Pharmacological tests in cardiology. Pharmacological test with isoproterenol, which causes an increase in heart rate and myocardial contractility Indications and contraindications

Functional stress tests are used in the diagnosis of IHD. They are divided into tests that improve metabolism in the myocardium (test with potassium, obzidan, rauwolfia preparations, ambosex), improve coronary circulation (tests with nitroglycerin), and increase the load on the myocardium and the myocardial oxygen demand (test with physical activity).

Medication tests Drug tests are prescribed to patients with suspected ischemic heart disease and with an altered terminal part of the ventricular complex. Before administering the drug, a baseline ECG is recorded, and after administration, a control ECG is recorded.

Test with potassium P When potassium is given to patients with metabolic disorders in the myocardium, there is an improvement in metabolic processes and normalization of the final part of the ventricular complex. Therefore, the test is positive when functional disorders in the myocardium. The potassium test is contraindicated in persons over 60 years of age and in patients with impaired atrioventricular and intraventricular conduction. After a light breakfast, the patient is given 5–6 g of potassium chloride dissolved in 100 ml of water. The control ECG is examined after 30, 60, 90 minutes.

Nitroglycerin test

When nitroglycerin is given to patients with coronary artery disease, an improvement in the terminal part of the ventricular complex is observed. Therefore, a positive test indicates the presence of ischemic heart disease. The patient is given 2-3 drops of a 1% solution of nitroglycerin under the tongue or 1 tablet of nitroglycerin. A control ECG is taken after 5 and 10 minutes. To prevent collaptoid reactions, the test is performed in a horizontal position.

Test with obsidan

The test is positive for functional disorders of the heart and is associated with blockade of β 1 - β 2 adrenergic receptors.

The test is carried out in the morning on an empty stomach, the patient is given 40–60 mg of ob-zidan or anaprilin. A control ECG is taken 30, 60, 90 minutes after taking the drug.

Isoprenaline test

The drug stimulates β 1 - and β 2 -adrenergic receptors, increases heart rate and myocardial oxygen demand. Isoprenaline (isadrin) 0.5 mg (1 ampoule) is diluted in 250 ml of saline or 5% glucose solution. The drug is administered intravenously dropwise until the pulse rate reaches 130–140 beats (more correctly, up to a submaximal rate of 200 - age in years). After reaching the required heart rate, hold it for 3 minutes. After the end of the test and after 5 and 10 minutes, a control ECG is taken. The test is assessed in the same way as for a test with physical activity. During the test, arterial hypertension and ventricular extrasystole may be observed. The test is carried out in a specialized department.

Ergometrine test

Ergometrine increases the tone of smooth muscles, including coronary vessels, and reveals variant Prinzmetal angina. Ergometrine is administered intravenously as a bolus of 0.15 and 0.3 mg, with a 5-minute break between administrations. The test is carried out under constant ECG control during the test and 15 minutes after its completion.

The assessment of the test is the same as for bicycle ergometry. The test is carried out in a specialized department.

Test with chimes (dipyridamole) The drug is a powerful vasodilator, dilates the

coronary arteries affected by atherosclerosis and does not expand those narrowed by atherosclerosis. As a result, there is an even greater decrease in blood flow in the ischemic areas of the myocardium, which is known as the steal phenomenon and is manifested by an attack of angina or an ischemic ECG change.

Dipyridamole (chirantil) is administered intravenously at the rate of 0.75 mg per 1 kg of body weight. The calculated dose is divided into 3 parts. The first third of the dose is administered over 3 minutes, the second third over 7 minutes. If an attack of angina or ischemic ECG changes occurs, further administration of the drug should be stopped; if they do not exist, a third of the dose is administered over 5 minutes. When an attack of angina occurs, a nitroglycerin tablet is given under the tongue and 5–10 ml of a 0.24% aminophylline solution is injected intravenously. Eufillin is a physiological antagonist of dipyridamole. Tests are carried out in cases where it is impossible to perform a VEP.

Breath-hold tests, orthostatic and sugar tests are less informative for identifying IHD.

Breath-hold test The test is performed in a supine position. The initial ECG is taken. The subject takes a deep breath and holds his breath. The duration of the breath hold is determined and a control ECG is taken at the end of the hold. In the presence of IHD, negative T readings appear. Normal minimum time hold your breath for 30 seconds.

Orthostatic test

Causes an increase in the tone of the sympathetic nervous system and reflex tachycardia. Increased heart rate increases the myocardial oxygen demand and the appearance of coronary disorders.

The initial ECG is recorded in a horizontal position, then the patient is asked to stand and the ECG is recorded in a vertical position after 30 seconds, 3, 5 and 10 seconds.

Sugar test The sugar test is performed on an empty stomach. The subject is taken with an initial ECG and 40 ml of a 40% glucose solution is administered intravenously. Control ECGs are taken immediately after glucose administration and at 10-minute intervals for an hour. In patients with coronary artery disease, negative T waves are recorded on the ECG; the mechanism of changes in T waves is unclear; apparently, it is associated with an increase in oxygen consumption of the heart muscle, which is necessary for the utilization of glucose in the heart muscle.

The frequency of positive samples increases with increasing severity of atherosclerotic cardiosclerosis.

Bicycle ergometer test

VEP is one of the options for exercise testing to detect coronary artery disease. The diagnostic value of VEP is 85% with high specificity. In addition to VEP, physical activity on the treadmill, Master's test, step test, abnormal physical activity in the form of climbing stairs, squats, running, walking, etc. are used to identify IHD.

The diagnostic value of treadmill load for identifying ischemic heart disease approaches that of VEP, but medical institutions do not have treadmills. The Master's test and the step test are of little use for the early diagnosis of IHD due to the low power of physical activity. Therefore, VEP is widely used in cardiology.

Indications:

1) detection of coronary artery disease (early and clinically pronounced forms);

2) determination of exercise tolerance in patients with coronary artery disease and the functional class of exertional angina;

3) monitoring the effectiveness of treatment for patients with coronary artery disease;

4) determination of the effectiveness of coronary agents;

5) identification of transient arrhythmias. In addition to diagnosing coronary heart disease, VEP is widely used for the rehabilitation of patients with cardiovascular pathology.

Most often, VEP is used to diagnose coronary artery disease. Contraindications to VEP in the diagnosis of coronary artery disease:

1) progressive angina, suspicion of myo
card;

2) rhythm disturbance ( frequent extrasystole, atrial fibrillation, paroxysmal tachycardia);

3) conduction disorders (atrioventricular blockade, complete blockade of the left or right leg His bundle).

VEP should not be prescribed if the initial blood pressure is 170/100 mmHg. Art. and higher as the temperature rises.

Currently, a continuously stepwise increase in VEP is generally accepted until the end points - submaximal pulse rate or positive test criteria.

180 kg/m/min, every 3 minutes the load power increases by 25–30 W (150–180 kg/m/min). The load is performed on an empty stomach or no earlier than 2 hours after eating. Smoking is prohibited during this period. Patients with coronary artery disease do not take nitrates, β-blockers, tranquilizers, cardiac glycosides, or diuretics on the day of the test.

Positive criteria VEP for identifying IHD:

1) angina attack during the test;

2) ST depression more than 1 mm horizontal;

3) oblique ST depression more than 1.5 mm through 0.08 from the junction point or QX more than 50;% QT;

4) frequent extrasystole (4:40 or more), transient atrioventricular and ventricular block;

5) deepening or broadening of previously existing Q.
Other criteria (decrease and inversion of T, increase in am
amplitudes R) have low specificity for identifying ischemic heart disease.

The test is considered negative when the subject reaches a submaximal pulse rate without signs of coronary insufficiency.

VEP stops when blood pressure decreases by 25–30% from the initial level, blood pressure increases to more than 220/120 mm Hg. Art., a feeling of lack of air, the appearance of general weakness, dizziness, and the patient’s refusal to carry out the test.

VEP should be performed in a stress test room equipped with a bicycle ergometer, a multichannel electrocardiograph with an oscilloscope, and equipment for studying oxygen consumption. It is necessary to have a defibrillator and a set of emergency medications (nitroglycerin, cardamine, mezaton, analgin, promedol, fentanyl, ammonia, etc.). There should be a syringe in the bag with alcohol. Medical personnel (doctor and technician conducting the study) must have the skills resuscitation measures. Before the start of the study, an ECG is recorded in 12 leads, every 3 minutes it is advisable to monitor the ECG III, avF, V 2, V 4 - V 6 leads, or chest V 1 - V 6, using an oscilloscope, observation is carried out in lead V 5. After the end of the load, the ECG is recorded in 12 leads, the ECG is monitored during the recovery period after 5 and 10 minutes.

In cardiology, the most frequently used functional tests are tests with physical activity (bicycle ergometer, treadmill). They are usually performed on patients for the purpose of diagnosis, determining prognosis and functional assessment. Continuous step-increasing load is given until the appearance of symptoms indicating its poor tolerance, or until the subject reaches a certain heart rate (submaximal, maximum). The amount of load performed is usually expressed in watts (W). The maximum oxygen consumption may also be indicated in MET units (metabolic equivalent) - in ml of oxygen used per 1 kg of body weight per minute. During exercise, ECG, blood pressure, and sometimes ventilation parameters are recorded. There are physiological and pathological reactions to stress. The pathological reaction that has the greatest clinical and diagnostic significance in CAD is the appearance of angina and ECG changes in the form of a horizontal or oblique decrease in the ST segment by 1 mm or more. Pathological changes in blood pressure include its insufficient increase or decrease during exercise, which indicates the development of severe left ventricular dysfunction, or an excessive increase in blood pressure (with arterial hypertension).

Keywords: diagnostics, coronary heart disease, tests with dosed physical activity, bicycle ergometry, dobutamine test, test with dipyridamole.

GENERAL CHARACTERISTICS

Functional or stress testing in cardiology is used to determine response of cardio-vascular system with increased demands on it (physical, psycho-emotional stress) or in artificial conditions (changes in body position in space, after the administration of pharmaceuticals) for diagnosis, determination of prognosis and functional assessment (Table 5.1).

Tests with physical activity, as the most physiological and informative, are used more often than others.

A psycho-emotional test consists of performing a logical, mathematical or mechanical task under unfavorable external conditions (limited time, noise, temperature, lighting, etc.).

Pharmacological tests are usually performed with drugs that cause hemodynamic reactions, for example, dobutamine, which has a rapid and pronounced inotropic effect, or dipyridamole, which causes coronary dilation and coronary steal syndrome.

For the first time, ECG changes in the occurrence of pain during physical activity in patients with angina pectoris were described by N. Feil and M. Segal in 1928 in the USA.

A year later, A. Master and F. Oppenheimer developed a standardized exercise protocol.

In 1993, D. Sherif and S. Goldhammer in Germany proposed a technique for conducting a stress test with simultaneous recording of an ECG.

In 1950, A. Master in the USA introduced a two-stage load test.

Table 5.1

Types of Load Tests

With physical activity:

Dynamic (bicycle ergometer, treadmill)

Isometric (wrist press) Psycho-emotional

Pharmacological (dobutamine, dipyridamole)

With changes in body position in space and during accelerations

Transesophageal pacing

Tests involving changes in body position in space and acceleration are used in aerospace medicine for the purpose of selecting and monitoring the training of pilots and astronauts.

Transesophageal pacing is used to assess sinus node function or provocation of myocardial ischemia caused by increased heart rate.

During exercise, hemodynamic (heart rate, blood pressure) and ventilation parameters (oxygen consumption, carbon dioxide emissions, respiratory rate, minute ventilation) can be measured. In special cases, stress tests are often combined with other studies: with echocardiography - for the purpose, for example, of identifying areas of myocardial asynergy or with myocardial scintigraphy with thallium-201 to assess its perfusion. Instrumental monitoring can be carried out in automatic mode (ECG, blood pressure). To evaluate the ECG, a computer is used, which, based on the average ECG complex, analyzes the position of the ST segment, the steepness of ST elevation or depression and other parameters. At the same time, oxygen consumption and carbon dioxide release can be determined, which makes it possible to calculate energy expenditure and aerobic capacity (the amount of oxygen absorbed in 1 minute per 1 kg of body weight).

PHYSIOLOGICAL AND PATHOLOGICAL RESPONSES TO LOAD

During exercise, heart rate increases rapidly, which depends on the intensity of the exercise and the muscle mass involved. As a result of this, as well as the Frank-Starling mechanism, cardiac output and oxygen uptake increases. Maximum oxygen consumption or maximum aerobic capacity is determined by the arteriovenous oxygen difference and cardiac output. With increasing age, this ability decreases. With cardiovascular disease or detraining, aerobic capacity also decreases due to limited cardiac output.

Maximum aerobic capacity can be determined with acceptable accuracy using empirical formulas that take into account gender, age, weight and height. With sufficient load power, achievable

reaching approximately 50-60% of maximum aerobic capacity, muscles switch to anaerobic metabolism. The lactate level in the blood begins to rise. Due to the interaction of lactate with buffered bicarbonate in the blood, the release of carbon dioxide increases, which becomes disproportionately large in relation to oxygen consumption. The respiratory coefficient reflects the ratio between the volume of carbon dioxide released and the amount of oxygen absorbed and usually at rest ranges from 0.7-0.85 depending on the substrate that is used for oxidation (1.0 - with the predominant use of carbohydrates and 0.7 - with the predominant use of fatty acids). If during exercise the subject reaches the anaerobic threshold, then the respiratory coefficient exceeds 1.1.

The term metabolic equivalent (MET) describes the resting oxygen consumption of a 40-year-old man weighing 70 kg. One MET unit is equal to the consumption of 3.5 ml of oxygen per 1 kg of body weight per minute. Therefore, work intensity can be expressed in MET units.

At maximum heart rate, the body uses 100% of its aerobic capacity, i.e. ability to capture and use oxygen.

Maximum heart rate is calculated using the formula:

Heart rate max = 220 - age.

The approximate values ​​of heart rate max are as follows: 20 years - 200; 30 years - 190; 40 years - 180; 50 years - 170; 60 years - 160. In addition, there is the concept of submaximal heart rate, which occurs during submaximal exercise, when not 100% aerobic capacity is achieved, but a smaller, predetermined one, for example, 70 or 80% of aerobic capacity. This predetermined target load corresponds to experimentally determined heart rate values, and the load continues until the subject has reached submaximal heart rate values. This will be the submaximal load.

Submaximal heart rate is determined by the equation:

Heart rate submax = 220 - (age? 0.65).

In some people, heart rate increases slightly in response to exercise, indicating dysfunction of the sinus node (sick sinus syndrome, hypothyroidism) or the influence of drugs (beta-blockers, ivabradine). Excessive acceleration of heart rate occurs with detraining, unusual anxiety, LV dysfunction, anemia, hyperfunction of the thyroid gland.

With increasing load, systolic blood pressure increases, reaching 200 mm Hg. and more. A more significant increase in blood pressure is typical for hypertensive patients. Diastolic blood pressure healthy people does not change significantly (with fluctuations of ±10 mm Hg), but increases in hypertensive patients.

If SBP does not increase or decreases during exercise, this may be due to insufficient cardiac output (myocardial dysfunction) or excessive systemic vasodilation. Insufficient increase in blood pressure during exercise or even its decrease occurs not only in cardiovascular diseases in which myocardial dysfunction develops during exercise (with the development of angina, myocardial disease, taking antihypertensive drugs, arrhythmias), but also in people with pronounced vasovagal reactions. A decrease in blood pressure during the onset of angina during exercise is typical of severe stenotic coronary lesions and asynergy in ischemic areas of the LV myocardium.

At a constant submaximal level of load, after 2-3 minutes a steady state is established, in which heart rate, blood pressure, cardiac output and pulmonary ventilation remain at a relatively stable level.

People with impaired cardiorespiratory function may not have a steady state, and the oxygen debt increases with exercise. After stopping the load, their oxygen consumption exceeds their normal consumption at rest by the amount of oxygen debt.

The product of heart rate and systolic blood pressure (double product) increases with increasing load and correlates with myocardial oxygen consumption. The calculation of this product is used

as an indirect index of myocardial oxygen consumption.

With detraining and with increasing age, the maximum myocardial oxygen consumption during exercise decreases due to an age-related decrease in maximum heart rate and systolic output.

The uptake of oxygen from the coronary bloodstream by the myocardium, even at rest, is maximum, and its increase during exercise is achieved due to coronary dilatation. With CAD, this dilatation is impossible in areas of stenosis. In addition, patients with variant Prinzmetal angina, which is rare, may experience coronary vasospasm during exercise. Therefore, in patients with angina pectoris during physical activity, there comes a period when, due to stenosis of the coronary vessels, an increase in oxygen delivery to the myocardium becomes impossible and cannot be higher than a certain level (internal angina threshold).

Therefore, myocardial oxygen consumption during the development of angina pectoris is maximum, which can be expressed by a double product, the value of which during the period of pain onset is also maximum for a given patient and characterizes his internal angina threshold.

Subendocardial areas of the myocardium are more susceptible to ischemia due to higher systolic tension. With the development of ischemia, the so-called ischemic cascade begins (Table 5.2).

Table 5.2

Ischemic cascade

Increased lactate production

Diastolic dysfunction:

Impaired diastolic filling;

Increased diastolic pressure Systolic dysfunction:

Impaired contractility of ischemic areas of the heart;

Decreased ejection fraction (EF) and systolic ejection ECG changes

Angina pectoris

The double product (heart rate and systolic blood pressure) is an index of myocardial oxygen consumption, and during the development of angina pectoris it is maximum for a given patient.

ECG CHANGES DURING LOAD

Under load as heart rate increases P-Q intervals, QRS and QT shorten, P voltage increases, the J point and ST segment decrease, the ST segment takes on an oblique-ascending appearance (functional decrease) (Fig. 5.1).

From top left to bottom: normal ECG, J-point of connection (“junction”, English) of the S wave and the ST segment; rapidly ascending ST segment depression, normal variant; deep horizontal ST depression indicating subendocardial myocardial ischemia.

From top right to bottom: downward-sloping ST depression, characteristic of subendocardial myocardial ischemia; ST segment elevation, indicating transmural myocardial ischemia; elevation of the ST segment in the scar area after Q-infarction, associated with asynergy of the left ventricular myocardium.

In patients with exertional angina, when subendocardial myocardial ischemia occurs, a decrease in the ST segment of a slowly ascending, horizontal or oblique type occurs (Fig. 5.1-5.4). The depth of depression increases with increasing ischemia.

As ischemia increases, slowly ascending depression can turn into horizontal and then downward. After the load is stopped, these changes disappear within a few minutes and the ECG becomes normal, but immediately after the load is stopped, the horizontal depression of the ST segment can turn into a downward depression. If changes in the position of the ST segment are already present at rest, this should be taken into account during subsequent assessment. With a large decrease in this segment at rest, the value of a stress test to assess changes in the position of the ST segment is significantly reduced.

To measure ST segment depression, the PQ segment is used as an isoline. It is advisable to have three consecutive

Rice. 5.1. Changes in the ST segment during exercise. Explanations in the text

Rice. 5.2. ECG in chest leads at rest (left) and at threshold load (right) in a patient with CAD. During exercise, slowly ascending ST segment depression (2 mm at ST60 in lead V5), indicating myocardial ischemia

Rice. 5.3. ECG in chest leads at rest (left) and at threshold load (right) in a patient with CAD. On the right, horizontal ST depression (1.8 mm in lead V5), indicating myocardial ischemia

Rice. 5.4. ECG in chest leads at rest (left) and at threshold load (right) in a patient with CAD. On the right - depression of the ST segment of an oblique type (by 1.6 mm in lead V5), indicating myocardial ischemia

ECG complex with a good isoline. Depression of the ST segment of a horizontal or oblique type by more than 1 mm at a distance of 80 milliseconds from the J point (ST 80) is considered nonphysiological and occurs with myocardial ischemia. When the heart rate exceeds 130 bpm, the ST 60 point is sometimes used to determine ST segment depression (some ECG machines always use the ST 60 point).

Points ST 60 and ST 80 are sometimes designated by the letter "i" (ischemia), and its offset from the isoline by the letter “h” (height, vertical dimension).

Rapidly rising ST depression (less than 1.5 mm at ST 80) during maximal exercise is considered a normal response. Slowly rising depression of 1.5 mm or more at ST 80 is considered an abnormal response and occurs in patients with stenotic atherosclerotic coronary artery disease and in people with a high pretest probability of CAD. In people with a low pretest probability of CAD, a definite assessment of such changes is difficult.

Sometimes in leads with a pathological Q wave (after a MI) or without such a Q, ST segment elevation is observed. In the first case, it is interpreted as an indicator of myocardial dysfunction (akinesia, dyskinesia) in the area of ​​former MI, usually in patients with reduced EF and poor prognosis. ST elevation in leads without pathological Q is regarded as an indicator of severe transmural myocardial ischemia (Fig. 5.5).

Changes in the ST segment during exercise in patients with CAD cannot be used to localize ischemia and coronary lesions.

In addition to coronary causes, there are also non-coronary causes of ST segment depression:

LV hypertrophy (aortic stenosis, arterial hypertension);

Hypokalemia;

Treatment with cardiac glycosides;

Hyperventilation;

Mitral valve prolapse;

WPW syndrome;

Intraventricular conduction disorders;

Severe volume overload (aortic, mitral insufficiency);

Supraventricular tachycardia.

Rice. 5.5. ECG in precordial leads V1-5 at rest (left) and at threshold load (right) in a patient with early post-infarction angina. A stress test was performed 3 weeks after the development of MI without a Q wave. With a low load (25 W), grade 3 angina developed with ST segment elevation of 2.5-3.0 mm in the precordial leads, indicating severe transmural myocardial ischemia

Changes in the T wave during exercise are nonspecific. Its form, even at rest and in healthy people, is highly variable and depends on many factors (body position, breathing). With hyperventilation, flattening of the T waves or the appearance of negative ones are often observed. If T waves are negative before exercise, they often become positive during exercise, and this is not considered a sign of disease.

Ventricular extrasystoles, including group ones, or ventricular “jogs” occur during exercise in healthy people. On the other hand, both in healthy people and in patients with CAD, ventricular extrasystole can disappear with exercise. Therefore, it does not have significant diagnostic value. In patients who have had an MI, group ventricular extrasystoles or periods of ventricular paroxysmal tachycardia during exercise are more common in patients at high risk of sudden death.

Supraventricular extrasystole during exercise is observed both in healthy people and in patients with heart disease. For the diagnosis of CAD, its appearance during the test is not significant.

During exercise, a blockade of the left or right bundle branch may occur, although rarely, which has no independent diagnostic or prognostic value.

With myocardial ischemia, the ECG shows depression of the ST segment (deep obliquely ascending, horizontal, obliquely descending) or elevation (rarely) of the ST segment (in leads without a post-infarction Q wave)

CARRYING OUT A TEST WITH DOSED PHYSICAL ACTIVITY

When studying cardiac patients, the most physiological and informative tests are exercise tests on a bicycle ergometer or treadmill, but a 6-minute walking test can also be used. The name "treadmill" comes from English verb "to thread"- step, put your foot down and noun "mill"- mill. In the Middle Ages, prisoners were forced to set the mill mechanism in motion by stepping on the steps of a large wheel.

The disadvantages of bicycle ergometry include learning difficulties for older women, as well as a large increase in blood pressure compared to walking on a treadmill. But a bicycle ergometer takes up less space, makes less noise and costs less. A device like a bicycle ergometer can also be adapted to work with your hands.

Before exercise, a 12-lead ECG is recorded in the supine and sitting position, and blood pressure is measured. Most loading tests are carried out in the form of a continuous step-increasing load. The duration of each load level is 1-5 minutes. It is advisable that the total examination time does not exceed 15 minutes, since otherwise most patients will not be able to continue working due to general fatigue and weakness in the legs.

The test begins with a warm-up for 1-2 minutes, followed by a loading period, during which the load gradually or intermittently (stepwise) increases.

At the end of each load stage, an ECG is recorded and blood pressure is measured.

The load is dosed either in watts (W) or in kilopond meters per minute, 1W = 6 kilopond meters/min.

Here are several bicycle ergometry protocols (Fig. 5.6), which may differ from those used in other countries and centers:

Rice. 5.6. Exercise protocols

1. The load starts at 10 watts for 1 minute and increases by 10 watts every minute.

2. The load starts at 20 watts for 2 minutes and increases by 20 watts every 2 minutes.

3. The load starts at 30 watts for 3 minutes and increases by 30 watts every 3 minutes.

4. The load starts at 25 or 50 watts for 5 minutes and increases by 25-50 watts every 5 minutes (“Scandinavian” protocol).

The threshold power of the performed load is calculated using the formula:

Power = A + [(V - A)/T]g,

where A is the power of the last fully completed load stage; B is the power of the load stage at which the test was stopped; T is the duration of each load step (min) according to the protocol; t is the duration of the load (min) at the last stage.

If the subject has completely completed the next stage of the load, but has not progressed further, this will be his threshold power. For example, if the subject completely completed the load stages of 50 and 100 watts for 5 minutes each stage and the test was stopped, then his threshold power is 100 watts.

If, after performing a load with a power of 100 watts, the subject performed the next load with a power of 150 watts for 1 minute, his threshold power is 110 watts, 2 minutes - 120 watts, 3 minutes - 130 watts, 4 minutes - 140 watts and 5 min - 150 watts, etc.

Or with a different protocol. For example, the subject performed sequential 3-minute load stages with a power of 60 and 90 watts, i.e. his threshold power is 90 watts, if there was the next load step with a power of 120 watts and he completed it within 1 minute, then his threshold power is 100 watts, 2 minutes - 110 watts, 3 minutes - 120 watts, etc.

The load on the bicycle ergometer is performed until subjective or objective signs of the inappropriateness or impossibility of continuing it appear, which are called the criteria for stopping the load (Table 5.3).

After stopping, the samples are recorded/or observed on an ECG monitor for 5 minutes or until it is completely normalized.

Evaluation of research results Test positive

This conclusion is based only on ischemic changes in the ST segment, which include:

Horizontal or downward ST segment depression (ST 80) of 1 mm or more;

Slowly rising ST segment depression (ST 80) of 1.5 mm or more;

ST segment elevation (ST 60) of 1 mm or more in leads without a post-infarction Q wave.

Table 5.3

Load termination criteria*

Subjective Angina pectoris, grade 3 on a 5-point scale:

1 - very light

2 - light

3 - quite strong

4 - strong

5 - intolerable fatigue

Severe shortness of breath (relative indication) Pain in legs, joints Dizziness

Pallor or cyanosis

Reluctance of the subject to continue the load Objective ECG changes

ST segment depression of 2 mm or more from baseline through 80 milliseconds from the J point (ST 80) of a horizontal or downward type (relative reading)

ST segment elevation of more than 2 mm in leads with a Q wave or more than 1 mm in leads without a pathological Q wave (ST 60)

The appearance of paroxysmal cardiac arrhythmias

Increasing frequency of ventricular extrasystoles, especially polymorphic, group ones (relative indication)

Supraventricular tachycardia (relative indication)

The appearance of new conduction disorders, bradyarrhythmias (relative indication)

Submaximal heart rate (approximately 85% of maximum, approximately equal to 200 - age):

20 years - 180

30 years - 170

40 years - 160

50 years - 150

60 years and older - 140-130 Changes in blood pressure

Increase in systolic blood pressure more than 220 mm Hg. or diastolic more than 115 mm Hg. (relative reading)

A decrease in systolic blood pressure by more than 10 mm Hg, despite an increase in load or no increase in two or more levels of load (relative reading)

Note:*may vary different countries and centers.

Test negative

This conclusion is possible when the patient reaches a submaximal heart rate without ischemic changes on the ECG. In a number of clinics they distinguish negative test with features - when rhythm and conduction disturbances appear during the study or when blood pressure increases above normal indicators for the corresponding load level, etc.

The test is questionable

This conclusion is justified when an ST 80 depression of less than 1 mm and (or) pain in the chest appears on the ECG.

If the test is stopped for other reasons, this is reflected in the conclusion. For example, the test is stopped because the systolic blood pressure reaches 230 mm Hg. or general fatigue, etc.

The second part of the conclusion characterizes exercise tolerance. To do this, it is necessary to calculate the threshold load power (see above).

When performing treadmill measurements, special tables are used, where power and aerobic capacity (in MET units) are determined by the level of load, or these parameters are issued automatically by a computer, as is the conclusion of the test.

The normal threshold load for untrained men 40-50 years old is 2 W/kg body weight, for women - 1.5 W/kg body weight.

It is believed that in men with angina pectoris of functional class 1, the threshold load is about 1.5 W/kg, with class 2 1-1.5 W/kg, with class 3 0.5-1 W/kg and class 4 0.5 W /kg body weight. These are average values.

Teddylometry

Multi-stage protocols are used (Naughton, Bruce, etc.), the duration of each load stage is 1-3 minutes. To increase the load power, the speed of the track and its elevation angle are increased. While walking along the path, subjects can hold onto handrails.

Wrist press

A form of static exercise that causes a greater increase in blood pressure and a smaller increase in heart rate compared to exercise

bicycle ergometer or treadmill. The increase in heart rate is often insufficient to provoke myocardial ischemia. First, the maximum compression force is recorded on a hand-held dynamometer, then the subject squeezes the dynamometer to 1/4-1/3 of the maximum force and holds the press for 3-5 minutes.

Indications and contraindications for stress tests

Stress tests are of greatest importance in diagnosis, functional and prognostic assessment in patients with CAD (Table 5.4).

Table 5.4

Indications for stress testing

Diagnosis of CHD

Establishing the functional class of angina pectoris, assessing the effectiveness of various interventions (medicines, surgeries, etc.)

Assessment of prognosis in cardiac patients

Selection of training load for physical rehabilitation

Determination of the cardiovascular system's response to stress

Since complications may develop during stress tests, the patient’s condition should be monitored during exercise (visually, ECG, blood pressure) and patients with a high risk of complications should not be tested (Table 5.5).

The physician recommending exercise testing should explain the purpose of the test and the possible response to exercise. It is advisable to obtain the patient's informed consent for the test. The study is carried out by a doctor trained in cardiac intensive care. The room for stress tests is equipped with a defibrillator and other resuscitation equipment.

Before the diagnostic test, antianginal drugs are discontinued (nitrates 24 hours before, calcium antagonists and β-blockers 48 hours before the test). Changes in the ST segment at rest and during exercise can be affected by cardiac glucosides (it is advisable to discontinue them 7 days before the test), saluretics, tricyclic antidepressants, and lithium salts. If possible, the latest medications should be discontinued 3-4 days before the test. Antianginal drugs are not discontinued when determining their effect on exercise tolerance in patients with angina pectoris.

Table 5.5

Contraindications for exercise testing*

Unstable angina

Acute MI (during the first days)

Dangerous arrhythmias

Decompensated heart failure

High degrees of sinoauricular or atrioventricular block

Acute myocarditis, pericarditis

Uncontrolled hypertension

Aortic aneurysm

Severe aortic or subaortic stenosis

Acute systemic disease

Acute thrombophlebitis

Acute cerebrovascular accident Note:* may vary by country and center.

THE IMPORTANCE OF EXERCISE TESTS

Use of exercise tests to diagnose CAD

When explaining the results of stress tests, you should consider the possible limitations inherent in these methods and learn a number of new concepts that are relevant to any research method (Table 5.6).

A 1998 European meta-analysis of bicycle ergometry compared with coronary angiography in 24,074 patients showed a sensitivity of 68% (23-100%) and a specificity of 77% (17-100%) in middle age.

The sensitivity of the test increases with the number of affected vessels: from 25-71% with damage to a single vessel to 81-86% (40-100%) with multi-vessel disease. Changes in the ST segment during exercise are more often detected with atherosclerotic changes in the anterior branch of the left coronary artery.

A positive stress test may occur in people with angiographically normal coronary vessels, e.g.

measures due to a violation of the mechanism of coronary vasodilation (coronary X syndrome), with LV hypertrophy, cardiomyopathies. In addition, the appearance of “ischemic” changes in the ST segment during physical activity is possible during treatment with cardiac glycosides, with hypokalemia, anemia, and mitral valve prolapse.

Table 5.6

Basic terminology when assessing physical test results

load

Ischemic ECG changes during exercise become more pronounced as multivessel coronary lesions develop in patients with CAD and with increasing load levels, with the most informative leads V4 - 6 (Table 5.7).

Table 5.7

Signs of severe coronary lesions during stress testing

Early onset of angina

No increase in systolic blood pressure as the level of exercise increases or its decrease

Deep depression of the ST segment of the oblique type,

persisting for more than 5 minutes after exercise

ST segment elevation during exercise

(in leads without pathological Q)

Prognostic value of exercise tests

The prognostic value of stress tests has been studied in healthy people and in patients with cardiovascular diseases (Table 5.8).

Table 5.8

Groups of subjects and features of the exercise test, characterizing an increased risk of developing cardiovascular diseases and complications

Use of graded physical exercise tests for functional assessment of cardiovascular patients

First of all, these are patients with coronary artery disease, chronic heart failure and heart defects.

Along with other research methods, stress tests are used to functionally assess patients with cardiac arrhythmias and test the effect of antiarrhythmic drugs. Thus, in patients with paroxysmal ventricular tachycardia, physical activity usually provokes ventricular arrhythmias, incl. and paroxysms of ventricular tachycardia. In patients with sick sinus syndrome, a stress test demonstrates that the heart rate does not increase sufficiently during exercise, although this is not the rule.

In patients with a tendency to hypertension, a more significant increase in blood pressure is detected during exercise.

Patients with heart defects undergo functional assessment before and after surgery.

PHARMACOLOGICAL TESTS

Dipyridamole

Used to provoke myocardial ischemia and mainly during myocardial perfusion studies with thallium-201. Dipyridamole blocks the metabolism of adenosine. Adenosine is formed from ATP, has a short half-life (10 s) and has a pronounced local arteriolodilating effect. Intravenous administration of dipyridamole increases the concentration of adenosine in the myocardium, increases coronary blood flow, slightly reduces systolic blood pressure and accelerates heart rate. In areas of the myocardium that are supplied with blood through stenotic arteries (85-90% stenosis), the coronary bed distal to the stenosis is maximally expanded already at rest. There is no coronary reserve in these areas. The administration of dipyridamole can lead to a redistribution of coronary blood flow towards less stenotic or healthy arteries and “intercoronary steal”, i.e. ischemia of myocardial areas distal to the stenosis. The appearance of ischemia is indicated by the development of angina pectoris and changes in the ECG.

Indications: impossibility of carrying out tests with physical activity (in persons with joint diseases, vessels lower limbs etc.) or stopping the exercise test before reaching the criteria for its evaluation, provoking myocardial ischemia during radionuclide studies.

Contraindications the same as for testing with physical activity.

Dipyridamole is administered intravenously at the rate of 0.75 mg/kg body weight (sometimes a dose of 0.84 mg/kg body weight is used), in a physiological solution of 20 ml for 5 minutes (4 ml/min). The endpoints and evaluation criteria of the dipyridamole test are similar to the exercise test.

Dipyridamole, causing coronary vasodilation, increases blood flow in unchanged vessels and reduces it (stealing) in stenotic ones, which creates ischemia in the area of ​​their blood supply.

Side effects when taking dipyridamole: headache, nausea, weakness.

The dipyridamole test provokes myocardial ischemia mainly in cases of severe stenosis of the coronary arteries and has low sensitivity (20-30%).

Dipyridamole infusion is often given before the radiotracer is inserted for myocardial scintigraphy.

Sometimes a dipyridamole test is combined with a low-power stress test.

Dobutamine

Dobutamine is a short-acting synthetic catecholamine, the intravenous administration of which increases heart rate, blood pressure, myocardial contractility and, as a result, myocardial oxygen demand. The occurrence of ischemia is recognized using myocardial scintigraphy with thallium-201 or stress echocardiography. During the latter, changes in local contractility are monitored, which is disrupted with the development of myocardial ischemia.

The dobutamine test is used for diagnostic purposes in patients who cannot perform a test with dosed physical activity or if such a test is not informative.

Diabetes mellitus, smoking, family history, hyperlipoproteinemia and elderly age– increase the likelihood that the cause of chest pain is myocardial ischemia.

Symptoms

Angina pectoris is characterized by the following qualities.

1. Localization

Unpleasant sensations or pain are usually localized behind the sternum, radiating to the neck, shoulders, arms, jaws, epigastrium or back. Sometimes there may be only radiating pain, without substernal pain.

2. Conditions of occurrence

Angina pectoris usually occurs during physical activity, emotional stress, cold, heavy eating or smoking.

Sometimes angina goes away despite continued exercise—this is called “working through the pain.” In other cases, a so-called “warm-up” is observed: first, angina pectoris occurs during physical activity, but when the same load is repeated, angina no longer occurs. Perhaps the disappearance of angina in these cases is due to an increase in collateral blood flow.

Angina pectoris that occurs in the supine position (angina decubitus) is quite rare. Ischemia in this case is thought to be due to volume overload. Nocturnal angina attacks can manifest as nightmares and tachycardia.

3. Nature of pain

Most patients describe angina as discomfort in the chest. This may be a feeling of squeezing, burning, tightness, suffocation, heaviness, and sometimes cold or heat. Many people do not consider these sensations to be pain. Sometimes angina presents with shortness of breath, extreme fatigue, weakness, dizziness, nausea, sweating, confusion, or fainting without any reason. discomfort in the chest. Such complaints are called angina equivalents.

4. Duration

An attack of angina usually lasts 3-5 minutes. Myocardial ischemia lasting more than 30 minutes usually causes infarction. Angina caused by emotional stress, usually lasts longer than that caused by physical activity. Chest pain lasting less than 1 minute is rarely caused by myocardial ischemia, especially if it is not accompanied by other characteristic symptoms.

5. Classification

Several classifications have been developed to assess severity and determine prognosis. The most commonly used classification is the Canadian Society of Cardiology.

Other classifications include the Specific Activity Scale, Duke Activity Status Index.

Physical examination

Allows you to identify risk factors for atherosclerosis and other heart diseases.

1. A high risk of atherosclerosis is indicated by high blood pressure, a lipoid arch of the cornea, xanthelasmas, changes in the retinal arteries, a diagonal fold of the earlobe, signs of damage to the carotid and peripheral arteries.

2. During a physical examination during an attack of angina, moist rales in the lungs, III and IV heart sounds and systolic murmur of ischemic mitral insufficiency can be detected. All these phenomena disappear at the end of the attack.

ECG at rest

1. The role of the ECG at rest is small; 60% of patients with chest pain have no ECG changes. In some cases, however, a resting ECG can help determine the etiology of chest pain and assess the risk of cardiovascular complications. Q waves and persistent ST segment depression indicate a less favorable prognosis. In addition, the ECG can detect other disorders: left ventricular hypertrophy, bundle branch block, and ventricular preexcitation syndrome.

2. An ECG during an attack is more informative. Transient changes in the T wave and ST segment, as well as conduction disturbances, indicate an ischemic origin of pain. However, a normal ECG in this case does not exclude angina pectoris.

Additional Research

For stable angina, testing is done to assess risk and guide treatment.

Load tests

Stress tests involve examining the heart using various methods against the background of myocardial ischemia, which is caused by stress on the heart or coronary vasodilation. Stress tests differ in the methods of inducing and detecting ischemia. stress tests depend on the composition of the study group and the experience of the researcher. The main parameters that determine the prognostic value of stress testing are listed below.

Methods of provoking ischemia

Physical activity is the most physiological and simplest method. If it is impossible to perform physical activity, pharmacological tests are used.

Exercise stress

Physiology

Physical activity increases myocardial contractility, preload and afterload, resulting in an increased myocardial oxygen demand.

Myocardial oxygen demand proportional to the double product (heart rate ∙ systolic blood pressure).

Since the increase in myocardial oxygen demand occurs mainly due to heart rate, the load is assessed precisely by it. The test is considered completed if the heart rate has reached 85% of the maximum for the corresponding age (220 - age).

Advantages

Physical activity allows you to objectively assess the patient’s capabilities; its tolerance has important prognostic significance. The prognosis for stable angina is largely determined by exercise tolerance and the level of stress at which ischemia occurs.

Chronotropic insufficiency

This is the inability to achieve 85% of the maximum heart rate at maximum tolerated physical activity in the absence of treatment with drugs with a negative chronotropic effect. This is a bad prognostic sign. While taking beta-blockers, it is impossible to identify chronotropic insufficiency.

Heart rate recovery

It is assessed by the decrease in heart rate 1 minute after cessation of exercise. It also has prognostic value. Normally, heart rate decreases by 12 beats in 1 minute; lower values ​​indicate an unfavorable prognosis.

Duke University Activity Index

The Duke University Treadmill ECG Activity Index takes into account the duration of exercise, the degree of ST segment deviation during or after exercise, and the severity of angina. It is calculated using the following formula:

Duke University Activity Index = (Test time, min) – (5 x maximum ST segment deviation, mm) – (4 x angina index)

A Duke index of -11 or lower indicates a high risk of complications, an index of -10 to 4 indicates a moderate risk, and 5 or higher indicates a low risk.

Flaws

Exercise tests are not suitable for intermittent claudication, severe lung disease, poor physical training and other conditions that prevent the load from being performed.

Pharmacological tests with adenosine and dipyridamole

Adenosine causes dilation of coronary vessels by activating adenosine receptors. It causes uneven coronary blood flow, which makes it possible to detect stenosis: the blood flow in the affected artery remains low, and in the rest it increases. With severe stenosis of the large coronary arteries, this leads to the steal phenomenon and causes ischemia.

Dipyridamole prevents the uptake of adenosine by cells, its effect is similar to that of adenosine, it acts more slowly, lasts longer, but is less predictable. Dipyridamole is used most widely because it acts within 20-30 minutes: this time is quite enough for the accumulation of the isotope. In addition, dipyridamole is less likely than adenosine to cause complete AV block.

Advantages

Pharmacological tests make it possible to assess the reserve of coronary blood flow, regardless of the increase in myocardial oxygen demand. This has its advantages, since a decrease in coronary flow reserve may precede the onset of ischemia. The unevenness of coronary blood flow significantly affects the accumulation of the isotope, so pharmacological tests are ideal for myocardial scintigraphy.

Flaws

Adenosine often causes I-II degree AV block. However, hemodynamic disturbances are rare. Since adenosine breaks down very quickly, it does not require any treatment.

Dipyridamole can cause bronchospasm, hypotension, chest pain, fever, lightheadedness and shortness of breath, sometimes requiring aminophylline to eliminate these reactions.

Because ECG changes and local contractility disturbances occur relatively rarely with the administration of adenosine and dipyridamole, they are not particularly suitable for stress echocardiography. The significance of the increased accumulation of the isotope in the lungs during the administration of dipyridamole remains unclear. The predictive value of a negative result of these tests is lower than that of exercise tests.

Pharmacological tests with dobutamine and arbutamine

Physiology

Dobutamine and arbutamine are beta-1 adrenergic stimulants; they increase the double product and increase the myocardial oxygen demand. The pharmacological load on the heart is considered adequate if the heart rate reaches 85% of the maximum. Atropine is used as an additional means to achieve the required heart rate, and a manual press is used to increase blood pressure.

Advantages

Physiological changes are similar to those that occur during exercise, but the double product usually increases less. There is evidence that chronotropic insufficiency during the dobutamine test indicates an unfavorable prognosis. ECG changes during the dobutamine test have approximately the same prognostic value as during the exercise test.

Flaws

Sometimes atrial fibrillation, ventricular tachycardia or arterial hypotension occurs, which requires discontinuation of the test. This most often occurs with aortic stenosis, severe left ventricular systolic dysfunction and mitral stenosis Therefore, dobutamine testing is not usually used in these patients. The test results may be unreliable due to the use of beta-blockers.

Methods for detecting ischemia

ECG

Advantages

An ECG test with physical activity is informative if the ECG is normal at rest and there is a high a priori probability of IHD. With a low prior probability, the value of this sample decreases. An ECG test with exercise can identify patients at high risk of cardiovascular complications. When test results indicate a high risk of complications, the one-year mortality rate exceeds 5%.

An exercise ECG test is used to determine permissible level physical activity for stable angina, sometimes to assess the effectiveness of treatment. In the latter case, antianginal drugs are not canceled before the test and a maximum stress test is performed to assess the patient's capabilities.

Flaws

The sensitivity and specificity of the ECG test is low at initial ECG changes, caused, in particular, by left ventricular hypertrophy, ventricular pacemaker, left bundle branch block, intraventricular conduction disorders, intake of cardiac glycosides and other drugs that affect conduction and depolarization.

Exercise ECG testing is not used to assess the significance of coronary stenoses because it does not localize ischemia. In addition, this test does not allow assessing myocardial viability.

Sensitivity and Specificity

The sensitivity of the ECG test with exercise varies from 48 to 94% (average 65%), specificity - from 58 to 98% (average 70%). The specificity of the test for detecting repeated stenoses is low. ECG changes during a pharmacological test with dipyridamole or adenosine are highly specific, but their sensitivity is low. When testing with dobutamine or arbutamine, the specificity and sensitivity of ECG changes is approximately the same as during exercise.

EchoCG

Advantages

Stress echocardiography is a relatively inexpensive test that allows localization of ischemia with good specificity. In addition, stress echocardiography is used to assess the severity and significance of valvular lesions.

If the patient can perform physical activity, then stress echocardiography is performed with exercise. Bicycle ergometry in the supine position is increasingly being used because it allows you to see the heart during exercise, and not immediately after it. Disturbances of local contractility against the background of load make it possible to localize ischemia.

If the patient is unable to perform physical activity, stress echocardiography with dobutamine or arbutamine is performed. Ischemia is indicated by a two-phase change in contractility: at low doses of dobutamine it increases, at higher doses it decreases. Dobutamine stress echocardiography is used to identify viable myocardium.

Some clinics use stress echocardiography with dipyridamole or adenosine. However, the sensitivity of this test is lower than that of stress echocardiography with dobutamine or exercise.

Flaws

The results of stress echocardiography may be uninformative if there is a marked increase in blood pressure in response to physical activity, as well as with severe mitral or aortic insufficiency. In addition, the test results are highly dependent on the quality of the image and the experience of the doctor.

Sensitivity and Specificity

The sensitivity of exercise stress echocardiography varies from 70 to 90% (average about 75%), and specificity - from 85 to 95% (average about 85%). The sensitivity and specificity of dobutamine stress echocardiography are approximately the same. These indicators decrease with poor image quality, with left bundle branch block, small volume of the left ventricle, severe valve damage, a strong increase in blood pressure in response to exercise and significant dilatation of the heart chambers. The decrease in sensitivity and specificity is due to poor visualization of the walls of the left ventricle, impaired local myocardial contractility not directly related to ischemia, and premature termination of the test.

Myocardial scintigraphy

Radiopharmaceuticals

Myocardial scintigraphy is performed with drugs labeled with thallium (thallium-201) and technetium (technetium-99m).

The accumulation of thallium-201 is directly proportional to regional blood flow, but since it is rapidly redistributed, images should be taken immediately after peak load is reached. For technetium-99m scintigraphy, assessment of coronary blood flow at rest requires reintroduction drug, but during physical activity, pictures do not have to be taken immediately.

The half-life of technetium-99m is shorter than that of thallium-201, and the emission energy is higher. This makes it possible to safely administer technetium-99m in doses 5-10 times higher than the dose of thallium-201 (in terms of radioactivity). This results in better quality images for obese patients and women with large breasts.

Rubidium-82 has an even shorter half-life and an even higher emission energy than technetium-99m. When using it, there is less scattering and signal attenuation.

Advantages

Myocardial scintigraphy allows one to assess the prognosis for stable angina. It is especially convenient when it is impossible to perform physical activity, permanent pacemaker, blockade of the left bundle branch, as well as when the results of tests with physical activity are ambiguous.

Among patients whose myocardial scintigraphy revealed perfusion abnormalities, mortality from cardiovascular diseases is 15 times higher. The more segments in which perfusion is impaired, the higher the mortality rate. The greatest prognostic value is the perfusion of the proximal part of the septal segment, which corresponds to the proximal part of the anterior descending artery.

In addition, dilatation of the left ventricle during exercise and accumulation of thallium-201 in the lungs indicate an unfavorable prognosis. With normal myocardial scintigraphy results, the risk of death or myocardial infarction within the next year does not exceed 1%.

Flaws

The sensitivity of myocardial scintigraphy is higher than that of stress echocardiography, but the specificity is lower. Signal attenuation and artifacts due to surrounding tissue reduce the sensitivity and specificity of the method.

Sensitivity and Specificity

Sensitivity ranges from 75 to 90% (average about 80%), and specificity ranges from 65 to 90% (average about 70%). Both indicators decrease with severe obesity, three-vessel disease and left bundle branch block.

EchoCG

EchoCG is a non-invasive study that allows you to evaluate the anatomical and functional features of the heart. This study is very valuable if CAD is suspected.

Abnormalities in local contractility of the left ventricle usually indicate ischemic heart disease. Moderate left ventricular systolic dysfunction, left ventricular hypertrophy, and severe mitral regurgitation indicate a poor prognosis. Drug treatment often depends on left ventricular systolic function.

EchoCG is the main method for excluding aortic stenosis and hypertrophic cardiomyopathy. For severe left ventricular systolic dysfunction, dobutamine stress echocardiography

and positron emission tomography allow assessment of myocardial viability.

MRI

MRI occupies an important place in cardiology. It gives an idea of ​​large vessels, the myocardium and pericardium, allows you to identify blood clots and heart tumors, congenital and acquired defects. MRI with gadolinium is used to assess local contractility and determine left ventricular ejection fraction. The data from this study correspond well to the results of myocardial scintigraphy. In addition, MRI allows you to see the coronary arteries.

MRI is usually used in addition to echocardiography. The disadvantages of MRI are its high cost and the inability to conduct the study at the patient’s bedside. In addition, MRI is contraindicated in the presence of a pacemaker or implantable defibrillator, and the number of such patients is increasing.

Positron emission tomography

Positron emission tomography does not provide an idea of ​​the morphology of structures such as the aorta, pericardium, and does not allow diagnosis volumetric formations hearts.

Electron beam CT

This is a non-invasive test that allows you to obtain cross-sectional images of the heart in a fraction of a second, while reducing artifacts caused by its movement. Electron beam CT makes it possible to quantify calcification of small arteries. The study is carried out quickly, in just 15 minutes, and does not require the introduction of contrast agents. Electron beam CT can detect significant coronary artery stenoses (>50% diameter) with a sensitivity of 90% and a specificity of 54%.

Electron beam CT cannot accurately determine the degree of stenosis. Despite the absence of artifacts associated with the movement of the heart, the image is not detailed enough to accurately assess the degree of stenosis and its location. Electron beam CT is convenient for mass examinations. When identifying pathology of the coronary arteries, a more thorough assessment of the risk of cardiovascular complications and an active fight against risk factors for atherosclerosis are indicated.

Coronary angiography

Advantages

Coronary angiography is the reference method for detecting coronary artery stenosis. Its results have important prognostic significance.

The degree of stenosis indicates a particular risk of myocardial infarction. With stenosis of more than 75% of the diameter in at least one artery, mortality is higher than with stenosis of less than 50%. Even with mild stenoses, the risk of myocardial infarction is significantly higher than in their absence.

The severity of the stenosis does not allow assessing the stability of the plaque; two-thirds of heart attacks are due to ruptured plaque that narrows the artery to less than 50% of its diameter. Nevertheless, a number of its angiographic characteristics indicate plaque instability.

1. Eccentric plaques with a narrow base, overhanging edges and uneven borders (type II plaques) are less stable than concentric plaques with smooth edges (type I plaques).

2. Plaques with irregular borders indicate a high risk of heart attack.

3. Angiographic features of the plaque allow us to assess the technical feasibility and risk of coronary angioplasty and coronary artery bypass grafting.

Ventriculography, which is performed simultaneously with coronary angiography, gives an idea of ​​​​the contractility of the left ventricle, which has additional prognostic value.

Indications

Coronary angiography for stable angina is not indicated for everyone. The American College of Cardiology and the American Heart Association have divided the indications for coronary angiography into three groups.

Flaws

Coronary angiography generally underestimates the extent of athersclerotic lesions in the coronary arteries, possibly due to vascular remodeling or extended lesions. In addition, coronary angiography does not allow assessment of coronary blood flow reserve and shows only that part of the plaque that faces the lumen of the vessel.

Intracoronary ultrasound

Intracoronary ultrasound provides cross-sectional views of the coronary artery. In this case, it is possible to calculate the area of ​​the plaque, the caliber of the artery and the degree of stenosis, examine areas of darkening of unknown origin on a coronary angiogram, questionable stenoses and their prevalence, and determine the calcium content of the plaque. Hypoechoic areas in the plaque may indicate high lipid content, which is typical of rapidly growing and unstable plaques. The findings may influence the choice of treatment. Intracoronary ultrasound provides clarity to unclear opacities on the coronary angiogram, which may be caused by calcification, thrombosis, severe eccentric stenosis, or intimal detachment. In addition, intracoronary ultrasound shows plaque growth both into the lumen of the vessel and beyond, which allows us to judge its stability. However, intracoronary ultrasound is not included in the standard examination for angina pectoris.

Invasive determination of the significance of stenoses

The hemodynamic significance of stenoses is assessed by coronary blood flow (using intracoronary Doppler) or by the pressure gradient on opposite sides of the stenosis.

1. The speed of blood flow in the coronary artery is determined using a pulsed Doppler study with an intracoronary ultrasound sensor passed along the coronary conductor.

Diastolic blood flow predominates in the left coronary artery. Normally, blood flow velocities in the proximal and distal segments of the artery are approximately equal. With significant stenosis, systolic blood flow begins to predominate, since stenosis primarily impairs diastolic blood flow.

The hemodynamic significance of stenosis is characterized by three indicators.

• The ratio of averaged peak velocities in diastole and systole distal to the stenosis is less than 1.8
• The ratio of average peak velocities proximal and distal to the stenosis is more than 1.7
• A decrease in coronary blood flow reserve with an increase in peak blood flow velocity of less than 2 times (coronary blood flow reserve is determined by the increase in blood flow in response to adenosine, which is administered after intracoronary administration of nitroglycerin).

2. Direct measurement The pressure gradient is carried out using a pressure sensor attached to the catheter. Pressure gradient more than 20 mm Hg. Art. indicates the hemodynamic significance of the stenosis. All these studies only complement coronary angiography. Their value in assessing the risk of cardiovascular events in addition to coronary angiography remains controversial.

Holter ECG monitoring

1. Frequent ventricular extrasystole after myocardial infarction is an unfavorable prognostic sign. In stable angina without a history of myocardial infarction, it is less important, so Holter monitoring is not necessary to assess the risk of complications. Moreover, treatment aimed at suppressing extrasystole does not affect the prognosis.

2. Holter monitoring may be useful if silent myocardial ischemia is suspected. Silent myocardial ischemia worsens the prognosis and indicates the need for more active examination and treatment.

Treatment

The goal of treatment is to eliminate angina attacks and improve exercise tolerance.

Tactics

Both drug treatment, coronary angioplasty, and coronary artery bypass grafting help eliminate angina attacks and increase the threshold of stress at which ischemia occurs, but the effectiveness of these methods varies. Medical treatment and coronary artery bypass surgery eliminate angina and improve survival, while coronary angioplasty eliminates angina but its effect on survival is not yet entirely clear.

Drug treatment

Antiplatelet agents

A meta-analysis including approximately 100,000 patients from 174 studies found that aspirin reduces the risk of stroke, myocardial infarction, and death in patients at high risk for cardiovascular events, including stable angina. According to some data, aspirin is effective in a dose of 75 to 160 mg, the currently recommended dose is from 81 to 325 mg/day.

Approximately 5-10% of patients with coronary artery disease have aspirin resistance, which means that their platelet aggregation is not sufficiently reduced by aspirin. Aspirin resistance increases the risk of thrombotic complications in peripheral arterial atherosclerosis. These patients have an increased risk of strokes, myocardial infarctions, and death from cardiovascular disease compared with those who are sensitive to aspirin.

For true allergy or intolerance to aspirin, use clopidogrel or ticlopidine; they also reduce the risk of thrombosis of peripheral, cerebral and coronary arteries. Clopidogrel is used for aspirin intolerance. In patients at high risk of complications who have undergone coronary artery bypass grafting in the past, clopidogrel was more effective than aspirin. However, these data have not yet been confirmed in large randomized trials. Clopidogrel is usually well tolerated and rarely causes side effects.

Ticlopidine can cause neutropenia, thrombocytopenia and pancytopenia, thrombotic thrombocytopenic purpura. When taking it, it is necessary to periodically repeat a general blood test. Because of these side effects, ticlopidine is rarely used.

Lipid-lowering drugs

Active treatment of hyperlipoproteinemia is effective for both primary and secondary prevention of coronary artery disease. In case of existing coronary artery disease, lipid-lowering drugs significantly slow down the progression of the disease and the risk of cardiovascular complications. Preference is given to HMG-CoA reductase inhibitors, which reduce the level of total cholesterol and LDL cholesterol. In the absence of contraindications, all patients with coronary artery disease should receive them.

Indications

A number of studies (4S, CARE, LIPID, HPS) have shown that HMG-CoA reductase inhibitors with increased or normal level total cholesterol levels reduce mortality, the incidence of myocardial infarction, and the need for coronary artery bypass grafting. After coronary artery bypass grafting, lipid-lowering drugs are necessary to prevent atherosclerosis of the grafts.

Efficiency

Studies using coronary angiography have shown that the clinical effectiveness of HMG-CoA reductase inhibitors extends well beyond their direct effect on the progression of coronary atherosclerosis. What is the matter here and whether there are any differences between different means from this group remains unclear. Probably, the effectiveness of HMG-CoA reductase inhibitors, in addition to their own lipid-lowering effect, is due to the fact that they stabilize plaques and have anti-inflammatory and antithrombotic effects.

Choice of drug

Apparently, all HMG-CoA reductase inhibitors are effective, so you need to choose a drug based on its cost. Measurement of lipoprotein(a), fibrinogen, apoprotein A and B100 levels is currently used mainly for scientific purposes.

Anion exchange resins primarily reduce LDL cholesterol and should not be used at triglyceride levels greater than 300 mg% because they may worsen hypertriglyceridemia.

Nicotinic acid lowers LDL cholesterol and triglycerides and is better than any other drug for raising HDL cholesterol. In addition, this is the only drug that reduces lipoprotein(a) levels.

Fibric acid derivatives are most effective for hypertriglyceridemia, they slightly increase HDL cholesterol and have little effect on LDL cholesterol. They are used when triglyceride levels are above 400 mg%.

For hypertriglyceridemia that cannot be treated nicotinic acid and fibric acid derivatives, use polyunsaturated omega-3 fatty acids.

Target LDL cholesterol level depends on the presence of coronary artery disease, risk factors and comorbidities

6 weeks after the prescription of HMG-CoA reductase inhibitors, the activity of liver enzymes and CPK must be measured, and then this analysis is repeated every six months.

Nitrates

Mechanism of action

Nitrates reduce the work of the myocardium and its oxygen demand by reducing preload and afterload on the left ventricle. In addition, they promote the redistribution of blood flow in favor of the subendocardial layers of the myocardium by reducing end-diastolic pressure in the left ventricle and dilatation of epicardial vessels. It is possible that nitrates also inhibit platelet aggregation.

Efficiency

Nitrates reduce myocardial ischemia during exercise, improve well-being and increase exercise tolerance in stable angina.

The addition of nitrates to well-selected beta-blocker therapy does not affect the frequency of angina attacks, the need for nitroglycerin, exercise tolerance, or the duration of silent ischemia.

Small studies have shown that the effect of nitrates on the incidence of angina pectoris was increased by ACE inhibitors.

There are no data on the effect of nitrates on mortality in stable angina.

Choice of drug

Nitrates act quickly, so nitroglycerin in the form of sublingual tablets or aerosol is used to relieve an attack of angina.

For short-term (up to 30 minutes) prevention of an attack, you can use nitroglycerin tablets. This is convenient if the patient knows well what stress causes his angina. The dosage regimen is selected individually, depending on the time of onset of angina. To prevent addiction to nitrates, take a break from taking them for at least 8 hours every day.

Long-acting nitrates, patches and ointments with nitroglycerin are more convenient for patients, but their use also requires breaks.

Side effect

Oral nitrates should not be taken with meals because they can cause heartburn.

Headaches are quite common and can be very severe. It weakens over time and may disappear when the dose is reduced.

There may be a short-term feeling of heat, lightheadedness, weakness and orthostatic hypotension; these phenomena disappear when moving to a supine position or increasing venous return by any other means.

Nitrates do not increase intraocular pressure and do not cause glaucoma.

Drug interactions

When taken concomitantly with other vasodilators, such as ACE inhibitors, hydralazine or calcium antagonists, nitrates can cause arterial hypotension. The simultaneous use of nitrates with sildenafil (Viagra) and other phosphodiesterase type V inhibitors is absolutely contraindicated, as it can lead to severe arterial hypotension.

Nitroglycerin IV high doses(> 200 mcg/min) may interfere with the binding of heparin to antithrombin III and cause relative resistance to heparin. If the rate of nitroglycerin infusion is high or changes frequently, aPTT should be determined more frequently.

Unresolved issues

addictive

With prolonged treatment with nitrates, their effect on blood vessels and platelets weakens. The mechanisms of addiction to nitrates have not been sufficiently studied; depletion of sulfhydryl groups, neurohumoral activation and an increase in blood volume probably play a role. Acetylcysteine, ACE inhibitors and diuretics do not prevent addiction. The only way to avoid it is to prescribe nitrates intermittently.

Withdrawal syndrome

When treated with beta-blockers, withdrawal of nitrates does not cause rebound angina. Maintaining long intervals without nitrates also does not cause rebound ischemia.

Beta blockers16

a-labetalol is also a powerful alpha-1-blocker

Mechanism of action

Blockade of cardiac beta-1 adrenergic receptors reduces the double product and myocardial oxygen demand. Reducing tension in the wall of the left ventricle promotes the redistribution of blood flow in the myocardium from the epicardium to the endocardium.

Coronary artery spasm due to beta-2 adrenergic receptor blockade is rare, however, if coronary artery spasm is established, these agents should not be used.

Beta blockers may have a quinidine-like (membrane stabilizing) effect.

Efficiency

Beta blockers reduce mortality after myocardial infarction. In stable angina without a history of heart attack, their effect on mortality has not been proven, but they significantly reduce angina.

Side effect

The heaviest side effects caused by blockade of beta-2 adrenergic receptors. However, some of these reactions occur much less frequently than previously thought, so given positive influence beta-blockers on survival, they should be prescribed even with high risk side effects.

Beta-blockers can cause bronchospasm, mask hypoglycemia in diabetes mellitus, aggravate intermittent claudication and have effects on the central nervous system (drowsiness, depression of consciousness, depression and nightmares). It is believed that the effect on the central nervous system is more typical for lipophilic beta-blockers.

If the conduction system of the heart is damaged, severe bradyarrhythmias may occur, and if heart failure occurs, its decompensation may occur.

Possible decreased libido, impotence and reversible alopecia.

Beta blockers can negatively affect lipid metabolism: increase LDL cholesterol and decrease HDL cholesterol. The clinical significance of this fact is not clear.

Drug interactions

When taken simultaneously with calcium antagonists, severe bradyarrhythmias and arterial hypotension are possible.

Choice of drug

When choosing a beta-blocker, they are guided by

• cardioselectivity,
• lipophilicity,
• routes of elimination and
• ease of reception.

Intrinsic sympathomimetic activity of great importance does not have it, although drugs that have it may be less effective in ischemic heart disease.

Calcium antagonists

The severity of the action is indicated by numbers from 0 (absent) to 5 (very pronounced effect)

Mechanism of action

These agents prevent the entry of calcium into smooth muscle cells and cardiomyocytes by blocking calcium channels. However, they do not affect the release of calcium from intracellular structures. As a result, the contractility of muscle cells decreases.

There are four types of calcium channels: L, T, N and P.

T-type channels are located in the atria and sinus node and are involved in phase 1 of the action potential.

L-type channels mediate calcium entry into cardiomyocytes during phase 3 of the action potential.

N- and P-type channels are found mainly in the central nervous system.

Dihydropyridines bind to the extracellular portion of L-type calcium channels. They do not interact with T-type channels and do not have negative chronotropic action. In addition, since dihydropyridines act outside the cell, they do not affect the release of calcium from intracellular stores.

Verapamil binds to L-type channels from the cytoplasmic side and blocks both L-type and T-type channels. It inhibits the release of calcium from intracellular stores and causes weaker sympathetic activation. Verapamil is characterized by frequency dependence: it binds to calcium channels when they are activated, so its effect increases with an increase in heart rate. The antianginal effect of verapamil is due to a decrease in the double product and an increase in oxygen delivery to the myocardium due to coronary vasodilation.

Efficiency

Calcium antagonists have been shown in a large number of controlled studies to reduce angina and increase the exercise threshold at which ST segment depression occurs.

For stable angina, calcium antagonists reduce mortality, heart attacks, and unstable angina to the same extent as beta-blockers.

A retrospective analysis showed that short-acting nifedipine may increase mortality in coronary artery disease. The reason for the increase in mortality remains unclear; it is possible that reflex tachycardia and the steal mechanism play a role. The combination of long-acting nifedipine with a beta-blocker is considered safer.

Side effect

The most common side effects are hypotension, fever, lightheadedness and headache. Due to the negative inotropic effect, calcium antagonists should not be prescribed for left ventricular systolic dysfunction. Conduction disturbances and severe bradycardia may occur when taking calcium antagonists that suppress the sinus and AV node.

When taking bepridil, you need to monitor the QT interval: it may be prolonged.

Drug interactions

Calcium antagonists may increase digoxin levels in the blood. In case of glycoside intoxication, calcium antagonists are contraindicated.

Choice of drug

Calcium antagonists vary in their inotropic effects.

Bibliography

1. B. Griffin, E. Topol “Cardiology” M. 2008
2. Aronov D.M., Lupanov V.P. “Current issues in the treatment of angina pectoris.” M, 2009
2. M. Fried, S. Grains “Cardiology” M. 1996
3. V.N. Kovalenko “Guide to Cardiology” K. 2008
4. Textbook of Cardiovascular Medicine (March 2002): By Eric J Topol MD, Robert M Califf MD, Jeffrey Isner MD, Eric N Prystowsky MD, Judith Swain MD, James Thomas MD, Paul Thompson MD, James B Young MD, Steven Nissen MD By Lippincott Williams & Wilkins

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• An ECG shows a deviation of the electrical axis of the heart to the right (in 79% of cases), signs of hypertrophy and overload of the RV (in 87% of cases), dilatation and hypertrophy of the RA (P-pulmonale). However, the sensitivity of the ECG is only 55% and the specificity is 70%, so this study is not considered the method of choice for screening patients. The absence of changes in the ECG does not exclude idiopathic pulmonary hypertension.
• Chest radiography is often one of the first methods of examination of patients with idiopathic pulmonary hypertension. In 90% of patients, at the time of diagnosis, an increase in the transparency of the pulmonary fields in the periphery is detected due to depletion of the pulmonary pattern. The main radiological signs of pulmonary hypertension are bulging of the pulmonary trunk and the left pulmonary artery, which form in a direct projection the 2nd arch along the left contour of the heart, expansion of the roots of the lungs, and in more late stages disease - enlargement of the right side of the heart.
• Transthoracic echocardiography is a non-invasive method for diagnosing pulmonary hypertension, thanks to which it is possible not only to assess the level of systolic pressure in the pulmonary artery, but to diagnose the causes and complications of increased pressure in the pulmonary circulation. In idiopathic pulmonary hypertension, dilatation of the superior vena cava, pancreas, and right pancreas, decreased contractile function of the pancreas, paradoxical movement of the interventricular septum, and the presence of pericardial effusion are detected.

In the absence of obstruction of the outflow tract of the pancreas, the degree of tricuspid regurgitation during a Doppler study can determine the value of systolic pressure in the pulmonary artery. The calculation is carried out using the modified Bernoulli equation.

where P is the pressure gradient through the tricuspid valve, mm Hg; V is the speed of tricuspid regurgitation, m/s.

If ΔР is less than 50 mmHg, then the systolic pressure in the pulmonary artery is equal to ΔР, with ΔР less than 85 mmHg. systolic pressure in the pulmonary artery exceeds ΔР by 10 mm Hg, and with ΔР more than 85 mm Hg. systolic pressure in the pulmonary artery exceeds ΔР by 15 mm Hg. Pulmonary artery pressure determined by echocardiography closely correlates with values ​​measured during catheterization.

• The “gold standard” for verifying idiopathic pulmonary hypertension is considered to be catheterization of the right heart with accurate measurement of pressure in the pulmonary artery and determination of cardiac output and total pulmonary vascular resistance. Idiopathic pulmonary hypertension is diagnosed when the mean pulmonary artery pressure is more than 25 mmHg. at rest or more than 30 mm Hg. during physical activity, pulmonary artery wedge pressure is less than 15 mm Hg. (precapillary pulmonary hypertension), total pulmonary vascular resistance more than 3 mm Hg. (l/min).
• Using acute tests with vasodilators (prostaglandin E1, inhalation of dinitrogen oxide), the reactivity of the pulmonary vessels can be assessed (Table 1). The criteria for a positive test are a decrease in the average pressure in the pulmonary artery by more than 10 mm Hg. with an increase or unchanged cardiac output. A positive test with a vasodilator is noted in 10-25% of patients with idiopathic pulmonary hypertension.
• With ventilation-perfusion scintigraphy of the lungs, no abnormalities are detected or the presence of small peripheral subsegmental perfusion defects without impaired ventilation is noted.
• Spiral CT and MRI play an important role in the diagnosis of idiopathic pulmonary hypertension. The main advantages of these methods are a three-dimensional (volumetric) method of obtaining images without artifacts from bones and lung fields, high spatial resolution, and non-invasiveness. The advantages of MRI are also considered to be the absence of radiation exposure and natural contrast from moving blood. With CT, you can assess the condition of the pulmonary fields, as well as the heart and blood vessels, by contrasting the cavities of the heart and the lumen of blood vessels with intravenous administration 80-120 ml of contrast agent.
• To determine exercise tolerance, a 6-minute walk test and a cardiopulmonary exercise test with gas exchange assessment are often performed.

The 6-minute walk test is a cheap, readily available method that is usually complemented by the Borg dyspnea assessment. In most multicenter studies in patients with pulmonary hypertension, distance in the 6-minute walk test was the primary endpoint.

The cardiopulmonary exercise test allows you to evaluate ventilation and gas exchange during dosed physical activity. Patients with idiopathic pulmonary hypertension have a reduced level of peak oxygen consumption index and anaerobic threshold.

• With idiopathic pulmonary hypertension, respiratory function indicators are within normal limits, although in some patients a moderate decrease in lung volumes is possible.

3. pharmacological test with isoproterenol, causing an increase Heart rate and myocardial contractility.

Other generally accepted pharmacological tests are based on provoking ischemia by changing the tone of the coronary arteries - their dilatation (dipyridomole) or narrowing (ergometrine). Each of these load testing techniques can be used various methods registration of ischemia: 1) electrocardiography; 2) myocardial scintigraphy; 3) two-dimensional echocardiography.

Indications for stress tests are: 1) diagnosis of coronary artery disease with atypical pain syndrome, nonspecific changes in ECG and GLP in the absence of typical anginal pain; 2) quantitation coronary reserve and functional state the cardiovascular system as a whole to assess prognosis, treatment tactics, and work recommendations; 3) optimization of the selection of antianginal drugs.

Absolute contraindications are: 1) early dates myocardial infarction and unstable angina; 2) severe disturbances of heart rhythm and conduction; 3) severe cardiac and respiratory failure, and for tests with physical activity - also acute thrombophlebitis.

The main relative contraindications are: high arterial hypertension (over 200/130 mm Hg), tachycardia more than 100 per minute, severe arrhythmias and a history of fainting.

Stress tests with electrocardiographic control are inappropriate for bundle branch blocks due to the inability to assess changes in the terminal part of the ventricular complex.

In clinical practice, the most widely used are simple tests with a dosed increase in the power of physical activity set by the researcher on a bicycle ergometer or treadmill with electrocardiographic monitoring. Throughout periods of exercise and rest, clinical symptoms and signs, blood pressure and ECG (heart rate, rhythm and conduction disturbances, changes in the ventricular complex) are monitored.

Submaximal or threshold tests are used. Submaximal is a load that is 75-85% of the maximum, that is, the one at which maximum aerobic capacity is achieved, assessed by the absence of a further increase in oxygen absorption. The determination of the submaximal level of exercise, which depends on age and gender, is based on the existence of a close connection between oxygen absorption and MOS and heart rate. He is judged by achieving a certain heart rate, which is determined using special tables or nomograms based on age and gender or, approximately, as 220 minus age for men and 200 minus age for women. If the criteria for stopping the test appear before the submaximal heart rate level is reached, it is considered threshold.

The criteria for a positive test are the following signs of an ischemic response: 1) the occurrence of an angina attack during or immediately after exercise; 2) decrease in systolic blood pressure by more than 15 mm Hg; 3) horizontal or oblique ST segment depression > 1 mm (so-called ischemic depression) lasting > 0.08 s, in at least one ECG lead; 4) ST segment elevation > 1 mm; 5) the duration of displacement registration is more than 3 minutes. Some authors consider an increase in the amplitude of the R wave, caused by impaired movement of the walls of the left ventricle or an increase in its EDP and EDV due to ischemic dysfunction, to be signs of ischemia.

The test is also stopped when other criteria for inadequate load appear: 1) clinical - shortness of breath, weakness, dizziness, cyanosis, sweating, sharp increase in blood pressure (over 230/130 mm Hg); 2) electrocardiographic - frequent (more than 1:10) ventricular extrasystoles, paroxysmal tachycardia and tachyarrhythmia, conduction disturbances, deepening and broadening of the Q and QS waves, decreased amplitude of the R wave. These electrocardiographic changes are considered nonspecific for IHD. Inversion (formation of negative) and reversion (positivization of initially negative) T waves are not grounds for stopping the test.

The test is considered negative when a submaximal heart rate is reached in the absence of clinical and electrocardiographic signs of myocardial ischemia and uninformative (uncertain) if it is terminated prematurely due to the appearance of signs of inadequate load not related to ischemia, as well as the patient’s refusal to continue the study.

The risk of an adverse outcome during exercise testing is very low - approximately 1 death per 20,000 studies and one heart attack 3,000.

The sensitivity of stress testing with electrocardiographic control, that is, the percentage of positive results among patients with coronary artery disease verified by coronary angiography, ranges from 65 to 75. With a three-vessel lesion, the sensitivity of the stress test is significantly higher than with a single-vessel lesion.

Its specificity, that is, the percentage of negative results among individuals who do not have coronary artery disease, is approximately in the same range (70-80%).

When assessing the likelihood of having IHD in cases positive result the nature of the test must be taken into account clinical manifestations diseases. Thus, in patients with typical attacks of angina, it is 98%, with atypical pain in chest- 88%, with non-anginal pain - 44% and in the absence pain syndrome - 33 %.

Since ST segment depression during exercise is not strictly pathognomonic for coronary insufficiency and indicates only changes in myocardial metabolism, which may also have a non-coronarogenic origin, false-positive test results are possible. Their frequency reaches 10-15% and increases in the presence of initial changes in the ST segment and T wave at rest, including those associated with taking cardiac glycosides and other drugs, as well as in young women. The likelihood of a false-positive result decreases with greater severity of ischemic depression of the ST segment - over 2 mm. A number of experts recommend using this criterion instead of > 1 mm, which, however, while increasing the specificity of the method, reduces its sensitivity.

The main reasons for false-positive results are: 1) hypersympathetic syndrome with neurocirculatory dystonia, mitral valve prolapse and other conditions (in this case, changes in the ECG do not depend on heart rate, occur at the very beginning of the load and disappear as it continues); 2) intracellular hypokalemia, including that developing during hyperventilation due to respiratory alkalosis; 3) severe hypoxemia (for example, with anemia); 4) low MOS and microcirculation disorders in non-coronary myocardial diseases, heart defects, etc.

False negative results are observed in 4-14% of cases. Their main reasons are: 1) insignificant severity of coronary atherosclerosis (stenosis< 50 % и хорошее развитие коллатералей); 2) нивелировка признаков ишемии при их локализации на противоположных стенках левого желудочка; 3) наличие исходных изменений сегмента ST и зубца Т; 4) предварительное лечение антиангинальными препаратами.

If there are doubts about the truth of a negative result of an electrocardiographic test with physical exercise, as well as if it is not informative, one should resort to other tests, in particular, transesophageal cardiac pacing and a dipyridamole test with electrocardiographic or scintigraphic control, coronary angiography.

The use of transesophageal pacing for the diagnosis of coronary artery disease is indicated for: 1) a questionable or uncertain result of an exercise test, for example, its termination due to an increase in blood pressure; 2) the inability to perform physical activity due to diseases of the blood vessels, joints or muscles of the lower extremities and detraining of patients.

Its sensitivity and specificity using electrocardiographic monitoring are the same as those for exercise testing. The disadvantage is a certain discomfort for the patient associated with the introduction of the electrode and sometimes with the stimulation itself.

Pharmacological tests with isoproterenol (isadrin) and dipyridamole are used to diagnose ischemic heart disease in the same cases as cardiac pacing. Isadrin (isoproterenol), stimulating B1 and B2 adrenergic receptors, increases myocardial oxygen consumption, which in case of stenotic atherosclerosis of the coronary arteries can cause ischemia.

Dipyridamole (chirantyl, persantine) causes dilatation of the coronary arteries due to the inhibition of adenosine deaminase and the accumulation of the powerful vasodilator adenosine. In the presence of hemodynamically significant stenosis, this leads to “intercoronary steal” and the development of isemia.

The sensitivity of both pharmacological tests with electrocardiographic control is similar to tests with physical exercise, and the specificity is slightly higher - 78-93%.

The ergometrine test is based on the ability of this ergot alkaloid to cause myocardial ischemia through coronary spasm due to stimulation of serotonergic and possibly α-adrenergic receptors. In this regard, it is used to diagnose vasospastic origin, or component, of angina. The drug is administered intravenously in small doses, usually 0.05-0.15-0.3 mg (total no more than 0.5 mg). The occurrence of an anginal attack with ST segment elevation is regarded as the result of a spasm of a large subepicardial coronary artery, characteristic of Prinzmetal's angina.

Anginal pain in combination with ST segment depression is explained by spasm of small coronary arteries as a cause of spontaneous angina or a component of exertional angina. To relieve the spastic reaction, nitroglycerin is used, which has a direct dilating effect on the large coronary arteries. For spasms of small vessels, however, it is ineffective. Due to the fact that the induced coronary spasm may be resistant to nitroglycerin taken sublingually and disappear only after intracoronary administration of this drug or nifedipine (Corinfar), an ergometrine test is recommended to be performed only during coronary angiography. The test is associated with an increased risk of developing severe complications associated with ischemia, including terminal rhythm and conduction disturbances, as well as myocardial infarction. This prevents its expanded use, despite its higher diagnostic value compared to other tests.

The sensitivity and specificity of all stress tests increases to 80-90% when using myocardial scintigraphy with 201T1 to detect foci of ischemia.

CORONAROGRAPHY

Coronary angiography is the recognized “gold standard” for detecting or excluding coronary heart disease. It allows you to determine the severity of narrowing of the coronary arteries, its location and the number of significantly stenotic coronary arteries (the criterion for such narrowing is a decrease in the lumen area by more than 70%)

In the 30s of the last century, Werner Forssman Cournand and Richards began to use cardiac catheterization for the first time as a method for diagnosing heart disease, which was a revolutionary step that determined the prospects and directions for the development of medicine for several decades to come, it became possible performing an invasive study of blood vessels, which made it possible to obtain their intravital visualization. In 1958, the first intravital selective coronary angiography was performed at the Cleveland Clinic (USA). It happened accidentally when, during cardiac catheterization of a patient with aortic valve disease, the catheter, instead of passing through the valve, ended up in the patient’s right coronary artery. Dr. Mason Sones, the pediatric cardiologist who conducted the study, waited in horror for the heart to fibrillate as the contrast agent filled the coronary artery within 30 seconds. But when this did not happen, Dr. Sones realized that the coronary arteries could be contrasted intravitally without endangering the patient's life. Mason Sones subsequently recalled: “That night I realized that I had finally found diagnostic method, defining the anatomical substrate of coronary artery disease." His creative work was a major achievement, allowing for the first time the accurate diagnosis of coronary artery disease and laying the foundation for subsequent myocardial revascularization operations: first for coronary artery bypass grafting, and later for coronary angioplasty. In 1967, Dr. Melvin Judkins modified the coronary angiography technique from Sones's technique. He inserted the catheter through a percutaneous puncture of the femoral artery just below the groin, while Sones performed the more complex and traumatic procedure of catheter insertion in the arm through the surgically exposed brachial artery. The use of this technique is limited in patients with simultaneous atherosclerosis of the femoral arteries, as well as in cases of abnormal location of the coronary arteries. In these cases, the use of the Sones technique, which involves inserting a catheter through the exposed right brachial artery, is indicated.

Premedication is not required. On the eve of CAG, medications are stopped, especially B-blockers. After inserting the catheter, 5000 units of heparin are simultaneously injected into the arterial bed. All stages of catheterization of the coronary arteries and their contrast are carried out under constant electrocardiographic control with periodic determination of pressure in the vessels. An X-ray contrast agent is injected into the left coronary artery in an amount of 4-6 ml at a rate of 4 ml/s, into the right artery 3-4 ml at a rate of 3 ml/s. Research is performed in several projections. KAG. always combined with left ventricular catheterization and ventriculography.

Complications include thromboembolism, bleeding from the puncture site of the vessel and the formation of false aneurysms, which are more often observed in patients with severe heart failure, arterial hypertension, with unstable angina, with arrhythmias. In 0.33% of cases it develops acute heart attack myocardium, in 0.9% - ventricular fibrillation. Fatalities are 0.24%. In a well-equipped angiography laboratory, where the examination is carried out by experienced doctor, the risk for life is less than 0.1% (that is, less than 1 death per 1000 examinations). The lowest number of complications from coronary angiography is recorded in those institutions where at least 200 examinations are performed during the year. With severe angina with poor left ventricular function in the elderly, the risk of death during coronary angiography increases to 1%.

Absolute contraindications to coronary angiography are:

1) febrile conditions;

2) severe damage to parenchymal organs;

3) severe heart rhythm disturbances;

4) severe cardiomegaly with tonal heart failure;

5) acute cerebrovascular accident;

6) untreatable polycythemia;

7) increased sensitivity to iodine preparations.

The development and development of the method of selective coronary angiography was the greatest incentive for the use of surgical methods treatment of ischemic heart disease. Since the issue of coronary bypass surgery cannot be resolved without angiographic data, the development of coronary surgery would be impossible without selective coronary angiography.

Wide Application selective coronary angiography and surgical interventions on the coronary arteries of the heart in recent years has made it possible to study anatomical features coronary circulation of a living person, to develop the functional anatomy of the arteries of the heart in relation to revascularization operations in patients with coronary heart disease.

Interventions on the coronary arteries with diagnostic and medicinal purposes place increased demands on the study of vessels at different levels, taking into account their variants, developmental anomalies, caliber, angles of origin, possible collateral connections, as well as their projections and relationships with surrounding formations.

The right and left coronary arteries were conventionally divided into three and seven segments, respectively.

The right coronary artery has three segments:

· a segment of the artery from the mouth to the origin of the branch - the artery of the acute edge of the heart (length from 2 to 3.5 cm);

· section of the artery from the branch of the acute edge of the heart to the origin of the posterior interventricular branch of the right coronary artery (length 2.2-3.8 cm);

· posterior interventricular branch of the right coronary artery. According to our data, only in 14% of patients it reached the apex of the heart, anastomosing with the anterior interventricular branch of the left coronary artery.

· The right coronary artery in most patients has a main type of division and plays an important role in the vascularization of the heart, especially its posterior diaphragmatic surface. In 25% of patients, the predominance of the right coronary artery was revealed in the myocardial blood supply.

The left coronary artery has seven segments:

· The initial section of the left coronary artery from the mouth to the place of division into the main branches is designated as segment I, its length is from 0.7 to 1.8 cm.

· The first 4 cm of the anterior interventricular branch of the left coronary artery are divided into two segments of 2 cm each - segments II and III. The diameter of the second segment of the artery ranges from 2 to 4.5 mm

· The distal portion of the anterior interventricular branch constituted segment IV. It can end at the apex of the heart, but usually (according to our observations, in 80% of patients) it continues on the diaphragmatic surface of the heart, where it meets the terminal branches of the posterior interventricular branch of the right coronary artery and participates in the vascularization of the diaphragmatic surface of the heart.

· The circumflex branch of the left coronary artery to the origin of the branch of the obtuse edge of the heart - segment V (length 1.8-2.6 cm).

· The distal portion of the circumflex branch of the left coronary artery is often represented by the artery of the obtuse edge of the heart - segment VI departs at a right angle to the main trunk and reaches the apex of the heart in 47.2%.

· The diagonal branch of the left coronary artery (VII segment) runs along the anterior surface of the left ventricle down and to the right, then plunging into the myocardium. The diameter of its initial part is from 1 to 3 mm. With a diameter of less than 1 mm, the vessel is poorly expressed and is more often considered as one of the muscular branches of the anterior interventricular branch of the left coronary artery.

James (1961) suggests calling the aortic sinuses from which the coronary arteries arise the right and left coronary sinuses. The orifices of the coronary arteries are located in the bulb of the ascending aorta at the level of the free edges of the semilunar valves of the aorta or 2-3 cm above or below them (V.V. Kovanov and T.I. Anikina, 1974). With a high position at the time of systole of the left ventricle, the orifice is under the impact of a stream of blood, not being covered by the edge of the semilunar valve. According to A.V. Smolyannikov and T.A. Naddachina (1964), this may be one of the reasons for the development of coronary sclerosis.

Thrombolytic therapy. Almost significant markers of myocyte death are the activities of enzymes - AST, CPK, LDH. Table 4 Some indicators of the lipid spectrum of blood serum of men from Kataysk, patients arterial hypertension I, II degrees and coronary heart disease, M±m Indicators Groups Total cholesterol, N – 5.2-6.5 mmol/l Triglycerides, N – 0.51-1.86 mmol/l...

Functional class of CHF. 12. The preliminary diagnosis can be formulated as follows: Main: Hypertonic disease III degree, III stage, very high risk group for complications. Complications: Ischemic disease heart: Stable angina at rest, functional class IV. Chronic heart failure stage I, functional class II. II. Plan for additional...

Drug therapy. Treatment is prescribed in repeated courses under the control of serum lipid levels (cholesterol, triglycerides, etc.) until a stable lipolytic effect is achieved. CORONARY HEART DISEASE The WHO Expert Committee defines coronary artery disease (CHD) as acute or chronic damage to the heart muscle caused by a decrease or cessation of blood delivery to the myocardium in...