reflects the time of repolarization of the ventricles of the heart. The normal length of the QT interval depends on your current heart rate. For diagnostic purposes, the absolute QTc indicator (corrected QT interval) is most often used, which is calculated by Bazett's formula. The calculation of this indicator includes a correction for the current heart rate.

– a disease accompanied by prolongation of the QT interval on the resting ECG (QTc>460 ms), syncope and a high risk of sudden death due to the development of polymorphic ventricular tachycardia. Hereditary forms of LQTS are inherited in both an autosomal dominant and autosomal recessive manner. Prolongation of the QT interval can be either genetically determined (primary) or secondary, as a result of exposure to unfavorable factors (taking a number of medications, hypokalemia, hypomagnesemia, hypocalcemia, low-protein diet and anorexia nervosa, myocarditis, cardiomyopathy, intracranial hemorrhage). Differential diagnosis between primary and secondary forms is extremely important for determining treatment tactics, assessing the risk of life-threatening arrhythmias and prognosis.

Recently, it has become obvious that the contribution of genetic factors to the occurrence of secondary prolongation of the QT interval cannot be underestimated. In a significant proportion of cases in patients with drug-induced QT prolongation, so-called “silent mutations,” or functional polymorphisms, are identified in the same genes that are responsible for the primary forms of LQTS.

Changes in the structure of ion channels of cardiomyocytes in such cases are minimal and can remain asymptomatic for a long time. Therefore, a person cannot know that some drugs widely available on the pharmaceutical market pose a danger to him. In most people, drug-induced depression of potassium current is minor and is not accompanied by any ECG changes.

However, the combination of genetic features of the structure of potassium channels and drug intake can cause clinically significant arrhythmias, up to the development of polymorphic ventricular tachycardia “Torsade des pointes” and sudden death. Therefore, for patients who have had polymorphic ventricular tachycardia caused by taking any medication at least once, consultation with a geneticist is recommended. In addition, all medications that prolong the QT interval should be avoided throughout your life.

The incidence of the primary form of long QT syndrome is about 1:3000. To date, at least 12 genes are known to be responsible for the development of the disease. A mutation in any of them can lead to the development of the disease.

Genes responsible for the development of long QT syndrome.

Possibilities of DNA diagnostics in Russia

You can apply for a direct DNA diagnosis of long QT syndrome in . Based on the results of DNA diagnostics, a written conclusion from a geneticist is issued with an interpretation of the results obtained. When analyzing all of these genes, it is possible to identify mutations and establish the molecular genetic form of the disease in 70% of probands. Mutations in these genes can also cause idiopathic ventricular fibrillation and sudden infant death syndrome (about 20% of cases).

Why do you need to carry out LQTS DNA diagnostics?

The use of molecular genetic methods for long QT syndrome may be critical in the following situations:

1. The need for confirmatory and/or differential diagnostics (for example, to resolve the issue of the primary or secondary nature of QT interval prolongation).
2. Identification of asymptomatic and low-symptomatic forms of the disease, for example, among relatives of patients with an established diagnosis. According to various authors, up to 30% of individuals with mutations in the genes involved do not have any signs of the disease (including electrocardiographic). At the same time, the risk of developing arrhythmias and sudden cardiac death remains high, especially when exposed to specific risk factors.
3. When choosing a treatment strategy for a disease. It has now been shown that patients with different molecular genetic forms of the disease respond differently to treatment. Accurate identification of the molecular genetic variant of the disease allows the patient to select adequate drug therapy, taking into account the dysfunction of a specific type of ion channel. The effectiveness of various treatment methods for various molecular genetic variants of LQTS syndrome. >

   	LQT1, LQT5	LQT2, LQT6	LQT3
   Sensitivity to sympathetic stimulation	+++	+	-
   Circumstances under which PVT is often observed	Fright	At rest/in sleep
   Specific factor that provokes syncope	Swimming	Sharp sound, postpartum period	-
   Limiting physical activity	+++	+	-
   b-blockers	+++	+	-
   Taking potassium supplements	+?	+++	+?
   Class IB antiarrhythmic drugs (sodium channel blockers)	+	++	+++
   Calcium channel blockers	++	++	+?
   Potassium channel openers (nicorandil)	+	+	-
   EX	+	+	+++
   ICD	++	++	+++

   ICD - implantable cardioverter-defibrillator, PVT - polymorphic ventricular tachycardia, pacemaker - pacemaker, +++ - maximum efficiency of the approach
4. Help with family planning. The serious prognosis of the disease, the high risk of life-threatening arrhythmias in the absence of adequate therapy, determines the relevance of prenatal DNA diagnosis of LQTS. The results of prenatal DNA diagnostics in families with an already established molecular genetic form of long QT syndrome make it possible to most successfully plan the management of pregnancy, childbirth and drug therapy in the postpartum period.

What to do if a mutation has been identified?

If you or your child have been diagnosed with a mutation that confirms the hereditary nature of the disease, you must remember the following:

1. You need to discuss the results of a molecular genetic study with a geneticist, what they mean, and what clinical and prognostic significance they may have.
2. Your relatives, even without clinical signs of the disease, may be carriers of a similar genetic change and be at risk of developing life-threatening arrhythmias. It is advisable to discuss with them and/or with a geneticist the possibility of consultation and DNA diagnostics for other members of your family.
3. It is necessary to discuss with a geneticist the features of this genetic variant of the disease, specific risk factors, and ways to best avoid them.
4. A number of medications must be avoided throughout your life.
5. You need an early consultation and long-term, usually lifelong, observation by an arrhythmologist. Our Center has a program for monitoring families with hereditary heart rhythm disorders

Questions that arise while reading the article can be asked to specialists using the online form.

Free consultations are available 24 hours a day.

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 ECG 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 is between the left leg and right arm, the third is 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 decipher it. This will be discussed further.

Decoding the cardiogram

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

1. The heart rhythm and myocardial conductivity 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. 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 heart rhythm patterns are observed:

1. The sinusoidal nature of the heart rhythm, in which the P waves in the second lead are positive and are located in front of the ventricular QRS complex, and the P waves in the same lead have an indistinguishable shape.
2. Atrial rhythm of the heart, in which the P waves in the second and third leads are negative and are located in front of the unchanged QRS complexes.
3. The ventricular nature of the heart rhythm, in which there is deformation of the QRS complexes and loss of connection 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 that the conduction velocity in the corresponding cardiac conduction section is too low.
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. To do this, the amplitude of the P wave is assessed and the duration of the P wave is measured. Afterwards, the shape and polarity of the P wave are determined.
4. The ventricular complex is analyzed. For this purpose, the QRS complex, RS-T segment, QT interval, T wave are assessed.

When assessing the QRS complex, the following is done: the characteristics of the Q, S and R waves are determined, 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 are compared.

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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.

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

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

Electrocardiogram norms

The table with ECG results has a visual appearance, consisting of rows and columns. In the 1st column, the rows list: heart rate, examples of contraction frequency, QT intervals, examples of axis displacement characteristics, P wave indicators, PQ indicators, examples of QRS indicator. ECG is performed in the same way 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;
• heart rate 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.

If deviations from the norm are observed in an adult, a conclusion is drawn about the presence of a 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 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 in all children: from 0.06 to 0.1;
• QT score in all children: 0.4 or less;
• the PQ indicator for all children: if the child is under 14 years old, then an example of the PQ indicator is 0.16, if the child is from 14 to 17 years old, then the PQ indicator is 0.18, after 17 years the normal PQ indicator is 0.2.

If any deviations from the norm are detected in children when interpreting the ECG, then treatment should not be started immediately. Some disturbances in the functioning of the heart disappear 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 at the stage of fetal development. For this purpose, electrocardiography is performed on women during pregnancy.

The normal electrocardiogram indicators in women during pregnancy are 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 functioning of the myocardium.

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 it exceeds a value of 0.42):

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

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

The distance between two R waves is 46 cells (0.92 seconds).

Square root of 0.92 = 0.96.

QT interval on ECG

The QT interval doesn't tell the average person much, but it can tell a doctor a lot about the patient's heart condition. Compliance with the norm of the specified interval is determined based on the analysis of the electrocardiogram (ECG).

Basic elements of an electrical cardiogram

An electrocardiogram is a recording of the electrical activity of the heart. This method of assessing the condition of the heart muscle has been known for a long time and is widespread due to its safety, accessibility, and information content.

The electrocardiograph records the cardiogram on special paper, divided into cells 1 mm wide and 1 mm high. At a paper speed of 25 mm/s, the side of each square corresponds to 0.04 seconds. A paper speed of 50 mm/s is also often found.

An electrical cardiogram consists of three basic elements:

A spike is a kind of peak that goes either up or down on a line graph. The ECG records six waves (P, Q, R, S, T, U). The first wave refers to the contraction of the atria, the last wave is not always present on the ECG, so it is called intermittent. The Q, R, S waves show how the heart ventricles contract. The T wave characterizes their relaxation.

A segment is a straight line segment between adjacent teeth. The intervals are a tooth with a segment.

To characterize the electrical activity of the heart, the PQ and QT intervals are of greatest importance.

1. The first interval is the time it takes for excitation to travel through the atria and the atrioventricular node (the conduction system of the heart located in the interatrial septum) to the ventricular myocardium.

1. The QT interval reflects the combination of processes of electrical excitation of cells (depolarization) and return to a resting state (repolarization). Therefore, the QT interval is called electrical ventricular systole.

Why is the length of the QT interval so significant in ECG analysis? Deviation from the norm of this interval indicates a disruption in the processes of repolarization of the ventricles of the heart, which in turn can result in serious disturbances of the heart rhythm, for example, polymorphic ventricular tachycardia. This is the name for malignant ventricular arrhythmia, which can lead to sudden death of the patient.

Normally, the duration of the QT interval is in the range of 0.35-0.44 seconds.

The length of the QT interval can vary depending on many factors. The main ones:

• age;
• heart rate;
• state of the nervous system;
• electrolyte balance in the body;
• Times of Day;
• the presence of certain medications in the blood.

If the duration of the electrical systole of the ventricles goes beyond 0.35-0.44 seconds, the doctor has reason to talk about the occurrence of pathological processes in the heart.

Long QT syndrome

There are two forms of the disease: congenital and acquired.

Congenital form of pathology

It is inherited in an autosomal dominant manner (one of the parents passes the defective gene to the child) and an autosomal recessive type (both parents have the defective gene). Defective genes disrupt the functioning of ion channels. Experts classify four types of this congenital pathology.

1. Romano-Ward syndrome. The most common occurrence is approximately one child in 2000 births. It is characterized by frequent attacks of torsades de pointes with an unpredictable rate of ventricular contraction.

The paroxysm may go away on its own, or it may develop into ventricular fibrillation with sudden death.

The following symptoms are typical for an attack:

Physical activity is contraindicated for the patient. For example, children are exempt from physical education lessons.

Romano-Ward syndrome is treated with medication and surgery. With the medication method, the doctor prescribes the maximum acceptable dose of beta-blockers. Surgical intervention is performed to correct the conduction system of the heart or install a cardioverter-defibrillator.

1. Jervell-Lange-Nielsen syndrome. Not as common as the previous syndrome. In this case we observe:

• more noticeable prolongation of the QT interval;
• increased frequency of attacks of ventricular tachycardia, fraught with death;
• congenital deafness.

Surgical treatment methods are mainly used.

1. Anderson-Tawil syndrome. This is a rare form of a genetic, inherited disease. The patient is susceptible to attacks of polymorphic ventricular tachycardia and bidirectional ventricular tachycardia. Pathology clearly makes itself known by the appearance of patients:

• short stature;
• curvature of the spine;
• low position of the ears;
• abnormally large distance between the eyes;
• underdevelopment of the upper jaw;
• deviations in the development of fingers.

The disease can occur with varying degrees of severity. The most effective method of therapy is the installation of a cardioverter-defibrillator.

1. Timothy syndrome. It is extremely rare. With this disease, a maximum prolongation of the QT interval is observed. Every six out of ten patients with Timothy syndrome have various congenital heart defects (tetralogy of Fallot, patent ductus arteriosus, ventricular septal defects). A variety of physical and mental abnormalities are present. The average life expectancy is two and a half years.

Acquired form of pathology

The clinical picture is similar in manifestations to that observed with the congenital form. In particular, attacks of ventricular tachycardia and fainting are characteristic.

Acquired prolonged QT interval on the ECG can be recorded for various reasons.

1. Taking antiarrhythmic drugs: quinidine, sotalol, ajmaline and others.
2. Electrolyte imbalance in the body.
3. Alcohol abuse often causes paroxysm of ventricular tachycardia.
4. A number of cardiovascular diseases cause prolongation of the electrical systole of the ventricles.

Treatment of the acquired form primarily comes down to eliminating the causes that caused it.

Short QT syndrome

It can also be either congenital or acquired.

Congenital form of pathology

It is caused by a rather rare genetic disease that is transmitted in an autosomal dominant manner. Shortening of the QT interval is caused by mutations in the genes of potassium channels, which ensure the flow of potassium ions through cell membranes.

• attacks of atrial fibrillation;
• attacks of ventricular tachycardia.

A study of families of patients with short QT syndrome shows that they have experienced sudden death of relatives at a young and even infancy due to atrial and ventricular fibrillation.

The most effective treatment for congenital short QT syndrome is the installation of a cardioverter-defibrillator.

Acquired form of pathology

1. The cardiograph may show on the ECG a shortening of the QT interval during treatment with cardiac glycosides in case of overdose.
2. Short QT syndrome can be caused by hypercalcemia (increased calcium levels in the blood), hyperkalemia (increased potassium levels in the blood), acidosis (a shift in the acid-base balance towards acidity) and some other diseases.

Therapy in both cases comes down to eliminating the causes of the short QT interval.

Decoding an ECG is the job of a knowledgeable doctor. This method of functional diagnostics evaluates:

• heart rhythm - the state of the generators of electrical impulses and the state of the heart system conducting these impulses
• the condition of the heart muscle itself (myocardium), the presence or absence of inflammation, damage, thickening, oxygen starvation, electrolyte imbalance

However, modern patients often have access to their medical documents, in particular, to electrocardiography films on which medical reports are written. With their diversity, these recordings can drive even the most balanced but ignorant person to panic disorder. After all, the patient often does not know for certain how dangerous to life and health is what is written on the back of the ECG film by the hand of a functional diagnostician, and there are still several days before an appointment with a therapist or cardiologist.

To reduce the intensity of passions, we immediately warn readers that with not a single serious diagnosis (myocardial infarction, acute rhythm disturbances), a functional diagnostician will not let a patient leave the office, but, at a minimum, will send him for a consultation with a fellow specialist right there. About the rest of the “open secrets” in this article. In all unclear cases of pathological changes in the ECG, ECG monitoring, 24-hour monitoring (Holter), ECHO cardioscopy (ultrasound of the heart) and stress tests (treadmill, bicycle ergometry) are prescribed.

• When describing an ECG, the heart rate (HR) is usually indicated. The norm is from 60 to 90 (for adults), for children (see table)
• The following are the various intervals and teeth with Latin designations. (ECG with interpretation, see Fig.)

PQ- (0.12-0.2 s) – atrioventricular conduction time. Most often it lengthens against the background of AV blockade. Shortened in CLC and WPW syndromes.

P – (0.1s) height 0.25-2.5 mm describes atrial contractions. May indicate their hypertrophy.

QRS – (0.06-0.1s) -ventricular complex

QT – (no more than 0.45 s) lengthens with oxygen starvation (myocardial ischemia, infarction) and the threat of rhythm disturbances.

RR - the distance between the apices of the ventricular complexes reflects the regularity of heart contractions and makes it possible to calculate heart rate.

The interpretation of the ECG in children is presented in Fig. 3

Sinus rhythm

This is the most common inscription found on an ECG. And, if nothing else is added and the frequency (HR) is indicated from 60 to 90 beats per minute (for example, HR 68`) - this is the best option, indicating that the heart works like a clock. This is the rhythm set by the sinus node (the main pacemaker that generates electrical impulses that cause the heart to contract). At the same time, sinus rhythm implies well-being, both in the state of this node and the health of the conduction system of the heart. The absence of other records denies pathological changes in the heart muscle and means that the ECG is normal. In addition to sinus rhythm, there may be atrial, atrioventricular or ventricular rhythm, indicating that the rhythm is set by cells in these parts of the heart and is considered pathological.

Sinus arrhythmia

This is a normal variant in young people and children. This is a rhythm in which impulses leave the sinus node, but the intervals between heart contractions are different. This may be due to physiological changes (respiratory arrhythmia, when heart contractions slow down during exhalation). Approximately 30% of sinus arrhythmias require observation by a cardiologist, as they are at risk of developing more serious rhythm disturbances. These are arrhythmias after rheumatic fever. Against the background of myocarditis or after it, against the background of infectious diseases, heart defects and in persons with a family history of arrhythmias.

Sinus bradycardia

These are rhythmic contractions of the heart with a frequency of less than 50 per minute. In healthy people, bradycardia occurs, for example, during sleep. Bradycardia also often occurs in professional athletes. Pathological bradycardia may indicate sick sinus syndrome. In this case, bradycardia is more pronounced (heart rate from 45 to 35 beats per minute on average) and is observed at any time of the day. When bradycardia causes pauses in heart contractions of up to 3 seconds during the day and about 5 seconds at night, leads to disturbances in the supply of oxygen to tissues and is manifested, for example, by fainting, an operation is indicated to install a cardiac pacemaker, which replaces the sinus node, imposing a normal rhythm of contractions on the heart.

Sinus tachycardia

Heart rate more than 90 per minute is divided into physiological and pathological. In healthy people, sinus tachycardia is accompanied by physical and emotional stress, drinking coffee, sometimes strong tea or alcohol (especially energy drinks). It is short-lived and after an episode of tachycardia, the heart rate returns to normal within a short period of time after stopping the load. With pathological tachycardia, heartbeats bother the patient at rest. Its causes are fever, infections, blood loss, dehydration, thyrotoxicosis, anemia, cardiomyopathy. The underlying disease is treated. Sinus tachycardia is stopped only in case of a heart attack or acute coronary syndrome.

Extarsystole

These are rhythm disturbances in which foci outside the sinus rhythm give extraordinary cardiac contractions, after which there is a pause of twice the length, called compensatory. In general, the patient perceives heartbeats as uneven, rapid or slow, and sometimes chaotic. The most worrying thing is the dips in heart rate. There may be unpleasant sensations in the chest in the form of tremors, tingling, feelings of fear and emptiness in the stomach.

Not all extrasystoles are dangerous to health. Most of them do not lead to significant circulatory disorders and do not threaten either life or health. They can be functional (against the background of panic attacks, cardioneurosis, hormonal imbalances), organic (with ischemic heart disease, heart defects, myocardial dystrophy or cardiopathy, myocarditis). They can also be caused by intoxication and heart surgery. Depending on the place of occurrence, extrasystoles are divided into atrial, ventricular and anthrioventricular (arising in the node at the border between the atria and ventricles).

• Single extrasystoles are most often rare (less than 5 per hour). They are usually functional and do not interfere with normal blood supply.
• Paired extrasystoles, two at a time, accompany a certain number of normal contractions. Such rhythm disturbances often indicate pathology and require further examination (Holter monitoring).
• Allorhythmias are more complex types of extrasystoles. If every second contraction is an extrasystole, this is bigymenia, if every third contraction is trigymenia, every fourth is quadrigymenia.

It is customary to divide ventricular extrasystoles into five classes (according to Lown). They are assessed during daily ECG monitoring, since the readings of a regular ECG in a few minutes may not show anything.

• Class 1 - single rare extrasystoles with a frequency of up to 60 per hour, emanating from one focus (monotopic)
• 2 – frequent monotopic more than 5 per minute
• 3 – frequent polymorphic (of different shapes) polytopic (from different foci)
• 4a – paired, 4b – group (trigymenia), episodes of paroxysmal tachycardia
• 5 – early extrasystoles

The higher the class, the more serious the violations, although today even classes 3 and 4 do not always require drug treatment. In general, if there are less than 200 ventricular extrasystoles per day, they should be classified as functional and not worry about them. For more frequent cases, ECHO CS is indicated, and sometimes cardiac MRI is indicated. It is not the extrasystole that is treated, but the disease that leads to it.

Paroxysmal tachycardia

In general, a paroxysm is an attack. A paroxysmal increase in rhythm can last from several minutes to several days. In this case, the intervals between heart contractions will be the same, and the rhythm will increase over 100 per minute (on average from 120 to 250). There are supraventricular and ventricular forms of tachycardia. This pathology is based on abnormal circulation of electrical impulses in the conduction system of the heart. This pathology can be treated. Home remedies to relieve an attack:

• holding your breath
• increased forced cough
• immersing face in cold water

WPW syndrome

Wolff-Parkinson-White syndrome is a type of paroxysmal supraventricular tachycardia. Named after the authors who described it. The appearance of tachycardia is based on the presence of an additional nerve bundle between the atria and ventricles, through which a faster impulse passes than from the main pacemaker.

As a result, an extraordinary contraction of the heart muscle occurs. The syndrome requires conservative or surgical treatment (in case of ineffectiveness or intolerance of antiarrhythmic tablets, during episodes of atrial fibrillation, and with concomitant heart defects).

CLC – syndrome (Clerk-Levi-Christesco)

is similar in mechanism to WPW and is characterized by earlier excitation of the ventricles than normal due to an additional bundle along which the nerve impulse travels. The congenital syndrome is manifested by attacks of rapid heartbeat.

Atrial fibrillation

It can be in the form of an attack or a permanent form. It manifests itself in the form of atrial flutter or fibrillation.

Atrial fibrillation

When flickering, the heart contracts completely irregularly (the intervals between contractions of very different durations). This is explained by the fact that the rhythm is not set by the sinus node, but by other cells of the atria.

The resulting frequency is from 350 to 700 beats per minute. There is simply no full contraction of the atria; contracting muscle fibers do not effectively fill the ventricles with blood.

As a result, the heart’s output of blood deteriorates and organs and tissues suffer from oxygen starvation. Another name for atrial fibrillation is atrial fibrillation. Not all atrial contractions reach the ventricles of the heart, so the heart rate (and pulse) will be either below normal (bradysystole with a frequency of less than 60), or normal (normosystole from 60 to 90), or above normal (tachysystole more than 90 beats per minute ).

An attack of atrial fibrillation is difficult to miss.

• It usually starts with a strong beat of the heart.
• It develops as a series of absolutely irregular heartbeats with a high or normal frequency.
• The condition is accompanied by weakness, sweating, dizziness.
• The fear of death is very pronounced.
• There may be shortness of breath, general agitation.
• Sometimes there is loss of consciousness.
• The attack ends with normalization of the rhythm and the urge to urinate, during which a large amount of urine is released.

To stop an attack, they use reflex methods, drugs in the form of tablets or injections, or resort to cardioversion (stimulating the heart with an electric defibrillator). If an attack of atrial fibrillation is not eliminated within two days, the risks of thrombotic complications (pulmonary embolism, stroke) increase.

With a constant form of heartbeat flicker (when the rhythm is not restored either against the background of drugs or against the background of electrical stimulation of the heart), they become a more familiar companion to patients and are felt only during tachysystole (rapid, irregular heartbeats). The main task when detecting signs of tachysystole of a permanent form of atrial fibrillation on the ECG is to slow down the rhythm to normosystole without trying to make it rhythmic.

Examples of recordings on ECG films:

• atrial fibrillation, tachysystolic variant, heart rate 160 b'.
• Atrial fibrillation, normosystolic variant, heart rate 64 b'.

Atrial fibrillation can develop in the course of coronary heart disease, against the background of thyrotoxicosis, organic heart defects, diabetes mellitus, sick sinus syndrome, and intoxication (most often with alcohol).

Atrial flutter

These are frequent (more than 200 per minute) regular contractions of the atria and equally regular, but less frequent contractions of the ventricles. In general, flutter is more common in the acute form and is better tolerated than flicker, since circulatory disorders are less pronounced. Fluttering develops when:

• organic heart diseases (cardiomyopathies, heart failure)
• after heart surgery
• against the background of obstructive pulmonary diseases
• in healthy people it almost never occurs

Clinically, flutter is manifested by rapid rhythmic heartbeat and pulse, swelling of the neck veins, shortness of breath, sweating and weakness.

Normally, having formed in the sinus node, electrical excitation travels through the conduction system, experiencing a physiological delay of a split second in the atrioventricular node. On its way, the impulse stimulates the atria and ventricles, which pump blood, to contract. If in any part of the conduction system the impulse is delayed longer than the prescribed time, then excitation to the underlying sections will come later, and, therefore, the normal pumping work of the heart muscle will be disrupted. Conduction disturbances are called blockades. They can occur as functional disorders, but more often they are the result of drug or alcohol intoxication and organic heart disease. Depending on the level at which they arise, several types are distinguished.

Sinoatrial blockade

When the exit of an impulse from the sinus node is difficult. In essence, this leads to sick sinus syndrome, slowing of contractions to severe bradycardia, impaired blood supply to the periphery, shortness of breath, weakness, dizziness and loss of consciousness. The second degree of this blockade is called Samoilov-Wenckebach syndrome.

Atrioventricular block (AV block)

This is a delay of excitation in the atrioventricular node longer than the prescribed 0.09 seconds. There are three degrees of this type of blockade. The higher the degree, the less often the ventricles contract, the more severe the circulatory disorders.

• In the first, the delay allows each atrial contraction to maintain an adequate number of ventricular contractions.
• The second degree leaves some of the atrial contractions without ventricular contractions. It is described, depending on the prolongation of the PQ interval and the loss of ventricular complexes, as Mobitz 1, 2 or 3.
• The third degree is also called complete transverse blockade. The atria and ventricles begin to contract without interconnection.

In this case, the ventricles do not stop because they obey the pacemakers from the underlying parts of the heart. If the first degree of blockade may not manifest itself in any way and can be detected only with an ECG, then the second is already characterized by sensations of periodic cardiac arrest, weakness, and fatigue. With complete blockades, brain symptoms (dizziness, spots in the eyes) are added to the manifestations. Morgagni-Adams-Stokes attacks may develop (when the ventricles escape from all pacemakers) with loss of consciousness and even convulsions.

Impaired conduction within the ventricles

In the ventricles, the electrical signal propagates to the muscle cells through such elements of the conduction system as the trunk of the His bundle, its legs (left and right) and branches of the legs. Blockades can occur at any of these levels, which is also reflected in the ECG. In this case, instead of being simultaneously covered by excitation, one of the ventricles is delayed, since the signal to it bypasses the blocked area.

In addition to the place of origin, a distinction is made between complete or incomplete blockade, as well as permanent and non-permanent blockade. The causes of intraventricular blocks are similar to other conduction disorders (ischemic heart disease, myocarditis and endocarditis, cardiomyopathies, heart defects, arterial hypertension, fibrosis, heart tumors). Also affected are the use of antiarthmic drugs, an increase in potassium in the blood plasma, acidosis, and oxygen starvation.

• The most common is blockade of the anterosuperior branch of the left bundle branch (ALBBB).
• In second place is right leg block (RBBB). This blockade is usually not accompanied by heart disease.
• Left bundle branch block is more typical for myocardial lesions. In this case, complete blockade (PBBB) is worse than incomplete blockade (LBBB). It sometimes has to be distinguished from WPW syndrome.
• Blockade of the posteroinferior branch of the left bundle branch can occur in persons with a narrow and elongated or deformed chest. Among pathological conditions, it is more typical for overload of the right ventricle (with pulmonary embolism or heart defects).

The clinical picture of blockades at the levels of the His bundle is not pronounced. The picture of the underlying cardiac pathology comes first.

• Bailey's syndrome is a two-bundle block (of the right bundle branch and the posterior branch of the left bundle branch).

With chronic overload (pressure, volume), the heart muscle in certain areas begins to thicken, and the chambers of the heart begin to stretch. On the ECG, such changes are usually described as hypertrophy.

• Left ventricular hypertrophy (LVH) is typical for arterial hypertension, cardiomyopathy, and a number of heart defects. But even normally, athletes, obese patients and people engaged in heavy physical labor may experience signs of LVH.
• Right ventricular hypertrophy is an undoubted sign of increased pressure in the pulmonary blood flow system. Chronic cor pulmonale, obstructive pulmonary diseases, cardiac defects (pulmonary stenosis, tetralogy of Fallot, ventricular septal defect) lead to RVH.
• Left atrial hypertrophy (LAH) – with mitral and aortic stenosis or insufficiency, hypertension, cardiomyopathy, after myocarditis.
• Right atrial hypertrophy (RAH) – with cor pulmonale, tricuspid valve defects, chest deformities, pulmonary pathologies and PE.
• Indirect signs of ventricular hypertrophy are deviation of the electrical axis of the heart (EOC) to the right or left. The left type of EOS is its deviation to the left, that is, LVH, the right type is RVH.
• Systolic overload is also evidence of hypertrophy of the heart. Less commonly, this is evidence of ischemia (in the presence of angina pain).

Early ventricular repolarization syndrome

Most often, this is a variant of the norm, especially for athletes and people with congenital high body weight. Sometimes associated with myocardial hypertrophy. Refers to the peculiarities of the passage of electrolytes (potassium) through the membranes of cardiocytes and the characteristics of the proteins from which the membranes are built. It is considered a risk factor for sudden cardiac arrest, but does not provide clinical results and most often remains without consequences.

Moderate or severe diffuse changes in the myocardium

This is evidence of a malnutrition of the myocardium as a result of dystrophy, inflammation (myocarditis) or cardiosclerosis. Also, reversible diffuse changes accompany disturbances in water and electrolyte balance (with vomiting or diarrhea), taking medications (diuretics), and heavy physical activity.

Nonspecific ST changes

This is a sign of deterioration in myocardial nutrition without severe oxygen starvation, for example, in case of disturbances in the balance of electrolytes or against the background of dyshormonal conditions.

Acute ischemia, ischemic changes, T wave changes, ST depression, low T

This describes reversible changes associated with oxygen starvation of the myocardium (ischemia). This can be either stable angina or unstable, acute coronary syndrome. In addition to the presence of the changes themselves, their location is also described (for example, subendocardial ischemia). A distinctive feature of such changes is their reversibility. In any case, such changes require comparison of this ECG with old films, and if a heart attack is suspected, troponin rapid tests for myocardial damage or coronary angiography. Depending on the type of coronary heart disease, anti-ischemic treatment is selected.

Advanced heart attack

It is usually described:

• by stages: acute (up to 3 days), acute (up to 3 weeks), subacute (up to 3 months), cicatricial (all life after a heart attack)
• by volume: transmural (large focal), subendocardial (small focal)
• By location, infarctions are: anterior and anterior septal, basal, lateral, inferior (posterior diaphragmatic), circular apical, posterobasal and right ventricular.

In any case, a heart attack is a reason for immediate hospitalization.

The whole variety of syndromes and specific changes on the ECG, the difference in indicators for adults and children, the abundance of reasons leading to the same type of ECG changes do not allow a non-specialist to interpret even the finished conclusion of a functional diagnostician. It is much wiser, having the ECG result in hand, to visit a cardiologist in a timely manner and receive competent recommendations for further diagnosis or treatment of your problem, significantly reducing the risks of emergency cardiac conditions.

Please decipher the electrocardiogram. Rhythm syn. heart rate 62/m deviation.o.s. left violation proc.ropol. at high levels lateral st.l.zh.

Hello! Please decipher the ECG. Heart rate-77.RV5/SV1 Amplitude 1.178/1. 334mV. P duration/PR Interval 87/119ms Rv5+sv1 Amplitude 2.512mV QRS duration 86ms RV6/SV2 Amplitude 0.926/0.849mv. QTC interval 361/399ms.P/QRS/T angle 71/5/14°

Good afternoon, please help me with deciphering the ECG: age 35 years.

Hello! Help me decipher the cardiogram (I’m 37 years old) by writing in “simple language”:

Reduced voltage. The rhythm is sinus, regular heart rate is 64 beats per minute.

EOS is located horizontally. QT prolongation. Pronounced diffuse metabolic changes in the myocardium.

Hello! Help me decipher 7 years old. Sinus rhythm, heart rate - 92 bpm, EOS - NORMAL POSITION, RBBB, pQ - 0.16 m.sec, QT - 0.34 msec.

Hello, Help me decipher the cardiogram, I am 55 years old, my blood pressure is normal, I have no diseases.

Heart rate 63 beats/min

PR interval 152 ms

QRS complex 95 ms

QT/QTc 430/441 ms

P/QRS/T axis (deg) 51.7 / 49.4 / 60.8

R(V5) / S(V) 0.77 / 1.07 mV

Sinus arrhythmia. A. in stage I blockade. Semi-horizontal EPS. Incomplete blockade of the left leg of the His. Change in/prev. conductivity. Enlargement of the left chambers of the heart.

Male 41 years old. Is consultation with a cardiologist required?

Sinus arrhythmia HR = 73 beats/min

EOS is located normally,

Disruption of repolarization processes and reduction of myocardial trophism (anterior apical sections).

Help me decipher the cardiogram: sinus rhythm, RBBB.

Male, 26 years old. Is consultation with a cardiologist required? Is treatment required?

Hello! Please tell me if, according to Holter kg per day, in a 12-year-old child, against the background of sinus rhythm, episodes of pacemaker migration at rest, in the daytime with a tendency to bradycardia were recorded. Supraventricular and ventricular activity was recorded, 2 episodes of NVT with aberrant conduction with chssuzh. per minute, episodes of 1st degree AV block, QT 0.44-0.51, can he play sports and what are the risks?

What does it mean? At night, 2 pauses of more than 200 ms (2054 and 2288 ms) were recorded due to the loss of QRST.

Hello. Passed the commission. Girl 13 years old.

conclusion: sinus arrhythmia with heart rate min. bradysystole, rhythm with pronounced irregularity, heart rate = 57 beats/min, RR: 810 ms - 1138 ms. normal position of the electrical axis of the heart. A passing phenomenon of WPW. RRav = 1054ms RRmin = 810ms RRmax = 1138. Interval: PQ = 130ms. Duration: P=84ms, QRS=90ms, QT=402ms QTcor=392ms

conclusion: migration of the pacemaker through the atria, heart rate 73 per minute. Normosystole, rhythm with pronounced irregularity, heart rate = 73 beats/min, RR: 652ms -1104ms. The PQRST form is a variant of the norm. normal position of the electrical axis of the heart. RRav = 808ms RRmin = 652ms RRmax = 1108. Interval: PQ = 140ms. Duration: P=88ms, QRS=82ms, QT=354ms QTcore=394ms.

There were no problems before. What could it be?

Progrostic mycocarditis of heart valve cysts

41 years weight 86kg. height 186

Hello, help me decipher the ECG

Duration P-96ms QRS-95ms

Intervals PQ-141ms QT-348ms QTc-383ms

Axles P-42 QRS-81 T-73

Rhythm irregularity 16%

Normal sinus rhythm

Left ventricular mass index 116 g/m2

Hello! Please decipher the cardiogram, I am 28 years old:

QT/QTB, sec.: 0.35/0.35

Accelerated sinus rhythm.

Single ventricular extrasystole with episodes of bigeminy (1:1)

Electrical axis deviation to the right

Hello. please decipher the ECG:

the position of the electrical axis is intermediate

incomplete blockade of PNPG

Hello, please decipher the child 2.5.

Hello. Decipher it please! 32 year old girl is normosthenic. HR = 75 beats! El. Axis 44_normal ind. juice. =23.0. PQ=0.106c. P=0.081c. QRS=0.073c. QT=0.353c. sp mind. At 1%(0.360) sinus rhythm. ShortenedPQ

Hello. Please decipher the cardiogram. I am 59 years old. There are 2 measurement results in the cardiogram, the first at 10.06 QRS 96ms QT/QTC 394/445ms PQ 168ms P 118ms RR/PP 770/775ms P/QRS/T 59/49/ -27 Degree and the second at 10.07 QRS 90ms QT/QTC 376/431ms PQ 174ms P 120ms RR /PP 768 / 755ms P/QRS/T 70/69/ -14 Degree

Hello, please decipher the cardiogram. HR 95, Qrs78ms. / Qts 338/424.ms interval PR122ms, duration P 106ms, RR interval 631ms, axes P-R-T2

Good afternoon, please help me decipher: a child is 3.5 years old. An ECG was done as preparation for surgery under general anesthesia.

Sinus rhythm with heart rate 100 beats/min.

Disturbance of conduction along the right bundle branch.

Hello, help me decipher the ECG, I am 27.5 years old, female (I complain about my pulse when lying down; during sleep it is 49).

Vent. ChChS 66 ChChS

QRS duration 90 ms

QT/QTc 362/379 ms

PR interval 122 ms

Duration P 100 ms

RR interval 909 ms

Hello, help me decipher the ECG, 31 years old, male

electrical axis of the heart 66 degrees

heart rate 73 beats/min

electric axis 66 degrees

Hello, help me decipher the ECG child 1 month heart rate-150 r-0.06 PQ-0.10 QRS-0.06 QT-0.26 RR-0.40 AQRS +130 sinusoidal voltage

Hello! SR 636 or (63 v) Acceleration. av-right. SRRSH.What is this?

Tell me, and we have a conclusion: sinus arrhythmia, vertical position, moderate disruption of myocardial reporization processes in the lower wall of the left ventricle (low-amplitude TV vf waves

Good evening! Please help me decipher the ECG:

QT/QTC 360/399 ms

P/QRS/T 66/59/27 degree

R-R: 893MS AXLE: 41 degrees

ORS: 97MS RV6:1.06mV

QT: 374MS SVI: 0.55mV

QTc: 395 R+S: 1.61mV I ask you to decipher the ECG

Good afternoon Today I received an ECG report for my son, 6 years 7 months old, and was confused by the report of CLC syndrome. Please decipher this conclusion, is there any reason to be afraid? Thanks in advance!

RR max-RR min 0.00-0.0

Conclusion: Sinus rhythm with heart rate = 75 per minute. Vertical EOS. Shortened PQ interval (CLC syndrome). In your article I learned that the heart rate in children aged 5 years is at the age of 8 years, and we are 6.7 years old and we are 75?

Hello, help me decipher. Heart rate:47min.

Good afternoon. Help me decipher the ECG

eos deviated to the left

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IN In recent years, in clinical cardiology, the problem of prolongation of the QT interval has attracted close attention of domestic and foreign researchers as a factor leading to sudden death. It has been established that both congenital and acquired forms of QT prolongation are predictors of fatal arrhythmias , which, in turn, lead to sudden death of patients.

Long QT syndrome is a combination of a prolonged QT interval on a standard ECG and life-threatening polymorphic ventricular tachycardias (torsade de pointes). Paroxysms of ventricular tachycardia of the “pirouette” type are clinically manifested by episodes of loss of consciousness and often end in ventricular fibrillation, which is the direct cause of sudden death.

The duration of the QT interval depends on the heart rate and gender of the patient. Therefore, they use not the absolute, but the corrected value of the QT interval (QTc), which is calculated using the Bazett formula

where: RR is the distance between adjacent R waves on the ECG in seconds;

K = 0.37 for men and K = 0.40 for women.

QT prolongation is diagnosed if the QTc duration exceeds 0.44 s.

In recent years, much attention has been paid to the study of the variability (dispersion) of the QT interval - a marker of the inhomogeneity of repolarization processes, since increased dispersion of the QT interval is also a predictor of the development of a number of serious rhythm disturbances, including sudden death. QT interval dispersion is the difference between the maximum and minimum values ​​of the QT interval measured in 12 standard ECG leads: D QT = QT max - QT min.

The most common method for detecting QT dispersion is recording a standard ECG for 3-5 minutes at a recording speed of 25 mm/hour. Holter ECG monitoring is also used, which makes it possible to analyze fluctuations in QTc dispersion (QTcd) throughout the day. However, a number of methodological aspects of this method are under development. Thus, there is no consensus on the upper limit of normal values ​​for the dispersion of the corrected QT interval. According to some authors, a predictor of ventricular tachyarrhythmia is a QTcd of more than 45; other researchers suggest that a QTcd of 70 ms and even 125 ms be considered the upper limit of normal.

There are two most studied pathogenetic mechanisms of arrhythmias in long QT interval syndrome. First - mechanism of “intracardiac disturbances” of myocardial repolarization , namely, increased sensitivity of the myocardium to the arrhythmogenic effect of catecholamines. The second pathophysiological mechanism is imbalance of sympathetic innervation (decreased right-sided sympathetic innervation due to weakness or underdevelopment of the right stellate ganglion). This concept is supported by animal models (QT prolongation after right stellectomy) and the results of left stellectomy in the treatment of refractory forms of QT prolongation.

Etiology of long QT syndrome

In healthy people at rest there is only a slight variability in the repolarization processes, so the dispersion of the QT interval is minimal. The causes of QT interval prolongation are conventionally divided into 2 groups - congenital and acquired.

Congenital forms

Congenital forms of long QT interval syndrome become one of the causes of death in children. The mortality rate for untreated congenital forms of this syndrome reaches 75%, with 20% of children dying within a year after the first loss of consciousness and about 50% in the first decade of life. Congenital forms of long QT syndrome include Gervell and Lange-Nielsen syndrome and Romano-Ward syndrome. Gervell and Lange-Nielsen syndrome - a rare disease, has an autosomal recessive type of inheritance and is a combination of congenital deaf-muteness with prolongation of the QT interval on the ECG, episodes of loss of consciousness and often ends in the sudden death of children in the first decade of life. Romano-Ward syndrome has an autosomal dominant mode of inheritance with a population frequency of 1:10,000-1:15,000 and a gene penetrance of 0.9. It has a similar clinical picture: cardiac arrhythmias, in some cases with loss of consciousness against the background of an extended QT interval in children without hearing or speech impairment.

The frequency of detection of a prolonged QT interval in school-age children with congenital deaf-muteness on a standard ECG reaches 44%, while almost half of them (about 43%) experienced episodes of loss of consciousness and paroxysms of tachycardia. During daily ECG monitoring, almost 30% of them recorded paroxysms of supraventricular tachycardia, and approximately every fifth had “jogs” of ventricular tachycardia of the “pirouette” type.

To diagnose congenital forms of long QT syndrome in the case of borderline prolongation and/or absence of symptoms, a set of diagnostic criteria has been proposed. “Major” criteria are a prolongation of the QT interval of more than 0.44 ms, a history of episodes of loss of consciousness, and the presence of long QT interval syndrome in family members. “Minor” criteria are congenital sensorineural hearing loss, episodes of T-wave alternans, slow heart rate (in children), and abnormal ventricular repolarization. The greatest diagnostic significance is a significant prolongation of the QT interval, paroxysms of tachycardia torsade de pointes and episodes of syncope.

Congenital long QT syndrome is a genetically heterogeneous disease involving more than 5 different chromosomal loci. At least 4 genes have been identified that determine the development of congenital prolongation of the QT interval.

The most common form of long QT syndrome in young adults is combination of this syndrome with mitral valve prolapse . The detection rate of QT interval prolongation in individuals with mitral and/or tricuspid valve prolapse reaches 33%. According to most researchers, mitral valve prolapse is one of the manifestations of congenital connective tissue dysplasia. Other manifestations of “connective tissue weakness” include increased skin extensibility, asthenic body type, funnel chest deformity, scoliosis, flat feet, joint hypermobility syndrome, myopia, varicose veins, hernias. A number of researchers have identified a relationship between increased variability of the QT interval and the depth of prolapse and/or the presence of structural changes (myxomatous degeneration) of the mitral valve leaflets. One of the main reasons for the formation of prolongation of the QT interval in individuals with mitral valve prolapse is genetically predetermined or acquired magnesium deficiency.

Acquired forms

Acquired prolongation of the QT interval can occur with atherosclerotic or post-infarction cardiosclerosis, with cardiomyopathy, against the background and after myo- or pericarditis. An increase in QT interval dispersion (more than 47 ms) may also be a predictor of the development of arrhythmogenic syncope in patients with aortic heart defects.

There is no consensus on the prognostic significance of an increase in the dispersion of the QT interval in patients with post-infarction cardiosclerosis: some authors have identified in these patients a clear relationship between an increase in the duration and dispersion of the QT interval (on the ECG) and the risk of developing paroxysms of ventricular tachycardia, other researchers have not found a similar pattern. In cases where the QT interval dispersion is not increased in patients with post-infarction cardiosclerosis at rest, this parameter should be assessed during an exercise test. In patients with post-infarction cardiosclerosis, assessment of QT dispersion against the background of stress tests is considered by many researchers to be more informative for verifying the risk of ventricular arrhythmias.

Prolongation of the QT interval can also be observed with sinus bradycardia, atrioventricular block, chronic cerebrovascular insufficiency and brain tumors. Acute cases of QT prolongation can also occur with injuries (chest, traumatic brain).

Autonomic neuropathy also increases the QT interval and its dispersion, so these syndromes occur in patients with diabetes mellitus types I and II.

Prolongation of the QT interval can occur with electrolyte imbalance with hypokalemia, hypocalcemia, hypomagnesemia. Such conditions arise under the influence of many reasons, for example, with long-term use of diuretics, especially loop diuretics (furosemide). The development of ventricular tachycardia of the “pirouette” type is described against the background of prolongation of the QT interval with a fatal outcome in women who were on a low-protein diet to reduce body weight.

The QT interval may be prolonged when using therapeutic doses of a number of drugs, in particular quinidine, procainamide, and phenothiazine derivatives. Prolongation of the electrical systole of the ventricles can be observed during poisoning with drugs and substances that have a cardiotoxic effect and slow down the processes of repolarization. For example, pachycarpine in toxic doses, a number of alkaloids that block the active transport of ions into the myocardial cell, and also have a ganglion-blocking effect. There are also known cases of prolongation of the QT interval in case of poisoning with barbiturates, organophosphate insecticides, and mercury.

Of interest are data on the daily rhythms of QT dispersion obtained from Holter ECG monitoring. A significant increase in the dispersion of the QT interval was found at night and in the early morning hours, which may increase the risk of sudden death at this time in patients with various cardiovascular diseases (myocardial ischemia and infarction, heart failure, etc.). It is believed that the increase in QT interval dispersion at night and in the morning is associated with increased sympathetic activity at this time of day.

It is common knowledge QT prolongation in acute myocardial ischemia and myocardial infarction . A persistent (more than 5 days) increase in the QT interval, especially when combined with early ventricular extrasystoles, has an unfavorable prognosis. These patients showed a significant (5-6 times) increase in the risk of sudden death.

With the development of acute myocardial ischemia, the dispersion of the QT interval also significantly increases. It has been established that the dispersion of the QT interval increases already in the first hours of acute myocardial infarction. There is no consensus on the magnitude of QT interval dispersion, which is a clear predictor of sudden death in patients with acute myocardial infarction. It has been established that in anterior myocardial infarction, a dispersion of more than 125 ms is a prognostically unfavorable factor, indicating a high risk of death. A number of authors have identified an even more significant increase in QT dispersion during reperfusion (after coronary angioplasty). However, other researchers, on the contrary, found a decrease in QT dispersion during reperfusion in patients with acute myocardial infarction, and an increase in QT dispersion was noted in cases where reperfusion was not achieved. Therefore, some authors recommend using a decrease in QT interval dispersion as a marker of successful reperfusion. In patients with acute myocardial infarction, the circadian rhythm of QT dispersion is also disrupted: it is increased at night and in the morning, which increases the risk of sudden death at this time of day.

Hypersympathicotonia undoubtedly plays a role in the pathogenesis of QT prolongation in acute myocardial infarction, which is why many authors explain the high effectiveness of b-blockers in these patients. In addition, the development of this syndrome is also based on electrolyte disturbances, in particular magnesium deficiency. The results of many studies indicate that up to 90% of patients with acute myocardial infarction have magnesium deficiency . An inverse correlation between the level of magnesium in the blood (serum and erythrocytes) and the QT interval and its dispersion in patients with acute myocardial infarction has also been revealed.

Treatment

First of all, the etiological factors that led to prolongation of the QT interval should be eliminated where possible. For example, you should discontinue or reduce the dose of medications (diuretics, barbiturates, etc.) that may increase the duration or dispersion of the QT interval. Adequate treatment of heart failure, according to international recommendations, and successful surgical treatment of heart defects will also lead to normalization of the QT interval. It is known that in patients with acute myocardial infarction, fibrinolytic therapy reduces the size and dispersion of the QT interval (although not to normal values). Among the groups of drugs that can influence the pathogenesis of this syndrome, two groups should be especially noted - b-blockers And magnesium preparations .

Clinical and etiological classification of prolongation of the QT interval ECG According to clinical manifestations: 1. With attacks of loss of consciousness (dizziness, etc.) 2. Asymptomatic By origin: I. Congenital: 1. Gervell and Lange-Nielsen syndrome 2. Romano-Ward syndrome 3. Sporadic II. Acquired 1. Drug-induced Antiarrhythmic drugs Class I A - quinidine, procainamide, disopyramide Class I C - encainide, flecainide Class III - amiodarone, sotalol, sematilide Other cardiotropic drugs(prenylamine, lyoflazin, probucol Psychotropic drugs(thioridazine, haloperidol) Tricyclic antidepressants Antihistamines(terfenadine, astemizole) Antibiotics(erythromycin, spiramycin, pentamidine, sulfamethoxazole-trimethoprim) Antifungal agents(ketoconazole, fluconazole, itraconazole) Diuretics(except potassium-sparing) 2. Electrolyte disturbances hypokalemia hypocalcemia hypomagnesemia 3. Central nervous system disorders subarachnoid hemorrhage thrombosis trauma embolism tumor infection 4. Heart disease sinus bradycardia, blockade myocarditis myocardial ischemia myocardial infarction mitral valve prolapse cardiopathy 5. Miscellaneous low protein diet chronic alcoholism osteogenic sarcoma lung carcinoma neck surgery familial periodic paralysis scorpion venom Conn's syndrome pheochromacytoma hypothermia vagotomy

Congenital long QT syndrome

Patients with Romano-Ward and Gervell and Lange-Nielsen syndromes require constant use of b-blockers in combination with oral magnesium supplements ( Magnesium orotate 2 tables each 3 times a day). Left-sided stellectomy and removal of the 4th and 5th thoracic ganglia may be recommended for patients who have failed pharmacological therapy. There are reports of successful combination of treatment with b-blockers with implantation of an artificial cardiac pacemaker.

For patients requiring emergency treatment, the drug of choice is propranolol intravenously (at a rate of 1 mg/min, maximum dose - 20 mg, average dose - 5-10 mg under the control of blood pressure and heart rate) or bolus intravenous administration of 5 mg of propranolol against the background of intravenous drip administration of magnesium sulfate (Cormagnesina) (at the rate of 1-2 g of magnesium sulfate (200-400 mg of magnesium) depending on body weight (in 100 ml of 5% glucose solution for 30 minutes).

In patients with idiopathic mitral valve prolapse, treatment should begin with the use of oral magnesium preparations (Magnerot 2 tablets 3 times a day for at least 6 months), since tissue magnesium deficiency is considered one of the main pathophysiological mechanisms of the formation of QT interval prolongation syndrome, and “weakness” of connective tissue. In these individuals, after treatment with magnesium preparations, not only does the QT interval normalize, but also the depth of prolapse of the mitral valve leaflets, the frequency of ventricular extrasystoles, and the severity of clinical manifestations (vegetative dystonia syndrome, hemorrhagic symptoms, etc.) decrease. If treatment with oral magnesium supplements after 6 months has not had a complete effect, the addition of b-blockers is indicated.

Acquired long QT syndrome

All drugs that can prolong the QT interval should be discontinued. Correction of serum electrolytes is necessary, especially potassium, calcium, magnesium. In some cases, this is sufficient to normalize the size and dispersion of the QT interval and prevent ventricular arrhythmias.

In acute myocardial infarction, fibrinolytic therapy and beta-blockers reduce the amount of QT interval dispersion. These appointments, according to international recommendations, are mandatory for all patients with acute myocardial infarction, taking into account standard indications and contraindications.

However, even with adequate management of patients with acute myocardial infarction, in a considerable part of them the value and dispersion of the QT interval do not reach normal values, therefore, the risk of sudden death remains. Therefore, the question of the effectiveness of the use of magnesium preparations in the acute stage of myocardial infarction is being actively studied. The duration, dosage and methods of administration of magnesium preparations in these patients have not been fully established. The following regimens are available: intravenous administration Cormagnesina-400 at the rate of 0.5-0.6 g of magnesium per 1 hour during the first 1-3 days, followed by switching to oral administration of Magnerot (2 tablets 3 times for at least 4-12 weeks). There is evidence that in patients with acute myocardial infarction who received such therapy, normalization of the value and dispersion of the QT interval and the frequency of ventricular arrhythmias were noted.

When stopping ventricular tachyarrhythmias in patients with acquired forms of prolongation of the QT interval, it is also recommended to add intravenous drip administration of Cormagnesin to the treatment regimen at the rate of 2-4 g of magnesium sulfate (400-800 mg of magnesium) in 100 ml of 5% glucose solution for 30 minutes. If necessary, it can be re-administered.

Conclusion

Thus, prolongation of the QT interval is a predictor of fatal arrhythmias and sudden cardiogenic death both in patients with cardiovascular diseases (including acute myocardial infarction) and in individuals with idiopathic ventricular tachyarrhythmias. Timely diagnosis of QT prolongation and its dispersion, including with Holter ECG monitoring and stress testing, will allow us to identify a group of patients with an increased risk of developing ventricular arrhythmias, syncope and sudden death. Effective means of preventing and treating ventricular arrhythmias in patients with congenital and acquired forms of long QT interval syndrome are b-blockers in combination with magnesium preparations.

Magnesium orotate -

Magnerot (trade name)

(Worwag Pharma)

Literature:

1. Shilov A.M., Melnik M.V., Sanodze I.D. Diagnosis, prevention and treatment of long QT interval syndrome. // Methodological recommendations - Moscow, 2001 - 28 p.

2. Stepura O.B., Melnik O.O., Shekhter A.B., Pak L.S., Martynov A.I. Results of the use of magnesium salt of orotic acid “Magnerot” in the treatment of patients with idiopathic mitral valve prolapse. // Russian medical news, 1999, No. 2, pp. 74-76.

3. Makarycheva O.V., Vasilyeva E.Yu., Radzevich A.E., Shpector A.V. Dynamics of QT dispersion in acute myocardial infarction and its prognostic significance // Cardiology - 1998 - No. 7 - P.43-46.

Long QT syndrome is a congenital or acquired pathology, which is manifested by an increase in the duration of the QT interval on the ECG by more than 50 ms from normal for a given heart rate or more than 440 ms.

Classification

1. Congenital long QT syndrome:

1.1. Genetic forms - Romano-Ward and Erwell-Lange-Nielsen syndrome.
1.2. Sporadic forms.

2. Acquired forms of the syndrome:

1.1. Consequences of taking medications - quinidine, procainamide, disopyramide, encainide, flecainide, cordarone, etacizine, propafenone, sotalol and others.
1.2. As a result of metabolic disorders.

1.3. On a low-calorie diet.

1.4. Diseases of the central and autonomic nervous system.
1.5. Diseases of the cardiovascular system - ischemic heart disease, mitral valve prolapse.

Romano-Ward syndrome characterized by a genetically determined combination of a prolonged QT interval and attacks of loss of consciousness.

Erwell-Lange-Nielsen syndrome differs from Romano-Ward syndrome in the presence of congenital deafness.

Etiology

It has been proven that congenital long QT syndrome is a consequence of mutations in the genes encoding potassium or sodium channels of cell membranes, which leads to an increase in the duration of the action potential, and, consequently, the processes of repolarization of the entire myocardium. There are 5 known genetic variants of the syndrome, each of which is responsible for its own genes, localized on different chromosomes. In three out of five cases, QT prolongation is caused by a decrease in the permeability of potassium channels, in one case - by sodium channels, and in one case, the exact mechanism of slowing repolarization remains unknown.

In patients with the congenital form of long QT syndrome, there is widespread damage to the conduction system of the heart (including the SA node) and the working myocardium in combination with damage to the sympathetic ganglia, which gives grounds to classify this condition as a cardioneuropathy.
In the acquired form of long QT syndrome, blockade of the transmembrane ion current is achieved due to the specific action of drugs, the influence of the autonomic nervous system, or electrolyte disorders.

Pathogenesis

In the pathogenesis of the syndrome, great importance is attached to the development of an imbalance of the sympathetic innervation of the heart. Let us recall that the innervation of the sinoatrial node is carried out by the right, and the atrioventricular node by the left sympathetic nerves. The ventricular myocardium has bilateral sympathetic innervation. In patients with a prolonged QT interval, the tone of the right-sided innervation of the heart decreases and the activity of the left-sided ganglia increases. As a result, an asymmetry of the innervation of the heart is formed, which leads to the appearance of dispersion of repolarization or the occurrence of late post-depolarizations. The change in the speed of transmembrane currents, which occurs as a result of disruption of the structure of ion channels, increases the sensitivity of individual cells to the presence of afterdepolarizations that previously did not reach the threshold level. In patients with slow ventricular repolarization (long QT syndrome), this provokes electrical instability of the myocardium with the development of ventricular tachycardia and ventricular fibrillation.

Clinic

Long QT syndrome is characterized by a combination of a virtually asymptomatic course and sudden death, which can occur against the background of complete health or periodic cases of loss of consciousness.

The most characteristic clinical sign of this disease is the presence of syncope. The duration of loss of consciousness during an attack is usually 1-2 minutes, but can reach 20 minutes. In some patients, the analogues of syncope include sudden weakness, darkening of the eyes, palpitations and chest pain. Syncope, leading to ischemia of the central nervous system, in some cases is accompanied by convulsions and can imitate an epileptic seizure, therefore such patients are often observed by neurologists with a diagnosis of epilepsy. Sometimes an increase in the duration of the QT interval on the ECG is combined with congenital deafness, and attacks of loss of consciousness in these patients are mistakenly associated with vestibular disorders.

Currently, there are four clinical variants of the syndrome:

1. A combination of syncope and prolongation of the QT interval more than 440 ms.

2. Isolated prolongation of the QT interval more than 440 ms without a history of syncope.

3. Syncope in the absence of QT prolongation.

4. Latent form - normal duration of the QT interval, sudden death during the first syncope.

On the ECG during attacks, ventricular tachycardia is most often recorded. Life-threatening is posed by bidirectional fusiform ventricular tachycardia of the "pirouette" type, which is often the result of the proarrhythmic effect of antiarrhythmic drugs. Cases of sudden death are usually associated with the transformation of ventricular tachycardia into ventricular fibrillation, which can occur either during the first attack of arrhythmia or as a result of repeated frequent episodes of ventricular tachycardia.

Diagnostics

A number of major and minor criteria have been proposed for the diagnosis of congenital long QT syndrome.

Major criteria include

Prolongation of the QT interval more than 440 ms,

Syncope,

Cases of QT prolongation in the family.

Among the small criteria -

Congenital deafness

T wave alternation

Bradycardia and disturbance of the processes of repolarization of the ventricular myocardium.

Long QT syndrome is diagnosed if the patient has two major or one major and two minor criteria.

To diagnose the disease, daily ECG monitoring is indicated, during which it is possible to identify:

1. Periods of severe rigid bradycardia associated with damage to the sinus node and the autonomic nervous system.

2. Change (alternation) in the morphology of the T wave.

3. Disturbance of repolarization processes in the ventricular myocardium (repolarization dispersion, T wave inversion).

4. Episodes of ventricular extrasystole of high gradations.

5. Paroxysms of ventricular tachycardia, including the “pirouette” type.

Forecast

The prognosis of the congenital form of the syndrome is in most cases unfavorable, due to the high likelihood of developing ventricular fibrillation and sudden death. Risk factors for sudden death in Romano-Ward syndrome among adult patients include a history of syncope, female gender, and documented episodes of ventricular fibrillation and torsade de pointes. Polytopic and early ventricular extrasystoles and T wave alternans also have an unfavorable prognostic value.

Treatment

In patients with acquired forms of long QT interval, elimination of etiological factors usually leads to normalization of ECG parameters and the patient's condition. Treatment may consist of discontinuing or reducing the dose of an antiarrhythmic or any other drug that has caused a significant increase in the duration of the QT interval, correction of metabolic disorders, treatment of diseases of the heart or central nervous system.

In patients with congenital long QT syndrome, it is necessary to examine close relatives to identify the syndrome and timely treatment.

Attacks of loss of consciousness are usually provoked by physical exertion or emotional arousal. It should be noted that there is a high incidence of syncope and sudden death in patients with prolonged QT interval during swimming. Therefore, such patients should be advised to limit exercise, including excluding swimming.

The basis of pathogenetic therapy in patients with long QT syndrome is the use of β-blockers. Their action is based on eliminating the imbalance of the autonomic (sympathetic) innervation of the heart and reducing the degree of dispersion of repolarization of the ventricular myocardium. It should be borne in mind that discontinuation of the drug may provoke the occurrence of arrhythmia due to increased sensitivity of β-receptors to the influence of catecholamines against the background of prolonged blockade.

Non-drug treatment methods include removal of the left stellate ganglion, which significantly reduces the incidence of arrhythmia. Considering the fact that life-threatening arrhythmias in patients with long QT syndrome often occur against the background of long pauses before the next sinus impulse, such patients are indicated for implantation of an IVR, which takes on the role of a pacemaker in the event of long pauses in its own rhythm control. To relieve attacks of ventricular tachycardia and ventricular fibrillation, implantation of a cardioverter-defibrillator is indicated.

Problem for students to solve independently

Patient V., 72 years old, was admitted with complaints of dizziness, weakness, and headache.

From the anamnesis it is known that for about 10 years he has been experiencing an increase in blood pressure to a maximum of 150/90 mmHg, accompanied by pain in the left half of the chest; 8 years ago he suffered a myocardial infarction. In subsequent years he suffered from angina pectoris. The real deterioration occurred around 1 month, when I began to notice unmotivated weakness, dizziness, palpitations, followed by “cardiac arrest.” Yesterday, while walking, the patient suddenly became dizzy and briefly lost consciousness. The fainting lasted no more than 10 seconds, according to those accompanying him, and was not accompanied by neurological symptoms. KSP was taken to the cardiology department.

On examination: the condition is satisfactory, consciousness is clear, the position is active. The skin is pale pink, there is no edema or cyanosis. Heart sounds are muffled, the rhythm is correct, heart rate is 45 per minute, blood pressure is 130/80 mm Hg. Vesicular breathing. The abdomen is soft, soft, the liver is not enlarged. Rectal examination: brown stool on the glove.

In general blood test: leukocytes 6.5 * 10 9 / l, erythrocytes 3.4 * 10 / 12 / l, hemoglobin 154 g / l, platelets 290 * 10 / 9 / l ESR 5 mm/h

In a biochemical blood test: cholesterol 7.2 mmol/l, LDL 2.5 mmol/l, HDL 1.4 mmol/l, CK 40 U/l (N), AST 23 U/l, troponin test negative

Stool occult blood test negative

An ECG study was performed:

1. Diagnosis?

2. What diseases of the cardiovascular system are accompanied by the development of MES syndrome?

3. Name the research methods necessary for the differential diagnosis of diseases causing MES syndrome.

4. Symptomatic and radical treatment of this patient.

Literature

1. Ardashev V.N., Steklov V.I. Treatment of heart rhythm disorders.-M.: Medpraktika, 2000.-165p.

2. Cardiac arrhythmias: in 3 volumes / Ed. V.D. Mandela.- M.: Medicine, 1996.

3. Bockeria L.A., Revishvili A.Sh., Ardashev A.V., Kochovich D.Z. Ventricular arrhythmias.-M.: Medpraktika, 2002.-272 p.

4 Gusak V.K., Kuznetsov A.S., Komissarov S.I., Basov O.I. Permanent electrocardiostimulation.-Donetsk: Donechchina, 2000.-225 p.

5. Doshchitsin V.L. Treatment of cardiac arrhythmias.- M., Medicine, 1993.-319 p.

6. Kushakovsky M.S. Cardiac arrhythmias. S.-Pb.: Foliant.-1998.-637 p.

7. Kushakovsky M.S., Zhuravleva N.B. Atlas of electrocardiograms. S.-Pb.: Foliant.-1999.-409 p.

8. Malaya L.T. Heart rhythms.-Kharkov, 1993.-656 p.

9. Atrial fibrillation. /Under the editorship of S.A. Boitsov.-S.-Pb.: Elbi-SPB.-2001.-334 p.

10. Murashko V.V., Strutynsky A.V. Electrocardiography. M.: MEDpress, 2000.-312 p.

11. Orlov V.N. Guide to electrocardiography.-M.: Medicine.-1983.-528 p.

12. Ruksin V.V. Emergency cardiology.-S.-Pb.: Nevsky dialect, 2001.-50

13. Long QT syndrome. /Ed. M.A. Shkolnikova.-M.: Medpraktika, 2001.-127p.

14. Fomina I. G. Emergency therapy in cardiology. Directory - M.: Medicine, 1997. - 256 p.

15. Shubik Yu.V. Daily ECG monitoring for cardiac rhythm and conduction disturbances. - St. Petersburg: Inkart, 2001. - 212 p.

The fact that drug antiarrhythmic therapy does not reduce overall mortality, but partially even leads to an increase in mortality, is due to the risk of a paradoxical increase in arrhythmias - that is, the proarrhythmic effect of Vaughan-Williams class I and III substances.
Indicative results of the CAST study (Cardiac Arrhytmia Suppression Trial), in which, in a comparative assessment, it was strikingly discovered that more post-infarction patients died under the influence of the IC antiarrhythmics Flecainid and Encainid than with placebo, which confirmed the proarrhythmic potential of sodium channel blocking substances.
But also antiarrhythmics acting through blockade of repolarizing potassium channels (class III) carry a risk of ventricular proarrhythmia. With these groups of substances, the prolongation of repolarization caused by early afterdepolarizations and Torsade-de-Pointes tachycardia (TdP) come to the fore.
The SWORD (Survival With Oral d-Sotalol) study was stopped because more new arrhythmias and deaths occurred with d-Sotalol (a pure class III antiarrhythmic without additional beta-blocking activity) in patients with cardiac infarction than with placebo. Even antiarrhythmic therapy with amiodarone in post-infarction patients does not provide benefit compared with placebo in terms of all-cause and cardiac mortality.
For some time, undesirable cardiovascular effects have also been described under certain circumstances of non-antiarrhythmic substances, which partially led to the withdrawal from the market by the manufacturer independently or by order of the government. We will discuss these adverse side effects of non-cardiac substances in more detail later.

QT interval

For ventricular repolarization, the time required can be measured on the ECG as the QT interval. Prolonged repolarization is recognized by prolongation of the QT interval.
Prolongation of the QT interval, on the one hand, can have an antiarrhythmic effect, and on the other hand, favor the onset of early post-repolarizations and is associated with the occurrence of TdP tachycardias, which either stop spontaneously or can lead to sudden cardiac death. Clearly prolongation of the QT time (or frequency corrected QT time (QRc)) is one of the main signs of TdP tachycardias.
QT intervals from 350 to 440 ms (men<430 ms, женщины <450 ms) являются нормальными, потенциально вызывающими озабоченность считаются значения от 450 до 500 ms, повышенный риск аритмий возникает со значений 500 ms.
Along with congenital forms of QT prolongation (with or without deafness), acquired forms play an important clinical role. Along with QT prolongation, an additional increase in QT dispersion, a measure of repolarization heterogeneity, is described.

QT prolongation by antiarrhythmics

QT prolongation and TdP tachycardia are typical side effects of various antiarrhythmics (Table 1). They occur partly in a dose-dependent manner and in the early phase of therapy.
Predominantly, TdP tachycardias are observed only after conversion of sinus rhythm (during relative bradycardia), and not during atrial flutter. The frequency of such rhythm disturbances ranges from 1% to 8%. Coplen conducted a meta-analysis of a number of randomized trials of quinidine to achieve sinus rhythm after cardioversion of atrial flutter. Quinidine therapy was associated with higher mortality (2.9% vs 0.8% of controls).
Some substances, such as amiodarone and Bepridil, even cause QT prolongation, but rarely TdP. Amiodarone is even used in patients who have developed TdP as a result of other drugs. This is due to the fact that amiodarone blocks not only K+ channels, but also Na+ - and Ca++ channels, as well as beta-adrenergic receptors, and reduces the risk of early post-repolarizations and triggered arrhythmias.

Table 1. QT-extension after antiarrhythmics (mod. Nach Thomas et al.)
Preparation	Mechanism of action
ClassI.A. Chinidin, Disopyramid ( Norpace, Rythmodul), Procainamid*	Na+ channel blockade Prolongation of repolarization
ClassIII N-Acetylprocainamid*, Amiodaron ( Amiobeta, Amiodarex, Amiohexal, Cordarex, Tachydarinetc..), Bretylium*, Sotalol ( Darob, Sotabeta, Sotagamma, Sotalexand d r.)	K+ channel blockade Prolongation of repolarization
ClassIV Bepridil*, Lidoflazin*, Prenylamin*	Calcium channel blockade
*No longer sold in Germany

Using the example of amiodarne, we can also draw attention to another problem. We are talking about the pharmacokinetic aspect. The half-elimination time for amiodarone is 15-100 days (average 30 days); for the active metabolites of desethylamiodarone, an average of 60 days.
Since the Kumulations-steady-state is established after almost 5 half-life values, it is easy to imagine that such substances are very difficult to control. In 27 patients (55.4 + 2.4 years) treated with amiodarone for 1 year, initial QTc values ​​were 453 + 7 ms. Between 9 and 12 months they quickly reached values ​​of 479 + 9 ms. Patient monitoring should appropriately include blood levels and ECG analysis.
The Drug Commission of the German Society of Physicians already pointed out quite early on the danger of QT prolongation with class I and III antiarrhythmics. Also, with regard to the fixed combination of Cordichin (160 mg Chinidin plus 80 mg Verapamil), the risk of developing TdP tachyarrhythmias and ventricular flutter was indicated.

QT prolongation with non-cardiac drugs

Along with Class IA and Class III antiarrhythmics, some other pharmacological drugs that are not considered antiarrhythmics or "cardiac drugs" may also lead to the development of QT prolongation and TdP tachycardias.

Withdrawals from the market
In recent years, some drugs have been withdrawn from both the German and American markets due to severe adverse cardiovascular effects.
Already in early 1998, the antihistamine Terfenadin (Teldane) was recalled in the United States. Astemizol followed in Germany and the USA in 1999, after the first indications of severe arrhythmias and cardiac arrest appeared - mainly in patients with severe liver dysfunction and/or while taking enzyme inhibitors.
In a "Rote-Hand" letter (October 27, 1999), Glaxo Wellcome in Germany and the US called attention to the withdrawal of Grepafloxacin after - although very rarely - it was associated with QT prolongation with a risk of severe arrhythmias (TdP). Also, the antipsychotic Sertindol was withdrawn from the German market due to the risk of severe adverse cardiovascular events (dose-dependent QT prolongation, sudden cardiac death). Sertindol has never been used in the United States.
In April 2000, Janssen withdrew the prokinetic drug Cisaprid from the market after the FDA documented more than 340 reports of cardiac arrhythmias, including 80 deaths. After which the German authorities revoked the approval of cisapride-containing drugs due to severe side effects. Janssen-Cilag protested about this.
In addition, other QT prolonging drugs have been described (Table 2), which have a wide variety of clinical implications. This often involved individual observations, sometimes probands or patients in clinical trials.

Table 2. ElongationQTafter "non-cardiac" drugs
Preparation	Notes
Antipsychotics/neuroleptics
Chlorpromazin (Propaphenin)*	Case description (100 mg/d)
Haloperidol (Haldol, etc.)*	4 mg orally to >100 mg i.v. (case description)
Primozid (Orap)*	Healthy probands (6 mg orally), TdP and fatal arrhythmias in patients
Quetiapin (Seroquel)*	Case description (comedication with the CYP3A4 inhibitor Lovastatin
Thioridazin (Melleril)*	Healthy probands (59 mg orally), overdose (500 mg)
Antidepressive drugs
Desipramin (Pertofran, Petylyl)*	Case description (2.5 mg/kg/d)
Doxepin (Aponal, Doneurin, etc.)*	Clinical study patients (169 mg/d)
Nortriptylin (Nortrilen)*	Case description (0.51 mg/kg/d)
Amitriptylin (Amineurin, Saroten, etc.)	Clinical trial patients. (150-200 mg/d)
Fluoxetin (Fluctin, Fluxet, etc.)	Patients wedge. Research (37 mg/d)
Maprotilin (Deprilept, Ludiomil, etc.)	Case description (patient 69 years old, severe heart failure)
Antihistamines (2nd generation)
Terfenadin (Histedin etc.)*	Healthy probands, patients with cardiovascular diseases (120-360 mg), Case description (combination with enzyme inhibitors), healthy probands (slow metabilizers)
Cetirizin (Alerid, Zyrtec)	Healthy probands (up to 60 mg/d)
Fexofenadin (Telfast)	Healthy probands, patients with allergic rhinitis (180-240 mg/d), description of a case with an attempt at reexposition
Loratadin) Lisino)	Healthy probands (10 mg/d in combination with erythromycin), case report of attempted suicide (300 mg)
Mizolastin (Mizollen, zolium)	Healthy probands (40 mg/d)
Antihistamines (1st generation)
Chlorphenamine (Codicaps, Contac, etc.)
Diphenhydramine (Emesan, etc.)
Hydroxyzin (AN 3 N, Atarax, etc.)
Promethazin (Atosil, Prothazin, etc.)
Macrolide antibiotics
Clarithromycin (Cylinid, Klacid, etc.)*	Case description (1000 mg/d orally)
	Patients (500-1000 mg i.v.) Case description (2000-4000 mg i.v.)
Spiramycin (Rovamycine, Selectomycin)*	Newborns (350,000 IE/kg/d orally
Gyrase inhibitors
Levoflaxin (Tavanic)*	Case description (500 mg/d)
Moxiflocxacin (Avalox)*	Patients in a clinical study (400 mg/d)
Beta-2 adrenergic agonists
Fenoterol (Berotec, Partsisten)*
Salbutamol (Apsomol, Sultanol, etc.)	Patients with mild asthma in a clinical study
Terbutalin (Bricanyl, Contimit, Terbul, etc.)	Patients with mild asthma in a clinical study
Antimalarial
	Patients (1800 mg/d i.v.), healthy probands, patients with hepatitis (10 mg/kg/i.v.)
Halofantrin (Halfan)*	Case description (1000 mg/d orally). Especially in women, high doses should be avoided.
Preparation	Notes
Others
	Patients in clinical trial (phase II), 0.15 mg/kg i.v./d max 60 days
Cyclophosphamide (Endoxan, etc.)*	5 out of 19 patients on high dose therapy
Ketoconazol (Nizoral, Terzolin)*	Healthy probands (400 mg/d orally)
Pentamidin (Pentacarinat)*	HIV-infected patients (4 mg/kg/d) Women in a clinical study in gynecological surgery
Tacrolimus (Prograf)*	Case description (5 mg i.v. daily, 0.25 mg/hour i.v.)
Tiaprid (Tiapridex)	Case description (300 mg/), 76 years old, additionally mild heart failure.
* We found the data to be particularly clinically significant

Antipsychotics
One very carefully conducted comparative study found that patients with schizophrenia who received antipsychotic medication (Chlorpromazin, Thioridazin, Levomepromazin and Haloperidol) at the conventional dosage (n=59) compared with patients not receiving antipsychotic medication (n=5) and with healthy people (n=45), both QTc values ​​and QTc dispersion increased. Ventricular tachycardias, however, were not observed in this study, possibly because other risk factors were absent.
In a recent review, abnormal QTc prolongation (>456 ms) was particularly common in patients over 65 years of age receiving Droperidol or Thioridazine. Thioridazin and Mesoridazin (not commercially available in Germany) have been classified by the FDA and WHO as having a particularly increased risk.
Droperidol intravenously has been primarily used for neuroleptanalgesia. Janssen-Cilag began producing it in 2001. Psychiatric emergency patients who received their psychotics parenterally and often experienced hypokalemia were particularly susceptible.
Conversely, QTc prolongations caused by the atypical antipsychotics Risperidon, Quetiapine or Olanzapine were not significant. Even comedication with enzyme inhibitors, such as Ketoconarazol, Fluvoxamine or Paroxetin, did not have a negative effect.

Antidepressants
Adverse cardiovascular events have been described with various tricyclic antidepressants (Clomidin, Imipramin, Desipramin, Doxepin, Nortriptylin) not only in overdoses, but in some cases also when using normal therapeutic doses. Reports of sudden cardiac death have been noted following Desipramin, Clomipramin, and Imipramin.
A 69-year-old female patient with severe heart failure developed TdP tachycardia (QTc=700 ms) while taking Maprotilin (50 mg/d for several years). In this case, comorbidity definitely played a decisive role. There should be clear indications of the meaning of comorbidity of “cardiovascular disease”.
In contrast, it appears that QT prolongation does not occur after Fluoxetin or after Amitriptylin at recommended dosages. Also, QT prolongation has not yet been described with the use of Citalopram.

Antihistamines
One of the case-controlled studies determined the incidence rates (95% confidentiality interval) of ventricular arrhythmias per 10,000 person/years, for example, for Astemizol 8.5 (2.8-26.5), for Cetrizin 3.6 (0 ,9-14.2), for Loratadin 1.5 (0.2-10.3) and for Terfenadin 1.0 (0.3-3.0). Women appeared to be slightly more susceptible than men, with patients >50 years of age clearly more affected than younger ones.
This risk assessment of the predominantly non-sedating 2nd generation H1 antihistamines has also been shared by other authors. It is necessary to point out especially the dose-dependence of these conditions, since it is with self-medication with antihistamines that the danger is especially great, since patients are “titrated” until the symptoms completely disappear.
The cardiotoxicity of Astemizol appears to be played by its two main metabolites Desmethylastemozol and Norastemizol.
The maternal substance is primarily responsible for cardiac incidents associated with Terfenadine. This is also supported by the fact that cardiotoxicity is enhanced by enzyme inhibitors, for example, macrolide antibiotics or antimycotics. In healthy men and women, it can be demonstrated that QTc values ​​can positively correlate with blood levels of Terfenadine and Loratadine. Blood levels increase with additional administration of the antidepressant drug Nefazodon. The latter is an inhibitor of cytochrome P-450-3A (CYP3A).
Currently, however, the lack of cardiotoxicity of Fexofenadine, a metabolite of Tefenadine, is questioned. In a 67-year-old man, the post-exposure and re-exposure QTc values ​​to Fexofenadine (180 mg/d) were 532 ms. - 512 ms. The baseline values ​​were however slightly prolonged (482-494 ms).
In addition, data from animal experiments and individual clinical observations deserve attention that even classical sedating antihistamines, and, above all, Diphenhydramine and even Hydrozysin in high dosages can induce QT prolongation and abnormal ventricular repolarization. Arrhythmogenic features have also been described for Promethazin, Pheniramin and Chlorphenamine. It is possible that with increased attention, such incidents could be identified and classified more often.

Macrolide antibiotics
Between 1970 and 1996, 346 observations of cardiac arrhythmias associated with erythromycin were reported to the FDA (58% women, 32% men, 10% missing data). In 49 patients, life-threatening arrhythmias (ventricular tachycardias, TdP, ventricular flutter) and death were reported (33). Risk factors were primarily high dosages and intravenous administration.
Erythromycin dose-dependently prolonged the duration of the action potential and decreased the maximum rise of the action potential in Purkinje fibers. These electrophysiological effects are very similar to those of Chinididn.
For Claritromycin, there were two incidents of QT prolongation and TdP as early as 1998. In healthy probands, QT prolongation was significant only in combination with the prokineticum Cisaprid.
In an animal experiment on rats, it was shown that Roxithromycin and Azithromycin were clearly less likely to provoke arrhythmias than erythromycin or clarithromycin. For this reason, Roxithromycin should be preferred in therapy.

Gyrase inhibitors
Of the new fluoroquinolones, Glaxo Wellcome's Grepafloxacin was withdrawn from the market due to the development of TdP. There have also been reports regarding Sparfloxacin and Moxifloxacin. Zagam was no longer listed in the Roten Liste 2002.
Also with regard to Moxifloxacin (Avalox), the manufacturer clearly indicates limitations of use and contraindications; Doses of 400 mg/d should not be exceeded. Comedication with other proarrhythmic drugs should not occur. Use is not recommended in patients with electrolyte disturbances and/or bradycardia.
There are separate descriptions of cardiac arrhythmias with the use of Ofloxacin, Levofloxacin and Enoxacin. The approval for the use of Clinafloxicin was withdrawn by the manufacturers Gödecke (or Parke-Davis) due to significant side effects, including QT prolongation.

Beta-2 adrenergic receptor agonists
An epidemic of asthma deaths in Japan was reported in the 1960s in association with Isoprenalin forte. 10 years later the same phenomenon was noted in connection with Fenoterol (200 mg per aerosol burst) in New Zealand, in Sasktchewan (Canada) and in Japan. The mechanisms of this association are not well known. However, cardiovascular effects cannot be excluded.
In a double-blind cross-over study, the effects of Fenoterol, Salbutamol and Terbutalin were compared with placebo on 8 patients with asthma. A pronounced dose-dependent prolongation of QT values ​​was detected with the use of Fenoterol. There was a slightly smaller, but obvious, prolongation of QTc when using the highest doses of Salbutamol and Terbutalin. There was a decrease in plasma potassium levels in almost the same proportions.
With restrained use of inhaled beta-agonists, such problems could be resolved in the future. The attitude of health officials towards this phenomenon varies from country to country. Fenoterol is not approved in the US.

Halofantin
21 healthy probands received 500 mg Halofantin daily for 42 days and were followed for a further 138 days. The average half-life was 7 + 5 days. It was possible to demonstrate a clear concentration-dependent prolongation of QTc intervals.

Cyclophosphamide, Ketoconazol
High doses (1400 mg/m2 for 4 days) of Cyclophosphamide caused prolongation of QT-dispersion values ​​(43.2-83.2 ms) in some patients; in this case, acute failure of the left heart then occurred. It is possible that these incidents mainly occur when additional anthracycline-related cardiac damage is at play.
Also, Ketoconazol (200 mg 12 hours for 5 days), an antimycotic, caused small but significant prolongations of QTc values ​​in healthy probands.

Vasodilatatoren
Also previously used as vasodilators, substances such as Lidoflazin, Prenylamin, Bepridil, now excluded from sale in Germany, have a dose-dependent class-1A effect, which was of particular clinical importance for elderly patients and could cause TdP tachycardias.

Serotonin antagonists
Also, during treatment with the serotonin antagonists Ketanserin and Zimedin, apparent prolongation of QT time and TdP tachycardia have been described; and almost always in the presence of additional favorable factors (hypokalemia, bradycardia). Both substances are not sold in Germany. Zimedin was abandoned worldwide in 1983.

Risk factors for QT prolongation and TdP

Gender dependent
In general, women are at higher risk for QT prolongation and TdP than men (Table 3).

Table 3 Congenital and acquired forms of alteredQT
Gender dependent Women have a greater risk of QT changes and the occurrence of Torsades de Pointes, clearly dependent on the menstrual cycle
Congenital forms* Romano-Ward-Syndrome Jervell-Lange-Nielsen-Syndrome (with inner ear deafness)
Acquired forms
Electrolyte disturbances	Hypokalemia, hypomagnesemia, hypocalcemia
Metabolic disorders	Hypothyroidism, hyperparathyroidism, hyperaldosteronism, pheochromocytoma, diabetes (autonomic neuropathy)
Central nervous system disorders	Intracranial, subarachnoid hemorrhages, acute sinus thrombosis, encephalitis, head injuries
Cardiac disorders	Myocarditis, cardiac tumor, high degree AV block, sinus node dysfunction, clinically significant bradycardia (<50 el|vby/)
Eating disorders	Fasting, liquid protein diet
* Ion channel diseases with cardiac arrhythmias

Of the 346 erythromycin-related arrhythmias, 58% occurred in women and 32% in men (10% had missing data). This effect was confirmed in isolated rabbit hearts perfused with erythromycin.
This effect has now been described again in relation to Chinidin. Among the participating probands, in any case, women already had higher baseline QTc values ​​(407 = 7 ms) than men (395 + 9 ms), Chinidin-induced prolongations ranged from 42 + 3 ms to 29 + 3 ms.
Using experimentally induced (antiarrhythmic Ibutilid 0.003 mg/kg i.v. 10 min.) QT prolongations in women, it was possible to show that the greatest changes were determined during the first half of the menstrual cycle (follicle maturation/proliferation phase).

Sudden death in childhood
There are indications that prolongation of the QT interval in newborns at 1 week of life is clearly associated with “sudden infant death syndrome”. Routine ECG screening of newborns, however, is not yet recommended.

Electrolyte changes
Electrolyte disturbances, whether drug-induced (eg, diuretics), or as concomitant diseases such as metabolic disorders, central nervous system disease, cardiac disease, and nutritional disorders, may favor the occurrence of TdP tachycardias. QTc prolongation secondary to pseudohypoparathyroidism-induced hypocalcemia was recently described in a 12-year-old girl.
It should be recalled that hypokalemia can be caused by diuretics (Thiazid, Furosemid), Amphotericin B i.v., corticosteroids and Laxanzien abuse. Hypomagnesiumemia known as "soft-water-factor". Causes can be varied, such as geographical areas with "soft water", phosphate-poor plant foods, modern cooking methods, phosphate-containing drinks such as cola, excessive sweating (sports, sauna), diseases and many medications.

Bradycardia
Bradycardias favoring the onset of early afterdepolarizations can, among other things, be caused by cardiac glycosides or beta-receptor blockers. Also, in bradycardias enhanced by antiarrhythmics (sinus bradycardia or AV block) and after His bundle ablation in patients with pre-intervention tachycardial superconducting atrial flutter, TdP tachycardias are described.

Overdose of drugs
Since toxic side effects occur depending on the dose, drug overdoses are always associated with special risks. The reasons for this are manifold: completely careless erroneous overdose by a doctor or patient, overdose of drugs as a result of underestimation when setting the dose of limited function of the kidneys, liver and/or thyroid gland. In old age, the often reduced volume of distribution plays a special role.
It may also be important that for many substances there are slow and fast metabolizers. Poor metabolizers are most at risk. In relation to the Cytochrome P-450 isoenzyme, among people of the Caucasian race there are 5-8% of slow excretors.
Drug interactions
In the early 90s, it became obvious that terfenadine-containing drugs are contraindicated not only in patients with severe liver dysfunction, but also the simultaneous use of other drugs, for example, Ketoconazol or the macrolide antibiotics erythromycin, Josamycin, Troleandomycin, which may be associated with a high risk life-threatening ventricular rhythm disturbances. Subsequently, relevant findings were again described, for example, QTc prolongation in healthy probands when Cisaprid was combined with Clarithromycin was significantly more intense than when using either substance separately.
Enzyme inhibitors include various macrolide antibiotics, primarily Erythromycin, Clarithromicin and Troleandomycin (and vice versa, not Rqxithromycin, Rulid), Chloramphenicol, Ciprofloxacin, Azol-Antmycotica, for example Fluvoxamin, Fluoxetin, HIV protease inhibitors, for example, Indinavir, Nelfinavir, Ritonavir , Saquinavir, an H2 receptor antagonist (but not Famotidin), and the HMG-CoA reductase inhibitor Lovastatin, which inhibits the CYP3A4 isoenzyme; here Pravastatin could be an alternative.
There is increasing interest in the fact that grapefruit juice inhibits the metabolism of many substances metabolized by CYP3A4, such as Dihydropyridine calcium antagonists, Cyclosporin, Midazolam, Triazolam, Terfenadin and Amiodaron. Complications may also develop.

Conclusion
If patients develop TdP while on treatment, all suspected medications should be discontinued and all electrolyte abnormalities corrected. If there are no alternative medications, it is necessary to conduct a very careful individual dose selection, taking into account the comorbidity and comedication of patients. The relevant incident must be reported to the pharmacological commission of the German Society of Physicians or to the pharmaceutical industry.