ECG interpretation: QT interval. Prolongation of the QT interval with the use of medications. Drug cardiotoxicity ECG qt prolongation

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

Changes in the structure of ion channels of cardiomyocytes in such cases are minimal, and may remain asymptomatic for a long time. Therefore, a person cannot be aware that some drugs that are widely represented on the pharmaceutical market are dangerous for him. For most people, drug-induced depression of potassium current is mild and does not cause any ECG changes.

However, the combination of genetic features of the structure of potassium channels and drug use can cause clinically significant arrhythmias, up to the development of polymorphic ventricular tachycardia "Torsade des pointes" and sudden death. Therefore, patients who have at least once recorded polymorphic ventricular tachycardia caused by taking any medication are advised to consult a geneticist. In addition, lifelong avoidance of all drugs that lead to prolongation of the QT interval.

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

Genes responsible for the development of long QT syndrome.

Possibilities of DNA diagnostics in Russia

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

Why is it necessary to carry out DNA diagnostics of LQTS?

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

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

   	LQT1, LQT5	LQT2, LQT6	LQT3
   Sensitivity to sympathetic stimulation	+++	+	-
   Circumstances in which PVT is often seen	fright	At rest / in sleep
   Specific factor provoking syncope	Swimming	Harsh sound, postpartum	-
   Limitation of physical activity	+++	+	-
   b-blockers	+++	+	-
   Taking potassium supplements	+?	+++	+?
   Class IB antiarrhythmic drugs (sodium channel blockers)	+	++	+++
   Calcium channel blockers	++	++	+?
   Potassium channel openers (nicorandil)	+	+	-
   THE EX	+	+	+++
   ICD	++	++	+++

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

What to do if a mutation has been identified?

If you or your child has a mutation that confirms the hereditary nature of the disease, you need to remember the following:

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

The size of the QT interval tells little about the average person, but it can tell a doctor a lot about the patient's heart condition. Compliance with the norm of the specified interval is determined on the basis of the analysis of the electrocardiogram (ECG).

Basic elements of an electrical cardiogram

An electrocardiogram is a record of the electrical activity of the heart. This method of assessing the state of the heart muscle has been known for a long time and is widely used because of its safety, accessibility, and information content.

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

An electrical cardiogram consists of three basic elements:

• teeth;
• segments;
• intervals.

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

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

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

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

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

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

Normal interval timeQTis in the range of 0.35-0.44 seconds.

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

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

The output of the duration of the electrical systole of the ventricles beyond 0.35-0.44 seconds gives the doctor reason to talk about the course of pathological processes in the heart.

Long QT Syndrome

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

Congenital form of pathology

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

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

Paroxysm can go away on its own, or it can turn into ventricular fibrillation with sudden death.

An attack is characterized by the following symptoms:

• pale skin;
• rapid breathing;
• convulsions;
• loss of consciousness.

The patient is contraindicated in physical activity. For example, children are exempted from physical education lessons.

Romano-Ward syndrome is treated with medical and surgical methods. With the medical method, the doctor prescribes the maximum acceptable dose of beta-blockers. Surgery is performed to correct the conduction system of the heart or install an cardioverter-defibrillator.

1. Jervell-Lange-Nielsen syndrome. Not as common as the previous syndrome. In this case, there is:

• more marked prolongation of the QT interval;
• an increase in the frequency of attacks of ventricular tachycardia, fraught with death;
• congenital deafness.

Mostly surgical methods of treatment are used.

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

• low growth;
• rachiocampsis;
• low position of the ears;
• abnormally large distance between the eyes;
• underdevelopment of the upper jaw;
• deviations in the development of the fingers.

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

1. Timothy Syndrome. It is extremely rare. In this disease, there is a maximum lengthening of the QT interval. Every six out of ten patients with Timothy's syndrome have various congenital heart defects (tetralogy of Fallot, patent ductus arteriosus, ventricular septal defects). There are a variety of physical and mental anomalies. The average life expectancy is two and a half years.

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

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

1. Taking antiarrhythmic drugs: quinidine, sotalol, aymaline and others.
2. Violation of the electrolyte balance in the body.
3. Alcohol abuse often causes a paroxysm of ventricular tachycardia.
4. A number of cardiovascular diseases cause lengthening of the electrical systole of the ventricles.

Treatment of the acquired form is primarily reduced to the elimination of the causes that caused it.

Short QT Syndrome

It can also be either congenital or acquired.

Congenital form of pathology

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

Symptoms of the disease:

• bouts of atrial fibrillation;
• episodes of ventricular tachycardia.

Study of families of patients with short interval syndromeQTshows that they have experienced sudden death of relatives at a young and even infancy due to atrial and ventricular fibrillation.

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

Acquired form of pathology

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

Therapy in both cases is reduced to the elimination of the causes of the appearance of a short QT interval.

More:

How to decipher the ECG analysis, the norm and deviations, pathologies and the principle of diagnosis

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

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

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

1. multiply by 1,0 at rhythm frequency ~60 bpm
2. multiply by 1,1 at rhythm frequency ~75 bpm
3. multiply by 1,2 at rhythm frequency ~85 bpm
4. multiply by 1,3 at rhythm frequency ~100 bpm

• If the ECG shows a heart rate of 60 bpm, 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 p an increased risk of developing potentially life-threatening torsade de pointes ventricular tachycardia (Torsades de Pointes).The QTc interval > 600 ms is very dangerous and requires not only the correction of provoking factors, but also active methods of treatment.

• NOTE! By eye, normal QT should be less than half of the previous RR interval(but this is true only for a rhythm rate of 60-100 bpm) .

• In the absence of the patient's baseline ECG on which the QT interval was measured, it is impossible to determine the rhythm of polymorphic ventricular tachycardia (PMVT) from Torsades de Pointes torsades tachycardia (which is TOV with a prolonged QT interval) and therefore their treatment should be the same - aimed at shortening the QT interval .

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

Long QT interval syndrome attracts close attention as a factor of sudden cardiovascular death, first described by the French cardiologist Dessertin in 1966. It has been established that both congenital and acquired forms of QT interval prolongation are harbingers of fatal heart rhythm disturbances, which turn lead to sudden death.

Long QT interval syndrome is a combination of a long QT interval on a standard ECG with life-threatening ventricular tachycardias (torsade de pointes - French pirouette). Paroxysms of ventricular tachycardia of the "pirouette" type are clinically manifested by episodes of dizziness, loss of consciousness and may result in ventricular fibrillation and sudden death.

The Q-T interval is the distance from the start of the QRS complex to the end of the T wave on the ECG waveform. 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. The duration of the Q-T interval depends on the heart rate and gender of the person. In normal women, the OT interval is on average slightly longer than in men of the same age. In healthy people at rest, there is only a slight variability in repolarization processes, so the change in the QT interval is minimal. Prolongation of the Q-T interval is diagnosed if the average Q-T duration exceeds 0.44 s.

There are two most studied mechanisms of arrhythmias in long QT syndrome.

• The first is intracardiac disorders of myocardial repolarization, namely, increased sensitivity of the myocardium to the arrhythmogenic effect of adrenaline, norepinephrine and other synthetic adrenomimetics. For example, the fact of Q-T prolongation in acute myocardial ischemia and myocardial infarction is well known.
• The second pathophysiological mechanism is an imbalance of sympathetic innervation (decrease in right-sided sympathetic innervation due to weakness or underdevelopment of the right stellate ganglion) and other genetic anomalies, especially against the background of congenital deafness. The most dangerous thing is that a person may not be aware of the existence of such a pathology for a long time and use drugs and their combinations that affect the Q-T interval.

DRUGS THAT PROLONG THE Q-T INTERVAL

Prolongation of the Q-T interval can occur with such electrolyte disorders as hypokalemia, hypocalcemia, hypomagnesemia. Such conditions occur under the influence of many factors, for example, with long-term use of diuretics, especially loop diuretics (furosemide), as well as strong laxatives. The development of ventricular tachycardia of the "pirouette" type against the background of a lengthening of the QT interval with a fatal outcome in women who were on a low-protein diet for weight loss and took furosemide is described. The Q-T interval can also be lengthened when using therapeutic doses of a number of drugs, in particular quinidine, novocainamide, phenothiazine derivatives, etc. (see table). 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, pachycarpine in toxic doses, a number of alkaloids that block active ion transport (K +, Mg 2+)

HEART AND MEDICINES

Recently, the pharmacovigilance authorities of various countries, including the FDA (USA), Australia and Canada, as well as the domestic State Expert Center, draw the attention of doctors and pharmacists to the risk of developing arrhythmias associated with taking well-known drugs, especially when they are combined with other drugs. drugs that prolong the Q-T interval in the myocardial cell and have a ganglioblocking effect. There are also cases of an extended Q-T interval and fatal arrhythmias in case of poisoning with barbiturates, organophosphorus insecticides and mercury, scorpion stings.

With arrhythmias or their threat, all drugs that can lengthen the Q-T interval should be canceled. Correction of electrolytes of blood serum is necessary, especially potassium, calcium and magnesium. In some cases, this is sufficient to normalize the magnitude and dispersion of the QT interval and prevent ventricular arrhythmias.

DOMPERIDONE AND SUDDEN CARDIAC DEATH

In December 2012, the Australian Health Products Regulatory Agency (TGA) published pharmacoepidemiological studies indicating that the use of domperidone may be associated with a risk of serious ventricular premature beats or sudden cardiac death, especially in patients taking daily doses of the drug. above 30 mg, and persons over 60 years of age. These findings confirmed the warnings of the Canadian pharmacovigilance authorities published in 2007. Therefore, domperidone should be avoided in the presence of cardiac arrhythmias, heart failure, coronary heart disease, myocardial infarction, heart defects, and in the absence of contraindications, start with the lowest dose. Domperidone, despite OTC status, should not be used in children. It is necessary to refuse sharing with inhibitors of CYP3A47, which can increase its level in plasma, such as itraconazole, amprenavir, atazanavir, fosamprenavir, indinavir, nelfinavir, ritonavir, saquinavir, diltiazem, verapamil, aprepitant, etc. In addition, domperidone is contraindicated for simultaneous use with other drugs that prolong the QT interval.

AZITHROMYCIN AND OTHER MACROLIDE ANTIBIOTICS

Also, special care should be taken when prescribing macrolides, in particular azithromycin preparations, available in the form of tablets, capsules, powders for the preparation of oral suspensions and a lyophilisate for injection solutions. The fact is that in relation to azithromycin, back in March 2013, the FDA informed about the risk of developing pathological changes in the electrical conduction of the heart, which can lead to potentially lethal arrhythmias. It must be remembered that the risk group consists of patients with a history of QT interval prolongation, hypokalemia or hypomagnesemia, bradycardia, as well as patients using class IA antiarrhythmic drugs (quinidine, procainamide) and class III (dofetilide, amiodarone, sotalol). Therefore, it is necessary to avoid the combined intake of these drugs with azithromycin and other macrolides in order to avoid the development of potentially dangerous arrhythmias. When choosing an alternative antibiotic therapy for such patients, it should be remembered that other macrolide drugs, as well as fluoroquinolones, can cause a prolongation of the QT interval.

Thus, when prescribing these drugs, it is necessary to ascertain the presence of contraindications and drug incompatibility. Patients taking these drugs who develop heart failure or abnormal heart rate and rhythm (particularly palpitations - tachycardia), dizziness, loss of consciousness or seizures should stop taking all drugs and seek immediate medical attention .

Drugs that can prolong the Q-T interval

Relevance. Lack of awareness of pediatricians, internists and neurologists about this disease often leads to tragic outcomes - sudden death of patients with long QT syndrome (Long-QT syndrome - LQTS). Also, such patients often have an overdiagnosis of epilepsy due to the clinical similarity of syncopal conditions (complicated by "convulsive syndrome"), which are incorrectly interpreted as classic epileptic seizures.

Definition. LQTS - is a prolongation of the QT interval on the ECG (more than 440 ms), against which there are paroxysms of ventricular tachycardia of the "pirouette" type. The main danger lies in the frequent transformation of this tachycardia into ventricular fibrillation, which often leads to loss of consciousness (fainting), asystole and death of the patient (sudden cardiac death [SCD]). Currently, LQTS is classified as a common rhythm disorder.

reference Information. QT interval - the time interval of the electrocardiogram (ECG) from the beginning of the Q wave to the return of the descending knee of the T wave to the isoline, reflecting the processes of depolarization and repolarization of the ventricular myocardium. The QT interval is a generally accepted, and, at the same time, widely discussed indicator that reflects the electrical systole of the ventricles of the heart. It includes the QRS complex (rapid depolarization and initial repolarization of the myocardium of the interventricular septum, the walls of the left and right ventricles), the ST segment (repolarization plateau), the T wave (final repolarization).

The most important factor in determining the length of the QT interval is HR (heart rate). The dependence is non-linear and inversely proportional. The length of the QT interval is variable both in the individual and in populations. Normally, the QT interval is at least 0.36 seconds and not more than 0.44 seconds. Factors that change its duration are: [ 1 ] HR; [ 2 ] state of the autonomic nervous system; [ 3 ] the action of the so-called sympathomimetics (adrenaline); [ 4 ] electrolyte balance (especially Ca2+); [ 5 ] some drugs; [ 6 ] age; [ 7 ] floor; [ 8 ] Times of Day.

Remember! The determination of QT prolongation is based on the correct measurement and interpretation of the QT interval relative to heart rate values. The duration of the QT interval normally varies with heart rate. To calculate (correct) the value of the QT interval, taking into account heart rate (= QTc) use various formulas (Bazett, Fridericia, Hodges, Framingham formula), tables and nomograms.

The prolongation of the QT interval 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 repeated circulation of the impulse in the same pathological focus. Such a center of impulse circulation (hyper-impulsation) can provoke a paroxysm of ventricular tachycardia (VT).

Pathogenesis. There are several main hypotheses for the pathogenesis of LQTS. One of them is the hypothesis of a sympathetic imbalance of innervation (decrease in right-sided sympathetic innervation due to weakness or underdevelopment of the right stellate ganglion and the predominance of left-sided sympathetic influences). The hypothesis of pathology of ion channels is of interest. It is known that the processes of depolarization and repolarization in cardiomyocytes arise due to the movement of electrolytes into the cell from the extracellular space and back, controlled by K+-, Na+- and Ca2+-channels of the sarcolemma, the energy supply of which is carried out by Mg2+-dependent ATPase. All LQTS variants are thought to be based on dysfunction of various ion channel proteins. At the same time, the reasons for the violation of these processes, leading to a lengthening of the QT interval, can be congenital and acquired (see below).

Etiology. It is customary to distinguish between congenital and acquired variants of the LQTS syndrome. The congenital variant is a genetically determined disease that occurs in one case per 3-5 thousand of the population, and from 60 to 70% of all patients are women. According to the International Registry, in about 85% of cases the disease is hereditary, while about 15% of cases are the result of new spontaneous mutations. To date, more than ten genotypes have been identified that determine the presence of different variants of the LQTS syndrome (all of them are associated with mutations in genes encoding the structural units of cardiomyocyte membrane channels) and designated as LQT, but three of them are the most frequent and clinically significant: LQT1, LQT2 and LQT3 .

Secondary etiological factors for LQTS may include drugs (see below), electrolyte disturbances (hypokalemia, hypomagnesemia, hypocalcemia); CNS disorders(subarachnoid hemorrhage, trauma, tumor, thrombosis, embolism, infection); heart disease (slow heart rhythms [sinus bradycardia], myocarditis, ischemia [especially Prinzmetal's angina], myocardial infarction, cardiopathy, mitral valve prolapse - MVP [the most common form of LQTS in young people is the combination of this syndrome with MVP; frequency of detection of prolongation of the QT interval in persons with MVP and / or tricuspid valves reaches 33%]); and other various reasons (low-protein diet, consumption of fatty animal foods, chronic alcoholism, osteogenic sarcoma, lung carcinoma, Kohn's syndrome, pheochromocytoma, diabetes mellitus, hypothermia, neck surgery, vagotomy, familial periodic paralysis, scorpion venom, psycho-emotional stress) . Acquired prolongation of the QT interval is 3 times more common in men and is typical for older people with diseases in which coronarogenic myocardial damage predominates.

Clinic. The most striking clinical manifestations of LQTS, which in most cases are the root cause of contacting a doctor, should include attacks of loss of consciousness, or syncope, which are caused by a life-threatening polymorphic VT specific for LQTS, known as "torsades de pointes" (ventricular tachycardia of the "pirouette" type), or ventricular fibrillation (VF). With the help of ECG research methods, a special form of VT with a chaotic change in the electrical axis of ectopic complexes is most often recorded during an attack. This fusiform ventricular tachycardia, turning into VF and cardiac arrest, was first described in 1966 by F. Dessertene in a patient with LQTS during syncope, who gave it the name "pirouette" ("torsades de pointes"). Often, paroxysms (VT) are short-lived, usually end spontaneously, and may not even be felt (LQTS may not be accompanied by loss of consciousness). However, there is a tendency for arrhythmic episodes to recur in the near future, which can cause syncope and death.

read also the article "Diagnosis of ventricular arrhythmias" by A.V. Strutynsky, A.P. Baranov, A.G. Elderberry; Department of Propaedeutics of Internal Diseases of the Medical Faculty of the Russian State Medical University (magazine "General Medicine" No. 4, 2005) [read]

In the literature, there is a stable relationship of provoking factors with syncopal episodes. When analyzing the factors involved in syncope, it was found that in almost 40% of patients, syncopal conditions are recorded against the background of strong emotional arousal (anger, fear). Approximately in 50% of cases, attacks are provoked by physical activity (excluding swimming), in 20% - by swimming, in 15% of cases they occur during awakening from a night's sleep, in 5% of cases - as a reaction to sharp sound stimuli (phone call, call in door, etc.). If syncope is accompanied by convulsions of a tonic-clonic nature with involuntary urination, sometimes with defecation, the differential diagnosis between syncope with a convulsive component and a grand mal seizure is difficult due to the similarity of clinical manifestations. However, a careful study will reveal significant differences in the post-attack period in patients with LQTS - a quick recovery of consciousness and a good degree of orientation without amnestic disturbances and drowsiness after the attack ends. LQTS does not exhibit personality changes typical of epilepsy patients. The main distinguishing feature of LQTS should be considered as a connection with established provoking factors, as well as pre-syncope states of cases of this pathology.

Diagnostics. The ECG is often of decisive importance in the diagnosis of the main clinical variants of the syndrome (the duration of the QT interval is determined on the basis of an assessment of 3-5 cycles). An increase in the duration of the QT interval by more than 50 ms in relation to the normal values ​​for a given heart rate (HR) should alert the investigator to the exclusion of LQTS. In addition to the actual lengthening of the QT interval, ECG also reveals other signs of electrical instability of the myocardium, such as alternation of the T wave (change in the shape, amplitude, duration or polarity of the T wave that occurs with a certain regularity, usually in every second QRST complex), an increase in the dispersion of the interval QT (reflects the heterogeneity of the duration of the repolarization process in the ventricular myocardium), as well as concomitant rhythm and conduction disturbances. Holter monitoring (HM) allows you to set the maximum duration of the QT interval.

Remember! The measurement of the QT interval is of great clinical importance, mainly because its prolongation may be associated with an increased risk of death, including SCD due to the development of fatal ventricular arrhythmias, in particular polymorphic ventricular tachycardia [ventricular tachycardia of the "pirouette" type - torsade de pointes , (TdP)]. Many factors contribute to the prolongation of the QT interval, among which the irrational use of medications that can increase it deserves special attention.

Drugs that can cause LQTS: [1 ] antiarrhythmic drugs: class IA: quinidine, procainamide, disopyramide, giluritmal; Class IC: encainide, flecainide, propafenone; Class III: amiodarone, sotalol, bretilium, dofetilide, sematilide; IV class: bepridil; other antiarrhythmic drugs: adenosine; [ 2 ] cardiovascular drugs: adrenaline, ephedrine, cavinton; [ 3 ] antihistamines: astemizole, terfenadine, diphenhydramine, ebastine, hydroxyzine; [ 4 ] antibiotics and sulfonamides: erythromycin, clarithromycin, azithromycin, spiramycin, clindamycin, anthramycin, troleandomycin, pentamidine, sulfamethaxosole-trimethoprim; [ 5 ] antimalarial drugs: nalofantrine; [ 6 ] antifungal drugs: ketoconazole, fluconazole, itraconazole; [ 7 ] tricyclic and tetracyclic antidepressants: amitriptyline, norttriptyline, imipramine, desipramine, doxepin, maprotiline, phenothiazine, chlorpromazine, fluvoxamine; [ 8 ] neuroleptics: haloperidol, chloral hydrate, droperidol; [ 9 ] serotonin antagonists: ketanserin, zimeldin; [ 10 ] gastroenterological preparations: cisapride; [ 11 ] diuretics: indapamide and other drugs that cause hypokalemia; [ 12 ] other drugs: cocaine, probucol, papaverine, prenylamine, lidoflazin, terodilin, vasopressin, lithium preparations.

Read more about LQTS in the following sources:

lecture "Long QT Syndrome" N.Yu. Kirkina, A.S. Volnyagin; Tula State University, Medical Institute, Tula (Journal "Clinical Medicine and Pharmacology" No. 1, 2018 ; pp. 2 - 10) [read ];

article "The clinical significance of prolongation of QT and QTC intervals while taking medications" N.V. Furman, S.S. Shmatova; Saratov Research Institute of Cardiology, Saratov (journal "Rational pharmacotherapy in cardiology" No. 3, 2013) [read];

article "Long QT syndrome - main clinical and pathophysiological aspects" N.A. Tsibulkin, Kazan State Medical Academy (Practical Medicine magazine No. 5, 2012) [read]

article "Long QT Syndrome" Roza Hadyevna Arsentieva, doctor of functional diagnostics of the center of psychophysiological diagnostics of the Medical and Sanitary Department of the Ministry of Internal Affairs of the Russian Federation in the Republic of Tatarstan (journal Bulletin of Modern Clinical Medicine No. 3, 2012) [read];

article "Long QT syndrome" heading - "Medicinal safety" (Zemsky doctor magazine No. 1, 2011) [read]

article “Acquired Long QT Syndrome” E.V. Mironchik, V.M. Pyrochkin; Department of Hospital Therapy of the Educational Establishment "Grodno State Medical University" (Journal of the GrGMU No. 4, 2006) [read];

article "Long QT syndrome - clinic, diagnosis and treatment" L.A. Bokeria, A.Sh. Revishvili, I.V. Pronicheva Scientific Center for Cardiovascular Surgery. A.N. Bakuleva RAMS, Moscow (magazine "Annals of Arrhythmology" No. 4, 2005) [read]

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