Prolongation of the QT interval when using medications. Cardiotoxicity of drugs

Human health is the main component of a normal and quality life. But we don’t always feel healthy. Problems can arise for various reasons, and their importance may also vary. For example, the common cold does not cause concern among people; it is quickly cured and does not cause much harm to overall health. But if problems arise with internal organs, this is already more life-threatening and worsens our well-being for a long time.

Recently, a lot of people have been complaining about heart problems, and most often these are common diseases that are easy to treat and diagnose. But there are cases when a patient has long QT syndrome. In medicine, this term refers to a pronounced or acquired condition of a person, accompanied by an increase in the duration of a given interval on a segment of the cardiogram. Moreover, only prolongations of more than 55 ms from normal values ​​are attributed to this syndrome. Moreover, when the disease develops, the deviation indicators of this interval can be more than 440 ms.

Manifestations

In most cases, this disease is asymptomatic for the patient himself, and it is almost impossible to detect it on his own. Basically, in people with this diagnosis, the processes of repolarization and depolarization are disrupted, due to changes in symmetrical This can only be noticed during research, based on data from various types of equipment. The main factor causing this condition is electrical instability of the heart muscle.

People with long QT syndrome may develop ventricular tachycardia if there is ineffective or no treatment. These complications are much more dangerous for the lives of patients and are detrimental to the general condition. In this regard, if you suspect the presence of this disease, you should immediately take care of your health, otherwise bad consequences may occur. In addition, the complications of this disease are quite serious. They can lead not only to impaired performance and deterioration of the patient’s general well-being, but also to death.

Species

This deviation has been studied in medicine for a long time, and over the years scientists have been able to learn more and more about it. This disease is divided into two types, namely acquired and congenital long QT syndrome. It is possible to determine which type a patient has only through research. With a congenital disorder, there is a problem with the failure of the genetic code. When acquired, the development of the disease can be influenced by various factors.

Forms

There are also certain types of disease progression:

• Hidden form. It is characterized by normal interval values ​​during examination, and the first attack of syncope causes sudden death.
• Syncope occurs, but the QT interval is not prolonged during testing.
• The prolongation of the interval is isolated and is not reflected in the anamnesis.
• Syncope occurs with a prolongation of the QT indicator, exceeding the norm by 440 ms or more.

Reasons

Many factors can influence the development of this disease. For example, it begins to develop due to hereditary diseases, including R-U syndrome. In this case, attacks of loss of consciousness are very common, which actually lead to the development of this disease. And also E-R-L syndrome, if the patient has congenital deafness. Scientists have not yet been able to figure out what causes this combination of symptoms and how exactly it provokes the development of the disease.

Also, gene mutations can cause the development of this disease. This is the most basic cause of congenital disease, but in some cases it does not appear immediately, but only in adulthood, after suffering stress. Typically, it is problems with protein synthesis in sodium and potassium channels that become factors that provoke long QT syndrome. The reason may lie in the side effects of taking certain medications. The greatest threat is posed by strong antibiotics, which the patient may take to treat other diseases.

The disease can be caused by metabolic disorders or diets aimed at reducing calories in food. Exhaustion of the body in such situations can affect not only the heart. Therefore, it is better to coordinate such diets with a doctor and constantly be under his supervision. Exhaustion can lead to complications of certain cardiovascular diseases, such as coronary disease or the syndrome sometimes develops due to pathologies of the central nervous system and with vegetative-vascular dystonia, as well as other disorders of the autonomic nervous system.

Symptoms

There are specific signs that indicate that the patient has long QT syndrome. The symptoms of this disease are as follows:

• Loss of consciousness lasting from a couple of minutes to a quarter of an hour. In some cases, an attack can last up to twenty minutes.
• Convulsions during synoptic conditions are similar to epileptic attacks in appearance, but the processes that provoke them are completely different.
• Sudden weakness in the body, accompanied by darkening of the eyes.
• Palpitations even in the absence of physical activity or emotional stress.
• Chest pain of various types, continuing during an accelerated heartbeat, as well as accompanying fainting or dizziness and numbness of the arms and legs.

Diagnostics

Very often, long QT syndrome, in children especially, occurs without symptoms. In such a situation, the patient may feel completely healthy and suddenly die. Therefore, if a person is at risk of the disease, it is necessary to be regularly examined by a doctor to exclude the possibility of developing the disease. To diagnose the disease, modern medicine uses several methods.

If there is a suspicion that a patient has long QT syndrome and health problems clearly indicate this, then electrocardiography is the most important test to determine the disease. Carrying it out during an attack, the device will show signs of ventricular tachycardia, turning into ventricular fibrillation. This method is the main one in determining the form of the disease.

There is also another test that can look for long QT syndrome. It is carried out throughout the day. Therefore, it is called 24-hour monitoring and allows you to record the patient’s cardiac activity during this period. A small device is attached to his body, which records the readings of the heart, and after it is removed, the specialist deciphers the data recorded by the device. They make it possible to determine whether the patient has severe rigid bradycardia, whether the morphology of the T wave is changing, and whether there are disturbances in the processes of myocardial repolarization and ventricular extrasystole.

Treatment

If a patient has been diagnosed with long QT interval syndrome, treatment must be comprehensive and adequate, because this is the only way to prevent the development of complications that are dangerous to health and can be fatal.

Drug therapy

The disease can be cured using antiarrhythmic drugs. A properly selected course of medication will not only eliminate the symptoms of this disease, but will also stabilize the functioning of the cardiovascular system for a long period. This is one of the methods to cure congenital long QT syndrome LQTS.

Surgical treatment

If a patient is at risk of life-threatening illness due to arrhythmia in this disease, experts recommend implantation of a pacemaker. Its job is to normalize the contraction frequency of the heart muscle. Modern medicine has developed special devices that detect pathological abnormalities in the functioning of the heart. The disease can be caused externally. During physical activity, for example, the device will not respond. But if the impulses are pathological in nature, it normalizes the functioning of the organ.

Surgery for a disease such as long QT syndrome is simple and quite safe. The pacemaker is attached to the left of the pectoralis major muscle. Electrodes come from it, which surgeons attach to the required area, passing them through the subclavian vein. The device can be configured using a programmer. With its help, you can change the parameters of cardiac stimulation, depending on the personal characteristics of the patient. The device will turn on every time the work of the heart muscle goes beyond the specified parameters.

Conclusion

This disease cannot always be diagnosed, since it rarely manifests itself clearly. But at the same time, the threat to the patient’s health is very great. Therefore, if there is even a slight risk of its occurrence, it is worth constantly undergoing examinations and consulting with specialists.

If the diagnosis is confirmed, then comprehensive and complete treatment of this disease is necessary, because it can be fatal.

Introduction

Hereditary long QT syndrome(LQT, in the English literature - Long QT syndrome - LQTS or LQT) is the most common and best studied of these diseases, manifested by prolongation of the QT interval on the ECG [in the absence of other causes causing this change], recurrent syncope and presyncope due to TdP paroxysms, as well as cases of sudden cardiovascular death.

Epidemiology

The prevalence of the disease in the population is about 1:2000 newborns. It should be noted that these data take into account only cases of “obvious” increase in the duration of the QT interval identified during ECG registration. In some patients, symptoms of the disease may be completely absent throughout life and appear only when additional factors occur that contribute to prolongation of the QT interval, such as hypokalemia, or when medications are prescribed that can prolong the QT interval. In addition, QT prolongation may be transient, so the true prevalence of this disease in the population is likely to be even greater.

Etiology

The main cause of ASUQT is dysfunction of ion channels and pumps, leading to an increase in the duration of the repolarization phases of cardiomyocytes. Impaired function of ion channels can be caused by mutations in the genes of the main pore-forming α-subunits, additional subunits that regulate their function, carrier proteins necessary for transporting molecules, as well as auxiliary proteins that mediate the “incorporation” of molecules into biological membranes and interaction with cellular membranes. structures.

Classification and clinical manifestations

IN table 1 a genetic classification of long QT interval syndrome is presented: genes in which mutations are found in the corresponding types of disease, proteins encoded by these genes and changes in ionic currents leading to prolongation of repolarization phases are indicated. It should be noted that when conducting molecular genetic screening of patients with SUIQT, in approximately 25% of cases, genetic disorders are not detected, which allows us to expect the further identification of new genetic mutations leading to the onset of the disease.
Table 1. Molecular genetic types of hereditary long QT syndrome

The following phenotypic forms of long QT syndrome have been described: Romano-Ward syndrome, Jervell and Lange-Nielsen syndrome, Andresen-Tawil syndrome, and Timothy syndrome.
The most common form of the disease with an autosomal dominant mode of inheritance is Romano-Ward syndrome, the characteristic clinical manifestations of which are an increase in the duration of the QT interval, recurrent syncope, most often caused by polymorphic ventricular tachycardia (VT) of the torsade de pointes type, and a hereditary pattern diseases. More than 90% of cases of Romano-Ward syndrome are represented by ASUQT of the 1st (ASUQT1), 2nd (ASUQT2) and 3rd (ASUQT3) types, which have features of clinical and electrocardiographic manifestations (Table 2, Fig. 1).
Table 2. Clinical characteristics of the main types of hereditary long QT syndrome.

Rice. 1. ECG changes in various types of hereditary long QT syndrome: (A) - wide smooth T wave with QT1 AIS; (B) - biphasic T-wave with SUIQT2; (B) - low-amplitude and shortened T-wave with an elongated, horizontal ST segment in SUIQT3.
AISQT1 is the most common type of syndrome, caused by a mutation in the KCNQ1 gene, which encodes the α-subunit of the potassium channel that generates the IKs current, which is the main repolarization current at high heart rates. A decrease in the strength of IKs leads to insufficient shortening of the QT interval as the heart rate increases. For these reasons, patients with SUIQT1 are characterized by the occurrence of TdP against the background of physical activity (Fig. 2) and emotional stress. A feature of the ECG in SUIQT1 is an elongated and smooth T wave (see Fig. 1A).

Rice. 2. Development of paroxysm of polymorphic ventricular tachycardia of the Torsade de Pointes type against the background of physical activity in a patient with Romano-Ward syndrome (a fragment of a continuous recording of 24-hour Holter ECG monitoring).
The cause of AISQT2 is a mutation in the KCNH2 gene, which encodes the α-subunit of the Kv11.1 potassium channel, which generates the IKr current. In AISQT2, TdP paroxysms can occur both during exercise and at rest. A characteristic provoking factor is a sharp loud sound. On the ECG of patients with SUIQT2, a short, biphasic T wave is recorded (see Fig. 1B).
SUIQT3 is a less common form of the disease caused by a mutation in the SCN5A gene, encoding the α-subunit of the sodium channel, which leads to impaired inactivation of sodium channels, continued entry of Na + ions into the cell and an increase in the duration of repolarization of cardiomyocytes. TdP in patients with SUIQT3 occurs against the background of bradycardia, mainly during sleep. Physical activity, on the contrary, is well tolerated and is accompanied by a shortening of the QT interval. A characteristic feature of the ECG in these patients is a prolonged ST segment with a delayed onset of a short, low-amplitude T wave (see Fig. 1B).
Much less common is the autosomal recessive form of the disease (Jervell and Lange-Nielsen syndrome), which is characterized by congenital sensorineural hearing loss, a more pronounced increase in the duration of the QT interval and a higher frequency of life-threatening ventricular arrhythmias. The disease is caused by mutations in the KCNQ1 or KCNE2 genes, encoding the main and accessory subunits of voltage-gated potassium channels Kv7.1, leading to a decrease in the current strength of IKs.
Andersen–Tawil syndrome is a rare form of the disease in which prolongation of the QT interval is accompanied by the appearance of a U wave, paroxysms of both polymorphic ventricular tachycardia of the TdP type and bidirectional ventricular tachycardia. In 60% of cases, the disease is caused by a mutation in the KCNJ2 gene, encoding the α-subunit of the abnormal inward rectifying potassium channels Kir2.1, generating a current IK1, the strength of which decreases. In 40% of cases, the genetic defect cannot currently be detected. Characteristic extracardiac manifestations of the disease, such as anomalies in the development of the skeletal system (short stature, micrognathia, large distance between the orbits, low position of the ears, scoliosis, clinodactyly), hypokalemia and periodic potassium-dependent paralysis, are not present in all patients. Andersen–Tawil syndrome is a disease with an autosomal dominant type of inheritance, but the familial nature of the disease is not always traceable due to diagnostic difficulties, nonspecific clinical manifestations of the disease and incomplete penetrance of mutant genes. Up to 50% of cases are caused by de novo mutation
Timothy syndrome is an extremely rare form of AISQT caused by a mutation in the CACNA1c gene, encoding the α-subunit of calcium channels CaV1.2. With this syndrome, the most pronounced prolongation of the QT and QTc intervals (up to 700 ms) is noted, accompanied by an extremely high risk of sudden cardiovascular death (average life expectancy is 2.5 years). Up to 60% of patients have various congenital heart defects [patent ductus arteriosus, tetralogy of Fallot, patent foramen ovale and ventricular septal defects] and various conduction disorders (characterized by transient and permanent forms of 2nd degree AV block with conduction to the ventricles 2:1). Among the extracardiac manifestations of the disease, cognitive impairment (retarded psychomotor development, autism), hypoglycemia, immunodeficiencies, abnormalities of the facial structure (smoothness of the nasolabial fold, low position of the ears), as well as partial or complete fusion of the fingers and toes (syndactyly) are described. Timothy syndrome is inherited in an autosomal dominant manner, but the vast majority of cases are caused by a de novo mutation.

Diagnostics

Criteria used for diagnosing hereditary AISQT proposed by J.P. Schwarz, are presented in table. 3.Table 3. Diagnostic criteria for hereditary long QT syndrome (as amended in 2006).


Hereditary AISQT is diagnosed if the total score is ≥3.5, in the presence of a mutation confirmed by molecular genetic methods, leading to an increase in the duration of the QT interval, with repeated registration on the ECG of a prolongation of the QTc interval ≥600 ms in the absence of other causes of prolongation of the QT interval .
The diagnosis of hereditary AISQT can also be made by repeated recording of an ECG prolongation of the QTc interval to 480–499 ms in patients with syncope of unknown origin, in the absence of a genetic mutation and other causes of prolongation of the QT interval.
Molecular genetic diagnostic methods are of great importance in diagnosing SUIQT and determining the prognosis of patients. When conducting complex genetic tests, mutations can be detected in approximately 75% of patients, so a negative result of a genetic test does not completely exclude the diagnosis of SUIQT.
Conducting a comprehensive genetic analysis to identify possible mutations in the KCNQ1 KCNH2 and SCN5A genes (QTS types 1, 2 and 3 are the most common forms of the disease) is recommended for all patients with clinical manifestations of QTS, a strong family history and prolongation of the QTc interval recorded on an ECG at rest or during provocative diagnostic tests, as well as in all patients who do not have characteristic QT symptoms, when an ECG prolongation of the QTc interval >500 ms is recorded in the absence of other possible causes of prolongation of the QT interval.
Carrying out a comprehensive genetic analysis to identify possible mutations in the KCNQ1, KCNH2 and SCN5A genes may be meaningful in patients who do not have characteristic AIS QT symptoms when an ECG prolongation of the QTc interval >480 ms is recorded in the absence of other possible causes of prolongation of the QT interval.
If a genetic mutation is detected in a patient with SUIQT, screening aimed at identifying this mutation is recommended for all close relatives, even if they do not have clinical manifestations or ECG changes characteristic of this disease.
Since the prolongation of the QT interval can be transient, long-term ECG recording is important in diagnosing the disease (for example, daily Holter ECG monitoring; this method is especially informative in patients with QTQT types 2 and 3, since patients with these forms of the disease have the greatest increase duration of the QT interval is usually noted at night) and provocative tests.
In order to ensure patient safety and increase diagnostic value, there are a number of requirements that must be taken into account when conducting these diagnostic studies. Since during research it is possible to induce life-threatening cardiac arrhythmias, all provocative tests should be carried out by experienced medical personnel with continuous ECG recording (ECG monitoring should be carried out until the ECG changes induced during the study are completely normalized; when conducting pharmacological provocative tests - for at least 30 minutes after completion of drug administration) and systematic measurement of the patient’s blood pressure, in conditions of immediate availability of the equipment necessary for cardiopulmonary resuscitation [including a defibrillator] and the possibility of immediately calling a resuscitator. Stress tests should be carried out by physically trained personnel who are able to protect the patient from falling in the event of hemodynamic collapse during induction of ventricular arrhythmias.
Provocative tests do not always cause ECG changes typical for a particular disease. Borderline changes should not be considered diagnostically significant. In the case of borderline ECG changes or a negative test result with a high probability of disease (characteristic clinical picture, results of genetic studies), it is advisable to conduct another provocative test.
To detect SUIQT, the following provocative tests are used.

• Active orthostatic test. Assessing the dynamics of the QT interval when recording an ECG during an orthostatic test has diagnostic significance, allowing in some cases to identify patients with ASQT. After moving to a vertical position, there is a moderate increase in sinus rhythm frequency, while in healthy patients the duration of the QT interval decreases, and in patients with ADS (especially type 2), the duration of the QT interval decreases less significantly, does not change or increases.
• Test with dosed physical activity on a bicycle ergometer or treadmill. The most informative assessment is the duration of the QT interval during the recovery period. The duration of the QTc interval >445 ms at the end of the recovery period (4 minutes after the end of the load) is typical for patients with type 1 and 2 SUIQT. In this case, the duration of the QTc interval<460 мс в начале периода восстановления позволяет отличить больных СУИQT 2-го типа от больных СУИQT 1-го типа.

Pharmacological provocative tests.

• Test with adrenaline (epinephrine). Allows us to identify patients with QT1 SUI, since in this form of the disease, during an adrenaline infusion, a paradoxical increase in the duration of the QT interval is noted. Two protocols have been proposed for this test: the Shimizu protocol, during which a bolus injection is followed by a short-term infusion of adrenaline, and the Mayo protocol, according to which an intravenous infusion of a gradually increasing dose of adrenaline is carried out. Both protocols have comparable sensitivity and specificity, are well tolerated, and are rarely associated with adverse reactions. The test is regarded as positive if the duration of the QT interval increases >30 ms against the background of an infusion of adrenaline at a dose of up to 0.1 mcg/kg per minute. It should be noted that correct measurement of QT duration during epinephrine infusion is often complicated by changes in the morphology of T waves, especially if high-amplitude U waves are recorded. Concomitant use of β-blockers reduces the diagnostic value of the test. Among the adverse reactions that occur during adrenaline infusion, it is necessary to mention arterial hypertension and the induction of life-threatening rhythm disturbances. Diagnostic testing should be stopped if systolic blood pressure increases >200 mm Hg. (or at lower values ​​in cases where arterial hypertension is accompanied by severe clinical manifestations), the occurrence of recurrent unstable runs or the induction of sustained paroxysm of VT. In case of clinically significant undesirable effects, it is advisable to use short-acting β-blockers administered intravenously.
• Test with adenosine. Patients with AISQT are characterized by an increase in the duration of the QT intervals >410 ms and QTc >490 ms, recorded during the minimum heart rate during adenosine-induced bradycardia. Currently, the diagnostic significance of this test has been studied in a limited number of patients with genetically confirmed SUIQT, so the interpretation of the results obtained during the study requires caution.

Differential diagnosis

SUIQT should be differentiated from other possible causes of syncope, taking into account the relatively young age of patients, primarily from epilepsy and vasovagal syncope, as well as from other congenital ventricular heart rhythm disorders.It is necessary to carry out differential diagnosis between congenital and acquired forms of AISQT, which can be caused by a number of factors leading to a slowdown in the processes of repolarization of the ventricular myocardium. These include:

• bradycardia caused by sinus node dysfunction or AV block;
• taking medications (list of drugs that prolong the QT interval).

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

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

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

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

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

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

In pathogenesis congenital QT syndrome Mutations of genes encoding ion channel proteins play a role, leading to insufficient activity of potassium channels or increased activity of sodium channels. Long QT syndrome may occur in the form of Jervell-Lange-Nielsen syndrome and Romano-Ward syndrome.

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

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

The first clinical manifestations of congenital QT syndrome appear in childhood. Repeated episodes of fainting are typical, appearing against a background of sympathicotonia, for example, when the child cries, experiences stress or screams.

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

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

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

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

Long QT syndrome (Romano-Ward syndrome).
Heart rate is 90 beats per minute, QT duration is 0.42 s, the relative duration of the QT interval is 128%, the corrected QTC interval is prolonged and equal to 0.49 s.

II. Acquired long QT syndrome

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

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

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

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

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

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Long QT syndrome

ROZA KHADIEVNA ARSENTIEVA, functional diagnostics doctor at the Center for Psychophysiological Diagnostics of the Medical and Sanitary Unit of the Ministry of Internal Affairs of the Russian Federation for the Republic of Tatarstan, e-mail: [email protected]

Abstract. This article highlights the current state of the problem of congenital and acquired long QT syndrome. Information is presented on its prevalence, etiology, pathogenesis, diagnostic methods, clinical picture, and possible ways to prevent life-threatening complications.

Key words: long QT syndrome.

long QT siNDRoME

R.K.H. ARSENTYEVA

Abstract. This article describes the current state of congenital and acquired Long QT syndrome problem. Provided the information about its prevalence, etiology, pathogeny, diagnostic methods, clinical picture and possible prophylaxis ways.

Key words: long QT syndrome.

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 interval prolongation are predictors of fatal rhythm disturbances, which, in turn, lead to sudden death of patients. The QT interval is the distance from the beginning of the QRS complex to the end of the T wave. From the point of view of electrophysiology, it reflects the sum of the processes of depolarization (electrical excitation with a change in cell charge) and subsequent repolarization (restoration of electrical charge) of the ventricular myocardium.

This parameter is often called electrical systole of the heart (Figure). The most important factor determining the duration of the QT interval is heart rate. The dependence is nonlinear and inversely proportional.

The history of the discovery of LQTS dates back to 1856, when T. Meissner described the sudden death of a young man during emotional stress, in whose family two other children died under similar circumstances. Only 100 years later, in 1957, A. Jervell and F. Lange-Nielsen presented a complete clinical description of LQTS in four members of one family, where all suffered from congenital deafness, frequent loss of consciousness and had persistent prolongation of the QT interval on the ECG. Soon C. Romano (1963) and

O. Ward (1964) presented an observation of a similar syndrome, but without congenital deafness. LQTS with high frequency

occurs in persons with paroxysmal conditions, and in children with congenital deafness - in 0.8%. When examining patients with cardiogenic syncope, LQTS was detected in 36% of cases. Bazett (1920), Fridericia (1920), Neddypn and Hotman (1937) were the first researchers of this phenomenon. NeddPp and Ho^tapp proposed a formula for calculating the proper value of the QT interval: QT=K/RR, where K is the coefficient

Electrical systole of the heart

0.37 for men and 0.40 for women. Since the duration of the QT interval depends on the heart rate (lengthening as it slows down), it must be corrected relative to the heart rate for assessment. The duration of the QT interval is variable both within individuals and across populations. The factors that change its duration are (only the main ones): heart rate (HR); state of the autonomic nervous system; the effect of so-called sympathomimetics (adrenaline, for example); electrolyte balance (especially Ca2+); some medications; age; floor; Times of Day. Long QT syndrome (LQTS) is a prolongation of the QT interval on the ECG, against the background of which paroxysms of ventricular tachycardia of the “pirouette” type occur. In children, the duration of the interval is shorter than in adults. There are tables that present the standards for electrical ventricular systole for a given gender and rhythm frequency. If the patient's QT interval duration exceeds the intervals by more than 0.05 s, then they speak of prolongation of the electrical systole of the ventricles, which is a characteristic sign of cardiosclerosis. The main danger is the frequent transformation of tachycardia into ventricular fibrillation, which often leads to loss of consciousness, asystole and death of the patient.

The most commonly used formulas are Bazett QT QT

QTc(B) = - and Frederic QTc(B) = - ,

where QTc is the corrected (relative to heart rate) value of the QT interval, a relative value; RR is the distance between this QRS complex and the one preceding it, expressed in seconds.

Bazett's formula is not entirely correct. There was a tendency toward over-correction at high heart rates (with tachycardia) and under-correction at low heart rates (with bradycardia). The proper values ​​are in the range of 300-430 for men and 300-450 for women. One of the reliable predictors of SCD can also be an increase in the dispersion of the QT interval (AQT), which is the difference between the maximum and minimum values ​​of the duration of the QT interval in 12 standard ECG leads: AQT = QTmax - QTmin. This term was first proposed by S.R. Day et al. in 1990. If the QT interval reflects the duration of the overall electrical activity of the ventricles, including both depolarization and repolarization, then in the absence of changes in the duration of the ventricular QRS complex, AQT reflects regional heterogeneity of repolarization. The AQT value depends on the number of ECG leads included in the assessment, so excluding several leads from the analysis could potentially affect the result downwards. To eliminate this factor, an indicator such as the normalized dispersion of the QT interval (AQT^, calculated by the formula AQ^ = AQ^ - the number of leads used was proposed. Normally, in healthy individuals in 12 ECG leads, this indicator does not exceed 20-50 ms.

Etiology of elongated syndrome

QT interval

The etiology of LQTS until recently remained unclear, although the presence of this syndrome in non-

how many members of one family allowed almost from the moment of the first description to consider it as a congenital pathology. There are several main hypotheses for the pathogenesis of LQTS. One of them is the hypothesis of a sympathetic imbalance of innervation (a decrease in right-sided sympathetic innervation due to weakness or underdevelopment of the right stellate ganglion and a predominance of left-sided sympathetic influences). The hypothesis of ion channel pathology is of interest. It is known that the processes of depolarization and repolarization in cardiomyocytes arise as a result of the movement of electrolytes into the cell from the extracellular space and back, controlled by the K+, Na+ and Ca2+ channels of the sarcolemma, the energy supply of which is carried out by the Md2+-dependent ATPase. It is believed that all LQTS variants are based on dysfunction of various ion channel proteins. Moreover, the causes of disruption of these processes leading to prolongation of the QT interval can be congenital and acquired. This is often preceded by a short-long-short sequence (SLS): alternation of supraventricular extrasystolia, post-extrasystolic pause and repeated ventricular extrasystoles. There are two most studied pathogenetic mechanisms of arrhythmias in long QT interval syndrome. The first mechanism of intracardiac disorders of myocardial repolarization, namely: increased sensitivity of the myocardium to the arrhythmogenic effect of catecholamines. The second pathophysiological mechanism is an 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 interval prolongation after right-sided stellectomy) and the results of left-sided stellectomy in the treatment of refractory forms of QT interval prolongation. According to the mechanism of development of ventricular tachycardias, all congenital LQTS syndromes are classified into the adrenergic-dependent group (ventricular tachycardia in such patients develops against the background of increased sympathetic tone), while acquired LQTS constitutes a pause-dependent group (ventricular extrasystole, predominantly pirouette, occurs after a change in the R-R interval in the form of SLS -sequences). This division is rather arbitrary, since there is evidence of the presence, for example, of pause-dependent congenital LQTS. Cases have been reported where taking medications leads to the manifestation of previously asymptomatic LQTS.

While Romano-Ward syndrome can result from any of 6 types of mutations, Jervell-Lange-Nielsen syndrome occurs when a child receives mutant genes from both parents. Some mutations cause more severe forms of the disease, while others cause less severe forms of the disease. It has been proven that Romano-Ward syndrome with the homozygous variant is more severe than with the heterozygous one. According to V.K. Gusak et al., of all cases of congenital LQTS, LQT1 accounts for 42%, LQT2 - 45%, LQT3 - 8%, LQT5 - 3%, LQT6 - 2%. It has been established that LQT1 is characterized by a widened T wave, LQT2 is characterized by a low-amplitude and double-humped wave, and LQT3 is characterized by a normal T wave. The longest QT duration s is observed in LQT3. Of interest is the difference in continuation

the duration of the QT interval at night: with LQT1, the QT interval is slightly shortened, with LQT2 it is slightly lengthened, with LQT3 it is significantly lengthened. The manifestation of clinical manifestations in LQT1 is most often observed at the age of 9 years, in LQT2 - at 12 years, in LQT3 - at 16 years. Of particular importance is measuring the interval after physical activity. With LQT1, syncope occurs more often during physical activity, and with LQT2 and LQT3 - at rest. Carriers of the LQT2 genes in 46% of cases have tachycardia and syncope induced by sharp sounds.

congenital forms

Congenital forms of long QT interval syndrome are becoming 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-Lange-Nielsen syndrome and Romano-Ward syndrome.

Gervell-Lange-Nielsen syndrome is a rare disease, has an autosomal recessive mode 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 pattern of inheritance. 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, paroxysms of supraventricular tachycardia were recorded in almost 30% of them, and in approximately every fifth “jog” ventricular tachycardia of the “pirouette” type was registered. To diagnose congenital forms of long QT interval syndrome in the case of borderline prolongation and/or absence of symptoms, a set of diagnostic criteria has been proposed. “Large” criteria are prolongation of the QT interval by 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 that involves more

5 different chromosome 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 people is a combination of this syndrome with mitral valve prolapse. The incidence 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 include weakness of connective tissue, 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 OT 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 OT interval in persons with mitral valve prolapse is genetically predetermined or acquired magnesium deficiency.

Acquired forms

Acquired prolongation of the OT interval can occur with atherosclerotic or post-infarction cardiosclerosis, with cardiomyopathy, against the background and after myo- or pericarditis. An increase in the dispersion of the OT interval (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 OT interval in patients with post-infarction cardiosclerosis: some authors have identified in these patients a clear relationship between the increase in the duration and dispersion of the OT interval (on the ECG) and the risk of developing paroxysms of ventricular tachycardia, other researchers have not found a similar pattern. In cases where in patients with post-infarction cardiosclerosis at rest the dispersion of the WC interval is not increased, this parameter should be assessed during an exercise test. In patients with post-infarction cardiosclerosis, many researchers consider the assessment of WC dispersion against the background of stress tests to be more informative for verifying the risk of ventricular arrhythmias.

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

Autonomic neuropathy also increases the value of the OT interval and its dispersion, therefore these syndromes occur in patients with diabetes mellitus types I and II. Prolongation of the OT interval can occur in case of 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 OT interval with a fatal outcome in women who were on a low-protein diet to reduce body weight. The OT interval can be lengthened 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 in case of poisoning with drugs and substances that have a cardiotoxic effect and slow down

repolarization processes. 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 cases of prolongation of the OT interval due to poisoning with barbiturates, organophosphorus insecticides, and mercury.

Prolongation of WC in acute myocardial ischemia and myocardial infarction is well known. A persistent (more than 5 days) increase in the OT interval, especially when combined with early ventricular extrasystoles, has an unfavorable prognosis. These patients showed a significant (56-fold) increase in the risk of sudden death. With the development of acute myocardial ischemia, the dispersion of the OT interval also significantly increases. It has been established that the dispersion of the OT interval increases already in the first hours of acute myocardial infarction. There is no consensus on the magnitude of the dispersion of the WC interval, which is a clear predictor of sudden death in patients with acute myocardial infarction. It has been established that if during anterior myocardial infarction the dispersion is more than 125 ms, then this is a prognostically unfavorable factor, indicating a high risk of death. In patients with acute myocardial infarction, the circadian rhythm of OT 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. In the pathogenesis of prolongation of OT in acute myocardial infarction, hypersympathicotonia undoubtedly plays a role, which is why many authors explain the high effectiveness of beta-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 red blood cells) with the value of the WC interval and its dispersion in patients with acute myocardial infarction was also revealed. Of interest are data on the daily rhythms of OT dispersion obtained from Holter ECG monitoring. A significant increase in the dispersion of the WC 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 the dispersion of the OT interval at night and in the morning is associated with increased sympathetic activity at this time of day. When it is carried out, along with a permanent or transient prolongation of the OT interval, patients may experience bradycardia during the day and a relative increase in heart rate at night, and a decrease in the circadian index (CI).

Characteristic signs are also prolongation of all parameters of the OT interval; identification of ventricular tachyarrhythmias or short paroxysms of ventricular tachycardia, which are not always manifested by fainting; T wave alternans; rigid circadian heart rate rhythm, often CI less than 1.2; identification of SLS sequence; decreased rhythm concentration function (increased rMSSD); signs of paroxysmal readiness of the heart rhythm (increase by more than 50% in periods of increased dispersion during sleep).

With Holter ECG monitoring, various conduction rhythm disturbances are much more common

are detected in systole-diastolic myocardial dysfunction, and the frequency of their detection is almost 2 times higher than the detection of rhythm disturbances in patients with isolated diastolic myocardial dysfunction. This indicates that rhythm disturbance and QT indicator are one of the criteria for the severity of myocardial dysfunction. Holter ECG monitoring in combination with VEM and everyday physical activity makes it possible to assess coronary reserve in patients with coronary artery disease - a relationship has been identified between prolongation of the QT interval, the degree of damage to the coronary arteries and a decrease in coronary reserve. In patients with less tolerance to physical activity and a more severe form of coronary artery disease, a significant prolongation of the corrected QT interval is observed, especially pronounced against the background of ischemic shift of the ST segment, which may indicate a high risk of fatal arrhythmias. According to modern approaches to assessing Holter ECG monitoring data, the duration of the QT interval should not exceed 400 ms in young children, 460 ms in preschool children, 480 ms in older children, 500 ms in adults.

In 1985, Schwarts proposed the following set of diagnostic criteria for LQTS syndrome, which are still used today:

1. “Large” diagnostic criteria for LQTS: prolongation of the QT interval (QT with more than 0.44 s); history of syncope; presence of LQTS in family members.

2. “Minor” diagnostic criteria for LQTS: congenital sensorineural deafness; episodes of T wave alternans; bradycardia (in children); pathological ventricular repolarization.

The diagnosis can be made if two “major” or one “major” and two “minor” criteria are present. Prolongation of the QT interval can lead to acute arrhythmias and sudden death in alcohol abusers. It is also possible that there may be early nonspecific changes in the ECG of the final part of the ventricular complex with negative dynamics of these changes with the “ethanol” test and the absence of positive dynamics when using a test with nitroglycerin and obsidan. The greatest diagnostic value has the measurement of the duration of the QT interval after the end of physical activity (and not during its implementation).

To date, there is no treatment method that would eliminate the risk of unfavorable outcome in patients with LQTS. At the same time, existing approaches to patient management can eliminate or significantly reduce the frequency of paroxysms of tachycardia and syncope, and reduce mortality by more than 10 times.

Drug treatments can be divided into acute and long-term therapy. The latter is based primarily on the use of p-blockers. The choice of these drugs is based on the theory of specific sympathetic imbalance, which plays a leading role in the pathogenesis of the disease. The preventive effect when using them reaches 80%. First of all, the etiological factors that led to prolongation of the QT interval should be eliminated in cases where this is possible. For example, you should stop or reduce the dose of medications

(diuretics, barbiturates, etc.), which 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: beta-blockers and magnesium drugs.

Clinical and etiological classification

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-Lange-Nielsen syndrome. 2. Romano-Ward syndrome.

3. ^radical. II. Acquired: caused by drugs.

congenital elongation syndrome

QT interval

Patients with Romano-Ward and Ger-vell-Lange-Nielsen syndromes require constant use of β-blockers in combination with oral magnesium supplements (magnesium orotate, 2 tablets 3 times a day). Left-sided stellectomy and removal of the 4th and 5th thoracic ganglia may be recommended in patients who have failed pharmacological therapy. There are reports of successful combination of p-blocker treatment with implantation of an artificial cardiac pacemaker. 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 long QT syndrome -interval, 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 did not have a complete effect; the addition of β-blockers is indicated.

Acquired elongation syndrome

QT interval

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 p-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.

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 cardiac arrhythmias in patients with congenital and acquired forms of long QT interval syndrome are p-blockers in combination with magnesium preparations.

The relevance of long QT syndrome is determined primarily by the proven association with syncope and sudden cardiac death, as indicated by the results of numerous studies, including the recommendations of the European Association of Cardiology. Awareness of this syndrome among pediatricians, cardiologists, neurologists, and family doctors, and the mandatory exclusion of LQTS as one of the causes of syncope will facilitate the diagnosis of the pathology under discussion and the prescription of adequate therapy to prevent an unfavorable outcome.

literature

1. Shilov, A.M. Diagnosis, prevention and treatment of long QT interval syndrome: method. rec. / A.M. Shilov, M.V. Melnik, I.D. Sanodze. - M., 2001. - 28 p. Shilov, A.M. Diagnostika, profilaktika i lechenie sindroma udlineniya QT-intervala: method. recom. / A.M. Shilov, M.V. Mel "nik, I.D. Sanodze. - M., 2001. - 28 s.

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

Stepura, O.B. Rezul"taty primeneniya magnievoi soli orotovoi kisloty "Magnerot" pri lechenii bol"nyh s idiopaticheskim prolapsom mitral"nogo klapana / O.B. Stepura O.O. Mel"nik, A.B. SHehter, L.S. Pak, A.I. Martynov // Rossiiskie medicinskie vesti. - 1999. - No. 2. - S.74-76.

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

Makarycheva, O.V. Dinamika dispersii QT pri ostrom infarkte miocarda i ee prognosticheskoe znachenie / O.V. Makarycheva, E. Yu. Vasil"eva, A.E. Radzevich, A.V. Shpektor // Kardiologiya. - 1998. - No. 7. - S.43-46.

• We pay less attention to the QT interval when other findings predominate on the ECG. But if the only abnormality on the ECG is a long QT interval, there are three common causes to think about:

DRUGS(antiarrhythmic drugs of groups Ia and III, tricyclic antidepressants) Drugs
ELECTROLYTE DISORDERS(hypokalemia, hypomagnesemia, hypocalcemia)
ACUTE CNS PATHOLOGY(extensive cerebral infarction, ICH, SAH and other causes of increased intracranial pressure)

• Hypercalcemia leads to shortening of the QT interval. Hypercalcemia is difficult to recognize on the ECG and begins to manifest itself only with very high serum calcium values ​​(>12 mg/dL).
• Other, less common causes of prolongation of the QT interval are ischemia, myocardial infarction, bundle branch block, hypothermia, alkalosis.
• To measure the QT interval, select the lead in which the end of the T wave is most clearly visible (usually lead II), or the lead in which the QT is longest (V2-V3).
• Clinically, it is often sufficient to distinguish between normal, borderline, or prolonged QT interval.
• Large U waves should not be included in QT interval measurements.

• Based on Bazett's formula, multipliers were calculated to more easily determine the QT correction to frequency:

1. Multiply by 1,0 at rhythm frequency ~60 beats/min
2. Multiply by 1,1 at rhythm frequency ~75 beats/min
3. Multiply by 1,2 at rhythm frequency ~85 beats/min
4. Multiply by 1,3 at rhythm frequency ~100 beats/min

The Bazett formula is the most commonly used because of its simplicity. Beyond the rhythm frequency of 60-100 beats/min, more accurate formulas are the Fredericia and Framingham formulas.

• If the ECG shows a rhythm frequency of 60 beats/min, no interval correction is required, QT=QTc.
• Normal QTc values ​​in men< 440ms, women< 460ms. Аномально короткий интервал QTc < 350 ms.
• QTc interval > 500 ms is associated with increased risk of developing potentially life-threatening torsade de pointes (Torsades de Pointes).A QTc interval > 600 ms is very dangerous and requires not only correction of provoking factors, but also active treatment methods.

• PAY ATTENTION! By eye, a normal QT should be less than half the previous RR interval(but this is only true for a rhythm frequency of 60-100 beats/min) .

• In the absence of a patient's baseline ECG to measure the QT interval, it is impossible to determine the rhythm of polymorphic ventricular tachycardia (PMVT) from Torsades de Pointes (which is PVT with a prolonged QT interval) and therefore they should be treated the same - aimed at shortening the QT interval .

• The longest QT interval occurs after the QRS that ends the compensatory pause after a ventricular extrasystole.
• If the QRS duration is more than 120 ms, this excess should be excluded from the QT interval measurement (that is, QT=QT-(QRS width-120 ms).