Extension of the q t interval. ECG interpretation: QT interval

Long QT syndrome (LQT) is a congenital or acquired cardiac pathology, which is characterized by prolongation of the corresponding interval by , the presence of repeated syncope and a high risk of sudden death due to the development of malignant arrhythmias. The congenital variant of the syndrome occurs in all ethnic groups with a frequency of 1:2000 to 1:2500. Females suffer from it somewhat more often. The prevalence of the acquired syndrome ranges from 2.5 to 4 cases per 1 million people. In our article we will look at why LQT occurs, what symptoms it causes, why it is dangerous, and how to treat it.

The disease has been known since the end of the 19th century, when the observation of a girl with congenital deafness and frequent fainting that occurs with strong excitement was first described in the medical literature (1856, Meissner). Later, his electrocardiographic picture was revealed (1953, Moller). Currently studying this syndrome and searching for effective methods his treatment is ongoing.

Causes of congenital syndrome

The hereditary variant of the syndrome is based on mutations in genes encoding the functions of protein molecules of ion channels in the heart muscle. Currently, more than 180 such mutations are known in 7 genes, which are located on chromosomes 3, 7, 11 and 21. In most cases, they disrupt the functioning of potassium and sodium channels, less often - calcium channels and specific building proteins. This leads to an increase in the duration of the action potential in cardiomyocytes, initiating the appearance of ventricular tachycardia of the “pirouette” type, which can develop into.

The processes of depolarization and repolarization that occur as a result of the movement of electrolytes into the cell from the extracellular space and back are reflected on the ECG by the QT interval, which lengthens with this pathology.

In clinical practice, there are 3 main variants of hereditary syndrome:

• Romano-Ward (characterized by isolated QT prolongation, transmitted from parents with dominant genes);
• Jervell-Lange-Nielsen (inherited in an autosomal recessive manner and combined with congenital deafness);
• autosomal dominant variant with extracardiac manifestations.

The last of them can manifest itself in the form:

• Andersen-Tawil syndrome (QT prolongation combined with pronounced U-wave, ventricular tachycardia, abnormalities of the skeletal system, hyper- or hypokalemic periodic paralysis);
• Timothy syndrome (syndactyly, congenital cardiac anomalies, various conduction disorders, extremely high risk of sudden death).

Acquired form

Previously, it was believed that the occurrence of acquired LQT syndrome is associated with a disruption in the functioning of ion channels, which is caused not by a mutation, but by the influence of some external or internal factors. This statement is true, but it has been proven that it contributes to the development pathological process genetic defect. At the same time, the acquired syndrome is difficult to distinguish from congenital pathology, since they have much in common. Usually, this pathology goes unnoticed for a long time and manifests itself in adverse conditions, for example, under the influence of stress or physical activity. Factors that contribute to prolongation of the QT interval include:

• taking medications (we’ll look at which ones below);
• electrolyte disturbances (lack of potassium, sodium, magnesium);
• heart rhythm disturbances;
• diseases nervous system(injuries, infections, tumors);
• change in hormonal status (pathology thyroid gland or adrenal glands)
• alcoholism;
• starvation, etc.

Of particular danger is the exposure of a susceptible organism to several risk factors.

Groups of drugs that can affect the length of the QT interval

Because LQT syndrome can be caused by direct exposure medicines, and their cancellation often leads to the normalization of all indicators, let’s take a closer look at what medicines can change the length of the QT interval:

• (amiodarone, procainamide, sotalol, propafenone, disopyramide);
• antibiotics (erythromycin, spiramycin, clarithromycin, isoniazid);
• (ebastine, astemizole);
• anesthetics;
• antimycotics (fluconazole, ketoconazole);
• antitumor drugs;
• psychotropic drugs (droperidol, amitriptyline);
• (indapamide), etc.

They should not be prescribed to persons who already have a prolongation of this interval. And with a late debut of the disease, their role as a provoking factor is necessarily excluded.

Clinical manifestations

Clinical picture syndrome is characterized by polymorphism of symptoms. Their severity can vary from mild dizziness to loss of consciousness and sudden death. Sometimes the latter can act as the first sign of illness. The most typical manifestations of this pathology are:

• bouts of loss of consciousness;
• congenital deafness;
• cases of sudden death in the family;
• changes on the electrocardiogram (QT more than 450 ms, T wave alternation, ventricular tachycardia of the "pirouette" type,).

With congenital variants of the syndrome, other symptoms characteristic only of it can be detected.

It should be noted that syncopal conditions in this pathology have their own characteristics:

• occur against a background of stress, under the influence of strong sound stimuli (alarm clock, phone call), physical activity, sports (swimming, diving), during a sharp awakening from a night's sleep, in women - after childbirth;
• the presence of symptoms preceding loss of consciousness (severe weakness, ringing in the ears, darkening of the eyes, feeling of heaviness in the chest);
• rapid restoration of consciousness with a favorable outcome;
• absence of amnesia and personality changes (as with epilepsy).

Sometimes loss of consciousness may be accompanied by convulsions and involuntary urination. In such cases, differential diagnosis with epileptic seizures is carried out.

The course of the pathological process in each patient may have certain differences. It depends both on the genotype and on living conditions. The following options are considered the most common:

• syncope occurring against the background of prolongation of the QT interval;
• isolated prolongation of this interval;
• syncope in the absence of changes on the ECG;
• complete absence of symptoms (high risk without phenotypic manifestations of the disease).

The most unfavorable course is complicated by the development of ventricular fibrillation and cardiac arrest.

With congenital variants of the disease, fainting appears in childhood(5-15 years). Moreover, their occurrence in children preschool age– a prognostically unfavorable sign. And paroxysm of ventricular tachycardia, which required treatment emergency care, increases the likelihood of a second cardiac arrest in the near future by 10 times.

Patients with asymptomatic long QT syndrome may be unaware of their diagnosis and have a normal life expectancy, but pass the mutation on to their children. This trend is observed very often.

Diagnostic principles

Diagnosis of the syndrome is based on clinical findings and electrocardiography results. Holter monitoring provides additional information to the doctor.

Given that it is not always easy to make a diagnosis, large and small diagnostic criteria. The latter include:

• lack of hearing from birth;
• variability of the T wave in different leads (on the electrocardiogram);
• disruption of the processes of repolarization of the ventricular myocardium;
• low heart rate.

Among the major criteria are:

• prolongation of the corrected QT interval more than 450 ms at rest;
• episodes of loss of consciousness;
• cases of illness in the family.

The diagnosis is considered reliable if two major or one major and two minor criteria are present.

Treatment

The main focus of treatment for such patients is the prevention of malignant arrhythmias and cardiac arrest.

All persons with prolonged QT interval should avoid:

• stressful situations;
• doing sports;
• heavy physical activity;
• taking medications that increase the length of this interval.

Medications for this syndrome are usually prescribed:

• β-blockers;
• magnesium and potassium preparations;
• mexiletine or flecainide (in low doses).

If ineffective conservative therapy resort to sympathetic denervation or implantation of a cardioverter-defibrillator. The latter is especially important in patients at high risk of sudden cardiac death and undergoing resuscitation.

Long QT syndrome is a heart condition that causes uncontrolled arrhythmias. It is the most common cause of unexplained deaths, affecting approximately 1 in every 2,000 people.

People with long QT syndrome have a structural defect in the ion channels of the heart muscle. A defect in these ion channels causes abnormalities in the electrical conduction system of the heart. This heart defect makes them prone to uncontrollable, rapid and chaotic heartbeats (arrhythmias).

With each heartbeat, an electrical signal is transmitted from the top to the bottom. An electrical signal causes the heart to contract and pump blood. This pattern for each heart rhythm can be seen on the ECG as five separate waves: P, Q, R, S, T.

The QT interval is a measurement of the time between the onset of the Q wave and the T wave and represents the time it takes for the heart muscles to relax after contracting to pump blood.

In people with long QT syndrome, this interval is longer than usual and disrupts the heart rhythm causing arrhythmias.

At least 17 genes are known to cause long QT syndrome. Mutations of these genes are associated with the structure and functioning of ion channels. There are 17 types of long QT syndrome, each associated with a single gene.

They are numbered sequentially as LQT1 (type 1), LQT2 (type 2) and so on.

LQT1 to LQT15 are known as Romano-Ward syndrome and are inherited in an autosomal dominant manner. In autosomal dominant inheritance, a mutation in one copy of the gene is sufficient to cause the disorder.

A rare form of long qt syndrome, known as Jervell and Lange-Nielsen syndrome, is associated with congenital deafness. It has two types: JLN1 and JLN2, depending on the gene involved.

Jervell and Lange-Nielsen syndrome is inherited in an autosomal recessive manner, meaning both copies of the gene must be mutated to cause the condition.

Causes and risk factors

Long QT syndrome is often inherited, which means it is caused by a mutation in one of 17 genes. Sometimes it is caused by a medicine.

More than 17 drugs, including some common ones, may prolong the QT interval in healthy people. Some of these include:

• antiarrhythmic drugs: Sotalol, Amiodarone, Dofetilide, quinidine, procainamide, disopyramide;
• Antibiotics: erythromycin, clarithromycin, levofloxacin;
• : Amitriptyline, Doxepin, desipramine, clomipramine, imipramine;
• Antipsychotic drugs: thioridazine, chlorpromazine, haloperidol, Prochlorpherazine, Fluphenazine;
• Antihistamines: terfenadine, astemizole;
• Diuretics, cholesterol medications, and some diabetes medications.

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Risk factors

Exist various factors, which determine a person's risk of having long QT syndrome.

You are at risk if:

• You or a family member have a history of unexplained fainting or seizures, drowning or near drowning incidents, unexplained accidents or deaths, or cardiac arrest at a young age.
• Your close relative has been diagnosed with long QT syndrome.
• You are taking medications that cause it.
• If you have low levels of calcium, potassium or magnesium in your blood.

People suffering from this condition often go undiagnosed or are misdiagnosed. Therefore it is important to consider key factors risk to ensure accurate diagnosis.

Symptoms

Symptoms of long QT syndrome are common in children. However, they can begin at any time in a person's life from birth to old age or never at all. These symptoms include:

• Fainting: Loss of consciousness is the most common symptom. It occurs when there is a limited supply of blood to the brain due to a temporary irregular heartbeat.
• Seizures: When the heart continues to beat erratically for a long period of time, the brain becomes deprived of oxygen, leading to seizures.
• Sudden death: If the heart does not return to normal rhythm immediately after an arrhythmic attack, sudden death may result.
• Arrhythmia during sleep: People who have long QT syndrome type 3 may experience irregular heartbeats during sleep.

Diagnostics

Not all people show symptoms of the condition, making diagnosis difficult. Therefore, it is important to use a combination of methods to identify individuals suffering from long qt syndrome.

Some methods used for diagnosis:

• Electrocardiogram (ECG);
• Medical and family history;
• Genetic test result.

Electrocardiogram

An ECG analyzes the electrical activity of the heart and helps determine the interval. This is done while the person is resting or while performing a stationary exercise. This test is performed several times as electrical activity may vary over time.

Some doctors attach a wearable heart monitor to the body to monitor heart activity for 24 to 48 hours.

Medical and family history

Medical history and family history of symptoms and signs of long QT syndrome can help determine the chances of having the condition. Therefore, the doctor examines a detailed family history of three generations to assess the risk.

Genetic results

A genetic test is done to check if there is a mutation in the gene associated with long-qt syndrome.

Treatment

The goal of treatment is to prevent arrhythmias and syncope. It may vary among individuals, depending on previous history of syncope and sudden stop heart, type of QT syndrome and family history.
Treatment options:

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Drugs

Beta blockers, medications that prevent the heart from beating at a high rate, are prescribed to prevent arrhythmias. In some cases, potassium supplements and fish oil prescribed to maintain a regular heart rhythm.

Implantable devices

Pacemakers or implantable cardioverter defibrillator (ICD) are small devices that help control your heart rhythm. They are implanted under the skin of the chest or stomach through a minor procedure.

If they detect any abnormalities in the heart rhythm, they send electrical impulses to teach the heart to correct its rhythm.

Surgery

In some people, the nerves that send messages to the heart to beat faster are surgically removed. This prevents the risk of sudden death.

How to prevent

Long QT syndrome is a lifelong condition and the risk of fainting or sudden cardiac arrest never goes away. However, there are several preventative options that people can incorporate into their lives to reduce the risk of complications associated with the syndrome.

To prevent abnormal heart rhythms, you should:

• Avoid activities that may cause irregular heart rhythm. For example, strenuous exercise such as swimming should be avoided as it causes arrhythmias.
• Medicines that cause arrhythmias should not be prescribed to persons with long QT syndrome. Ask your doctor for a list of medications to avoid.
• If you have an implanted pacemaker or ICD device, be careful when playing sports not to move the device from its location.
• Let people you see regularly about your condition so they can help you if an emergency arises.
• Visit your cardiologist regularly.

• Know your body: Keep checking for symptoms and see your doctor if you notice anything unusual.
• Visit your doctor regularly: follow the advice carefully.
• Support healthy image life, avoid smoking, drinking alcohol to avoid the risk of heart disease.
• Reduce sporting events: Avoid or reduce sports activities that cause your heart rate to fluctuate constantly.
• Medications: Be very careful to avoid drugs that cause long QT syndrome. You should tell all doctors you see about your condition so that they do not prescribe medications that may cause arrhythmia.

If I have a heartbeat, what does it mean?

Palpitation is the feeling that the heart is beating quickly. It is not necessarily a symptom of arrhythmia. If you feel this sensation, get checked by a cardiologist.

Long QT syndrome is characterized by 2 signs: prolongation of the QT interval (the duration of the estimated QT interval exceeds 0.44 s) and ventricular tachycardia with syncope.

In addition to these signs, a tall U wave, a flattened or negative T wave, and sinus tachycardia are noted.

The congenital form of this syndrome is less common and is a genetically heterogeneous disease; the acquired form is often caused by antiarrhythmic therapy.

The congenital form of long QT syndrome is treated with beta-adrenergic receptor blockers, and if there is no effect of drug therapy, a cardioverter/defibrillator is implanted if necessary. In the acquired form, you should first of all discontinue medications that could cause prolongation of the QT interval.

(synonym: QT syndrome) are divided into congenital, genetically heterogeneous form and acquired, or drug-induced, form. The congenital form is extremely rare (1 case per 10,000 births). The clinical significance of QT syndrome is that both its congenital and acquired forms are manifested by ventricular tachycardia.

I. Congenital long QT syndrome (Jervell-Lange-Nielsen and Romano-Ward syndromes)

In pathogenesis congenital QT syndrome play a role in mutations of genes encoding ion channel proteins, leading to insufficient activity of potassium channels or increased activity sodium channels. Long QT syndrome can manifest as Jervell-Lange-Nielsen syndrome and Romano-Ward syndrome.

Characteristic features Jervell-Lange-Nielsen syndrome are:
QT prolongation
deaf-mute
episodes of fainting and sudden death.

At Romano-Ward syndrome There is no deaf-muteness.

First clinical manifestations Congenital QT syndrome appears already in childhood. Characterized by repeated episodes of fainting that appear against the background of sympathicotonia, for example, when the child cries, is stressed, or screams.

To the most important signs of QT syndrome relate:
prolongation of the QT interval, i.e. the duration of the estimated QT interval exceeds 0.44 s (normally it is 0.35-0.44 s)
ventricular tachycardia (torsade de pointes: fast and polymorphic form)
sinus bradycardia at rest and during exercise
flattened or negative T wave
tall or biphasic U wave and fusion of T wave and U wave
dependence of the duration of the QT interval on heart rate

At measuring the QT interval care must be taken not to include the U-wave (corrected QT interval; Bazett's QTC interval) in the interval. The relative QT interval (for example, according to Lepeshkin or Hegglin and Holtzman) is easier to measure, but its value is less accurate. Normally it is 100±10%.

At QT syndrome There is an uneven lengthening of the repolarization phase, which facilitates the mechanism of re-entry of the excitation wave, contributing to the appearance of ventricular tachycardia (torsade de pointes, torsade de pointes) and ventricular fibrillation.

Treat QT syndrome beta-adrenergic receptor blockers, and in case of resistance to these drugs, a cardioverter/defibrillator is implanted.

II. Acquired long QT syndrome

Reasons causing acquired long QT syndrome, may be different. Only those with the greatest clinical significance are listed below:
antiarrhythmic drugs (eg, quinidine, sotalol, amiodarone, ajmaline, flecainide)
violation electrolyte balance(eg, hypokalemia)
blockade of the PG branch and widening of the QRS complex
hypothyroidism
IHD
antibiotic therapy (eg, erythromycin)
alcohol abuse
myocarditis
cerebral hemorrhage

In typical cases acquired QT syndrome may be associated with the use of antiarrhythmic drugs, especially quinidine and sotalol. The clinical significance of this syndrome is great, given that, as with the congenital form, acquired QT syndrome is accompanied by attacks of ventricular tachycardia.

Frequency of occurrence episodes of ventricular tachycardia in patients with acquired long QT syndrome is 2-5%. A typical example is the so-called quinidine syncope. ECG changes are the same as with congenital QT syndrome.

Treatment implies, first of all, the abolition of the “causal” drug and the introduction, among other things, of a lidocaine solution.

ECG features in long QT syndrome:
Change in the QT interval (normal QTC interval<0,44 с)
Tendency to ventricular tachycardia
Congenital form: for some patients who faint, implantation of a cardioverter/defibrillator is indicated
Acquired form: withdrawal of antiarrhythmic drugs (common cause of the syndrome)

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What is an ECG?

Electrocardiography is a method used to record electrical currents that occur during contractions and relaxations of the heart muscle. An electrocardiograph is used to conduct the study. Using this device, it is possible to record electrical impulses that come from the heart and convert them into a graphic drawing. This image is called an electrocardiogram.

Electrocardiography reveals disturbances in the functioning of the heart and disruptions in the functioning of the myocardium. In addition, after decoding the results of the electrocardiogram, some non-cardiac diseases can be detected.

How does an electrocardiograph work?

The electrocardiograph consists of a galvanometer, amplifiers and a recorder. Weak electrical impulses that arise in the heart are read by electrodes and then amplified. The galvanometer then receives data on the nature of the pulses and transmits them to the recorder. In the recorder, graphic images are printed on special paper. The graphs are called cardiograms.

How is an EKG done?

Electrocardiography is performed according to established rules. Below is the procedure for taking an ECG:

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• The person removes metal jewelry, removes clothing from the legs and upper body, and then assumes a horizontal position.
• The doctor treats the contact points between the electrodes and the skin, and then places the electrodes in certain places on the body. Next, he fixes the electrodes on the body with clips, suction cups and bracelets.
• The doctor attaches the electrodes to the cardiograph, after which the impulses are recorded.
• A cardiogram is recorded, which is the result of electrocardiography.

Separately, it should be said about the leads used for ECG. The following leads are used:

• 3 standard leads: one of them is located between the right and left arms, the second – between the left leg and right arm, the third – between the left leg and left arm.
• 3 limb leads with enhanced character.
• 6 leads located on the chest.

In addition, additional leads can be used if necessary.

After the cardiogram is recorded, it is necessary to decrypt it. This will be discussed further.

Deciphering the cardiogram

Conclusions about diseases are made on the basis of heart parameters obtained after deciphering the cardiogram. The following is the procedure for decoding the ECG:

1. The heart rhythm and myocardial conduction are analyzed. To do this, the regularity of contractions of the heart muscle and the frequency of myocardial contractions are assessed, and the source of excitation is determined.
2. The regularity of heart contractions is determined as follows: the R-R intervals between successive cardiac cycles are measured. If the measured R-R intervals are the same, then a conclusion is made about the regularity of contractions of the heart muscle. If the duration of the R-R intervals is different, then a conclusion is drawn about the irregularity of heart contractions. If a person exhibits irregular contractions of the myocardium, then a conclusion is drawn about the presence of arrhythmia.
3. The heart rate is determined by a certain formula. If a person’s heart rate exceeds the norm, then a conclusion is drawn about the presence of tachycardia, but if a person’s heart rate is below normal, then a conclusion is drawn about the presence of bradycardia.
4. The point from which the excitation comes is determined as follows: the movement of contraction in the cavities of the atria is assessed and the relationship of the R waves to the ventricles is established (according to the QRS complex). The nature of the heart rhythm depends on the source that causes the excitation.

The following patterns of heart rhythms are observed:

1. The sinusoidal nature of the heart rhythm, in which the P waves in the second lead are positive and are in front of the ventricular QRS complex, and the P waves in the same lead have an indistinguishable shape.
2. Atrial rhythm of the nature of the heart, in which the P waves in the second and third leads are negative and are in front of the unchanged QRS complexes.
3. The ventricular nature of the heart rhythm, in which there is a deformation of the QRS complexes and a loss of communication between the QRS (complex) and the P waves.

Cardiac conductivity is determined as follows:

1. Measurements of P wave length, PQ interval length, and QRS complex are assessed. Exceeding the normal duration of the PQ interval indicates too low conduction velocity in the corresponding cardiac conduction section.
2. The rotations of the myocardium around the longitudinal, transverse, anterior and posterior axes are analyzed. To do this, the position of the electrical axis of the heart in the general plane is assessed, after which the presence of rotations of the heart along one or another axis is determined.
3. The atrial P wave is analyzed. For this, the amplitude of the P bison is assessed, the duration of the P wave is measured. After that, the shape and polarity of the P wave are determined.
4. The ventricular complex is analyzed - For this, the QRS complex, the RS-T segment, the QT interval, the T wave are evaluated.

During the assessment of the QRS complex, do the following: determine the characteristics of the Q, S and R waves, compare the amplitude values ​​of the Q, S and R waves in a similar lead and the amplitude values ​​of the R/R waves in different leads.

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At the time of evaluation of the RS-T segment, the nature of the displacement of the RS-T segment is determined. The displacement can be horizontal, oblique and oblique.

During the period of analysis of the T wave, the nature of the polarity, amplitude and shape are determined. The QT interval is measured by the time from the beginning of the QRT complex to the end of the T wave. When assessing the QT interval, do the following: analyze the interval from the starting point of the QRS complex to the end point of the T wave. To calculate the QT interval, use the Bezzet formula: the QT interval is equal to the product of the R-R interval and a constant coefficient.

The coefficient for QT depends on gender. For men, the constant coefficient is 0.37, and for women – 0.4.

A conclusion is made and the results are summed up.

In conclusion, the ECG specialist draws conclusions about the frequency of the contractile function of the myocardium and heart muscle, as well as the source of excitation and the nature of the heart rhythm and other indicators. In addition, an example of the description and characteristics of the P wave, QRS complex, RS-T segment, QT interval, T wave is given.

Based on the conclusion, it is concluded that a person has heart disease or other ailments of internal organs.

Electrocardiogram norms

The table with ECG results has a visual appearance, consisting of rows and columns. In the 1st column, the lines list: heart rate, beat rate examples, QT intervals, examples of axis displacement characteristics, P-wave readings, PQ readings, QRS reading examples. ECG is carried out equally in adults, children and pregnant women, but the norm is different.

The ECG norm for adults is presented below:

• heart rate in a healthy adult: sinus;
• P wave index in a healthy adult: 0.1;
• the frequency of contractions of the heart muscle in a healthy adult: 60 beats per minute;
• QRS indicator in a healthy adult: from 0.06 to 0.1;
• QT score in a healthy adult: 0.4 or less;
• RR in a healthy adult: 0.6.

In the case of observation of deviations from the norm in an adult, a conclusion is made about the presence of the disease.

The norms of cardiogram indicators in children are presented below:

• P wave index in a healthy child: 0.1 or less;
• heart rate in a healthy child: 110 beats per minute or less in children under 3 years old, 100 beats per minute or less in children under 5 years old, no more than 90 beats per minute in children in adolescence;
• QRS indicator in all children: from 0.06 to 0.1;
• QT score in all children: 0.4 or less;
• PQ in all children: if the child is under 14 years old, then the example PQ is 0.16, if the child is from 14 to 17 years old, then the PQ is 0.18, after 17 years the normal PQ is 0.2.

If in children, when deciphering the ECG, any deviations from the norm were found, then treatment should not be started immediately. Some heart problems improve with age in children.

But in children, heart disease can also be congenital. It is possible to determine whether a newborn child will have a heart pathology even at the stage of fetal development. For this purpose, electrocardiography is performed on women during pregnancy.

The norm of electrocardiogram indicators in women during pregnancy is presented below:

• heart rate in a healthy adult child: sinus;
• P wave index in all healthy women during pregnancy: 0.1 or less;
• heart muscle contraction frequency in all healthy women during pregnancy: 110 or less beats per minute in children under 3 years of age, 100 or less beats per minute in children under 5 years of age, no more than 90 beats per minute in adolescent children;
• QRS indicator for all expectant mothers during pregnancy: from 0.06 to 0.1;
• QT index in all expectant mothers during pregnancy: 0.4 or less;
• PQ indicator for all expectant mothers during pregnancy: 0.2.

It is worth noting that during different periods of pregnancy, ECG readings may differ slightly. In addition, it should be noted that performing an ECG during pregnancy is safe for both the woman and the developing fetus.

Additionally

It is worth saying that under certain circumstances, electrocardiography can give an inaccurate picture of a person’s health status.

If, for example, a person subjected himself to heavy physical activity before an ECG, then when deciphering the cardiogram, an erroneous picture may be revealed.

This is explained by the fact that during physical activity the heart begins to work differently than at rest. During physical activity, the heart rate increases, and some changes in the rhythm of the myocardium may be observed, which is not observed at rest.

It is worth noting that the work of the myocardium is affected not only by physical stress, but also by emotional stress. Emotional stress, like physical stress, disrupts the normal course of myocardial function.

At rest, the heart rhythm normalizes and the heartbeat evens out, so before electrocardiography you must be at rest for at least 15 minutes.

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ECG interpretation: QT interval

QT interval (ventricular electrical systole) is the time from the beginning of the QRT complex to the end of the T wave. The QT interval depends on gender, age (in children the interval is shorter), and heart rate.

Normally, the QT interval is 0.35-0.44 s (17.5-22 cells). The QT interval is a constant value for the rhythm frequency (separately for men and women). There are special tables that present QT standards for a given gender and rhythm frequency. If the result on the ECG exceeds 0.05 seconds (2.5 cells) of the table value, then they speak of prolongation of the electrical systole of the ventricles, which is a characteristic sign of cardiosclerosis.

Using Bazett's formula, you can determine whether the QT interval in a given patient is normal or pathological (the QT interval is considered pathological if the value exceeds 0.42):

For example, the QT value calculated for the cardiogram presented on the right (calculation using standard lead II:

• The QT interval is 17 cells (0.34 seconds).

– a genetically heterogeneous hereditary condition characterized by a violation of the structure and functionality of some ion channels of cardiomyocytes. The severity of the manifestations of the pathology varies over a very wide range - from a practically asymptomatic course (only electrocardiological signs are detected) to severe deafness, fainting and arrhythmias. The definition of long QT interval syndrome is based on data from electrocardiological studies and molecular genetic tests. Treatment depends on the form of the pathology and may include constant or course use of beta-blockers, magnesium and potassium supplements, as well as the installation of a defibrillator-cardioverter.

General information

Long QT syndrome is a group of cardiac disorders of a genetic nature in which the passage of ionic currents in cardiomyocytes is disrupted, which can lead to arrhythmias, fainting and sudden cardiac death. A similar condition was first identified in 1957 by Norwegian doctors A. Jervell and F. Lange-Nielsen, who described a patient’s combination of congenital deafness, syncope, and prolongation of the QT interval. Somewhat later, in 1962-64, similar symptoms were identified in patients with normal hearing - such cases were described independently by K. Romano and O. Ward.

This, as well as further discoveries, determined the division of long QT syndrome into two clinical variants - Romano-Ward and Jervell-Lange-Nielsen. The first is inherited by an autosomal dominant mechanism, its frequency in the population is 1 case per 5,000 population. The incidence of long QT syndrome of the Jervell-Lange-Nielsen type ranges from 1-6:1,000,000; it is characterized by an autosomal dominant mode of inheritance and more severe manifestations. According to some data, all forms of long QT syndrome are responsible for a third of cases of sudden cardiac death and about 20% of sudden infant death.

Causes and classification

Currently, it has been possible to identify 12 genes in which mutations lead to the development of long QT interval syndrome; all of them encode certain proteins that are part of the ion channels of cardiomyocytes responsible for sodium or potassium ion current. It was also possible to find the reasons for the differences in the clinical course of this disease. Autosomal dominant Romano-Ward syndrome is caused by a mutation in only one gene and therefore can be asymptomatic or, at a minimum, without hearing impairment. With the Jervell-Lange-Nielsen type, there is a defect in two genes - this option, in addition to cardiac symptoms, is always accompanied by bilateral sensorineural deafness. Today it is known which gene mutations cause the development of long QT syndrome:

1. Long QT syndrome type 1 (LQT1) caused by a mutation in the KCNQ1 gene located on chromosome 11. Defects in this gene are most often detected in the presence of this disease. It encodes the sequence of the alpha subunit of one of the varieties of cardiomyocyte potassium channels (lKs)
2. Long QT syndrome type 2 (LQT2) is caused by defects in the KCNH2 gene, which is localized on chromosome 7 and encodes the amino acid sequence of a protein - the alpha subunit of another type of potassium channel (lKr).
3. Long QT syndrome type 3 (LQT3) caused by a mutation in the SCN5A gene located on chromosome 3. Unlike previous variants of the pathology, the functioning of sodium channels in cardiomyocytes is disrupted, since this gene encodes the sequence of the alpha subunit of the sodium channel (lNa).
4. Long QT syndrome type 4 (LQT4)– a rather rare variant of the condition caused by a mutation of the ANK2 gene, which is located on the 4th chromosome. The product of its expression is the ankyrin B protein, which in the human body is involved in stabilizing the structure of myocyte microtubules, and is also secreted in neuroglial and retinal cells.
5. Long QT syndrome type 5 (LQT5)– a type of disease that is caused by a defect in the KCNE1 gene, localized on chromosome 21. It encodes one of the ion channel proteins, the beta subunit of potassium channels of the lKs type.
6. Long QT syndrome type 6 (LQT6) is caused by a mutation in the KCNE2 gene, also located on chromosome 21. The product of its expression is the beta subunit of potassium channels of the lKr type.
7. Long QT syndrome type 7(LQT7, another name is Andersen syndrome, in honor of the pediatrician E. D. Andersen, who described this disease in the 70s) is caused by a defect in the KCNJ2 gene, which is localized on the 17th chromosome. As in the case of previous variants of the pathology, this gene encodes one of the protein chains of potassium channels.
8. Long QT syndrome type 8(LQT8, another name is Timothy syndrome, in honor of K. Timothy, who described this disease) is caused by a mutation in the CACNA1C gene, which is located on the 12th chromosome. This gene encodes the alpha 1 subunit of the L-type calcium channel.
9. Long QT syndrome type 9 (LQT9) caused by a defect in the CAV3 gene, localized on chromosome 3. The product of its expression is the caveolin 3 protein, which is involved in the formation of many structures on the surface of cardiomyocytes.
10. Long QT syndrome type 10 (LQT10)– the cause of this type of disease lies in a mutation of the SCN4B gene, which is located on chromosome 11 and is responsible for the amino acid sequence of the beta subunit of sodium channels.
11. Long QT syndrome type 11 (LQT11) is caused by defects in the AKAP9 gene, located on chromosome 7. It encodes a specific protein - A-kinase of the centrosome and Golgi complex. The functions of this protein have not been sufficiently studied to date.
12. Long QT syndrome type 12 (LQT12) caused by a mutation in the SNTA1 gene, localized on chromosome 20. It encodes the alpha-1 subunit of the syntrophin protein, which is involved in the regulation of the activity of sodium channels in cardiomyocytes.

Despite the wide genetic diversity of long QT interval syndrome, the general links of its pathogenesis are generally the same for each of the forms. This disease is classified as a channelopathy due to the fact that it is caused by disturbances in the structure of certain ion channels. As a result, the processes of myocardial repolarization occur unevenly and not simultaneously in different parts of the ventricles, which causes prolongation of the QT interval. In addition, the sensitivity of the myocardium to the influences of the sympathetic nervous system increases significantly, which becomes the cause of frequent tachyarrhythmias that can lead to life-threatening ventricular fibrillation. At the same time, different genetic types of long QT interval syndrome have different sensitivity to certain influences. For example, LQT1 is characterized by syncope attacks and arrhythmia during physical activity, with LQT2 similar manifestations are observed with loud and sharp sounds, for LQT3, on the contrary, the development of arrhythmias and fibrillations in a calm state (for example, in sleep) is more typical.

Symptoms of a Long QT Interval

The manifestations of long QT syndrome are quite varied. With the more severe clinical type of Jervell-Lange-Nielsen, patients experience deafness, frequent fainting, dizziness, and weakness. In addition, in some cases, epilepsy-like seizures are recorded in this condition, which often leads to incorrect diagnosis and treatment. According to some geneticists, 10 to 25% of patients with long QT syndrome are treated incorrectly and experience sudden cardiac or infant death. The occurrence of tachyarrhythmias and syncope depends on external influences - for example, with LQT1 this can occur against the background of physical activity, with LQT2 loss of consciousness and ventricular fibrillation can occur from sharp and loud sounds.

A milder form of long QT syndrome (Romano-Ward type) is characterized by transient syncope (fainting) and rare attacks of tachyarrhythmia, but there is no hearing impairment. In some cases, this form of the disease does not manifest itself at all, with the exception of electrocardiographic data, and is an accidental finding during a medical examination. However, even with this course of long QT syndrome, the risk of sudden cardiac death due to ventricular fibrillation is many times higher than in a healthy person. Therefore, this type of pathology requires careful study and preventive treatment.

Diagnostics

Diagnosis of long QT interval syndrome is made based on a study of the patient's medical history, electrocardiological and molecular genetic studies. When questioning the patient, episodes of fainting, dizziness, and palpitations are often detected, but in mild forms of the pathology they may not be present. Sometimes similar manifestations occur in one of the patient’s relatives, which indicates the family nature of the disease.

With any form of long QT interval syndrome, changes will be detected on the ECG - an increase in the QT interval to 0.6 seconds or more, possibly an increase in the amplitude of the T wave. The combination of such ECG signs with congenital deafness indicates the presence of Jervell-Lange-Nielsen syndrome. In addition, Holter monitoring of heart function throughout the day is often necessary to identify possible attacks of tachyarrhythmias. Determination of long QT interval syndrome using modern genetic methods is now possible for almost all genetic types of this disease.

Treatment of long QT syndrome

Therapy for long QT syndrome is quite complex; many experts recommend some regimens for this disease and reject others, but there is no single protocol for the treatment of this pathology. Beta-blockers are considered universal drugs, they reduce the risk of developing tachyarrhythmias and fibrillations, and also reduce the degree of sympathetic effects on the myocardium, but in LQT3 they are ineffective. In the case of long QT syndrome type 3, it is more reasonable to use class B1 antiarrhythmic drugs. These features of the treatment of the disease increase the need for molecular genetic diagnostics to determine the type of pathology. In case of frequent attacks of tachyarrhythmias and a high risk of developing fibrillation, implantation of a pacemaker or defibrillator-cardioverter is recommended.

Forecast

The prognosis of long QT syndrome, according to most experts, is uncertain, since this disease is characterized by a wide range of symptoms. In addition, the absence of manifestations of pathology, with the exception of electrocardiographic data, does not guarantee the sudden development of fatal ventricular fibrillation under the influence of external or internal factors. When long QT interval syndrome is detected, it is necessary to perform a thorough cardiac examination and genetic determination of the type of disease. Based on the data obtained, a treatment regimen is developed to reduce the likelihood of sudden cardiac death, or a decision is made to implant a pacemaker.