heart contractions are disrupted, and arrhythmia develops. In more than half of the clinical cases, supraventricular and reciprocal paroxysmal tachyarrhythmias, atrial flutter or fibrillation occur. Often, the Wolff-Parkinson-White syndrome is caused by Ebstein's hypertrophic cardiac anomaly, mitral valve prolapse, and cardiomyopathy.

Wolff-Parkinson-White syndrome is a phenomenon in which premature excitation of the ventricles of the heart occurs. The development of the syndrome is usually not accompanied by the appearance of any symptoms expressed to a sufficient extent for its detection. Often, it is possible to determine the presence of Wolff-Parkinson-White syndrome solely by electrocardiogram data.

Symptoms of WPW syndrome

Symptoms of WPW syndrome may not manifest themselves in any way until its presence is definitely established by the results of an electrocardiogram as the main method of confirmation. This can happen at any time, regardless of a person's age, and until then the course of this cardiac symptom is mostly not accompanied by the appearance of any pronounced symptoms inherent to it.

The main characteristic signs indicating that WPW syndrome is present are disturbances in the heart rhythm. In 80 percent of cases, reciprocal supraventricular tachycardia occurs against its background, with a frequency of 15 to 30%, atrial fibrillation occurs, 5% of patients experience atrial flutter, when the number of beats per minute reaches 280-320.

In addition, there is a possibility of developing non-specific arrhythmias – ventricular tachycardia and ecchysystole: ventricular and atrial.

Arrhythmic attacks are often caused by conditions caused by emotional overstrain or the consequences of significant physical exertion. Alcohol abuse can also be one of the causes, and sometimes cardiac arrhythmia is spontaneous, and it is impossible to determine exactly why it occurs.

When an attack of arrhythmia occurs, it is accompanied by sensations of the heart stopping and palpitations, cardialgia, the patient may feel that he is suffocating. In the state of atrial flutter and fibrillation, fainting often occurs, shortness of breath, dizziness, arterial hypotension occur. If the transition to ventricular fibrillation occurs, the possibility of sudden cardiac death is not excluded.

Such symptoms of WPW syndrome as arrhythmic paroxysms can last from several seconds to several hours. They can be stopped either by performing reflex techniques or independently. Long duration of paroxysms calls for the need for hospitalization and involvement of a cardiologist to monitor these conditions of the patient.

Latent WPW syndrome

The course of WPW syndrome in some cases can be completely latent, hidden. It is possible to make an assumption about its presence in a patient based on the detected tachyarrhythmia, and the main diagnostic measure is the study of the heart by an electrophysiological method, in which the ventricles receive artificial stimulation with an electric current. The need for this is due to the fact that additional conduction pathways can conduct impulses exclusively retrogradely and they do not have the ability to follow in the antegrade direction.

Latent WPW syndrome is also stated on the basis that the sinus rhythm is not accompanied by manifestations indicating premature excitation of the ventricles, that is, in the electrocardiogram, the PQ interval does not have a deviation from the values that are normal. In addition, the delta wave is also not observed, but the presence of atrioventricular reciprocal tachycardia is noted, which is characterized by retrograde conduction through additional atrioventricular connections. In this case, the spread of the depolarization area occurs in sequence - from the sinus node to the atria, and then, passing through the atrioventricular node with the bundle of His, reaches the ventricular myocardium.

In conclusion, it should be noted that latent WPW syndrome can be detected either by recording the time of retrograde impulse conduction or when the ventricles are stimulated during endocardial examination.

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Manifesting WPW syndrome

The key feature that distinguishes the manifesting WPW syndrome is that the direction of excitation passage can be not only antegrade, but also retrograde. Purely retrograde conduction of the impulse by additional ventricular excitation pathways exceeds anterograde conduction in the frequency of cases encountered.

The syndrome is said to be of an antegrade-manifesting type because it “manifests,” declares its existence in the form of characteristic changes appearing in the patient’s electrocardiogram. The ability of the impulse to follow in the antegrade direction actually determines the specific manifestations that distinguish this syndrome in the results of electrocardiography. In particular, with signs of pre-excitation of the ventricles, the appearance of a delta wave in standard leads is noted, the PQ interval becomes shorter, and a widened QRS complex is observed. With regard to the delta wave, it should be noted separately that its magnitude is the greater, the larger the area of the ventricular myocardium to which excitation from the Kent bundle is transmitted.

Manifesting WPW syndrome is characterized by the above-mentioned properties outside of a paroxysmal reciprocal attack of tachycardia. The degree of danger, if it means a danger to the patient's life, is associated primarily not with the presence of this cardiac syndrome, but primarily with such attacks, with tachycardia and atrial fibrillation.

WPW syndrome type B

The WPW syndrome type B is in many ways similar to type A of the same cardiac syndrome. In it, as a result of the passage of the sinus impulse through the right bundle of Paladino-Kent, excitation of part of the right ventricle occurs, ahead of the usual activation of both ventricles, which occurs from the impulse from the atrioventricular junction.

The similarity with the similar syndrome of type A is in the premature excitation of the ventricles, or more precisely, part of the right ventricle. This phenomenon is reflected in the shortening of the PQ interval. Further, the WPW syndrome is characterized by the activation of muscle tissues in the right ventricle, which occurs from one layer to another sequentially. This causes the formation of a delta wave. And finally, the excitation processes of the right and left ventricles do not coincide in time. First, the right is activated, after which the excitation is transmitted to the interventricular septum, and ultimately the left ventricle is involved.

This sequence of ventricular excitation also has similarities to the left bundle branch block.

There are often cases that do not fall under the definition of WPW syndrome type B, and at the same time do not completely correspond to type A of such a syndrome. Some of them are classified as a transitional form of A-B. The occurrence of WPW syndrome is not always necessarily associated with the presence of additional Paladino-Kent pathways. It can also be caused by the simultaneous activation of the James bundle and the Mahaim bundle. If activation occurs only with the James bundle, the LGL syndrome is formed.

Transient WPW syndrome

Transient WPW syndrome occurs in a certain number of patients. In such cases, ventricular pre-excitation is transient. In this form of the syndrome, specific deviations from normal cardiac complexes on the resting electrocardiogram occur episodically, and there may be a fairly long period of time between their appearances, during which the ECG indicators of cardiac activity are not changed.

It is possible to determine the WPW syndrome of the transient type mainly only as a result of a certain targeted effect: when transesophageal stimulation of the atria is performed, ATP or finoptin was administered intravenously. Often, the detection of signs that ventricular pre-excitation is taking place is also possible only if a temporary conduction block through the atrioventricular node is artificially induced. In this case, the syndrome is called latent WPW syndrome.

Transient WPW syndrome is characterized by the occurrence of attacks of tachycardia.

If the transient WPW syndrome is not associated with the occurrence of cardiac arrhythmia, it is called the WPW phenomenon. The possible transition of the disease during its course from syndrome to phenomenon is a factor indicating a favorable trend.

Intermittent WPW syndrome

Intermittent WPW syndrome is also known as intermittent. This name is an accurate reflection of the very essence of the processes that take place in it. And the following happens - the pathways for conducting excitation alternately become its passage through the atrioventricular node, then the antegrade direction of the impulse through the Kent bundle. Due to this circumstance, a standard electrocardiogram outside a paroxysmal attack of tachycardia shows either the presence of signs of premature excitation of the ventricles, or no manifestations of this are detected. ECG indicators are characterized by the presence of signs of ventricular pre-excitation against the background of sinus rhythm and verified atrioventricular reciprocal tachycardia. Difficulties in diagnosing intermittent WPW syndrome can be caused by the fact that it is not always possible to determine it on the basis of a single electrocardiogram of the resting state.

In the intermittent type of WPW syndrome, a transient appearance of a characteristic delta wave is observed on the electrocardiogram.

Intermittent WPW syndrome is thus characterized by a constantly changing direction of the sinus impulse from retrograde through the atrioventricular node to antegrade in the bundle of Kent. For this reason, this type of syndrome can often be difficult to diagnose.

WPW syndrome in adolescents

Adolescence is a time when there is a high probability of occurrence of various anomalies of heart activity and development of its pathologies. One of them is WPW syndrome in adolescents.

This heart syndrome occurs most often in the age group from 10 to 15 years. After the age of 10, adolescent boys are more susceptible to this disease. The age of a teenager, or as it is also called - adolescence, along with the first year of a child's life, is one of the two main periods when tachycardia and all sorts of other heart rhythm disorders can occur.

When this occurs due to the presence of WPW syndrome in a teenager, no characteristic physical signs are found except for its only manifestations in the form of tachyarrhythmia symptoms. Moreover, in adolescence, the severity of these symptoms is often extremely weak. However, if an attack occurs, it is accompanied by intense sweating, cold extremities, hypotension and pulmonary congestion may occur. The risk of such negative phenomena increases if there are heart defects, acquired or congenital.

In 70% of adolescents, WPW syndrome leads to paroxysmal tachycardia with a pulse rate reaching 200 beats per minute and a decrease in blood pressure to 60-70 mm Hg and further down to critically minimal values.

WPW syndrome in adolescents, and especially the arrhythmia it provokes, is closely associated with the possibility of sudden cardiac death. From 3 to 13 years of age, the frequency of such cases is 0.6%, and among young people under 21 years of age, it is 2.3%, respectively.

Atypical WPW syndrome

It becomes possible to say that there is an atypical WPW syndrome based on the fact that, according to electrocardiography data, while all other characteristic features are preserved, an incomplete presence of the complex of ECG signs characteristic of it is noted.

In particular, the conclusion about atypical WPW syndrome is made if the P-Q interval has an unchanged value. The justification for this fact can be that after the atrioventricular delay of the impulse, its abnormal conduction is observed in the fibers of Mahayma, which branch off from the main trunk of the bundle of His.

In addition, the P-O interval may not be shortened due to the phenomenon of atrial block. Diagnosis of this form of the syndrome is carried out on the basis of the form that the ventricular cardiac complexes with the delta wave take.

Changes occurring in the QRS complexes that reflect characteristic rhythm disturbances are also taken into account.

In its typical form, WPW syndrome has a short PR interval of less than 120 ms and a wide QRS complex of over 120 ms, and also has a slow initial part and signs of altered repolarization.

As for the additional conduction pathways of the left-sided location, it should be noted that they are pre-excited to a lesser extent than the shunting tracts of the free wall on the right.

Atypical WPW syndrome is considered when pre-excitation is clearly observed (by a sufficiently competent ECG specialist), while the PR interval is greater than or equal to 120 ms, and the QRS complex, accordingly, does not reach 120 ms. Pre-excitation is not expressed or obvious, both due to a non-shortened PR interval and when there is evidence of ventricular pre-excitation. Here, however, atypical WPW syndrome should be distinguished from the existence of hidden additional conduction pathways.

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Diagnosis of WPW syndrome

Diagnosis of WPW syndrome involves conducting a Holter electrocardiogram and 12-lead ECG, the use of electrical cardiac stimulation through the esophagus, and an electrophysiological examination of the heart.

Transesophageal cardiac pacing provides reliable confirmation that there are additional impulse conduction pathways characteristic of WPW syndrome, and also induces arrhythmic paroxysms.

Conducting an endocardial electrophysiological study provides an opportunity to establish the exact area of localization and the number of additional pathways. The use of this method is also a way to verify the clinical form of WPW syndrome and helps to select drugs for therapy, and in addition, it allows to assess the effectiveness of their use or radiofrequency ablation.

Determination of all possible heart defects and karyomyopathy associated with the existence of WPW syndrome occurs through an ultrasound examination of the heart.

The main criteria of electrocardiography in WPW syndrome are shortening of the PQ interval to a value less than 0.12 s, the presence of deformation of the fusion QRS complex, and the presence of delta waves. In addition, to establish transient rhythm disturbances, daily ECG monitoring is used.

To perform differential diagnosis of this cardiac syndrome, bundle branch block is required.

Diagnosis of WPW syndrome is based on a comprehensive approach using various clinical and instrumental diagnostic methods. However, the first detection of this disease occurs mainly in the process of decoding the patient's electrocardiogram by a cardiologist.

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WPW syndrome on ECG

WPW syndrome on ECG manifests itself as follows.

The passage of the sinus impulse in the left bundle of Paladino-Kent leads to the activation of part of the left ventricle earlier than the other parts of the ventricles are excited under the action of the impulse following the normal path along the atrioventricular junction. As a result, the ventricles, namely part of the left ventricle, are excited ahead of the normal time. This phenomenon is reflected on the cardiogram as a shortening of the P-Q interval. In this case, it does not reach 0.10 s.

The next thing that is inherent in the WPW syndrome on the ECG is the sequential transition of excitation from one muscle layer in the left ventricle to another. As a result, the delta wave is displayed on the electrocardiogram. The delta wave is a pathologically altered initial part in the ascending knee of the R wave, which has a jagged and widened appearance.

And another characteristic feature of the ECG results in WPW syndrome is not the simultaneous excitation of both ventricles, as is normal, but the sequential transfer of excitation from one to the other. The process begins with an abnormally early activation of the left ventricle, then the impulse moves to the interventricular septum, and only after that ends up in the right ventricle.

Thus, the excitation process is similar to what occurs in the case of right bundle branch block.

Thus, among the main signs of WPW syndrome on ECG we can name, firstly, shortening to less than 0.10 of the P-Q (P-R) interval; secondly, the existence of a positive delta wave in the leads of the anterior wall of the left ventricle and a negative one, respectively, in the posterior. This is similar to a pathological Q wave. And another characteristic phenomenon is a widening of more than 0.12 s and deformation of the QRS complex of a type similar to the block of the right leg of the His bundle.

The above mentioned features refer to the ECG indicators of WPW syndrome type A.

Type B of this syndrome has almost identical characteristics. It is characterized by shortening of the P-Q interval to less than 0.10 s, the presence of a delta wave negative in the right chest leads and positive in the left, respectively, the QRS complex in a widened state of more than 0.12 s and deformed in the way that is characteristic of the left bundle branch block.

In addition, there are a considerable number of forms of WPW syndrome that are transitional from type A to type B, as well as the unification of these types into the so-called type A-B of this syndrome. This is what determines the diversity of the picture of what WPW syndrome looks like on the ECG.

Treatment of WPW syndrome

Treatment of WPW syndrome, depending on the clinical picture of the disease and based on the data obtained from instrumental diagnostic studies, involves choosing one of the most appropriate existing methods.

Medical measures are limited to the use of a number of the following therapeutic measures.

First of all, this is the implementation of antiarrhythmic therapy with the appointment of a course of treatment with medications. Here, however, there is one important point, namely, it should be taken into account that the use of drugs acting as Ca-blockers is unacceptable, and digitalis drugs are also unacceptable.

The use of electrophysiological methods can show a high level of efficiency. Among them is the implementation of cardioversion/defibrillation, which means external defibrillation performed in synchronization with electrocardiography.

In addition, in the treatment of WPW syndrome, they resort to the use of catheter ablation of additional conduction pathways. This method is a non-surgical procedure aimed at the destruction of these pathological impulse transmission pathways that cause cardiac arrhythmia and determine WPW syndrome. In this case, special catheters are inserted into the heart through the circulatory system, which does not require opening the patient's chest. For this reason, this method, while being a fairly radical and effective treatment measure, is also minimally invasive.

Treatment of WPW syndrome can only be entrusted to a relevant medical specialist, since self-medication and self-prescription of all kinds of medications and the use of various methods can pose a threat to the patient's life. Since a person incompetent in the field of medicine is not able to independently establish the objective causes, nature and mechanism of heart rhythm disturbances. Especially when surgical intervention is required to treat this syndrome. Here you cannot do without an experienced surgeon.

Surgery for WPW syndrome

Surgery for WPW syndrome is a modern method of radical treatment, which implies catheter ablation, that is, destruction of the existing pathological additional pathway.

The procedure for this operation involves first inserting a special catheter into the heart cavity through the subclavian vein. It contains various sensors, the data collected by which is analyzed using complex software. Thanks to this, it becomes possible to determine with maximum accuracy the area in which the additional conduction path is localized.

Based on the diagnostic information obtained at this stage, which is called electrophysiological examination of the heart, the accurately established additional conduction path is treated with high-frequency current. The consequence of this is the destruction of such a path.

The result of this operation for WPW syndrome with a 97% probability is complete relief of the patient from this cardiac syndrome. In the remaining 3% of cases, another such surgical intervention may be necessary. After repeated surgery, the success rate of this treatment method reaches 100%.

Patients who are indicated for surgery for WPW syndrome are hospitalized in a specialized department. The "cauterization", as catheter ablation is often called, is bloodless and takes no more than one hour. The patient can often be discharged within 24 hours in the shortest possible time.

Prevention of WPW syndrome

Today, it is impossible to say with any certainty that there is any special prevention of WPW syndrome, and there are a number of measures that are 100% guaranteed to prevent the disease.

The development of this cardiac syndrome in many cases can be largely due to congenital factors. This means that if a person has predispositions to cardiac disorders (including WPW syndrome), the latter will sooner or later manifest themselves under certain unfavorable circumstances.

Even if no obvious symptoms of heart rhythm disturbances are observed, and, nevertheless, the electrocardiogram indicates a disease, this should be sufficient reason for consultation with a cardiologist.

If a person is diagnosed with WPW syndrome, their relatives should also undergo a comprehensive examination with electrocardiography, daily ECG monitoring, echocardiography. There may also be a need for an electrophysiological study. It is recommended to do this in order to minimize the possibility of their disease.

Prevention of WPW syndrome essentially boils down to promptly identifying alarming symptoms, determining what exactly causes them, and deciding what should be done to prevent further progression of negative phenomena.

Prognosis of WPW syndrome

The prognosis for WPW syndrome in cases where its presence in a person is not accompanied by the appearance of a full range of characteristic symptoms is favorable.

Carrying out treatment measures and registering with a cardiologist is advisable only for those patients who have a family history aggravated by sudden cardiac death of one of the relatives of such patients. Certain professional indications also cause such a need, for example, with regard to pilots, people professionally involved in sports, etc.

If patients complain or experience life-threatening arrhythmias, a full comprehensive diagnosis is required to select the necessary treatment measures. After radiofrequency catheter ablation, these patients must be observed by a cardiac surgeon and a cardiologist-arrhythmologist.

About 80% of people with WPW syndrome experience paroxysms of reciprocating tachycardia, with a 15-30% chance of atrial fibrillation, and 5% of cases of atrial flutter. There is also a small risk of sudden cardiac death. It occurs in 0.1% of patients.

When a person with WPW syndrome is not bothered by any negative manifestations associated with its presence, this seems to be a positive prognostic factor.

The prognosis of WPW syndrome is significantly improved by radiofrequency catheter ablation of pathological accessory pathways.

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