RU2265391C2 - Method for detecting endothelium-dependent arterial vasodilation due to evaluating alterations in pulse wave distribution rate at the background of reactive hyperemia - Google Patents

Abstract

FIELD: medicine, cardiology.

SUBSTANCE: one should detect pulse wave distribution rate (PWR) at rest by standard technique, then one should squeeze brachial artery with manometer's gasket to measure arterial pressure (AP) for 3 min. Pressure should be increased by not less than 50 mm mercury column against systolic AP. Immediately on removing the air out of manometer's gasket one should detect PWR after restoration of arterial circulation. Normally one should state upon significant PWR decrease, by 21.2%, on an average. In patients with ICD alterations of PWR are expressed in considerably lower degree and corresponded to 3.9%, in one portion of patients with ICD one may observe increased PWR. The method suggested could be applied as functional probe for evaluating endothelial arterial function being the routine trial in clinical practice.

EFFECT: higher accuracy of detection.

2 ex, 4 tbl

Description

The invention relates to medicine, for the use of a diagnostic functional test based on the determination of the pulse wave propagation velocity (SPS) and the change in SPS that developed after arterial occlusion. The method can be used as a functional test in patients with various cardiovascular pathologies to study the vasoregulatory function of arterial endothelium during treatment.

It is known that vascular endothelium regulates local processes of hemostasis, proliferation, migration of blood cells into the vascular wall and affects vascular tone. Endothelial dysfunction implies an imbalance between the factors that provide these interactions (A. A. Quyyumi. Endothelial function in health and disease: new insights into the genesis of cardiovascular disease // Am. J. Med. - 1998. - V.105. - P. 32S-39S).

It has been proven that, normally, with a change in blood flow velocity, the diameter of large arteries changes: with an increase in blood flow, the arteries expand, and with a decrease, they narrow. It is believed that the regulation of the lumen of the arteries is a local reaction (D.A. Zateishchikov, L.O. Minushkina, O.Yu. Kudryashova and others. The functional state of the endothelium in patients with arterial hypertension and ischemic heart disease // Cardiology. - 2000. - No. 6 . - S.14-17).

The relationship between the onset and progression of endothelial dysfunction with age has been established. The increase in dilatation of the brachial artery in response to increased blood flow is normal, in people aged 40 to 55 years remains stable, and subsequently decreases by 0.21% per year. In patients with coronary artery disease, a decrease in the dilatation of the brachial artery is also detected, which is explained by impaired lipid metabolism, heart failure, and possible concomitant arterial hypertension. A number of studies have shown that endothelial dysfunction in patients with coronary artery disease occurs in most cases, including at a young age (up to 45 years), and in the early stages of myocardial infarction, patients often experienced more paradoxical vasoconstriction (V.A. Almazov , OA Berkovich, M.Yu. Sitnikova and others. Endothelial dysfunction in patients with the onset of coronary heart disease at different ages // Cardiology - 2001. - No. 5. - P.26-29).

In the studied literature, we came across data on developed tests for evaluating endothelial function, based on ultrasound diagnostic methods. Using an ultrasound apparatus, a portion of the brachial artery was visualized, the diameter of which was determined in diastole. Endothelium-dependent artery dilatation is caused by reactive hyperemia that occurs in response to the cessation of blood flow imposed by a cuff proximal to the measurement site. The diameter and velocity of blood flow were evaluated before and after clamping the artery. The normal response of the brachial artery to reactive hyperemia is its expansion of more than 10%. A lesser degree of vasadilation or paradoxical vasoconstriction is considered a pathological reaction and may indicate the presence of endothelial dysfunction (D.A. Zateishchikov, L.O. Minushkina, O.Yu. Kudryashova and others. Functional state of endothelium in patients with arterial hypertension and coronary heart disease // Cardiology. - 2000. - No. 6. - S.14-17).

The proposed methods for assessing the endothelial function of arteries have obvious advantages, but cannot be used for routine use for a large number of studies, as they require expensive equipment, highly qualified specialists and a sufficiently long time for the procedure itself. Most authors noted that an increase in the diameter of the artery in response to increased blood flow is due to a decrease in the tone of the arterial wall. It can be assumed that when determining the speed of the pulse wave (SST), changes will also be observed during the test, namely its decrease in response to increased blood flow.

The aim of the present invention is to develop a method for evaluating the endothelium-dependent dilatation of the brachial artery by recording changes in SST on the background of reactive hyperemia.

To achieve this goal, the standard method for assessing SST was used, for which simultaneous recording of sphygmograms from the carotid, femoral and radial arteries is performed. The receivers (sensors) of the pulse are installed: on the carotid artery - at the level of the upper edge of the thyroid cartilage (it is better to palpate the pulsation on the neck in the place where the trachea and sternocleid muscle are in contact), on the femoral artery - at the place where it leaves the pupar ligament (better slightly lower than the ligament, for better registration of the signal), on the radial artery - in the place of palpation of the pulse. The correctness of the imposition of heart rate sensors is carried out under the visual control of the monitor.

If simultaneous recording of all three pulse curves is not possible due to technical reasons, then the pulse of the carotid and femoral arteries, and then the carotid and radial arteries are simultaneously recorded simultaneously. To calculate the propagation speed of a pulse wave, you need to know the length of the segment of the artery between the pulse receivers. Conventionally, in the study of SST, the carotid-radial section corresponds to the muscular type of arteries and is measured as follows: the sum of the distances from the position of the sensor on the carotid artery to the head of the humerus and from the head of the humerus to the place of the best pulse recording in the radial artery. The length of an artery of an elastic type was determined by the sum of the distances from the jugular notch of the sternum to the navel and to the place of pulse recording on a.femoralis.

During manual processing of the sphygmogram, it is necessary to determine another indicator - the time of the delay of the pulse in the distal segment of the artery with respect to the central pulse, which is usually determined by the distance between the beginning of the rise of the curves of the central and peripheral pulse or by the distance between the bending points on the ascending part of the sphygmogram.

Knowing the length of the section of the studied artery (D) and the delay time (t), we can calculate the SST for this vessel (D / t, m / s). In automatic systems, such as the Colson computer console (Camplior), the determination of the time indicator is carried out by the corresponding program. Measurements are repeated and an average delay time of at least 10 cardiac cycles is calculated. When conducting a study using this instrument, it must be taken into account that the results can be considered objective with a representativeness coefficient of at least 0.890 and a repeatability coefficient of 0.935, respectively (Asmar R., Benetos A., Topouchian J. et al. Assessment of Arterial Distensibility by Automatic Pulse Wave Velocity Measurement (Validation and Clinical Application Studies) // Hypertension - 1995 - V.26 - P.485-490).

When conducting a test against a background of reactive hyperemia, the SST is determined on the carotid-radial site, namely, the response of muscle type arteries is assessed. We intentionally conducted a study on a large segment of an arterial vessel, since the atherosclerotic lesion may be local, which may affect the final result of the test. Preliminarily determine SPV at rest by a standard method. As in the evaluation of endothelium-dependent vasodilation under ultrasound guidance, the brachial artery is pinched with the cuff of the pressure gauge for 3 min, increasing the pressure by more than 50 mm Hg. from systolic blood pressure, or to the disappearance of complexes on the radial artery (in the case of constant recording of the sphygmogram on the monitor). Immediately after the air is released from the cuff of the manometer and after 3 minutes, the SPV in the artery under investigation is determined, the difference between the indicators is indicated in percent.

The study included patients (n = 16) with coronary heart disease, in whom the diagnosis was confirmed by anamnestic data (the presence of post-infarction cardiosclerosis) or coronary angiography results (revealed hemodynamically significant stenoses of the coronary arteries). The control group consisted of practically healthy people (n = 14) who did not have indications of the presence of cardiac pathology.

In both groups, the determination of SPV was carried out under the same conditions, all patients were men, the age of the patients was comparable. The study did not include patients with concomitant arterial hypertension, diabetes mellitus, obesity, or another pathology that could affect the test results. When comparing the results obtained (Table 1), it turned out that in the group with coronary artery disease, the baseline SST for elastic type arteries (C _e ) was not significantly higher than in the comparison group (7.1 ± 0.4%). Differences for muscle-type arteries were even less pronounced (3.2 ± 0.5%). Virtually all of the examined, and according to the SST, were comparable. Only the C _m / C _e ratio differed significantly, normally it turned out to be more than 18% higher, which, according to P.N. Fofonov, 1977 can be one of the confirming signs of the atherosclerotic process in the test vessel.

Table 1
Source data of the speed of propagation of a pulse wave Indicators Control (n = 14) Patients with coronary heart disease (n = 16) Age years 46.7 ± 2.7 49.8 ± 1.8 S _e , m / s 9.21 ± 0.4 9.95 ± 0.6 S _m , m / s 9.27 ± 0.3 9.48 ± 0.5 S _e / S _m 1.11 ± 0.04 0.99 ± 0.04 Notes: С _e - pulse wave propagation speed for elastic type arteries; C _m - pulse wave velocity for muscle type arteries

During the test, statistically significant changes in C _m decrease were revealed in patients with coronary artery disease (Table 2). Normally, the decrease in С _m averaged 21.2%, while in the coronary heart disease group this indicator turned out to be 3.9%, by 3 minutes after restoration of blood flow, in healthy individuals, C _m did not reach the initial figures, and in patients increased even more significantly.

table 2
Changes in the pulse wave propagation velocity against the background of reactive hyperemia are normal and with concomitant coronary heart disease Indicators Control (n = 14) Patients with coronary heart disease (n = 16) Initial C _m , m / s 9.27 ± 0.3 9.48 ± 0.5 C _m after restoration of blood flow 8.18 ± 0.2 8.92 ± 0.4 % reduction C _m , after sample 21.21 ± 0.9 3.9 ± 0.4 C _m , 3 min after restoration of blood flow 9.16 ± 0.4 9.9 ± 0.5 Notes: C _m is the pulse wave propagation speed for muscle type arteries.

In addition, we noted that normally, no patient had a paradoxical reaction - an increase in PST, in all cases a decrease in C _m from 7% to 41% was observed, and in patients with coronary artery disease, three changes were not observed, and practically in one third (5 patients) we observed an increase in PST.

Examples of specific application.

Example 1. The assessment of endothelium-dependent artery dilatation is normal.

As an example, we give the results of observations of 2 practically healthy people. Subjects KN and MS were 44 and 56 years old, respectively, with no signs of cardiovascular disease. Both carried out the determination of SPV at rest and against the background of a sample with reactive hyperemia. The results are shown in table 3.

Table 3
Pulse wave velocity indices in patients are normal before and during the test with reactive hyperemia Indicators Age years S _e , m / s S _m , m / s C _m after restoration of blood flow, m / s % reduction C _m C _m , 3 min after restoration of blood flow, m / s Kn 44 7.92 8.65 7.01 twenty 7.79 Ms 56 10.8 10.8 8.2 24 8.9

As can be seen from the data presented, in response to increased blood flow in the arteries, the SVR significantly decreased (by 20% and 24%) due to a decrease in vascular tone, which will indirectly indicate the preserved vasodilating ability of the vascular endothelium.

Example 2. Evaluation of endothelium-dependent artery dilatation in coronary artery disease.

The parameters of PST were estimated in patients with coronary artery disease. As an example, we present the results of 2 patients corresponding in age to the previous observation. Patients with CT and RK 47 and 57 years old, respectively, both had a confirmed diagnosis of coronary heart disease (history of myocardial infarction 4 and 2 years ago), angina pectoris FC II, heart failure II FC according to NYHA, without signs of arterial hypertension. The results of the study are shown in table 4.

Table 4
Pulse wave velocity indices in patients with coronary heart disease before and during the test with inactive hyperemia Indicators Age years C _uh
m / s S _m
m / s C _m after restoration of blood flow, m / s SPV change C _m , 3 min after restoration of blood flow, m / s CT 47 7.36 9.53 8.92 6.4% decrease 10.81 Rk 57 7.53 8.58 9.26 8% increase 9.11

In the first patient with coronary heart disease, we observed a decrease in PTS, but to a much lesser extent than normal - only 6.4%, and the second one had a paradoxical reaction in the form of an increase in PPS, probably associated with paradoxical vasoconstriction, which would indicate a violation of edothelial function endothelial lining of the vessel.

Thus, we can say that changes in the pulse wave propagation velocity against the background of reactive hyperemia can reflect the state of endothelial function of arteries. Evaluation of SST is quite informative when conducting a test on an automatic computer instrument of the Colson type. Normally, in response to reactive hyperemia, the propagation velocity of the pulse wave through the muscular arteries will decrease by no less than 20%. With atherosclerotic lesions of the vascular wall, the changes are significantly leveled and the percentage of reduction will be much lower, in addition, the occurrence of a paradoxical reaction in the form of an increase in PST in patients with coronary artery disease was observed to a greater extent.

Claims (1)

A method for determining endothelium-dependent vasodilation by assessing changes in the pulse wave velocity (PWV) against the background of reactive hyperemia, while the PWV is determined on the site of the carotid artery - the radial artery at rest and immediately after stopping the clamping of the brachial artery, and a normal decrease in the PWV by an average of 21 , 2% in patients with coronary heart disease - a decrease in SST by an average of 3.9%, while in some patients there was an increase or absence of changes in SPS, clamping of the brachial artery was carried out by the cuff of the manometer measuring blood pressure (BP) for 3 minutes, increasing the pressure by at least 50 mmHg from systolic blood pressure.