Acquired long qt interval syndrome. Prolongation of the QT interval with the use of medications. Cardiotoxicity of drugs. Possibilities of DNA diagnostics in Russia

ECG analysis is not always an easy task even for experienced doctors. What can we say about novice doctors, because they need to decipher the ECG with such violations, which were sometimes mentioned in textbooks only in a few words.

Nevertheless, the ECG signs of some diseases, and even more so their clinical manifestations, need to be known to a doctor of any specialty, since in the absence of treatment they can lead to sudden death of the patient. Such a disease is long QT syndrome.

What is the QT interval responsible for?

Each contraction of the atria and ventricles of the heart, providing a cardiac cycle, is reflected on the electrocardiogram. So, the P wave on the cardiogram reflects the contraction of the atria, and the QRST complex reflects the contraction of the ventricles. At the same time, the QT interval characterizes atrioventricular conduction, that is, the conduction of an electrical impulse through the connection between the atria and ventricles (via the AV node).

Thus, the QT interval on the ECG characterizes the conduction of an impulse along the Purkinje fibers in the wall of the ventricles, more precisely, the time during which electrical excitation of the myocardium provides systole (contraction) of the ventricles.

Normally, the QT interval is at least 0.36 seconds and not more than 0.44 seconds. Typically, students and doctors use this cheat sheet - on a conventional ECG with a tape speed of 50 mm / sec, each small cell (1 mm of graph paper) corresponds to a time period of 0.02 seconds, and each large cell (including five small ones) corresponds to 0.1 second. In other words, the QT interval should normally be at least three and a half large cells and no more than four and a half large cells.

Due to the fact that the time of the QT interval depends on the heart rate, for a more accurate calculation, the definition of the corrected QT interval is used. For patients with normal heart rate (from 60 to 100 per minute), the Bazett formula is used:

QTс = QT/ √RR,

For patients with bradycardia or tachycardia (heart rate less than 60 or more than 100 per minute, respectively), use the Frederick formula:

QTc = QT/ 3 √RR, where RR is the distance between the R waves of two neighboring complexes.

What is the difference between short and long QT and PQ intervals?

Medical students and patients can sometimes get confused with terminology. To prevent this, it is necessary to clearly understand what the PQ interval is responsible for, and what the QT interval is responsible for, and what is the difference between shortening and lengthening the interval. As already mentioned, analysis of the PQ interval is necessary to assess conduction between the atria and ventricles, and the QT interval is necessary to assess intraventricular conduction.

So, elongation PQ in another way, it can be regarded as, that is, the longer the interval, the longer the impulse is conducted through the atrioventricular connection. With a complete block, hemodynamics can be significantly impaired, accompanied by an extremely low heart rate (less than 20-30 per minute), as well as low cardiac output, insufficient to ensure blood flow to the brain.

PQ interval shortening (more) means a decrease in the time of impulse conduction through the atrioventricular connection - the shorter the interval, the faster the impulse passes, and in the normal rhythm of heart contractions there is a constant “reset” of impulses from the atria to the ventricles. More often, this phenomenon is characteristic of Clerk-Levy-Christesco syndrome (CLC syndrome) and Wolff-Parkinson-White syndrome (). The latter syndromes are also fraught with the risk of developing paroxysmal ventricular tachycardias with a heart rate of more than 200 per minute.

QT interval prolongation reflects an increase in the time of conduction of excitation through the ventricles, but such a delay in the impulse leads to the emergence of prerequisites for the formation of the re-entry mechanism (the mechanism for re-entry of the excitation wave), that is, for the repeated circulation of the impulse in the same pathological focus. Such a center of impulse circulation (hyper-impulsation) is capable of provoking paroxysm.

QT shortening characteristic of the rapid conduction of the impulse through the ventricles, again with the occurrence of paroxysmal and ventricular tachycardia. For the first time this syndrome (Short QTS) was described in 2000, and its prevalence among the population is still poorly understood.

Causes of a Long QT Interval

The causes of this disease are currently well understood. There are two forms of long QT syndrome - due to congenital and acquired factors.

congenital form is a rare pathology (about 1 case per 10 thousand newborns) and, as a rule, is combined with congenital deafness. It is caused by genetic changes in the structure of genes encoding the corresponding proteins on the membranes of cardiomyocytes. In this regard, the permeability of the membrane changes, contributing to the change in cell contractility. As a result, electrical excitation is carried out more slowly than normal - there is a re-circulation of the pulse in the focus.

The genetically determined form of long QT syndrome, combined with congenital deaf-mutism, is called Jervell-Lange-Nielsen syndrome, and the form that is not accompanied by deaf-mutism is called Roman-Ward syndrome.

Acquired form of long QT interval may be due to side effects used for the basic therapy of other arrhythmias - atrial fibrillation, atrial flutter, etc. Quinidine and sotalol (sotalex, sotahexal and other trade names) usually have arrhythmogenic side effects. In addition to taking antiarrhythmics, the occurrence of a prolonged QT interval can occur with, intracranial hemorrhages, alcohol poisoning, and also with.

How is long QT syndrome clinically manifested?

The symptomatology of the congenital form of the syndrome begins to manifest itself in childhood. If the child was born deaf and dumb, the doctor already has the right to suspect Jervell-Lange-Nielsen syndrome. If the child hears well and is able to make sounds (cooing, speech), but he has episodes of loss of consciousness, you need to think about the Roman-Ward syndrome. Loss of consciousness can be observed during screaming, crying, stress or during physical exertion. Usually, fainting is accompanied by a rapid pulse (more than 150-200 per minute) and a feeling of rapid heartbeat - the heart flutters in the chest. Episodes of fainting can occur rarely or up to several times a day.

As they get older, these symptoms persist if left untreated, and can lead to sudden cardiac death.

The clinical manifestations of the acquired form are also characterized by syncope with tachycardia, and in the interictal period there is dizziness, general weakness and fatigue due to sinus bradycardia (pulse less than 50 per minute).

Long QT Diagnosis

To clarify the diagnosis, a standard ECG is sufficient. Even in the absence of paroxysm of ventricular tachycardia on the cardiogram, one can see signs characteristic of the syndrome. These include:

• Prolongation of the QT interval from the beginning of the Q wave to the end of the T wave.
• Very high heart rate (150-200 or more) with wide, deformed QRST complexes with paroxysmal ventricular tachycardia.
• Sinus bradycardia in the interictal period.
• Negative or flattened T wave, as well as depression of the ST segment.

Long QT Syndrome Treatment

The tactics of treating congenital forms of the disease implies the appointment of drug therapy, and in the absence of the effect of treatment -.

Medical therapy consists in taking beta-blockers (metoprolol, bisoprolol, nebivalol, etc.) according to the age dosage, which can prevent paroxysms of ventricular tachycardia. If there is resistance to the therapy, the patient is shown installation of a stimulator, which has the function . That is, the pacemaker detects the onset of ventricular tachycardia and, by electrically “rebooting” the heart, helps to maintain a normal heart rate and adequate cardiac output.

A cardioverter-defibrillator requires an annual examination by an arrhythmologist and a cardiac surgeon, but in general it can remain operational for several years, perfectly preventing paroxysms of ventricular tachycardia. Thanks to the pacemaker, the risk of sudden cardiac death is minimized, and the patient, whether a child or an adult, can perform normal household activities without fear of losing consciousness or dying.

With the acquired form, it is quite enough discontinuation of an antiarrhythmic with correction of antiarrhythmic therapy with other drugs.

Complications and prognosis

Of the complications of this syndrome, of course, it should be noted sudden cardiac death caused by ventricular tachycardia, which turned into followed by asystole (cardiac arrest).

According to the research, the prognosis of this syndrome without treatment is unfavorable, since long QT syndrome causes the development of sudden cardiac death in 30% of all cases. That is why this syndrome requires close attention of cardiologists and arrhythmologists, since in the absence of the effect of ongoing drug therapy, the only method that can prolong the life of a child with a congenital form of the syndrome is the implantation of a pacemaker. When it is installed, the prognosis for life and health becomes favorable, since life expectancy increases significantly, and its quality improves.

Video: about long QT syndrome

July 20, 2018 No comments

Long QT syndrome is a congenital disorder characterized by prolongation of the QT interval on the electrocardiogram (ECG) and a tendency to ventricular tachycardia, which can lead to syncope, cardiac arrest, or sudden cardiac death (SCD). See image below.

The QT interval on the ECG, measured from the beginning of the QRS complex to the end of the T wave, represents the duration of activation and recovery of the ventricular myocardium. A heart rate-adjusted QT interval greater than 0.44 seconds is generally considered abnormal, although a normal QTc may be longer in women (up to 0.46 seconds). The Bazett formula is the formula most commonly used to calculate QTc, as follows: QTc = QT / square root of the R-R interval (in seconds).

To accurately measure the QT interval, the relationship between QT and R-R interval must be reproducible. This issue is especially important when the heart rate is below 50 beats per minute (bpm) or over 120 bpm, and when athletes or children have marked R-R variability. In such cases, long ECG recordings and multiple measurements are required. The longest QT interval is usually seen in the right atrial leads. When a marked change is present in the R-R interval (atrial fibrillation, ectopia), QT interval correction is difficult to pinpoint.

Signs and symptoms

Long QT syndrome is usually diagnosed after a person has a fainting spell or a heart attack. In some situations, this condition is diagnosed after the sudden death of a family member. In some people, the diagnosis is made when the ECG shows a prolongation of the QT interval.

Diagnostics

Physical examination results do not usually indicate a diagnosis of long QT syndrome, but some people may have excessive bradycardia for their age, and some patients may have hearing loss (congenital deafness), suggesting the possibility of Jervell and Lange-Nielsen syndrome. Skeletal abnormalities such as short stature and scoliosis are seen in Andersen's syndrome. Congenital heart defects, cognitive and behavioral problems, musculoskeletal disorders, and immune dysfunction may be seen in Timothy syndrome.

Research

Diagnostic tests in people with suspected syndrome include the following:

• Measurement of the level of potassium and magnesium in serum;
• Study of thyroid function;
• Pharmacological provocative tests with epinephrine or isoproterenol;
• Electrocardiography of the patient and family members;
• Genetic testing of the patient and family members.

A prolonged corrected QT interval in response to a standing test, which is associated with increased sympathetic tone, may provide more diagnostic information in patients with the syndrome. This increase in QT as a result of standing may persist even after the heart rate returns to normal.

Treatment

No treatment can eliminate the cause of long QT syndrome. Antiadrenergic therapeutic measures (eg, use of beta-blockers, left-sided cerucotracal stellectomy) and device therapy (eg, use of pacemakers, implantable cardioverter defibrillators) are aimed at reducing the risk and mortality of heart attacks.

Medical

Beta-adrenergic blocking agents are drugs that may be prescribed to treat the syndrome and include the following drugs:

• Nadolol
• propranolol
• metoprolol
• Atenolol

That being said, Nadolol is the preferred beta-blocker, which should be used at a dose of 1-1.5 mg/kg/day (once a day for patients over 12 years of age, twice a day for younger people).

Surgery

Surgery for people with long QT syndrome may include the following procedures:

Implantation of cardioverter-defibrillators

Placement of the pacemaker

Left cervicothoracic stellectomy

People who have the syndrome should avoid participating in competitive sports, doing heavy physical exercise, and try not to avoid emotional stress.

In addition, the following drugs should also be avoided:

Anesthetics or asthma medications (such as adrenaline)

Antihistamines (eg, diphenhydramine, terfenadine, and astemizole)

Antibiotics (eg, erythromycin, trimethoprim and sulfamethoxazole, pentamidine)

Cardiac drugs (eg, quinidine, procainamide, disopyramide, sotalol, probucol, bepridil, dofetilide, ibutilide)

Gastrointestinal drugs (eg, cisapride)

Antifungals (eg, ketoconazole, fluconazole, itraconazole)

Psychotropic drugs (eg, tricyclic antidepressants, phenothiazine derivatives, butyrophenones, benzisoxazole, diphenylbutylpiperidine)

Potassium-losing medications (eg, indapamide, other diuretics, vomiting/diarrhea medications)

Causes

The QT interval represents the duration of activation and recovery of the ventricular myocardium. Prolonged recovery from electrical stimulation increases the likelihood of dispersive refractoriness, where parts of the myocardium may be immune to subsequent depolarization.

From a physiological point of view, dispersion occurs during repolarization between the three layers of the heart, and the phase of repolarization tends to increase in the middle myocardium. This is why the T-wave is usually wide and the Tpeak-Tend (Tp-e) interval represents the transmural dispersion of repolarization. With prolonged QT syndrome, it increases and creates a functional opportunity for transmural re-initiation.

Hypokalemia, hypocalcemia, and the use of loop diuretics are risk factors for QT prolongation.

The syndrome is divided into two clinical variants - Romano-Ward syndrome (familial origin with autosomal dominant inheritance, QT prolongation and ventricular tachycardias) or Jervell and Lang-Nielsen syndrome (familial origin with autosomal recessive inheritance, congenital deafness, QT prolongation and ventricular arrhythmias). Two other syndromes have been described: Andersen's syndrome and Timothy's syndrome, although there is some debate among scientists about whether these should be included in long QT syndrome.

Tachyarrhythmia

QT prolongation can lead to polymorphic ventricular tachycardia, which itself can lead to ventricular fibrillation and sudden cardiac death. It is widely believed that Torsade de pointes is activated by reactivation of calcium channels, reactivation of delayed sodium current, or a decrease in chamber current that leads to early post-depolarization, in a state of increased transmural dispersion of repolarization, usually associated with a prolonged QT interval, serves as a functional auxiliary substrate to maintain tachycardia.

The transmural dispersion of repolarization not only provides a substrate for the reentry mechanism, but also increases the likelihood of early post-depolarization, the trigger event for tachyarrhythmia, by prolonging the time window for calcium channels to remain open. Any additional condition that accelerates calcium channel reactivation (eg, increased sympathetic tone) increases the risk of early post-depolarization.

Genetics

Long QT syndrome is known to be caused by mutations in the genes for potassium, sodium, or calcium cardiac channels; at least 10 genes have been identified. Based on this genetic background, 6 types of Romano-Ward syndrome, type 1 Andersen syndrome and type 1 Timothy syndrome and 2 types of Jervell-Lange-Nielsen syndrome are characterized.

The syndrome is the result of mutations in genes encoding cardiac ion channel proteins that cause abnormal ion channel kinetics. The shortened opening of the potassium channel in type 1, type 2, type 5, type 6, type 1 and type 1 Jervell-Lange-Nielsen syndrome and the delayed closure of the sodium channel in type 3 syndrome recharges the myocardial cell with positive ions.

In people with the syndrome, various adrenergic stimuli, including exercise, emotion, loud noise, and swimming, can accelerate the arrhythmic response. However, arrhythmias can also occur without such prior conditions.

Drug-induced QT interval prolongation

Secondary (drug-induced) prolongation of the QT interval may also increase the risk of ventricular tachyarrhythmias and sudden cardiac death. The ionic mechanism is similar to the ionic mechanism seen in the congenital syndrome (i.e., internal blockade of potassium release).

In addition to drugs that can potentially prolong the QT interval, several other factors play a role in this disorder. Important risk factors for drug-induced QT prolongation are:

Electrolyte disorders (hypokalemia and hypomagnesemia)

Hypothermia

Abnormal thyroid function

Structural heart disease

Bradycardia

Drug QT prolongation may also have a genetic background consisting of an ion channel predisposition to abnormal kinetics caused by a gene mutation or polymorphism. However, there is insufficient evidence to state that all patients with drug-induced QT prolongation have a genetic basis for the syndrome.

Forecast

The prognosis for people suffering from the syndrome is good, which is treated with beta-blockers (and, if necessary, using other therapeutic measures). Fortunately, episodes of torsade de pointes are usually self-limiting in patients with QT syndrome; only about 4-5% of heart attacks are fatal.

People at high risk (i.e., those who have had a cardiac arrest or recurrent heart attacks despite beta-blocker therapy) have a significantly increased risk of sudden cardiac death. For the treatment of such patients, an implantable cardioverter-defibrillator is used; the prognosis after ICD implantation is good.

Mortality, morbidity, and responses to pharmacological treatment vary across different types of syndrome.

Long QT syndrome can lead to syncope, sudden cardiac death, which usually occurs in healthy young people.

Although sudden cardiac death usually occurs in symptomatic patients, it can also occur during the first episode of syncope in about 30% of patients. This emphasizes the importance of diagnosing the syndrome in the presymptomatic period. Depending on the type of mutation present, sudden cardiac death can occur during exercise, emotional stress, rest, or sleep. Type 4 syndrome is associated with paroxysmal atrial fibrillation.

Scientific studies have shown an improved response to pharmacological treatment with a reduced incidence of sudden cardiac death in types 1 and 2 QT syndrome compared to type 3.

Neurological deficits after interrupted cardiac arrest may complicate the clinical course of patients after successful resuscitation.

Video: Long QT Syndrome

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

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

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

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

In individuals with long qt syndrome, this interval is longer than usual, it disrupts the rhythm of the heart, causing arrhythmias.

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

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

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

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

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

Causes and risk factors

Long qt syndrome is often inherited, meaning that it is caused by a mutation in one of 17 genes. Sometimes it is caused by a drug.

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

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

To learn more Signs, treatment and prognosis of the Waterhouse Friederiksen syndrome in meningococcal infection in children

Risk factors

There are various factors that determine a person's risk of having long QT syndrome.

You are at risk if:

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

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

Symptoms

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

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

Diagnostics

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

Some methods used for diagnosis:

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

Electrocardiogram

ECG analyzes the electrical activity of the heart, helps determine the interval. This is done while the person is resting or while doing a stationary exercise. This test is carried out several times, as the electrical activity may change over time.

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

Medical and family history

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

Genetic Results

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

Treatment

The goal of treatment is to prevent arrhythmia and syncope. It may vary among individuals, depending on a previous history of syncope and sudden cardiac arrest, the type of QT syndrome, and family history.
Treatment options:

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Preparations

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

Implantable Devices

Pacemakers or an implantable cardioverter defibrillator (ICD) are small devices that help control your heart rate. They are implanted under the skin of the breast or stomach with a minor procedure.

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

Surgery

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

How to prevent

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

To prevent abnormal heart rhythms, you should:

• Avoid activities that can cause irregular heart rhythms. For example, strenuous exercise such as swimming should be avoided because it causes arrhythmias.
• Drugs that cause arrhythmias should not be given to individuals with long QT syndrome. Ask your doctor for a list of medications to avoid.
• If you have an implanted pacemaker or ICD, be careful when playing sports not to move the device from your location.
• Let the people you meet regularly about your condition so they can help you if there is an emergency.
• See your cardiologist regularly.

• Know your body: keep checking for symptoms, see your doctor if you notice anything unusual.
• Visit your doctor regularly: follow the advice carefully.
• Maintain a healthy lifestyle, avoid smoking, drinking alcohol to avoid the risk of heart disease.
• Reduce sports activities: Avoid or reduce sports activities that cause constant fluctuations in heart rate.
• Medications: Be very careful to avoid drugs that cause long QT syndrome. You must tell all the doctors you see about your condition so that they do not prescribe you drugs that can cause an arrhythmia.

If I have a heartbeat, what does it mean?

Palpitations is the feeling that the heart is beating rapidly. It is not necessarily a symptom of an arrhythmia. If you feel this sensation, check with your cardiologist.

I. N. Limankina

The frequency of negative cardiovascular effects of psychotropic therapy, according to large-scale clinical studies, reaches 75%. The mentally ill have a significantly higher risk of sudden death. So, in a comparative study (Herxheimer A. et Healy D., 2002) a 2-5-fold increase in the frequency of sudden death in patients with schizophrenia was shown in comparison with two other groups (patients with glaucoma and psoriasis). The US Food and Drug Administration (USFDA) has reported a 1.6-1.7-fold increased risk of sudden death with all current antipsychotics (both classic and atypical). One of the predictors of sudden death during psychotropic drug therapy is long QT interval syndrome (QTQS).

The QT interval reflects the electrical systole of the ventricles (time in seconds from the beginning of the QRS complex to the end of the T wave). Its duration depends on gender (QT is longer in women), age (QT lengthens with age) and heart rate (hcc) (inversely proportional). For an objective assessment of the QT interval, the corrected (corrected for heart rate) QT interval (QTc) is currently used, determined by the formulas of Bazett and Frederick:

Normal QTc is 340-450 ms for women and 340-430 ms for men.

It is known that QT SUI is dangerous for the development of fatal ventricular arrhythmias and ventricular fibrillation. The risk of sudden death in congenital SUI QT in the absence of adequate treatment reaches 85%, while 20% of children die within a year after the first loss of consciousness and more than half in the first decade of life.

In the etiopathogenesis of the disease, the leading role is played by mutations in the genes encoding potassium and sodium channels of the heart. Currently, 8 genes have been identified that are responsible for the development of clinical manifestations of SUI QT. In addition, it has been proven that patients with SUI QT have a congenital sympathetic imbalance (asymmetry of the innervation of the heart) with a predominance of left-sided sympathetic innervation.

Genes responsible for the development of SUI QT

The clinical picture of the disease is dominated by attacks of loss of consciousness (syncope), the relationship of which with emotional (anger, fear, sharp sound stimuli) and physical stress (physical activity, swimming, running) emphasizes the important role of the sympathetic nervous system in the pathogenesis of SUI QT.

The duration of loss of consciousness averages 1-2 minutes and in half of the cases is accompanied by epileptiform, tonic-clonic convulsions with involuntary urination and defecation. Since syncope can also occur in other diseases, such patients are often treated as patients with epilepsy, hysteria.

Features of syncope in SUI QT:

As a rule, they occur at the height of psycho-emotional or physical stress.
typical precursors (sudden general weakness, darkening of the eyes, palpitations, heaviness behind the sternum)
fast, without amnesia and drowsiness, recovery of consciousness
lack of personality changes characteristic of patients with epilepsy

Syncopal conditions in SUI QT are due to the development of polymorphic ventricular tachycardia of the "pirouette" type ("torsades de pointes") (TdP). TdP is also called “cardiac ballet”, “chaotic tachycardia”, “ventricular anarchy”, “cardiac storm”, which is essentially a synonym for circulatory arrest. TdP - unstable tachycardia (the total number of QRS complexes during each attack ranges from 6 to 25-100), prone to relapse (in a few seconds or minutes the attack may repeat) and the transition to ventricular fibrillation (refers to life-threatening arrhythmias). Other electrophysiological mechanisms of sudden cardiogenic death in patients with QT SUI include electromechanical dissociation and asystole.
ECG signs of SUI QT.

1 Prolongation of the QT- interval exceeding the norm for a given heart rate by more than 50 ms, regardless of the reasons underlying it, is generally accepted as an unfavorable criterion for electrical myocardial instability.
The Patent Medicines Committee of the European Agency for the Evaluation of Medical Products offers the following interpretation of QTc interval duration

An increase in QTc of 30-60ms in a patient taking new drugs should raise suspicion of a possible drug association. An absolute QTc duration greater than 500ms and a relative increase greater than 60ms should be considered as a threat to TdP.
2. Alternation of the T wave - a change in the shape, polarity, amplitude of the T wave indicates electrical instability of the myocardium.
3. Variance of the QT interval - the difference between the maximum and minimum value of the QT interval in 12 standard ECG leads. QTd = QTmax - QTmin, normally QTd = 20-50ms. An increase in the dispersion of the QT interval indicates the readiness of the myocardium for arrhythmogenesis.
The growing interest in the study of acquired QT SUI over the past 10–15 years has expanded our understanding of external factors, such as various diseases, metabolic disorders, electrolyte imbalance, drug aggression, causing dysfunction of the heart ion channels, similar to congenital mutations in idiopathic QT SMI.

Clinical conditions and diseases closely associated with QT prolongation

According to the data given in the report of the Centers for Disease Control and Prevention (Centers for Disease Control and Prevention) dated March 2, 2001, the incidence of sudden cardiac death among young people is increasing in the United States. It is suggested that among the possible reasons for this increase, drugs play an important role. The volume of drug consumption in economically developed countries is constantly increasing. Pharmaceutics has long become the same business as any other. The pharmaceutical giants spend on average about $800 million just to develop a new product, which is two orders of magnitude higher than in most other areas. There has been a clear negative trend in pharmaceutical companies marketing an increasing number of drugs as status or prestigious (lifestyle drugs). Such drugs are taken not because they are needed for treatment, but because they fit a certain lifestyle. These are Viagra and its competitors Cialis and Levitra; "Xenical" (a means for weight loss), antidepressants, probiotics, antifungal and many other drugs.

Another worrying trend can be described as Disease Mongering. The largest pharmaceutical companies, in order to expand the sales market, convince completely healthy people that they are sick and need medical treatment. The number of imaginary ailments, artificially inflated to the extent of serious diseases, is constantly increasing. Chronic fatigue syndrome (manager's syndrome), menopause as a disease, female sexual dysfunction, immunodeficiency states, iodine deficiency, restless legs syndrome, dysbacteriosis, "new" infectious diseases are becoming brands for increasing sales of antidepressants, immunomodulators, probiotics, hormones.
Independent and uncontrolled drug intake, polypharmacy, unfavorable drug combinations and the need for long-term drug use create prerequisites for the development of SUI QT. Thus, drug-induced prolongation of the QT interval as a predictor of sudden death is acquiring the scale of a serious medical problem.

A variety of drugs of the widest pharmacological groups can lead to prolongation of the QT interval.

Drugs that prolong the QT interval

The list of drugs that prolong the QT interval is constantly updated.

All centrally acting drugs prolong the QT interval, often clinically significant, which is why the problem of drug-induced QT SUI in psychiatry is most acute.

In a series of numerous publications, the relationship between the prescription of antipsychotics (both old, classic and new, atypical) and SUI QT, TdP and sudden death has been proven. In Europe and the US, several neuroleptics were denied or delayed licensing, and others were discontinued. After reports of 13 cases of sudden unexplained death associated with taking pimozide, in 1990 it was decided to limit its daily dose to 20 mg per day and treatment under ECG control. In 1998, after the publication of data on the association of sertindole with 13 cases of serious but not fatal arrhythmia (36 deaths were suspected), Lundbeck voluntarily stopped the sale of the drug for 3 years. In the same year, thioridazine, mesoridazine, and droperidol received a black box warning for QT interval prolongation, and ziprasidone in bold. By the end of 2000, after the death of 21 people due to taking prescribed thioridazine, this drug became a second-line drug in the treatment of schizophrenia. Shortly thereafter, droperidol was withdrawn from the market by its manufacturers. In the United Kingdom, the atypical antipsychotic drug ziprasidone is being delayed because more than 10% of patients taking the drug experience mild QT prolongation.

r /> Of the antidepressants, the cardiotoxic effect is most pronounced in cyclic antidepressants. According to a study of 153 cases of TCA poisoning (of which 75% were due to amitriptyline), a clinically significant prolongation of the QTc interval was observed in 42% of cases.
Of 730 children and adolescents receiving antidepressants at therapeutic doses, prolongation of the QTc interval > 440 ms accompanied treatment with desipramine in 30%, nortriptyline in 17%, imipramine in 16%, amitriptyline in 11% and clomipramine in 11%.

Cases of sudden death, closely associated with QT SUI, have been described in patients receiving tricyclic antidepressants for a long time, incl. with postmortem identification of the “slow-metabolizer” CYP2D6 phenotype due to drug accumulation.

New cyclic and atypical antidepressants are safer in relation to cardiovascular complications, demonstrating prolongation of the QT interval and TdP only when therapeutic doses are exceeded.

Most psychotropic drugs widely used in clinical practice belong to class B (according to W. Haverkamp 2001), i.e. against the background of their use, there is a relatively high risk of TdP.

According to experiments in vitro, in vivo, sectional and clinical studies, anticonvulsants, antipsychotics, anxiolytics, mood stabilizers and antidepressants are able to block fast HERG potassium channels, sodium channels (due to a defect in the SCN5A gene) and L-type calcium channels, thus causing functional insufficiency of all channels of the heart.

In addition, well-known cardiovascular side effects of psychotropic drugs are involved in the formation of QT SUI. Many tranquilizers, antipsychotics, lithium preparations, TCAs reduce myocardial contractility, which in rare cases can lead to the development of congestive heart failure. Cyclic antidepressants are able to accumulate in the heart muscle, where their concentration is 100 times higher than the level in the blood plasma. Many psychotropic drugs are inhibitors of calmodulin, which leads to dysregulation of myocardial protein synthesis, to structural damage to the myocardium and to the development of toxic cardiomyopathy and myocarditis.

It should be recognized that clinically significant prolongation of the QT interval is a formidable but rare complication of psychotropic therapy (8-10% with antipsychotics). Apparently, we are talking about a latent, latent form of congenital SUI QT with clinical manifestations due to drug aggression. An interesting hypothesis is the dose-dependent nature of the effect of the drug on the cardiovascular system, according to which each antipsychotic has its own threshold dose, the excess of which leads to a prolongation of the QT interval. It is believed that for thioridazine it is 10 mg / day, for pimozide - 20 mg / day, for haloperidol - 30 mg / day, for droperidol - 50 mg / day, for chlorpromazine - 2000 mg / day. It has been suggested that QT interval prolongation may also be associated with electrolyte disturbances (hypokalemia).

its meaning and method of drug administration.
The situation is aggravated by the complex comorbid cerebral background of the mentally ill, which in itself is capable of causing QT SUI. It must also be remembered that mentally ill patients receive drugs for years and decades, and the vast majority of psychotropic drugs are metabolized in the liver, with the participation of the cytochrome P450 system.

Cytochrome P450: drugs metabolized by certain isomers (according to Pollock B.G. et al., 1999)

There are 4 statuses of a genetically determined metabolic phenotype:

o extensive (fast) metabolizers (Extensive Metabolizers or fast) - having two active forms of microsomal oxidation enzymes; in therapeutic terms, these are patients of standard therapeutic doses.
o Intermediate Metabolizers - having one active form of the enzyme and, as a result, somewhat reduced drug metabolism
o low metabolizers or slow (Poor Metabolizers or slow) - do not have active forms of enzymes, as a result of which the concentration of the drug in the blood plasma can increase by 5-10 times
o Ultra-extensive Metabolizers - having three or more active forms of enzymes and accelerated drug metabolism

Many psychotropic drugs (especially neuroleptics, phenothiazine derivatives) have a hepatotoxic effect (up to the development of cholestatic jaundice) due to a complex (physicochemical, autoimmune and direct toxic) effect on the liver, which in some cases can be transformed into chronic liver damage with impaired enzymatic metabolism by the type of "poor metabolizing" ("poor" metabolism).

In addition, many neurotropic drugs (sedatives, anticonvulsants, neuroleptics and antidepressants) are inhibitors of microsomal oxidation of the cytochrome P450 system, mainly enzymes 2C9, 2C19, 2D6, 1A2, 3A4, 5, 7.

Drugs that block the CYP 3A4 isoenzyme of the cytochrome P450 system. (A. John Camm, 2002).

Inhibitors 1A

2C9 inhibitors

2C19 inhibitors

2D6 inhibitors

Thus, prerequisites are created for cardiovascular complications with an unchanged dose of a psychotropic drug and with unfavorable drug combinations.
Allocate a group of high individual risk of cardiovascular complications in the treatment of psychotropic drugs.

These are elderly and pediatric patients with concomitant cardiovascular pathology (heart disease, arrhythmias, bradycardia less than 50 beats per minute), with genetic damage to the ion channels of the heart (congenital, including latent, and acquired SUI QT), with electrolyte imbalance (hypokalemia, hypocalcemia, hypomagnesemia, hypozincemia), with a low level of metabolism (“poor”, “slow”-metabolizers), with dysfunction of the autonomic nervous system, with severe impaired liver and kidney function, simultaneously receiving drugs that lengthen the QT interval, and/or inhibiting cytochrome P450. In the study by Reilly (2000), risk factors for prolongation of the QT interval are recognized:

A modern doctor faces difficult tasks of the correct choice of a drug from a huge number of drugs (in Russia it is 17,000 items!) According to the criteria of effectiveness and safety.

Competent monitoring of the QT interval will avoid serious cardiovascular complications of psychotropic therapy.

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LONG QT SYNDROME AND SAFETY ISSUES OF PSYCHOPHARMACOTHERAPY
© Limankina, I. N.
St. Petersburg Psychiatric Hospital No. 1 named after P.P. Kashchenko

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

Long QT interval syndrome is a combination of a prolonged QT interval on a standard ECG and life-threatening polymorphic ventricular tachycardias (torsade de pointes - "pirouette"). 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, not the absolute, but the corrected value of the QT interval (QTc), which is calculated according to the Bazett formula, is used.

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.

Prolongation of the QT interval is diagnosed if the duration of QTc 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 an increased dispersion of the QT interval is also a predictor of the development of a number of serious arrhythmias, including sudden death. The dispersion of the QT interval 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 variance is to record a standard ECG for 3-5 minutes at a recording speed of 25 mm/hour. Holter ECG monitoring is also used, which allows analyzing fluctuations in QTc dispersion (QTcd) during the day. However, a number of methodological aspects of this method are under development. Thus, there is no consensus on the upper limit of the normal values ​​of the dispersion of the corrected QT interval. According to some authors, a QTcd of more than 45 is a predictor of ventricular tachyarrhythymia, other researchers suggest that the upper limit of the normal QTcd is 70 ms and even 125 ms.

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

Etiology of long QT syndrome

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

congenital forms

Congenital forms of QT prolongation syndrome are becoming one of the causes of death in children. Mortality in untreated congenital forms of this syndrome reaches 75%, while 20% of children die 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-mutism with lengthening 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 pattern 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 a prolonged QT interval in children without hearing and speech impairment.

The frequency of detecting a prolonged QT interval in school-age children with congenital deaf-mutism on a standard ECG reaches 44%, while almost half of them (about 43%) had episodes of loss of consciousness and paroxysms of tachycardia. With 24-hour ECG monitoring, almost 30% of them had paroxysms of supraventricular tachycardia, approximately one in five had "runs" of ventricular tachycardia of the "pirouette" type.

A set of diagnostic criteria has been proposed for diagnosing congenital forms of QT syndrome in the case of borderline prolongation and/or absence of symptoms. "Large" criteria are QT prolongation 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. "Small" criteria are congenital sensorineural hearing loss, episodes of T-wave alternation, slow heart rate (in children), and abnormal ventricular repolarization. Significant prolongation of the QT interval, paroxysms of tachycardia torsade de pointes and episodes of syncope are of the greatest diagnostic value.

Congenital long QT syndrome is a genetically heterogeneous disorder 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 frequency of detection of prolongation of the QT interval in individuals with prolapse of the mitral and / or tricuspid valves reaches 33%. According to most researchers, mitral valve prolapse is one of the manifestations of congenital connective tissue dysplasia. Among other manifestations of “weakness of the connective tissue” are increased extensibility of the skin, 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 in the QT interval and the depth of prolapse and/or the presence of structural changes (myxomatous degeneration) of the mitral valve cusps. One of the main reasons for the formation of QT prolongation in individuals with mitral valve prolapse is a 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 and after myo- or pericarditis. An increase in the dispersion of the QT interval (more than 47 ms) may also be a predictor of the development of arrhythmogenic syncope in patients with aortic heart disease.

There is no consensus on the prognostic value of an increase in the dispersion of the QT interval in patients with postinfarction cardiosclerosis: some authors have revealed 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 such a pattern. In cases where in patients with postinfarction cardiosclerosis at rest, the magnitude of the dispersion of the QT interval is not increased, this parameter should be evaluated during an exercise test. In patients with postinfarction cardiosclerosis, the assessment of QT dispersion against the background of exercise 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 in sinus bradycardia, atrioventricular block, chronic cerebrovascular insufficiency and brain tumors. Acute cases of QT prolongation can also occur with trauma (chest, craniocerebral).

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

Prolongation of the QT interval can occur with electrolyte imbalance with hypokalemia, hypocalcemia, hypomagnesemia. Such conditions occur 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 against the background of prolongation of the QT interval with a fatal outcome in women who were on a low-protein diet in order to reduce body weight is described.

The QT interval can be lengthened with the use of therapeutic doses of a number of drugs, in particular, quinidine, novocainamide, phenothiazine derivatives. Elongation of the electrical systole of the ventricles can be observed in case of poisoning with drugs and substances that have a cardiotoxic effect and slow down the repolarization processes. For example, pahikarpin in toxic doses, a number of alkaloids that block the active transport of ions into the myocardial cell, and also have a ganglioblocking effect. There are also cases of prolongation of the QT interval in case of poisoning with barbiturates, organophosphorus insecticides, mercury.

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

It's common knowledge QT prolongation in acute myocardial ischemia and myocardial infarction . Persistent (more than 5 days) increase in the QT interval, especially when combined with early ventricular extrasystoles, is unfavorable prognostically. These patients showed a significant (5-6 times) increased 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 the dispersion of the QT interval, which is a clear predictor of sudden death in patients with acute myocardial infarction. It has been established that in case of 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 revealed an even more significant increase in QT dispersion during reperfusion (after coronary angioplasty). However, other researchers, on the contrary, found a decrease in QT variance during reperfusion in patients with acute myocardial infarction, and an increase in QT variance was noted in cases where reperfusion was not achieved. Therefore, some authors recommend using a decrease in QT variance as a marker of successful reperfusion. In patients with acute myocardial infarction, the circadian rhythm of QT dispersion is also disturbed: it is increased at night and in the morning, which increases the risk of sudden death at this time of day.

In the pathogenesis of QT prolongation in acute myocardial infarction, hypersympathicotonia undoubtedly plays a role, and this is precisely what many authors explain the high effectiveness of b-blockers in these patients. In addition, the development of this syndrome is 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 was also found between the level of magnesium in the blood (serum and erythrocytes) and the QT interval and its dispersion in patients with acute myocardial infarction.

Treatment

First of all, the etiological factors that led to the lengthening of the QT interval should be eliminated in cases where this is possible. For example, medications (diuretics, barbiturates, etc.) that may increase the duration or variance of the QT interval should be discontinued or reduced. 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 magnitude 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 ECG QT interval prolongation According to clinical manifestations: 1. With bouts of loss of consciousness (dizziness, etc.) 2. Asymptomatic 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, novocainamide, 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) Antifungals(ketoconazole, fluconazole, itraconazole) Diuretics(except potassium-sparing) 2. Electrolyte disorders hypokalemia hypocalcemia hypomagnesemia 3. CNS 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 osteosarcoma lung carcinoma neck surgery familial periodic paralysis scorpion venom Conn's syndrome pheochromocytoma hypothermia vagotomy

Congenital long QT syndrome

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

For patients requiring emergency treatment, the drug of choice is propranolol intravenously (at a rate of 1 mg / min, the maximum dose is 20 mg, the average dose is 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 of magnesium sulfate (Kormagnezina) (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 for the formation of both the syndrome of lengthening the QT interval, and "weakness" of the connective tissue. In these individuals, after treatment with magnesium preparations, not only the QT interval normalizes, but also the depth of mitral valve prolapse, the frequency of ventricular extrasystoles, and the severity of clinical manifestations (vegetative dystonia syndrome, hemorrhagic symptoms, etc.) decrease. If treatment with oral magnesium preparations after 6 months has not had a full 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 electrolytes of blood serum is necessary, especially potassium, calcium, magnesium. In some cases, this is sufficient to normalize the magnitude and dispersion of the QT interval and prevent ventricular arrhythmias.

In acute myocardial infarction, fibrinolytic therapy and b-blockers reduce the magnitude of the dispersion of the QT interval. These appointments, according to international recommendations, are mandatory in 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 magnitude 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. Duration, dosages and methods of administration of magnesium preparations in these patients have not been finally established. The following schemes are available: intravenous administration Kormagnezina-400 at the rate of 0.5-0.6 g of magnesium per hour for the first 1-3 days, followed by the transition to oral administration of Magnerot (Table 2, 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 magnitude and dispersion of the QT interval and the frequency of ventricular arrhythmias was noted.

When stopping ventricular tachyarrhythmias in patients with acquired forms of QT interval prolongation, it is also recommended to add an intravenous drip of Kormagnesin 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 reintroduced.

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 ECG Holter monitoring and exercise tests, will allow identifying a group of patients with an increased risk of developing ventricular arrhythmias, syncope, and sudden death. Effective means of prevention and treatment of ventricular arrhythmias in patients with congenital and acquired forms of QT interval prolongation 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. // Guidelines - Moscow, 2001 - 28s.

2. Stepura O.B., Melnik O.O., Shekhter A.B., Pak L.S., Martynov A.I. The 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., Vasil'eva E.Yu., Radzevich A.E., Shpektor A.V. Dynamics of QT dispersion in acute myocardial infarction and its prognostic value // Cardiology - 1998 - No. 7 - P.43-46.