RU2294137C2 - Method for predicting the development of paroxysms of atrial flutter and fibrillation in patients at supraventricular extrasystolia - Google Patents

Abstract

FIELD: medicine, cardiology.

SUBSTANCE: it is necessary to register dispersion of P wave at carrying out electrocardiography simultaneously in 12 standard leads. Moreover, at detecting supraventricular extrasystolia (SVE) at preectopic interval (PEI) range being above or equal 10% at least in 10 extrasystolic complexes and at the presence of P wave dispersion being of below 10 msec one should fulfill peresophageal electrocardiostimulation at frequency being 50% above that of basic sinus rhythm. At registering P wave dispersion before or after stimulation being above 10 msec or at registering SVE at PEI range being up to or equal 10% at least in 10 extrasystolic complexes at P wave dispersion being above 10 msec one should predict the development of paroxysms of atrial flutter and fibrillation. PEI range should be calculated by the following formula:

where PEI - preectopic interval in %; PEImax, PEImin - maximal, minimal preectopic SVE interval in sec; PEIav. - average preectopic SVE interval in sec; RRsr - RR interval of sinus rhythm before extrasystole in sec. Dispersion of P wave should be calculated by the following formula: Pd = Pmax - Pmin, where Pd - dispersion of P wave in msec, Pmax and Pmin - maximal and minimal interval of P wave in msec.

EFFECT: higher accuracy and efficiency of diagnostics.

4 ex, 2 tbl

Description

The invention relates to medicine, namely to cardiology, in particular to methods for predicting the development of supraventricular cardiac arrhythmias (NDS), in particular paroxysms of atrial fibrillation and atrial flutter (MP and TP) in patients with supraventricular extrasystole (NER).

An analogue of the proposed solution is a method for predicting the development of MP and TP paroxysms in patients with NJE, which consists in determining the width and amplitude of the P wave of the electrocardiogram (ECG), moreover, if the P wave is detected more than 0.12 s and (or) the amplitude is more than 2.5 mm the development of paroxysms of these arrhythmias within a few years after the first examination (Kushakovsky MS Heart arrhythmias. - L .: Medicine, 1993).

Based on the closest technical nature, as a prototype, we have chosen a method for predicting the development of MP and TP paroxysms in patients with NJE, which consists in determining the size or volume of the right and (or) left atrium, and with atrial dilatation of more than 4.0 cm, development is predicted (during 1-3 years) of paroxysms of MP and TP (Kushakovsky M.S. Cardiac arrhythmias. - L .: Medicine, 1993).

The disadvantage of analogue and prototype is the lack of accuracy of forecasting and the absence of specific terms for the development of MP and TP paroxysms.

The objective of the invention is to improve the accuracy of predicting the development of paroxysms of MP and TP in patients with NJE by determining the specific timing of the development of paroxysms of MP and TP.

The technical solution of the problem lies in the fact that the patient undergoes an ECG study at the same time in 12 standard leads and determines the dispersion of the P wave, and when detecting an NRE with a spread of the preectopic interval (PEI) of ≥10% in at least 10 extrasystolic complexes and in the presence of a dispersion of the P wave less than 10 ms conduct transesophageal electrocardiostimulation (CPEX) at a frequency of 50% more than the frequency of the basic sinus rhythm, and when detecting tooth dispersion P≥10 ms after stimulation or when registering NJE with times Wolverine PEI to 10% at least 10 extrasystolic complexes dispersive wave R≥10 ms predict the development of MP and TP paroxysms, the PEI scatter calculated by the formula:

where PEI is the preectopic interval in%, PEImax, PEImin is the maximum, minimum preectopic interval of NJE in sec, PEIred is the average pre-idiotic interval of NJE in sec, RRcp is the RR interval of the sinus rhythm before the extrasystole in sec;

the dispersion of tooth P is calculated by the formula: Pd = Pmax-Rmin, where Pd is the dispersion of tooth P in ms, Pmax and Rmin are the maximum and minimum interval of tooth P in ms.

The salient features of the proposed method are the following: when detecting an NLC with a PEI spread of ≥10% in at least 10 extrasystolic complexes and in the presence of a P wave dispersion of less than 10 ms, CPEX is performed at a frequency of 50% more than the frequency of the basic sinus rhythm, and if tooth dispersion P≥10 ms after stimulation or upon registration of NJE with PEI scatter of up to 10% in at least 10 extrasystolic complexes with tooth dispersion P≥10 ms predict the development of MP and TP paroxysms, and the PEI scatter is calculated according to rmule:

where PEI is the preectopic interval in%, PEImax, PEImin is the maximum, minimum preectopic interval of NJE in sec, PEIred is the average pre-idiotic interval of NJE in sec, RRcp is the RR interval of the sinus rhythm before the extrasystole in sec;

the dispersion of the tooth P is calculated by the formula: Pd = Pmax-Rmin,

where Pd is the dispersion of the P wave in ms, Pmax and Rmin are the maximum and minimum interval of the P wave in ms.

Currently, it is known that when registering excitations on the myocardium of the atria or ventricles, the conduct of excitation (PV) obeys the law of "flow" from one cardiomyocyte to another (Physiology and pathophysiology of the heart: T.1 .; translated from English - Ed. N. Sperelaxis. - M .: Medicine, 1990, Olshansky B., Okumura K., Hess PG, Waldo AL Demonstration of the area of slow conduction in human atrial flytter. // J. Amer. Coll. Cardiol. - 1991. - Vol.16, N.6. - P.1639-1648, Shimisu A., Nosaki A., Rudy Y., Waldo AL Multiplexing studies of effects of rapid atrial pacing on the area of slow conduction during atrial flutter in canine pericarditis model. // Circulation. - 1991. - Vol. 83, N.3. - P.983-994). Therefore, by directly applying electrodes to the myocardium, the nature and direction of PV in the heart muscle is recorded. In addition, the atrial myocardium is a tissue with a quick response, i.e. the membrane potential of atrial contractile fibers is characterized by rapid depolarization (Physiology and pathophysiology of the heart: T.1 .: transl. from English. - Ed. by N. Sperlaksis. - M .: Medicine, 1990). The onset of depolarization corresponds to electrical excitation of the myocardium and is recorded on the ECG as the beginning of the P wave or QRS complex, and the input of calcium current through the membrane of cardiomyocytes to the development of mechanical contraction of the myocardium (Physiology and pathophysiology of the heart: T.1 .: transl. From English - Ed. N.Sperelaksisa. - M .: Medicine, 1990). It should be noted that the interval from the onset of electrical excitation of the myocardium to the beginning of its mechanical contraction in both clinical and experimental studies is designated as the time of asynchronous contraction (Physiology and Pathophysiology of the Heart: T.1 .: transl. From English - Ed. N. Sperelaksisa. - M .: Medicine, 1990).

The presence of supraventricular arrhythmias in patients with coronary artery disease is due to the fact that there is a slowdown in PV in the upper and middle parts of the atria, which reflects the variance of the excitability of the myocardium of the atria (Bokeria L.A. Tachyarrhythmias: Diagnosis and surgical treatment.-L.: Medicine, 1989, Olshansky V. , Okumura K., Hess PO, Waldo AL Demonstration of the area of slow conduction in human atrial flytter. // J. Amer. Coll. Cardiol. - 1991. - Vol.16, N.6. - P.1639-1648 , Shimisu A., Nosaki A., Rudy Y., Waldo AL Multiplexing studies of effects of rapid atrial pacing on the area of slow conduction during atrial flutter in canine pericarditis model. // Circulation. - 1991. - Vol. 83, N .3. - P.983-994, Zipes DP Genesis of cardiac arrhythmias: electrophysiological consideraton // Heart Dis ease / Ed.E. Braunwald. 1984. - P.605-647), and in these patients atrial conduction disturbance is noted long before the increase in atria and other predictors of MP and TP development (Shabrov A.V., Olesin A.I., Golub Y.V., Golub V.I. Clinical evaluation of the use of a non-invasive method for determining intra and atrial conduction in patients with coronary heart disease. // Ter. archive. - 1999. - No. 1. - S. 34-39). When comparing the localization of sites of slowing down the spread of excitation and retrograde PV in the atria with the zones of hypokinesia, a positive correlation between them was revealed, averaging r = 0.89 and r = 91, respectively (Shabrov A.V., Olesin A.I., Golub Ya .V., Golub V.I. Clinical evaluation of the use of the non-invasive method for determining intra and atrial conduction in patients with coronary heart disease // Ter. Archive. - 1999. - No. 1. - P.34-39).

In our proposed method, it is assumed that with uneven PV in the atrial myocardium, i.e. with uneven depolarization of cardiomyocytes, there will be uneven repolarization of atrial myocardiocytes, which can be detected by determining the dispersion of the P wave during registration of a standard ECG simultaneously in 12 leads, which is highly correlated with the frequency of clinical relapses of MP and TP paroxysms (Aytemir K., Ozer N. , Atalar E. et al. P wave dispersion on 12-lead electrocardiography in patients with paroxysmal atrial fibrillation // Pacing Clin. Electrophysiol. - 2000. - Vol.23. - No. 7. - P.1109-1112).

An example of a specific implementation.

Example 1

IS No. 948. Patient A., 54 years old, was admitted to a day hospital on January 11, 2002, in the direction of a local doctor regarding coronary heart disease: angina pectoris, periodic heart attacks. From the anamnesis it is known that the patient suffers from coronary heart disease: angina pectoris of functional class II over the past 4-5 years. Constantly takes nitrong, aspirin at a dose of 300-400 mg per day, anaprilin at a dose of 60-80 mg per day. In the last 3-4 months, I began to notice the appearance of interruptions in the work of the heart. With daily ECG monitoring performed on an outpatient basis on December 10, 2001, a single and paired atrial extrasystole (PE) was detected with a frequency of up to 15-35 extrasystoles per hour.

According to the clinical and instrumental examination, the patient’s condition was regarded as coronary heart disease in a hospital: stable angina pectoris of functional class II, data for the presence of “fresh” focal myocardial changes were not detected. The patient was continued with nitrogom therapy at 6.4 mg per day, aspirin at a dose of 300 mg per day, enalopril (ednit) at a dose of 5 mg per day.

On the second day of the patient’s stay in the hospital, ECG was recorded simultaneously in 12 standard leads for 15 minutes using the Polyspectrum-Rhythm computer complex (Neurosoft, Ivanovo). An ECG revealed 5-8 PE per minute. Then, the spread of PEI PE was calculated by the formula:

where PEI is the preectopic interval in%, PEImax, PEImin is the maximum, minimum preectopic interval of NJE in sec, PEIred is the average pre-idiotic interval of NJE in sec, RRcp is the RR interval of the sinus rhythm before the extrasystole in sec;

составил - 452 мс/

;

составил - 432 мс/

мс;

составил - 433 мс/

.Patient A., 54 years old according to ECG studies in 85 extrasystolic complexes

amounted to 452 ms /

;

amounted to 432 ms /

ms;

amounted to 433 ms /

.

PEI = [(16.50 ms-17.21 ms) ÷ 16.14 ms] × 100% = 4.40%.

Then, the dispersion of the P wave was calculated by the formula:

Pd = Pmax-Rmin,

where Pd is the dispersion of the P wave in ms, Pmax and Rmin are the maximum and minimum interval of the P wave in sec.

According to the ECG data, Rmax was 122 ms, Rmin was 104 ms, Pd = 122 ms-104 ms = 18 ms.

Patient A., 54 years old, was predicted to develop MP and TP. The patient was induced with MP by the method of volley super-frequent stimulation using NPEX, and the threshold for arrhythmia induction (PIA) was 650 imp / min. Arrhythmia stopped on its own after 5 minutes. It should be noted that with CPEX, indicators reflecting the function of the sinus node, such as the time of restoration of the function of the sinus node, the corrected time of restoration of the function of the sinus node, the time of sinoatrial conduction, determined by the generally accepted technique (Kushakovsky M.S. Cardiac arrhythmias. -L .: Medicine , 1993), did not go beyond the limits of fluctuations of normal values. Subsequently, the patient was treated with nitrates, aspirin, renitec (enalopril) at the doses indicated above. Antiarrhythmic drugs were not prescribed. Spontaneous seizures of MP and TP lasting from 3-6 seconds to 10-15 minutes were detected during daily monitoring of the ECG 3 months after the above examination, and when performing PEEX in the same period (3 months after the first stimulation), the PIA was 320 imp / min

This example showed that when registering PE with a PEI spread of extrasystoles of less than 10% and with a P wave dispersion of more than 10 seconds, it is possible to predict MP and TP paroxysms within 3 months after the examination.

Example 2

IS No. 211138. Patient S., 58 years old, was admitted to the hospital on 06/19/2002 in the direction of an ambulance doctor about coronary heart disease: progressive angina pectoris. From the anamnesis it is known that the patient suffers from coronary heart disease: angina pectoris of functional class II over the past 3 years. Constantly takes nitrosorbide, antiplatelet agents. Two days before hospitalization, the patient sore anginal pain in frequency, duration, intensity, and the nature of the pain syndrome changed. Hospitalization in hospital.

In a hospital, according to clinical and instrumental examination, the patient's condition was regarded as coronary heart disease: progressive angina pectoris, data for the presence of "fresh" focal myocardial changes were not detected. The patient was continued with nitrosorbide therapy at a dose of 30 mg per day, aspirin at a dose of 300 mg per day, renitec at a dose of 5 mg per day, a polarizing mixture with nitroglycerin.

On the third day of the patient's stay in the hospital, the nature of anginal pain stabilized.

On the third day of the patient’s stay in the hospital, ECG was recorded simultaneously in 12 standard leads for 20 minutes using the Polyspectrum-Rhythm computer complex (Neurosoft, Ivanovo). On the ECG, 3-5 PE per minute were detected. Then, the spread of PEI PE was calculated by the formula:

where PEI is the preectopic interval in%, PEImax, PEImin is the maximum, minimum preectopic interval of NJE in sec, PEIred is the average pre-idiotic interval of NJE in sec, RRcp is the RR interval of the sinus rhythm before the extrasystole in sec;

составил - 637 мс/

;

составил - 468 мс/

;

составил - 522 мс/

.According to ECG studies in 55 extrasystolic complexes

amounted to 637 ms /

;

amounted to 468 ms /

;

amounted to 522 ms /

.

PEI = [(22.38 ms-15.43 ms) ÷ 17.85 ms] × 100% = 38.94%.

Then, the dispersion of the P wave was calculated by the formula:

Pd = Pmax-Rmin,

where Pd is the dispersion of the P wave in ms, Pmax and Rmin are the maximum and minimum interval of the P wave in sec.

In patient S., 58 years old, according to the ECG data, Rmax was 112 ms, Rmin was 106 ms, Pd = 112 ms-106 ms = 6 ms.

The average heart rate was 70 beats per minute. Then the patient underwent CPEX at a frequency of 105 pulses. in min (which is 50% more than the frequency of the basic sinus rhythm). After CHPEX, ECG was re-recorded simultaneously in 12 standard leads for 15 minutes using the Polyspectrum-Rhythm computer complex (Neurosoft, Ivanovo). On an ECG, 2-3 PE per minute were detected.

составил - 656 мс/

;

составил - 488 мс/

;

составил - 534 мс/

.Patient S., 58 years old, after CPEX according to ECG data in 34 extrasystolic complexes

amounted to 656 ms /

;

amounted to 488 ms /

;

amounted to 534 ms /

.

PEI = [(22.91 ms-15.92 ms) ÷ 18.15 ms] × 100% = 38.51%.

Then, the dispersion of the P wave was calculated by the formula:

Pd = Pmax-Rmin,

where Pd is the dispersion of the P wave in ms, Pmax and Rmin are the maximum and minimum interval of the P wave in sec.

According to the ECG data, Rmax was 116 ms, Rmin was 108 ms, Pd = 116 ms-108 ms = 8 ms.

In patient S., 58 years old, development was not predicted by MP and TP. The patient was attempted to induce MP by the method of volley super-frequent stimulation using CPEX, but arrhythmia was not induced. It should be noted that with CPEX, indicators reflecting the function of the sinus node, such as the time of restoration of the function of the sinus node, the corrected time of restoration of the function of the sinus node, the time of sinoatrial conduction, determined according to the generally accepted technique (Kushakovsky M.S. Cardiac arrhythmias. - L .: Medicine , 1993), did not go beyond the limits of fluctuations of normal values.

Subsequently, the patient was treated with nitrates, aspirin, renitec (enalopril) at the doses indicated above. Antiarrhythmic drugs were not prescribed.

The patient was discharged from the hospital 14 days after admission.

During follow-up for 6 years, including daily ECG monitoring once every 3 months, the development of MP and TP paroxysms was not observed.

This example showed that when registering PE with a PEI spread of extrasystoles of more than 10% and with a P wave dispersion of less than 10 seconds, the development of MP and TP paroxysms is not observed.

Example 3

IS No. 2698. Patient O., 60 years old, was admitted to the hospital on April 21, 2002, in the direction of a doctor at the polyclinic about coronary heart disease: first-time angina. From the anamnesis it is known that the patient previously considered himself practically healthy.

In the hospital, according to clinical and instrumental examination, the patient's condition was regarded as coronary heart disease: the first angina pectoris, data for the presence of "fresh" focal myocardial changes were not detected. The patient was started therapy with erinitis at 40 mg per day, aspirin at a dose of 300 mg per day, zoocor 20 mg per day, a polarizing mixture with nitroglycerin.

On the third day of the patient’s stay in the hospital, characteristic anginal pains stopped and did not recur in the future.

On the third day of the patient’s stay in the hospital, ECG was recorded simultaneously in 12 standard leads for 15 minutes using the Polyspectrum-Rhythm computer complex (Neurosoft, Ivanovo). An ECG revealed 2 PE per minute. Then, the spread of PEI PE was calculated by the formula:

where PEI is the preectopic interval in%, PEImax, PEImin is the maximum, minimum preectopic interval of NJE in sec, PEIred is the average pre-idiotic interval of NJE in sec, RRcp is the RR interval of the sinus rhythm before the extrasystole in sec;

составил - 568 мс/

;

составил - 416 мс/

;

составил - 476 мс/

.Patient O., 68 years old, according to an ECG study in 30 extrasystolic complexes

amounted to 568 ms /

;

amounted to 416 ms /

;

amounted to 476 ms /

.

PEI = [(21.31 ms-14.53 ms) ÷ 17.20 ms] × 100% = 39.42%.

Then, the dispersion of the P wave was calculated by the formula:

Pd = Pmax-Rmin,

where Pd is the dispersion of the P wave in ms, Pmax and Rmin are the maximum and minimum interval of the P wave in sec.

Patient O., 68 years old, according to the ECG study Rmax. amounted to 114 ms, Rmin. amounted to 106 ms, Pd = 114 ms-106 ms = 8 ms.

The average heart rate was 78 beats. in minutes Then the patient underwent CPEX at a frequency of 118 pulses. in min (which is 50% more than the frequency of the basic sinus rhythm). After CHPEX, ECG was re-recorded simultaneously in 12 standard leads for 15 minutes using the Polyspectrum-Rhythm computer complex (Neurosoft, Ivanovo). An ECG revealed 2 PE per minute.

составил - 478 мс/

;

составил - 406 мс/

;

составил - 456 мс/

.Patient O., 68 years after CHPEX according to ECG studies in 30 extrasystolic complexes

amounted to 478 ms /

;

amounted to 406 ms /

;

amounted to 456 ms /

.

PEI = [(17.57 ms-16.31 ms) ÷ 17.68 ms] × 100% = 7.10%.

Then, the dispersion of the P wave was calculated by the formula:

Pd = Pmax-Rmin,

where Pd is the dispersion of the P wave in ms, Pmax and Rmin are the maximum and minimum interval of the P wave in sec.

According to the ECG data, Rmax was 126 ms, Rmin was 106 ms, Pd = 126 ms-106 ms = 20 ms.

In patient O., 68 years old, the development of MP and TP was predicted. The patient was induced with MP by the method of volley super-frequent stimulation using CPEX, with a PIA of 450 imp./min. Arrhythmia stopped on its own after 5 minutes. It should be noted that with CPEX, indicators reflecting the function of the sinus node, such as the time of restoration of the function of the sinus node, the corrected time of restoration of the function of the sinus node, the time of sinoatrial conduction, determined by the generally accepted technique (Kushakovsky M.S. Cardiac arrhythmias. -L .: Medicine , 1993), did not go beyond the limits of fluctuations of normal values. Subsequently, the patient was treated with nitrates, aspirin, zoocor in the doses indicated above. Antiarrhythmic drugs were not prescribed.

Spontaneous seizures of MP and TP lasting from 15 seconds to 10-15 minutes were detected during 24-hour ECG monitoring 4 months after the above examination, and when performing PEEX in the same period (3 months after the first stimulation), the PIA was 260 pulses / min.

This example showed that when registering PE with a spread of PEI, extrasystoles are less than 10% and when the dispersion of the P wave is more than 15 seconds. After CPEKS, which is carried out by 50% more in comparison with the frequency of the basic sinus rhythm, it is possible to predict MP and TP paroxysms within 4 months after the examination.

Example 4

IS No. 1056. Patient K., 68 years old, was admitted to the hospital on 02.21.2002 in the direction of the district doctor regarding coronary heart disease: angina pectoris, periodic heart attacks. From the anamnesis it is known that the patient suffers from coronary heart disease: angina pectoris of functional class II over the past 6 years. Constantly takes monochinqua at a dose of 50 mg per day, aspirin at a dose of 300-400 mg per day, enalapril (renitec) at a dose of 20 mg per day. In the last 3-4 months, I began to notice the appearance of interruptions in the work of the heart. During daily ECG monitoring performed on an outpatient basis on December 10, 2001, a single PE was detected with a frequency of up to 26 extrasystoles per hour.

According to the clinical and instrumental examination, the patient’s condition was regarded as coronary heart disease in a hospital: stable angina pectoris of functional class II, data for the presence of “fresh” focal myocardial changes were not detected. The patient was continued with monocinque therapy at a dose of 50 mg per day, aspirin at a dose of 300-400 mg per day, enalapril (renitec) at a dose of 20 mg per day.

On the second day of the patient’s stay in the hospital, ECG was recorded simultaneously in 12 standard leads for 15 minutes using the Polyspectrum-Rhythm computer complex (Neurosoft, Ivanovo). An ECG revealed 24-26 PE per minute. Then, the spread of PEI PE was calculated by the formula:

where PEI is the preectopic interval in%, PEImax, PEImin is the maximum, minimum preectopic interval of NJE in sec, PEIred is the average pre-idiotic interval of NJE in sec, RRcp is the RR interval of the sinus rhythm before the extrasystole in sec;

составил - 468 мс/

;

составил - 454 мс/

;

составил - 466 мс/

.Patient K., 68 years old, according to an ECG study in 85 extrasystolic complexes

amounted to 468 ms /

;

amounted to 454 ms /

;

amounted to 466 ms /

.

PEI = [(16.76 ms-17.02 ms) ÷ 16.96 ms] × 100% = 1.50%.

Then, the dispersion of the P wave was calculated by the formula:

Pd = Pmax-Rmin,

where Pd is the dispersion of the P wave in ms, Pmax and Rmin are the maximum and minimum interval of the P wave in sec.

According to the ECG data, Rmax was 128 ms, Rmin was 106 ms, Pd = 128 ms-106 ms = 22 ms.

Patient K., 68 years old, was predicted to develop MP and TP. Subsequently, the patient was treated with nitrates, aspirin, renitec (enalopril) at the doses indicated above. Antiarrhythmic drugs were not prescribed. A spontaneous attack of MP and TP developed a day after the examination (on the third day after admission to the hospital), stopped by the intravenous administration of procainamide at a dose of 1000 mg. As an anti-relapse treatment of MP and TP paroxysms, the patient was prescribed sotalol in a dose of 120 mg per day in addition to the therapy. Arrhythmia did not recur for 2 years.

This example showed that when registering PE with a PEI spread of extrasystoles of less than 10% and with a P wave dispersion of more than 10 seconds, MP and TP paroxysms can be predicted for several days after the examination.

There were 119 patients with coronary artery disease complicated by PE. All patients underwent prolonged-action nitrate therapy, antiplatelet agents, angiotensin-converting enzyme inhibitors (renitec, enalopril, enap). Antiarrhythmic drugs were not prescribed. In all patients, the prognosis of MP and TP paroxysms was carried out according to the proposed method and, according to the prototype, the prognosis of MP and TP paroxysms was predicted depending on the size or volume of the right and (or) left atrium, and with dilatation of one or both atria of more than 4.0 cm, paroxysms are predicted MP and TP (Kushakovsky M.S. Arrhythmias of the heart. -L.: Medicine, 1993).

Statistical analysis of the results is carried out on a computer. In 87 (73.11%) of all examined patients, according to the prototype (Kushakovsky MS, Cardiac arrhythmias. -L .: Medicine, 1993), an increase in the left atrium of more than 4.0 cm was revealed. All patients, according to the proposed method , ECG was recorded simultaneously in 12 standard leads for 15-20 minutes using the Polyspectrum-Rhythm computer complex (Neurosoft, Ivanovo). The ECG was recorded at a speed of 50 mm / s, and the determination of the P wave dispersion was carried out when the ECG was recorded at a speed of 200 mm / s with a gain of 80 mm / μV. An ECG revealed 2-28 PE per minute (an average of 14 ± 1 PE per minute). Then, the spread of PEI PE and the dispersion of the P wave were calculated using the formulas:

where PEI is the preectopic interval in%, PEImax, PEImin is the maximum, minimum preectopic PE interval in sec, PEIred is the average pre -opic PE interval in sec, RRcp is the RR interval of the sinus rhythm before the extrasystole in sec;

the dispersion of the tooth P was calculated by the formula:

Pd = Pmax-Rmin,

where Pd is the dispersion of the P wave in ms, Pmax and Rmin are the maximum and minimum interval of the P wave in ms.

In 40 (33.61%) of 119 examined patients, PE was observed with a PEI spread of more than 10% in 10 or more extrasystolic complexes, ranging from 18% to 46% (average 34 ± 3%) with P wave dispersion of less than 10 ms, averaging 6 ± 1 ms, and the rest showed PE with a spread of PEI of less than 10% in 10 or more extrasystolic complexes, ranging from 1% to 9% (average 4 ± 1%) with a P wave dispersion of more than 10 ms, averaging 42 ± 1 ms (p <0.001). All patients with PEI PE scatter of more than 10% in 10 or more extrasystolic complexes and with P wave dispersion of less than 10 ms underwent CPEX at a frequency 50% higher than the baseline sinus rhythm frequency, followed by PEI PE and P wave dispersion determination using the method described above (see. above).

The results of the study showed that 20 (50.00%) of 40 patients after PEEX maintained PEI PE of more than 10% in 10 or more extrasystolic complexes with P wave dispersion of less than 10 ms (on average 6 ± 1%), while in other patients, after pacemaking, a P wave dispersion of more than 15 ms was observed, averaging 46 ± 4 ms (p <0.001).

In all patients with PEI PE more than 10% in 10 or more extrasystolic complexes and with P wave dispersion less than 10 ms after CPEX, MP and TP paroxysms were not observed during 6 years of observation, while in the remaining 95 (95.96%) of 99 patients in whom the development of these arrhythmias was predicted by the proposed method, their development was noted within 1 year (on average 5 ± 2 months) after the first examination, while only 10 (11.49%) of 87 patients with dilatation of the atria, the development of paroxysms of MP and TP was observed (P <0.001).

Most accurately (on average 7.4-8 times), it is possible to predict the development of MP and TP paroxysms within 1 year using the proposed method in comparison with the prototype (see tables 1, 2).

Thus, more accurately (on average 7.7 times), it is possible to predict the development of MP and TP paroxysms using the proposed method in comparison with the prototype, which will ensure the appointment of adequate therapy to prevent paroxysms of these NDS.

Table 1
Comparison of the accuracy of predicting the paroxysms of MP and TP of the proposed method in comparison with the prototype. Patient groups The proposed method Prototype ΔM BUT B BUT B Predictable value,% 100.00 95.96 100.00 11.49 +7.4 times Note: A is the predicted, B is the real result of the development of MP and TP paroxysms, ΔM is the forecast accuracy in comparison with the prototype. table 2
Comparison of the accuracy of prediction of MP and TP paroxysms of the proposed method in comparison with the prototype in patients with detection of tooth dispersion P> 15 ms after CPEX Patient groups The proposed method n = 20 Prototype n = 10 ΔM BUT B BUT B Predictable value,% 100.00 90.00 100.00 10.00 +8 times Note: A is the predicted, B is the real result of the development of MP and TP paroxysms, ΔM is the forecast accuracy in comparison with the prototype.

Claims (1)

A method for predicting the development of paroxysms of atrial fibrillation and flutter in patients with supraventricular extrasystole (NJE) by determining the dispersion of the P wave during electrocardiography simultaneously in 12 standard leads, characterized in that when detecting NJE with a spread of the preectopic interval (PEI) more than or equal to 10% as in at least 10 extrasystolic complexes and in the presence of a P wave dispersion of less than 10 ms, transesophageal cardiac pacing is performed at a frequency of 50% more than the frequency of the basal sinus about the rhythm and when detecting the dispersion of the P wave before or after stimulation for more than 10 ms or when registering an NRE with a PEI spread of up to or exactly 10% in at least 10 extrasystolic complexes with a P wave dispersion of more than 10 ms, the development of paroxysms of atrial fibrillation and flutter is predicted PEI is calculated by the formula

where PEI - preectopic interval,%; PEIMax., PEIMin. - maximum, minimum preectopic interval of NJE, s; PEI Avg. - averaged preectopic interval of NJE, s; RRcp. - the interval RR of the sinus rhythm before the extrasystole, s, the dispersion of the P wave was calculated by the formula Pd = Pmax.-Rmin., where Pd is the dispersion of the P wave, ms; Rmax and rmin. - the maximum and minimum interval of the P wave in ms.