Angina pectoris d. What is angina pectoris? Stable exertional angina

Angina pectoris (angina pectoris, angina pectoris) is one of the clinical forms of IHD, characterized by discomfort or pain in the chest (most often behind the sternum, but other localization is possible) due to myocardial ischemia as a result of physical or emotional stress, which quickly passes after taking nitroglycerin or after cessation of stress.

According to the clinical course and prognosis, angina pectoris can be divided into several options:

Stable angina pectoris of various (I-IV) functional classes;

New-onset angina pectoris;

Progressive angina pectoris;

Angina at rest;

Spontaneous (special) angina (vasospastic, variant, Prinzmetal's angina).

Currently, new-onset, progressive angina pectoris and angina at rest are classified as clinical variants of unstable angina and are considered within the framework of acute coronary syndrome without segment elevation ST(see relevant sections of the textbook).

Stable exertional angina

Angina pectoris is considered stable if it occurs in a patient for at least 1 month with a more or less certain frequency (1-2 attacks per week or month). In most patients, angina occurs with the same physical activity and can be stable for many years. This clinical variant of the disease has a relatively favorable prognosis.

The prevalence of angina depends on age and gender. Thus, among the population aged 45-54 years, angina pectoris is registered in 2-5% of men and 0.5-1% of women, and in those aged 65-74 years - in 11-20% of men and 10-14% of women. Before myocardial infarction, angina pectoris is observed in 20% of patients, after myocardial infarction - in 50% of patients.

Etiology

The cause of angina in the vast majority of patients is atherosclerosis of the coronary arteries. Non-coronarogenic causes of its development include hypertension, aortic stenosis, HCM, anemia, thyrotoxicosis, changes in the blood coagulation and anticoagulation system, as well as insufficient development of collateral circulation. Angina attacks occur much less frequently with unchanged coronary arteries.

Pathogenesis

In most cases, the basis of coronary artery disease, including angina pectoris, is atherosclerosis of the coronary arteries. Unmodified coronary arteries during maximum physical activity due to a decrease in resistance are capable of increasing the volume of coronary blood flow by 5-6 times. The presence of atherosclerotic plaques in the coronary arteries leads to the fact that during physical activity there is no adequate increase in coronary blood flow, resulting in the development of myocardial ischemia, the degree of which depends on the severity of the narrowing of the coronary arteries and the myocardial oxygen demand. Narrowing of the coronary arteries by less than 40% has little effect on the ability of the coronary circulation to provide maximum physical activity, and therefore is not accompanied by the development of myocardial ischemia and does not manifest itself as angina attacks. At the same time, in patients with a narrowing of the coronary arteries by 50% or more, physical activity can lead to the development of myocardial ischemia and the occurrence of angina attacks.

As is known, normally there is a clear correspondence between the delivery of oxygen to cardiomyocytes and the need for it, ensuring normal metabolism and, consequently, the normal functioning of heart cells. Coronary atherosclerosis leads to the development of an imbalance between oxygen delivery to cardiomyocytes and the need for it: impaired perfusion and myocardial ischemia occur. Episodes of ischemia lead to changes in the metabolism of cardiomyocytes and cause short-term reversible impairment of myocardial contractile function (“stunned myocardium”). Frequently recurring episodes of myocardial ischemia can lead to the development of chronic myocardial dysfunction (hibernating myocardium), which can also be reversible.

Cellular acidosis, disturbance of ionic balance, decrease in ATP synthesis first lead to diastolic and then to systolic myocardial dysfunction, as well as electrophysiological disorders expressed in changes in the wave T and segment ST on the ECG, and only later do chest pains arise. The main mediator of pain, which plays a role in the development of an angina attack, is considered to be adenosine, which is released from the cells of the ischemic myocardium and stimulates A 1 receptors located at the endings of the nerve fibers innervating the heart muscle. This sequence of changes is called the ischemic cascade. Thus, angina pectoris - its final stage, in fact, is the “tip of the iceberg”, which is based on changes in myocardial metabolism that have arisen as a result of perfusion disorders.

It should be noted that silent myocardial ischemia also exists. The absence of pain during an ischemic episode may be due to its short duration and severity, which is not sufficient to cause damage to the endings of the afferent nerves of the heart. In clinical practice, silent myocardial ischemia is most often recorded in patients with diabetes mellitus (diabetic polyneuropathy), in elderly patients, women, people with a high pain sensitivity threshold, as well as in diseases and injuries of the spinal cord. In patients with silent myocardial ischemia, so-called angina equivalents often occur in the form of attacks of shortness of breath and palpitations caused by the development of systolic and (or) diastolic myocardial dysfunction or transient mitral regurgitation against the background of left ventricular myocardial ischemia.

Clinical picture

The main symptom of angina is a characteristic pain attack. The first classical description of angina was given by Heberden in 1772. He wrote that angina is “... pain in the chest that occurs while walking and forces the patient to stop, especially while walking shortly after eating; it seems that this pain, if it continues or intensifies, can take a person’s life; the moment you stop, all unpleasant sensations disappear. After the pain continues to occur for several months, it ceases to immediately disappear when stopped, and in the future it will continue to occur not only when a person walks, but also when lying down...”

Typical angina has a number of characteristic clinical signs.

Nature, localization and duration of pain. Typical angina is characterized by pressing, squeezing, cutting and burning pain. Sometimes patients perceive an attack not as obvious pain, but as a difficult to express discomfort, which can be characterized as heaviness, compression, tightness, compression or dull pain. An attack of typical angina is often also called anginal, by analogy with the Latin name for angina - "angina pectoris"

With typical angina, pain is localized mainly behind the sternum. Irradiation of pain into the lower jaw, teeth, neck, interscapular area, left (less often, right) shoulder, forearm and hand is often noted. The more severe the angina attack, the wider the area of pain irradiation may be.

Despite the fact that the intensity and duration of anginal pain can vary significantly in different patients, a typical attack of angina does not last more than 15 minutes. Most often it lasts about 2-5 minutes and is interrupted after the cessation of physical or emotional stress. If a typical angina attack lasts more than 20 minutes and is not eliminated by taking nitroglycerin, then first of all you should think about the possibility of developing acute coronary syndrome (myocardial infarction) and register an ECG.

Provoking factors. In typical situations, the factor that provokes angina is physical or emotional stress. After its influence ceases, the attack passes. If the load (fast walking, climbing stairs) does not cause retrosternal discomfort, then it can most likely be assumed that the patient does not have significant damage to the large coronary arteries of the heart. An anginal attack is also characterized by its occurrence in frost or cold wind, which especially often occurs in the morning, when leaving the house. Cooling the face stimulates vasoregulatory reflexes aimed at maintaining body temperature. As a result, vasoconstriction and systemic hypertension occur, which increases myocardial oxygen consumption and provokes an attack of angina.

The effect of taking nitroglycerin. Usually, sublingual administration of nitroglycerin in the form of one tablet or one dose of spray quickly (within 1-2 minutes) and completely relieves an attack of angina. If the patient does not have experience using this drug, then for the first time it is better for him to take nitroglycerin in the supine position, which will avoid a possible sharp decrease in blood pressure caused by orthostatic arterial hypotension. The patient can independently take two tablets (two doses of spray) of nitroglycerin with an interval of 10 minutes. If after this the angina attack does not stop, then to exclude developing myocardial infarction, medical assistance and ECG registration are necessary. Often an attack of angina is accompanied by vegetative symptoms: increased breathing, pallor of the skin, increased dry mouth, increased blood pressure, the occurrence of extrasystole, tachycardia and the urge to urinate.

Angina is considered typical (certain), if the pain attack meets all three of the above criteria. The typical nature of the pain syndrome (pain, localization of pain, its duration, provoking factors, effectiveness of nitroglycerin) in combination with male gender and age over 40 years allows us to say with a high probability (85-95%) that the patient has coronary artery disease and myocardial ischemia against the background of atherosclerosis of the main (subepicardial) coronary arteries with a narrowing of their lumen by more than 50%.

Angina is considered atypical (possible) if the clinical characteristics of a painful attack satisfy only two of the three above criteria. To confirm that atypical pain in the heart is a sign of atypical angina pectoris, objective confirmation of the relationship between myocardial ischemia and a pain attack is necessary at the third stage of the diagnostic search, while the likelihood of detecting coronary artery disease and myocardial ischemia (i.e., objective confirmation that the pain syndrome has the character of angina pectoris, although atypical) in men over 40 years of age is significantly lower and ranges from 45 to 65% (Table 2-10). Most often, atypical angina is recorded in patients with diabetes mellitus, women and elderly patients.

If pain in the chest does not meet any of the above criteria, then it is regarded as non-cardiac.

Table 2-10. The probability of the existence of coronary heart disease depending on the nature of the pain syndrome, gender and age of patients

Thus, typical angina pectoris is one of the few internal diseases that can be diagnosed with a high degree of probability already at the first stage of the diagnostic search, after carefully questioning the patient.

According to the classification of the Canadian Society of Cardiology, adopted in 1976, stable angina pectoris, depending on the severity of physical activity that causes it, can be divided into four functional classes.

Functional class I - normal physical activity (walking, climbing stairs) does not cause angina. It occurs only during very intense, “explosive” or prolonged physical activity.

Functional class II - slight limitation of physical activity. Angina is caused by normal walking over a distance of more than 500 m, climbing stairs more than one floor or uphill, walking after eating, in the wind or in the cold. Angina pectoris may occur under the influence of emotional stress.

Functional class III - severe limitation of physical activity. Angina occurs when walking normally at a distance of 200-400 m or when climbing to the first floor.

Functional class IV - inability to perform any physical work without developing angina. Rare attacks of resting angina are possible.

The main clinical symptom - a painful attack (angina attack) - is not considered specific only for coronary artery disease. In this regard, the diagnosis of angina pectoris as a form of chronic ischemic heart disease can be made only in cases where, taking into account all the data obtained at various stages of examination of the patient (mainly using objective examination methods at the third stage of the diagnostic search), the connection between the occurrence of pain in chest with the existence of myocardial ischemia.

At the same time, the clinical picture of angina pectoris with ischemic heart disease has its own characteristics, which are detected already at the first stage of the diagnostic search. Task first stage of diagnostic search- definition:

Typical angina;

Other signs of chronic ischemic heart disease (rhythm disturbances, heart failure);

Risk factors for coronary heart disease;

Atypical cardiac pain and its assessment taking into account age, gender, risk factors for the development of coronary artery disease and concomitant diseases;

The effectiveness and nature of the drug treatment;

Diseases manifesting as angina pectoris.

The first stage of the diagnostic search is extremely important for diagnosing angina pectoris. In its classic version, correctly collected information about the nature of the pain syndrome makes it possible to make a diagnosis in more than 70% of cases, even without the use of instrumental methods of examining the patient.

All complaints are assessed taking into account the age, gender, constitution, psycho-emotional background and behavior of the patient, so that often, already at the first communication with the patient, you can reject or verify the correctness of the preliminary diagnosis of IHD. Thus, with classic complaints over the past year and the absence of cardiovascular diseases in the past, a man aged 50-60 years can be diagnosed with chronic ischemic heart disease with a very high probability.

Nevertheless, a detailed diagnosis indicating the clinical variant of the disease and the severity of damage to the coronary arteries and myocardium can be made only after completing the entire basic diagnostic search scheme, and in some situations (described below) - after additional examination.

It is sometimes difficult to differentiate between angina pectoris and various pain sensations of cardiac and extracardiac origin. The characteristics of pain in various diseases are described in numerous manuals. It should only be emphasized that stable angina is characterized by a constant, identical nature of pain during each attack, and its occurrence is clearly related to certain circumstances.

With NCD and a number of other diseases of the cardiovascular system, the patient notes the varied nature of the pain, its different localization and the absence of any pattern in its occurrence. In a patient with angina pectoris, even in the presence of other pain (caused, for example, by damage to the spine), it is usually possible to identify characteristic ischemic pain.

In patients with diseases such as hypertension and diabetes mellitus, complaints characteristic of angina pectoris, arrhythmia and circulatory disorders should be actively identified. The patient himself may not present them if the corresponding phenomena are insignificantly expressed or he considers them insignificant compared to others.

Patients often describe angina not as pain, but talk about a feeling of discomfort in the chest in the form of heaviness, pressure, tightness, or even burning and heartburn. In older people, the sensation of pain is less pronounced, and clinical signs are more often represented by difficulty breathing and a sudden feeling of lack of air, combined with severe weakness.

In some cases, there is no typical localization of pain; they arise only in those places where they usually radiate. Since the pain syndrome during angina pectoris can occur atypically, for any complaints of pain in the chest, arms, back, neck, lower jaw and epigastric region (even in young men), one should find out whether the circumstances of their occurrence and disappearance correspond to the patterns of pain syndrome with angina pectoris. With the exception of localization, in such cases the pain retains all the features of typical angina (cause of occurrence, duration of the attack, effect of nitroglycerin or stopping when walking, etc.).

Thus, at the first stage of the diagnostic search, the nature, localization and duration of the pain syndrome, its relationship with physical and emotional stress, the effectiveness of taking nitroglycerin (if the pain disappears after 5 minutes or later, the effect of the drug is very doubtful) and other previously taken medications (important not only for diagnosis, but also for creating an individual plan for further treatment).

Second stage of diagnostic search uninformative for the diagnosis of stable angina pectoris. There are no data from an objective examination of the patient specific to her. Often, during a physical examination, you may not find any abnormalities at all (with recent onset of angina). However, in a patient with angina pectoris, the second stage of the diagnostic search makes it possible to clarify the nature of the damage to the cardiovascular system (heart defects, hypertension), the existence of concomitant diseases (anemia) and complications (heart failure, arrhythmias). That is why at the second stage of the diagnostic search, despite its relatively low information content in patients with stable angina pectoris, one should actively look for symptoms of diseases that may be accompanied by myocardial ischemia.

Extracardiac localization of atherosclerosis is considered important for diagnosis (with damage to the aorta - an accent of the second tone and systolic murmur in the aorta, with disease of the lower extremities - a sharp weakening of the pulsation of the arteries), symptoms of left ventricular hypertrophy with normal blood pressure and the absence of any diseases of the cardiovascular system.

On third stage of diagnostic search perform instrumental and laboratory studies to determine risk factors for coronary artery disease, objective signs of myocardial ischemia and its connection with painful attacks. Thus, the diagnosis of coronary artery disease and angina pectoris is confirmed as one of the signs of ischemia.

Laboratory research. In all patients in whom, based on the results of the first and second stages of the diagnostic search, the existence of stable angina pectoris is suspected, it is advisable to:

Clinical blood test with assessment of the number of erythrocytes, leukocytes and hemoglobin concentration;

Biochemical blood test with assessment of the lipid spectrum (concentration of total cholesterol, LDL, HDL and triglycerides), glucose and creatinine levels.

In patients with severe and prolonged attacks of angina, in order to exclude the development of a heart attack, it is recommended to determine biochemical markers of myocardial necrosis (cardiac troponin T or I, activity of the MB fraction of creatine phosphokinase (see “Myocardial infarction)).

Chest X-ray. This routine test, performed in patients with suspected cardiovascular or respiratory disease, detects extracardiac signs of aortic atherosclerosis. In patients with angina, chest x-ray does not provide any specific information, so it is justified if there are clinical signs of heart failure or respiratory disease.

ECG- one of the leading non-invasive methods of instrumental diagnosis of coronary artery disease, which is associated with its simplicity, accessibility and ease of implementation.

A resting 12-lead ECG should be recorded in all patients with suspected exertional angina. It should be remembered that, outside of a painful attack, in many patients with angina (if they have not previously suffered a myocardial infarction), the ECG at rest may be normal. At the same time, cicatricial changes detected on the ECG at rest, with complaints of characteristic pain in the heart, are considered an important argument in favor of the diagnosis of coronary artery disease (Fig. 2-12).

Rice. 2-12. Standard 12-lead ECG at rest in a patient with coronary artery disease who suffered an anterolateral myocardial infarction with a Q-wave, after which exertional angina persisted (ST segment unchanged)

It is quite difficult to register a regular 12-lead ECG during an attack of pain in the heart area, but if it is possible, it brings a lot of valuable information. First of all, it allows you to detect and associate objective signs of myocardial ischemia (changes in the ST in the form of depression or elevation) with pain in the chest, i.e. makes it possible to objectively diagnose coronary artery disease and angina pectoris as one of its clinical signs. In addition, a 12-lead ECG recorded during an attack of pain in the cardiac region makes it possible to determine transient rhythm and conduction disturbances caused by myocardial ischemia, which is essential for risk stratification and prognosis. That is why, if possible (especially if the patient is in a hospital), one should strive to register an ECG during a painful attack.

Load tests. These include ECG tests with physical activity (treadmill test, bicycle ergometry), stress echocardiography, myocardial stress scintigraphy with physical activity or pharmacological drugs (dobutamine, dipyridamole, trifosadenine) and transesophageal electrical stimulation of the atria.

ECG tests with exercise are more sensitive and specific in diagnosing myocardial ischemia than ECG at rest. That is why, taking into account the ease of implementation, availability and low cost, ECG tests with exercise are considered the method of choice for detecting inducible myocardial ischemia in patients with suspected stable angina pectoris.

The most common indication for ECG testing with exercise is the occurrence of chest pain, reminiscent of angina pectoris, in people who, based on age, gender and other risk factors, have a moderately high or low probability of having coronary artery disease (see Table 2 -10). At the same time, the diagnostic value of ECG tests with exercise in patients who, based on clinical assessment, have a high probability of coronary artery disease, is minimal: a 65-year-old man with typical severe attacks of exertional angina has a 95% probability of suffering from coronary artery disease. Their implementation is advisable both from the point of view of objective verification of myocardial ischemia, and from the point of view of determining the prognosis and choosing treatment tactics. In addition, performing ECG tests with physical activity is advisable if:

Typical pain syndrome in the absence of changes in the ECG recorded at rest;

Pain in the heart area of an atypical nature;

ECG changes uncharacteristic of myocardial ischemia in middle-aged and elderly people, as well as in young men with a preliminary diagnosis of coronary artery disease;

No changes in the ECG if CHD is suspected.

An ECG test with physical activity is considered positive if, during its conduct, an attack of angina occurs, accompanied by horizontal or oblique depression or elevation of the segment ST>1 mm (0.1 mV), spaced >=60-80 ms from the end point of the complex QRS(Figure 2-13).

If during an ECG test with physical exercise a typical attack of angina occurs (serves as a basis for its termination), not accompanied by changes in the ECG characteristic of myocardial ischemia, then such test results are regarded as doubtful. They usually require other instrumental methods for diagnosing coronary artery disease (pharmacological stress tests in combination with echocardiography, myocardial perfusion scintigraphy, multislice CT with contrast of the coronary arteries or coronary angiography).

An important condition for interpreting an ECG test with physical activity as negative is the absence of an angina attack and the above-described changes in the ECG when the patient reaches a submaximal heart rate for his age. For each patient, the latter is approximately calculated as 200 minus the patient’s age.

The sensitivity of exercise ECG tests averages 68% and the specificity is 77%.

The main contraindications to testing with physical activity:

Acute MI;

Frequent attacks of angina pectoris between exertion and rest;

Heart failure;

Prognostically unfavorable disturbances of heart rhythm and conduction;

Thromboembolic complications;

Severe forms of hypertension;

Acute infectious diseases.

If it is impossible to carry out a treadmill test or bicycle ergometry (diseases of the musculoskeletal system, severe obesity, detraining of the patient, etc.), increased heart function can be achieved using a test of frequent transesophageal electrical stimulation of the atria (the method is not traumatic and is quite easy to perform).

In patients who initially have changes in the ECG at rest, which complicate its interpretation when performing exercise tests (complete block of the left bundle branch, depression of the segment ST>1 mm, WPW syndrome, implanted pacemaker), stress echocardiography and myocardial perfusion scintigraphy can be used in combination with physical activity.

Stress echocardiography and myocardial perfusion scintigraphy in combination with physical activity can also be used to detect objective signs of myocardial ischemia in patients with a high probability of coronary artery disease, in whom ECG tests with physical activity did not give clear results and the diagnosis remained unclear.

Rice. 2-13. ECG of a patient with coronary artery disease during an exercise test (treadmill test), segment ST sharply reduced in leads V 2 -V 6. Before the load, the ST segment was not changed

Pharmacological stress tests. Despite the fact that it is considered preferable to use physical activity as stress, since this makes it possible to induce myocardial ischemia and more physiologically cause a painful attack, pharmacological stress tests with various drugs that can affect the coronary bed and the functional state of the myocardium can also be used to diagnose IHD. .

Thus, if there are initial changes in the final part of the ventricular complex on the ECG and the need for differential diagnosis of IHD and NCD, pharmacological tests with propranolol and potassium chloride are used. Changes obtained on the ECG are always assessed taking into account other data from the examination of the patient.

The use of pharmacological stress tests in combination with echocardiography (stress echocardiography) or myocardial perfusion scintigraphy (stress scintigraphy) is advisable in patients who cannot fully perform an exercise test.

In clinical practice, two variants of pharmacological stress tests are used.

Using short-acting sympathomimetics (dobutamine), which are administered intravenously with a gradual increase in dose, which helps to increase the myocardial oxygen demand, acting similarly to physical activity.

Less commonly used is intravenous infusion of drugs that dilate the coronary arteries (trifosadenine or dipyridamole). These drugs have different effects on the areas of the myocardium that are supplied by normal and atherosclerotic stenotic coronary arteries. Under the influence of these drugs, perfusion increases significantly or may increase slightly or even decrease (the “steal” phenomenon).

If a patient has coronary artery disease during stress echocardiography with dobutamine or dipyridamole, an imbalance occurs between the delivery of oxygen and the need for it in a certain area of the myocardium, supplied with blood from a branch of the affected coronary artery. As a result, local disturbances in myocardial contractility and perfusion occur, which are detected either using ultrasound (stress echocardiography) or using radioisotope (myocardial perfusion scintigraphy) studies. With stress echocardiography, changes in local contractility may precede or be combined with other signs of myocardial ischemia (ECG changes, pain, cardiac arrhythmias).

The sensitivity of the dobutamine ultrasound stress test ranges from 40 to 100% and the specificity from 62 to 100%. The sensitivity of the ultrasound stress test with vasodilators (triphosadenine, dipyridamole) is 56-92%, and the specificity is 87-100%. The sensitivity and specificity of the radioisotope pharmacological stress test with trifosadenine are 83-94% and 64-90%, respectively.

At the third stage of the diagnostic search in patients with stable angina pectoris, ultrasound of the heart at rest should be performed when listening to pathological murmurs in the heart, suspicious of valvular heart disease or HCM, clinical signs of chronic heart failure, previous MI and pronounced ECG changes (complete blockade of the left bundle branches, pathological waves Q,

signs of significant hypertrophy of the left ventricular myocardium). Ultrasound of the heart at rest allows you to assess the contractility of the myocardium and determine the size of its cavities. In addition, if a heart defect, dilated or obstructive cardiomyopathy is detected, the diagnosis of coronary artery disease becomes unlikely, but in elderly people a combination of these diseases is possible.

Holter 24-hour ambulatory ECG monitoring in patients with stable angina pectoris allows you to determine objective signs of myocardial ischemia that occur during the normal, daily activities of patients, but can rarely add anything significant to the diagnostic information obtained during ECG tests with physical activity. load. However, Holter 24-hour ambulatory ECG monitoring in patients with stable angina pectoris is recommended to determine possible rhythm disturbances associated with it, “silent” myocardial ischemia and if vasospastic angina is suspected (Prinzmetal angina).

With the introduction of new intravenous contrast agents and modern MSCT, which allows performing up to 320 slices per second, the role of CT in the diagnosis of coronary artery disease and atherosclerotic lesions of the coronary arteries is significantly increasing. Despite the fact that the sensitivity of MSCT with contrast of the coronary arteries in diagnosing their atherosclerotic lesions reaches 90-95%, and the specificity is 93-99%, the final place of this examination method in the hierarchy of others has not yet been fully determined. Currently, it is believed that MSCT is recommended for patients in whom, based on a clinical assessment, a low (less than 10%) probability of the existence of coronary artery disease has been determined and in whom ECG tests with physical activity, as well as ultrasound and radioisotope stress tests were not sufficiently informative to establish diagnosis. In addition, MSCT, a non-invasive research method, is used for screening the population to diagnose the initial stages of coronary artery disease.

Selective coronary angiography is the gold standard for diagnosing coronary artery disease. It is recommended to carry it out for the purpose of diagnosing stable angina pectoris:

If angina pectoris is more than functional class III and there is no effect from full-fledged drug treatment;

When angina returns after previously performed myocardial revascularization operations (coronary artery bypass grafting, percutaneous transluminal angioplasty);

In case of previous circulatory arrest;

Severe ventricular arrhythmias (episodes of sustained and unsustained VT, frequent polytopic ventricular ventricular reflux, etc.);

Patients in whom, based on a clinical assessment, an intermediate or high probability of the existence of coronary artery disease was noted, and the results of using non-invasive research methods were insufficiently informative to establish a diagnosis or brought conflicting information.

Risk stratification in patients with stable angina pectoris

Depending on the risk of death within the next year, all patients with stable angina pectoris are divided into patients with low (risk of death less than 1%), high (risk of death more than 2%) and intermediate risk (risk of death 1-2%).

An effective way to stratify the risk of death in patients with stable angina pectoris is a combination of clinical assessment (severity of angina, frequency of attacks, changes in the resting ECG) and the results of ECG exercise tests (Duke treadmill index). The latter is calculated using the following formula:

Duke index = A--, where A is the duration of physical activity (min), B is the maximum deviation of the segment ST(mm), C - angina index.

Angina index score: 0 - no angina, 1 - angina, 2 - angina leads to study stop.

With a Duke treadmill index of more than +5, the patient is classified as a low-risk group, with a four-year survival rate of 99% and an annual probability of death of 0.25%. If the Duke Treadmill Index is in the range of +4 to -10, then he is classified as intermediate risk and has a four-year survival rate of 95% and an annual probability of death of 1.25%. If the Duke treadmill index is less than -10, the patient is classified as a high-risk group, his four-year survival rate is 79%, and the annual probability of death is more than 5.0%.

Patients who, according to the results of stratification, have an intermediate and high risk of death are recommended to undergo coronary angiography to decide on the advisability of performing myocardial revascularization.

It should be noted that normal results of coronary angiography indicate only the absence of significant narrowing of the large coronary arteries and their branches, while changes in small arteries (fourth and fifth order) may remain undetected. This situation is typical for patients with the so-called IHD with normal coronary arteries. This category includes patients with coronary syndrome X and vasospastic (variant) angina (Prinzmetal angina).

Coronary syndrome X. Although there is no generally accepted definition of this syndrome, it is characterized by a classic triad of symptoms: typical exercise-induced angina attacks; positive results of an ECG test or other tests with physical activity and unchanged coronary arteries (according to coronary angiography). The most recognized cause of coronary syndrome X is the occurrence of functional disorders of the coronary circulation at the level of the microvasculature during physical or emotional stress. Possible causes of pain and ischemic changes on the ECG include endothelial dysfunction with inadequate coronary vasodilation and excessively pronounced coronary vasoconstriction during physical activity at the level of the microvasculature. The prognosis is relatively favorable.

Vasospastic (variant, spontaneous) angina. A characteristic sign of this form of angina is the occurrence of typical anginal attacks at rest in their absence during physical and emotional stress. Less commonly, spontaneous angina is combined with exertional angina.

If, during an attack of spontaneous angina, a transient elevation of the segment is recorded on the ECG ST, This type of angina is called Prinzmetal angina.

Most often, spontaneous attacks of angina occur at night or early in the morning, without connection with physical or emotional stress, last from 5 to 15 minutes and are eliminated by taking nitroglycerin within a few minutes.

Spontaneous angina is based on spasm of normal or atherosclerotic coronary arteries. The mechanism of development of the spasm of the latter is not fully understood, but hyperactivity of the smooth muscle elements of the vascular wall and endothelial dysfunction may play a significant role in its occurrence.

In typical situations, an attack of vasospastic angina is accompanied by a transient elevation of the segment ST on the ECG, which reflects the occurrence of transmural myocardial ischemia, which disappears immediately after the cessation of pain and is not accompanied by a subsequent increase in the concentration of biochemical markers of myocardial necrosis (cardiac troponin T or I, CF fraction of CK), i.e. does not end with the development of MI.

Vasospastic angina can be triggered by smoking, cold, hyperventilation, drug use (cocaine) and electrolyte disturbances.

In order to prove the occurrence of coronary artery spasm and thus objectively confirm the existence of vasospastic angina, a provocative test is used with the introduction of acetylcholine (less commonly, ergonovine) into the coronary arteries during coronary angiography.

The prognosis for patients with vasospastic angina that occurs against the background of unchanged coronary arteries is relatively favorable; their risk of death does not exceed 0.5% per year. In patients with vasospastic angina on the background of hemodynamically significant stenosis of the coronary arteries, the prognosis is much more serious.

Diagnostics

When establishing a diagnosis of stable angina pectoris, the main and additional diagnostic criteria are taken into account.

Main criteria:

Attacks of angina pectoris typical in terms of the nature of the pain syndrome (history, observation);

Reliable indications of a previous MI (history, signs of chronic cardiac aneurysm or scar changes on the ECG and according to ultrasound of the heart);

Positive results of ECG tests with physical activity (treadmill test, bicycle ergometry), pharmacological stress tests (stress echocardiography, myocardial stress scintigraphy);

Positive results of coronary angiography (hemodynamically significant stenoses of the coronary arteries).

Additional diagnostic criteria:

Signs of chronic heart failure;

Heart rhythm and conduction disturbances (in the absence of other diseases causing them).

Formulation of a detailed clinical diagnosis should take into account:

Statement of the existence of IHD (provided that there is objective evidence of its presence);

Determination of the clinical variant of coronary artery disease (often a combination of two or even three variants is noted in one patient; if a patient is diagnosed with stable angina pectoris, then its functional class is indicated in accordance with the classification of the Canadian Cardiovascular Society; 1979);

The nature of rhythm and conduction disturbances (if any);

If chronic heart failure is detected, its severity (according to the classification of the New York Heart Association and N.D. Strazhesko-V.Kh. Vasilenko);

The main localization of atherosclerosis (the absence of coronary atherosclerosis with convincing evidence according to coronary angiography is necessarily reflected in the diagnosis);

If detected - hypertension (including hypertension, indicating the stage of its progression);

If detected - diabetes mellitus;

Other background and concomitant diseases.

Treatment

The main goals of treatment for patients with stable angina are:

Increasing the life expectancy of patients by reducing the risk of developing MI and sudden death;

Improving the quality of life by reducing the severity of clinical symptoms of the disease.

Similar goals can be achieved through the combined use of:

Non-drug measures aimed at correcting existing risk factors for coronary artery disease;

Drug and surgical treatment.

Considering the relatively favorable prognosis in patients with stable angina, for most patients drug treatment is considered a real alternative to interventional (balloon coronary angioplasty and coronary artery stenting) and surgical treatment methods (coronary artery bypass grafting, etc.).

The use of interventional and surgical methods for the treatment of patients with stable angina pectoris is justified in patients at high risk for the development of MI and sudden death, as well as in persons in whom full-fledged drug treatment is not sufficiently effective.

Risk factor correction should be carried out in all patients and at any stage of disease development.

Smoking is an important risk factor for the development of coronary artery disease, so it is necessary to ensure that patients permanently quit smoking. This often requires the participation of a qualified psychologist or psychotherapist. Significant help can be provided by the use of nicotine-containing preparations (nicotine) in the form of skin patches, chewing gum and in the form of an inhaler with a mouthpiece (most preferable, since it simulates the act of smoking).

It is advisable to change the nature of your diet, focusing on the so-called Mediterranean diet, which is based on vegetables, fruits, fish and poultry. In case of hyperlipidemia (the lipid profile must be assessed in all patients with angina), adherence to a strict lipid-lowering diet becomes especially important. The concentration of total cholesterol should be maintained below 5.0 mmol/l (192 mg/dl), LDL - less than 2.6 mmol/l (100 mg/dl). The choice of drugs for lipid-lowering therapy depends on the lipid profile, but in most cases preference is given to drugs from the group of statins (simvastatin, atorvastatin, rosuvastatin), taking into account their proven positive effect on the prognosis in patients with coronary artery disease.

Patients with angina pectoris should definitely maintain feasible physical activity, as this can help increase exercise tolerance, as well as normalize blood pressure, lipid concentrations, improve glucose tolerance and insulin sensitivity. This will also help reduce excess body weight.

Of particular importance is the treatment of concomitant hypertension and diabetes mellitus, which serve as risk factors for the development of coronary artery disease. You should not only strive to achieve target blood pressure, but also try to use drugs that simultaneously have antihypertensive and antianginal activity (beta-blockers, slow calcium channel blockers). In patients with diabetes mellitus, the most justified use of ACE inhibitors, slow calcium channel blockers, as well as highly selective beta-blockers with vasodilating properties (nebivolol)).

Drug treatment

There are two main areas of drug treatment for stable angina:

Treatment aimed at preventing the occurrence of MI and death;

Treatment aimed at reducing myocardial ischemia and the severity of clinical signs of the disease.

The first direction includes the use of antiplatelet drugs, beta-blockers, statins and ACE inhibitors.

The second direction includes the use of beta-blockers, nitrates, slow calcium channel blockers and cytoprotectors.

All patients with angina pectoris should be recommended to use short-acting nitrates to relieve anginal attacks. Patients should always carry one or another short-acting nitro-containing drug with them. Traditionally, nitroglycerin tablets are used for this purpose, but they are small in size, often crumble, and therefore their use is often difficult (especially in elderly patients and patients with motor impairments). More convenient are short-acting nitrates in the form of metered aerosols (isosorbide dinitrate, isomac), which are sprayed into the oral cavity. An alternative is isosorbide dinitrate 10 mg tablets, administered in a similar manner to nitroglycerin (sublingually). It should be remembered that the effect occurs somewhat later (after 10-15 minutes), but also lasts longer (up to 1.5 hours). It is often useful to take isosorbide dinitrate in advance before planned increased physical and (or) emotional stress. It is important to explain to patients the need for timely replacement of the drug packaging even before its expiration date, as well as the danger of repeated uncontrolled use of short-acting nitrates, which is fraught with the development of hypotension and indicating the insufficient effectiveness of antianginal therapy in general.

Treatment to prevent myocardial infarction and death

All patients with angina pectoris, in the absence of contraindications, should receive acetylsalicylic acid at a dose of 75-160 mg/day (the optimal dose is 100 mg/day), which reduces the relative risk of developing MI and sudden death by at least 30%. The main contraindications to the use of the drug: peptic ulcer, erosive gastritis, duodenitis. In such cases, clopidogrel can be used.

Beta blockers are widely used in the treatment of angina. The improvement in their prognosis while taking these drugs is associated with a reduced risk of developing MI and death. It is especially recommended to prescribe beta-blockers to patients with angina who have had an MI, since the ability of these drugs to reduce the relative risk of MI and death by 30-35% has been shown.

In the treatment of angina, preference is given to cardioselective beta-blockers. The most widely used drugs are metoprolol (50-200 mg/day), bisoprolol (2.5-5 mg/day), carvedilol (25-50 mg/day), betaxolol (10-40 mg/day). day), etc. Atenolol is used much less frequently (100-200 mg/day), while an adequate dose of beta-blockers is considered to be the one at which it is possible to reduce heart rate at rest to 50-60 per minute.

The non-selective beta-blocker propranolol is still used at a dose of 40-200 mg/day, but it is usually less tolerated by patients. In addition, the drug requires 3-4 doses, which reduces patient adherence to treatment.

The main adverse reactions when taking beta-blockers are: bradycardia, atrioventricular conduction disorders, arterial hypotension, deterioration of exercise tolerance, bronchospasm and erectile dysfunction.

The use of beta-blockers should be avoided in patients with bronchial obstruction (especially with poorly controlled asthma), peripheral arterial disease and diabetes mellitus. In a number of such cases, it is possible to use highly selective beta-blockers such as metoprolol and bisoprolol, but this should be done with extreme caution. The safest use of drugs that have the ability to peripherally vasodilate as a result of modulating the release of nitric oxide, in particular nebivolol and carvedilol.

Attention should be paid to the use of beta-blockers in patients with angina pectoris with concomitant chronic heart failure. In such a situation, it is recommended to use metoprolol, bisoprolol, carvedilol and nebivolol.

Treatment with β-blockers in patients with angina pectoris due to chronic heart failure should begin with the use of small doses and only against the background of adequate intake of ACE inhibitors and diuretics, and at first it is natural to expect some worsening of the symptoms of heart failure.

Long-term treatment with statins is recommended for patients with stable angina with elevated concentrations of cholesterol, LDL and triglycerides in the blood, which can reduce the relative risk of MI and death by 20-40%.

Patients with stable angina, regardless of the presence of hypertension, heart failure and diabetes mellitus, are recommended to undergo long-term treatment with one of two ACE inhibitors - ramipril or perindopril. These drugs also reduce the likelihood of their developing MI and death by 20%. This effect is not considered class-dependent, since other ACE inhibitors have not demonstrated this ability in large clinical trials.

Treatment aimed at reducing myocardial ischemia and the severity of clinical signs of the disease

To prevent angina attacks, drugs with hemodynamic action are traditionally used, which, by influencing the parameters of central hemodynamics, reduce the myocardial oxygen demand or increase its delivery. Three main groups of drugs are used: beta-adrenergic blockers, slow calcium channel blockers and long-acting nitrates.

Slow calcium channel blockers are used in the treatment of angina in cases where the use of beta-blockers is impossible or in combination with the latter to enhance the antianginal effect. The positive effect of treatment with them on the life expectancy of patients with stable angina has not been proven. The most preferred non-dihydropyridine drugs are verapamil (120-320 mg/day) and its prolonged form isoptin CP 240, as well as diltiazem (120-320 mg/day).

For the treatment of patients with stable angina pectoris, short-acting dihydropyridines (nifedipine) and long-acting second and third generation dihydropyridines (amlodipine, felodipine, etc.) should not be used.

In patients with stable angina pectoris, long-acting nitrates are widely used as drugs that reduce the degree of myocardial ischemia and the severity of clinical signs of angina. It must be remembered that this class of antianginal drugs does not affect the life expectancy of patients with stable angina. For this purpose, isosorbide dinitrate (40-240 mg/day) and isosorbide mononitrate (40-240 mg/day) are used. These drugs are better tolerated by patients and cause headaches to a lesser extent. The use of sustak mite, sustak forte and pentaerythrityl tetranitrate is not justified due to low efficiency and inconvenience of use (multiple doses).

The main side effects of treatment with nitrates: headache, arterial hypotension, redness of the skin, and sometimes syncope. Significant disadvantages of this class of drugs include the development of tolerance, which can be overcome by temporary withdrawal of these drugs. The development of tolerance to nitrates can be avoided by rational dosing, ensuring a “nitrate-free interval” lasting at least 8 hours (usually at night).

If nitrates are poorly tolerated, molsidomine can be prescribed at a dose of 2-24 mg/day (especially in patients with concomitant lung diseases, cor pulmonale).

Often in the treatment of angina pectoris it is not possible to achieve success with monotherapy. In such cases, it is advisable to use combinations of antianginal drugs with different mechanisms of action. The most rational combinations are: beta blockers + nitrates, beta blockers + slow calcium channel blockers (dihydropyridine), slow calcium channel blockers + nitrates, beta blockers + slow calcium channel blockers + nitrates. It is not advisable to combine drugs of the same class due to ineffectiveness and a sharply increasing risk of side effects. Caution should be exercised when combining beta-blockers with verapamil or diltiazem, as the likelihood of conduction disturbances and left ventricular dysfunction sharply increases.

Although combination antianginal therapy is used everywhere, its effectiveness is not always sufficient. It can be enhanced by adding metabolic drugs to treatment: trimetazidine, nicorandil or the sinus node pacemaker ion current blocker Ir ivabradine. Trimetazidine is a cytoprotective drug with metabolic action that has proven its antianginal effectiveness. The most important advantage of trimetazidine is its lack of any effect on hemodynamics. It also does not affect automaticity and conduction, and does not aggravate bradycardia. Trimetazidine is usually very well tolerated by patients. It is prescribed at a dose of 20 mg 3 times a day with meals. Currently, a new dosage form of trimetazidine is used - preductal MB *, which makes it possible to maintain constant antianginal effectiveness of the drug for 24 hours (one tablet of the drug, taken 2 times a day, contains 35 mg of trimetazidine).

Patients with coronary syndrome X are recommended to use long-acting nitrates, beta-blockers and slow calcium channel blockers as monotherapy or a combination thereof. For hyperlipidemia, it is advisable to prescribe statins, and for hypertension - ACE inhibitors. If the effectiveness is insufficient, metabolic drugs (nicorandil, trimetazidine) can be used.

Treatment of patients with variant (vasospastic) angina consists of eliminating provoking factors (smoking, cocaine use, etc.) and using medications such as slow calcium channel blockers (verapamil at a dose of up to 480 mg/day, diltiazem at a dose of up to 260 mg/day day, nifedipine at a dose of up to 120 mg/day) and prolonged nitrates.

Myocardial revascularization. Currently, there are two methods of myocardial revascularization (including in patients with stable angina pectoris): surgical (coronary artery bypass grafting) and interventional (percutaneous coronary angioplasty and stenting of the coronary arteries).

Choosing a treatment strategy in patients with stable angina pectoris is a rather difficult task. It should be decided strictly individually and take into account many factors: the clinical picture, the severity and extent of areas of myocardial ischemia according to stress tests, the severity, localization and prevalence of atherosclerotic lesions of the coronary arteries according to coronary angiography, the desire of the patient himself, and much more.

When choosing a treatment strategy for patients with stable angina, it is necessary to remember that recent clinical studies comparing the immediate and long-term results of optimal drug treatment and myocardial revascularization in patients with stable angina pectoris have shown that five-year survival does not depend on the chosen strategy, but quality of life (frequency and severity of angina attacks) was significantly better in patients who underwent myocardial revascularization.

Clinical indications for myocardial revascularization in patients with stable angina pectoris:

Ineffectiveness of optimal drug treatment, in which the patient’s quality of life is not satisfactory;

The results of the use of non-invasive examination methods, indicating that a large volume of myocardium subject to ischemia is at risk;

High probability of successful myocardial revascularization with an acceptable risk of short-term and long-term mortality;

The patient’s informed choice of a surgical treatment method, taking into account his full information about the possible risks of the intervention.

At the same time, there are certain indications for myocardial revascularization in order to improve the prognosis of the development of MI. They are associated primarily with the severity, prevalence and localization of atherosclerotic lesions of the coronary arteries, which are determined using coronary angiography.

Percutaneous coronary angioplasty and stenting are recommended for:

Severe (>=75%) stenosis of one coronary artery in patients with angina pectoris I-IV functional class and ineffectiveness of optimal drug treatment;

Severe (>=75%) stenosis of several coronary arteries in patients with angina pectoris of functional class I-IV (without diabetes mellitus) and ineffectiveness of optimal drug treatment.

For angina pectoris I-IV functional class in patients with hemodynamically significant (>50%) stenosis of the trunk of the left coronary artery or its equivalent (pronounced (>=75%) stenosis of the ostia or proximal parts of the anterior interventricular and circumflex arteries);

Angina pectoris I-IV functional class and ineffectiveness of optimal drug treatment in patients with severe (>75%) stenoses of all three coronary arteries (anterior interventricular, circumflex and right), especially their proximal sections, as well as in diabetes mellitus, left ventricular dysfunction and objective proven large zone of myocardial ischemia.

Forecast

The prognosis depends on the results of risk stratification. In most patients, it is relatively favorable, but it should always be assessed with caution, since the chronic course of the disease can suddenly worsen, be complicated by the development of myocardial infarction, and sometimes by sudden death.

Prevention

Primary prevention comes down to the prevention of atherosclerosis. Secondary prevention should be aimed at carrying out rational anti-atherosclerotic treatment and optimal relief of pain, arrhythmias and heart failure.

Good day, dear readers!

In today's article we will look at a heart disease such as angina, as well as its symptoms, causes, types, diagnosis, treatment, medications, folk remedies and prevention of angina. So…

What is angina?

Angina pectoris– a clinical syndrome characterized by discomfort or severe pain in the chest, the main cause of which is a violation of the coronary blood supply to the heart muscle.

Other names for angina - "angina pectoris"(obsolete name).

Angina is included in the classification, being a clinical manifestation (symptom) of this disease. It is often accompanied by cardiac arrest, for example - in which the heart rate increases to 90 or more beats per minute, shortness of breath,.

Pain during angina pectoris appears suddenly, more often during physical exertion or stressful situations, less often when the person is at rest. In terms of time, the attack can last no more than 10-15 minutes, but disappears after removing the provoking factor, as well as when taking nitroglycerin (under the tongue).

The main cause of angina in most cases is the appearance and development of atherosclerotic plaques in the coronary arteries. The presence of plaques, which are based on cholesterol deposits, narrows the lumen of blood vessels, and sometimes even blocks them, thereby disrupting blood flow and, accordingly, the nutrition of the organ cut off from the blood supply. In our case, nutrition is limited by the “human engine” - the heart, which, with a lack of oxygen and other substances supplied with the blood, begins to hurt. Pain in the heart under such circumstances is angina.

It is also important to understand that the section of the heart cut off from the blood circulation begins to starve after a few minutes, then dies and develops, a complication of which can be cardiac arrest and even death. That is why discomfort and pain in the heart should be taken extremely seriously, especially if angina attacks periodically make themselves felt.

Development of angina

As we have already said, the main cause of angina is a violation of the blood supply to the heart muscle (myocardium) due to the presence of atherosclerotic plaques in the coronary vessels of the heart.

Before looking at plaque formation, let's take a quick look at what it consists of.

The fact is that for the normal functioning of the body, for its cells, in particular their protection, cholesterol is necessary. Cholesterol itself cannot spread throughout the body, so this role is played by transporter proteins - apolipoproteins, which deliver it through the blood and blood vessels to all organs.

Depending on the “target” where cholesterol needs to be delivered, different types of apolipoproteins are used - high density (HDL), low density (LDL), very low density (VLDL) and chylomicrons.

The cause of the formation of atherosclerotic plaques is low-density lipoproteins (LDL), because. they have the bad property of precipitating, sticking to the walls of blood vessels along the way. Over time, cholesterol deposits accumulate in the walls of blood vessels, reducing the lumen of the bloodstream at the site of accumulation, and sometimes even blocking it. The following images perfectly illustrate this pathological process:

An area or organ cut off from the blood experiences starvation, because along with the blood, it receives both oxygen and nutrients necessary for their normal functioning.

Moreover, in this case there is another dangerous condition - the formation of a blood clot. Indeed, over time, in the place where cholesterol deposits accumulate, the wall of the blood vessel can break through, and a dense clot in the form of a plaque with other substances is thrown into the riverbed. The thrombus, moving through the vessels, reaching the point of narrowing, clogs the bloodstream, thereby causing a sharp cessation of blood supply to subsequent parts of the organs.

The most dangerous is the formation of blood clots in the vessels of the brain, provoking the development of the brain, as well as blood clots in the area of the heart muscle, causing myocardial infarction and sometimes cardiac arrest.

In fact, angina attacks are the “first bell” that tells us about developmental processes in a person, especially if pain in the heart area appears during physical exertion and emotional experiences. After all, when running or under stress, a person’s heart begins to work faster and, accordingly, needs a larger portion of blood and oxygen. If it does not receive enough nutrition, we will definitely find out about it.

Of course, the above model of angina development is very superficial. After all, there are other causes of an attack of angina, for example, spasm of the coronary vessels of the myocardium, but this is a rarer phenomenon, and I think I was able to describe the main one in a simple form accessible to every person.

Angina pectoris - statistics

The prevalence of angina pectoris is increasing from year to year, which is primarily due to the deterioration in the quality of modern food, as well as the deterioration of the psycho-emotional state of many people.

A sharp increase in angina attacks has been observed in adults aged 45 years and over, especially in men, approximately 1 to 2, sometimes to 3. This is due to the characteristics of the female body, which produces hormones that inhibit the development of atherosclerosis and its consequences.

If we talk about percentages, then at the age of 45 to 54 years, angina attacks affect 2-5% of people, while among 65-74 year olds, it increases to 10-20%.

Angina pectoris - ICD

ICD-10: I20;
ICD-9: 413.

Symptoms of angina

Main symptom of angina- sharp, squeezing, pressing, sometimes with burning pain behind the sternum. Its location is shown in the picture on the right. The pain associated with angina pectoris is short-term in nature - from 3 to 15 minutes. Very often, the painful effect radiates (gives) to the left arm, shoulder, shoulder blade, half of the neck, and rarely to the jaw.

Other signs of angina

Feeling short of air, difficulty breathing;
Feelings of anxiety, fear, similar to a panic attack;
, confusion;
- increase in heart rate to 90 beats per minute or more;
Rarely - and.
A characteristic feature is also the effect of nitroglycerin, which, when used, helps to abruptly stop an attack of angina.

Important! If the chest pain does not go away for more than 15 minutes, even when using nitroglycerin, immediately call an ambulance, because Possible more serious damage to the heart, for example, myocardial infarction.

Complications of angina

Heart failure;
Death.

The main cause of angina attacks is, the mechanism of development of which we partially discussed at the beginning of the article. In short, the cause of angina is damage to the coronary vessels by atherosclerotic plaques that reduce or completely block the lumen of the bloodstream. At the same time, the heart (myocardium) does not receive the required amount of blood, and along with it oxygen and nutrients, this is especially expressed during loads on the heart muscle, when it especially needs an additional portion of blood.

Other causes of angina include:

Spasms of the coronary or coronary vessels;
Anomalies in the development of the coronary vessels of the heart muscle;
Thrombosis and thromboembolism of the coronary arteries;

Factors that contribute to the occurrence of angina attacks are:

Strong emotional experience;

Tachycardia;

Exit from a warm room into cold, cold and windy weather;

Genetic predisposition.

The reasons for the development of atherosclerotic plaques are:

Consumption of low-health and - lemonades, fast food, unnatural food with a large number of substitutes (food additives - E***);
Bad habits – smoking, alcohol;
Hyperlipidemia (increased levels of lipids and lipoproteins in the blood);
Dysfunction of the endothelium (the inner wall of blood vessels);
Hormonal imbalance (, etc.);
Violation of metabolic processes in the body;
Increased blood clotting;
Damage to blood vessels by infection - herpes virus, cytomegalovirus, chlamydia;
Drug abuse.

Those most prone to angina attacks are:

Males;
Overweight persons;
Elderly persons;
Hypertensive patients;
Addicted to smoking, alcohol, drugs;
Fast food lovers;
People with a sedentary lifestyle;
People often exposed to stress;
Persons with diseases such as,.

Angina is divided into 2 main groups – stable and unstable angina.

1. Stable angina (angina pectoris)

Angina pectoris usually develops during a person’s physical exertion, strong experiences, stress, i.e. in cases where the heartbeat quickens and the heart muscle needs an increased amount of blood and oxygen.

Depending on the level of physical activity at which a person experiences chest pain, exertional angina is divided into 4 functional classes (FC):

Angina pectoris FC 1 (FC I)– characterized by rare attacks of pain, mainly with significant or excessive physical stress on the body;

Angina pectoris FC 2 (FC II)– characterized by frequent attacks of pain during minor physical exertion – climbing stairs to the 1st floor, brisk walking of about 300 meters or more. An attack can also begin in the first hours of a person’s wakefulness, when, turning on from a state of rest to normal mode, the rhythm of the heart increases, blood circulation increases and antifibrinolytic ability decreases (circadian rhythm of angina).

Angina pectoris FC 3 (FC III)- characterized by frequent attacks of pain with minor physical exertion - climbing the stairs to the 1st floor at the usual slow pace, brisk walking of about 150 meters or more.

Angina pectoris FC 4 (FC IV)– characterized by frequent attacks with minimal physical activity of a person or a state of rest (rest).

2. Unstable angina

Unstable angina is characterized by painful attacks of varying intensity, duration, and unpredictable occurrence, for example, at rest. Pain syndrome is more difficult to relieve when taking nitrates (nitroglycerin). The risk of developing myocardial infarction is higher, in contrast to the stable form of this pathology. Due to its properties, unstable angina has been divided into several different types:

2.1. New-onset angina (AF)– the development of a repeated attack occurs 30-60 days after the first manifestation of pain.

2.2 Progressive angina (PA)– development occurs more often against the background of a stable form of angina, with an increase in the functional class (FC).

2.3. Early post-infarction, postoperative angina– the development of pain syndrome occurs in the period from 3 to 28 days after myocardial infarction (according to the classification of domestic doctors), or from 1 to 14 days (NYHA classification).

2.4. Spontaneous angina (vasospastic, variant, Prinzmetal)– characterized by sudden attacks of chest pain for no apparent reason, most often at rest. Typically, vasospastic angina is not associated with atherosclerotic lesions of the coronary vessels. Its cause is predominantly spasms of the coronary vessels.

Diagnosis of angina pectoris

Diagnosis of angina pectoris includes the following examination methods:

Anamnesis;
Measuring blood glucose levels (determination of glycemia);
at rest and during physical activity;
Daily monitoring of heart function using ECG;
Echocardiography (EchoECG) at rest and during exercise;
Scintigraphy during physical or pharmacological stress.
Coronary angiography (in some cases, at the discretion of the doctor).

How to treat angina? Treatment of angina pectoris is aimed at relieving pain, preventing the development of myocardial infarction, as well as stopping the development of atherosclerosis and cleansing blood vessels of atherosclerotic plaques.

Treatment of angina pectoris includes the following therapy methods:

1. Limitation of human physical activity;
2. Drug treatment (drugs for angina):
2.1. Pain relief;
2.2. Maintenance therapy;
2.3. Anti-atherosclerotic therapy;
3. Diet;
4. Surgical treatment;
5. Compliance with preventive measures.

1. Limiting physical activity

As we have repeatedly mentioned in this article, any physical activity of a person, including strong emotional experiences, makes the heart work faster, the pulse increases and the heart begins to pump blood faster for normal functioning, and accordingly needs more blood. If there are obstacles in the blood vessels to normal blood flow, in our case - the presence of atherosclerotic plaques in the coronary vessels, the heart begins to experience a lack of oxygen and nutrients. In this case, the person feels a pain attack.

To prevent such situations, the patient needs rest, and the higher the functional class (FC) of angina, the more you need to protect yourself from physical activity and stressful situations.

Physical activity is necessary and prescribed by the attending physician at the rehabilitation stage, after additional examination of the patient.

2. Drug treatment (drugs for angina pectoris)

Important! Before using any drugs or medications to treat angina, be sure to consult your doctor!

2.1. Pain relief

Relief (relief) of pain caused by angina pectoris is carried out by the following groups of drugs:

Nitrates– drugs with antianginal and vasodilating effects. There are short, medium and long acting. Assigned depending on the functional class.

To quickly relieve an attack of angina, Nitroglycerin is used under the tongue. If the remedy does not help, it is necessary to examine the person for myocardial infarction or non-cardiac pain.

During the treatment period, if a person has to exercise, depending on the functional class (FC), nitrates are prescribed 5-10 minutes beforehand.

Angina pectoris FC 1 is prevented with the help of short-acting nitrates (less than 1 hour) - “Nitroglycerin”.

Angina pectoris 2 FC is prevented with the help of short-acting (less than 1 hour) or medium-acting nitrates (from 2 to 6 hours) - “Nitroglycerin”, “Isosorbide dinitrate”.

Angina pectoris FC 3 is prevented with the help of long-acting nitrates (more than 6 hours) - “Isosorbide mononitrate”.

Angina pectoris FC 4 is prevented by the combined use of long-acting nitrates (Isosorbide mononitrate) and other antianginal drugs (β-blockers, etc.). This combination is also used in the evening, before bed.

β-blockers (beta blockers)- contribute to a decrease in heart rate (HR) and, accordingly, the heart’s need for an increased amount of blood and oxygen. Thus, beta-blockers relieve angina pain.

Among the β-blockers we can distinguish: bisoprolol (Biprol, Cordinorm), carvedilol (Dilatrend, Coriol), metoprolol (Betalok, Vazocardin, Egilok).

Calcium channel blockers– have an antianginal effect, which is why they are often prescribed for the treatment of angina pectoris. They are divided into 2 groups - dihydropyridine derivatives and non-dihydropyridine derivatives.

Dihydropyridine derivatives (“Amlodipine”, “Nifedipine”) have a prolonged antianginal effect, often used in combination with β-blockers to increase the effectiveness of treatment.

Non-dihydropyridine derivatives (Verapamil, Diltiazem) are used in case of contraindications to taking beta-blockers - in the presence of severe atherosclerosis of the lower extremities, chronic obstructive pulmonary disease (COPD).

Angiotensin-converting enzyme (ACE) inhibitors– block the conversion of angiotensin II from angiotensin I, thereby preventing spasms of blood vessels. In addition, ACE inhibitors normalize and protect the heart muscle from pathological processes.

Among the ACE inhibitors are: Captopril, Lisinopril, Enalapril.

2.2. Maintenance therapy

Maintenance therapy is aimed at improving the course and preventing subsequent attacks of angina, as well as the development of myocardial infarction.

Anticoagulants– protect blood vessels from thrombosis, inhibit the development of existing blood clots and the formation of fibrin threads.

Anticoagulants include: Heparin.

Antiarrhythmic drugs- help normalize heart rate, improve respiratory function, alleviate angina pectoris, coronary heart disease and many others.

Among the antiarrhythmic drugs we can highlight: “Ajmalin”, “Lidocaine”, “Novocainamide”.

Sedatives– calm the nervous system, which is especially important during strong emotional experiences leading to attacks of angina pectoris, as well as during pain syndrome, when a person begins to be attacked by fear.

Among the sedative drugs one can highlight: “Valerian”, “Persen”, “Tenoten”.

2.3. Anti-atherosclerotic therapy

Anti-atherosclerotic therapy is aimed at stopping and preventing the development of atherosclerotic plaques in blood vessels.

Statins And fibrates– have a hypocholesterolemic (cholesterol-lowering) effect. These groups of drugs lower the level of “bad” cholesterol in the blood, thereby reducing the amount of cholesterol deposits and, accordingly, the “building material” for the formation of atherosclerotic plaques. To achieve maximum effect, statins and fibrates are taken simultaneously.

Fibrates increase the amount of high-density lipoprotein (HDL) in the blood, which actually counteracts low-density lipoprotein (LDL), from which cholesterol actually precipitates. Fibrates are also used to treat coronary heart disease (CHD) and dyslipidemia. These drugs minimize the number of deaths from coronary artery disease.

Among the fibrates, one can highlight Fenofibrate.

Statins, unlike fibrates, directly lower the level of low-density lipoprotein (LDL) in the blood.

Statins include Atorvastin, Lovastatin, and Rosuvastin.

Total blood cholesterol levels should be reduced to 4.5 mmol/L (175 mg/dL) or lower, and LDL cholesterol levels to 2.5 mmol/L (100 mg/dL) or lower.

Antiplatelet agents- prevent the gluing of red blood cells and platelets, as well as their sedimentation on the inner walls of blood vessels (endothelium), thereby improving blood flow (blood circulation) in the body.

Antiplatelet agents include: Dipyridamole, Clopidogrel.

Diet for angina pectoris is an important and integral part of the course of treatment. After all, the level of cholesterol in the blood, the presence of atherosclerosis and its derivative cardiovascular diseases largely depend on the quality of food.

Key points of the diet for angina pectoris:

The calorie content of food is 10-15% less than your daily diet, and in case of obesity - 20%;
The amount of fat is no more than 60-80 g per day;
The amount of protein is no more than 1.5 g per 1 kg of human body weight per day;
The amount of carbohydrates is no more than 350-400 g per day;
The amount of salt is no more than 8 g per day.

What not to eat if you have angina

Spicy, fatty, fried, salted and smoked foods - ham, sausages, sausages, fatty dairy products, mayonnaise, ketchup and other unhealthy foods;
Animal fats, large amounts of which are found in fatty meats (pork, domestic duck, goose, carp and others), lard, butter, margarine;
High-calorie foods, as well as foods rich in easily digestible carbohydrates - cakes, pastries, chocolate, candies, marmalade, marshmallows, jams.

What can you eat if you have angina?

Food of animal origin - lean meats (lean fish, chicken), low-fat dairy products, egg whites;

Cereals – oatmeal, buckwheat;
Vegetables and fruits – mostly green vegetables and orange fruits;
Bakery products - rye or bran bread;
Drink - mineral waters, unsweetened tea,...

Vitamins

4. Surgical treatment

Surgical treatment (operation) of angina pectoris is prescribed only in cases where non-invasive therapy has not led to the desired result, as well as in cases where the coronary vessel has too small a lumen or a blood clot has formed in it.

Among the surgical methods of treating angina pectoris are:

Coronary artery bypass grafting (CABG)– “reconnection” of the coronary vessel with another section of the blood vessel, below its blockage;

Balloon angioplasty– the operation is based on the introduction of a special balloon into a blood vessel, at the site of its narrowed lumen, which is then inflated, thereby expanding the lumen of the bloodstream. Next, the balloon is deflated and removed from the vessel. For a longer and more reliable effect, a stent is installed in place of the vessel lumen expanded by the balloon. This method is called vessel stenting.

5. Compliance with preventive measures

Prevention of angina pectoris is aimed not only at preventing pain, but also at stopping possible complications of this pathological process, which is why such things as quitting smoking, alcohol and other measures are mandatory for the patient. We will talk about prevention in more detail a little later, but now let’s look at folk methods and remedies for angina.

Important! Before using folk remedies for angina, be sure to consult your doctor!

Lemon. While following the diet that we talked about just above in the article, eat thoroughly washed peel before each meal.

Garlic, lemon and honey. Put 1 liter of juice from 10 lemons and 5 heads (not cloves) squeezed through a garlic press into a 3-liter jar, mix everything thoroughly, close the jar with a lid and leave for 7 days to infuse in a dark, cool place. You need to take 2 tbsp. spoons in the morning, 1 time per day, on an empty stomach, slowly dissolving the product for a couple of minutes. The course of treatment is until the prepared product runs out.

Hawthorn. Pour 4 tbsp into a thermos. spoons and pour 1 liter of boiling water over it, leave the product to infuse overnight. Drink the infusion throughout the day as tea.

Mint and valerian. 4 tbsp. spoons and 1 tbsp. add a spoonful to the thermos, pour 1 liter of boiling water over the plants and leave to steep for a couple of hours. The infusion should be drunk throughout the day.

To increase the effectiveness of the product, you can also add a couple of teaspoons of fruits, which will add a portion to the drink that directly counteracts the formation of atherosclerotic plaques.

Fir oil. To relieve pain in the heart area, you need to rub 6-7 drops of fir oil into this area.

Prevention of angina pectoris includes compliance with the following rules and recommendations:

Complete cessation of smoking and alcoholic beverages;
Minimizing the consumption of unhealthy and unhealthy foods, including fatty, fried, spicy, salty, smoked foods, as well as foods that increase the level of “bad” cholesterol in the blood;
Eating foods enriched with and;
Move more so that blood circulation is always “playing”. Do exercises, if necessary, consult a physical therapy doctor so that he can prescribe a group of exercises to strengthen the cardiovascular system;
Watch your weight, don't let it happen;

– a form of ischemic heart disease, characterized by paroxysmal pain in the heart region, due to acute insufficiency of blood supply to the myocardium. A distinction is made between angina pectoris, which occurs during physical or emotional stress, and angina pectoris at rest, which occurs outside of physical effort, often at night. In addition to pain behind the sternum, it is manifested by a feeling of suffocation, pallor of the skin, fluctuations in pulse rate, and sensations of interruptions in the functioning of the heart. May cause the development of heart failure and myocardial infarction.

General information

Progressive, as well as some variants of spontaneous and new-onset angina, are combined into the concept of “unstable angina”.

Symptoms of angina

A typical sign of angina is pain behind the sternum, less often to the left of the sternum (in the projection of the heart). Painful sensations can be squeezing, pressing, burning, and sometimes cutting, pulling, drilling. Pain intensity can be from tolerable to very pronounced, causing patients to moan and scream, and experience fear of imminent death.

The pain radiates mainly to the left arm and shoulder, lower jaw, under the left shoulder blade, and to the epigastric region; in atypical cases - to the right half of the body, legs. The irradiation of pain during angina pectoris is due to its spread from the heart to the VII cervical and I-V thoracic segments of the spinal cord and further along the centrifugal nerves to the innervated zones.

Pain with angina pectoris often occurs during walking, climbing stairs, exertion, stress, and can occur at night. An attack of pain lasts from 1 to 15-20 minutes. Factors that alleviate an attack of angina are taking nitroglycerin and standing or sitting.

During an attack, the patient experiences a lack of air, tries to stop and freeze, presses his hand to his chest, turns pale; the face takes on a pained expression, the upper limbs become cold and numb. At first, the pulse quickens, then slows down, arrhythmia, often extrasystole, and an increase in blood pressure are possible. A prolonged attack of angina can develop into a myocardial infarction. Long-term complications of angina include cardiosclerosis and chronic heart failure.

Diagnostics

When recognizing angina pectoris, the patient’s complaints, nature, localization, irradiation, duration of pain, conditions of their occurrence and factors of attack relief are taken into account. Laboratory diagnostics include blood tests for total cholesterol, AST and ALT, high and low density lipoproteins, triglycerides, lactate dehydrogenase, creatine kinase, glucose, coagulogram and blood electrolytes. Of particular diagnostic importance is the determination of cardiac troponins I and T - markers indicating myocardial damage. Identification of these myocardial proteins indicates that a microinfarction or myocardial infarction has occurred and makes it possible to prevent the development of post-infarction angina.

An ECG taken at the height of an angina attack reveals a decrease in the ST interval, the presence of a negative T wave in the chest leads, conduction and rhythm disturbances. Daily ECG monitoring allows you to record ischemic changes or their absence with each attack of angina, heart rate, and arrhythmia. An increasing heart rate before an attack suggests exertional angina; a normal heart rate suggests spontaneous angina. EchoCG for angina pectoris reveals local ischemic changes and disturbances in myocardial contractility.

Myocardial scintigraphy is performed to visualize the perfusion of the heart muscle and identify focal changes in it. The radioactive drug thallium is actively absorbed by viable cardiomyocytes, and in angina pectoris accompanied by coronary sclerosis, focal areas of impaired myocardial perfusion are identified. Diagnostic coronary angiography is performed to assess the location, extent and extent of damage to the arteries of the heart, which allows one to determine the choice of treatment method (conservative or surgical).

Treatment of angina

Aimed at relieving and preventing attacks and complications of angina pectoris. The first aid drug for an angina attack is nitroglycerin (keep it in your mouth on a piece of sugar until completely absorbed). Pain relief usually occurs within 1-2 minutes. If the attack is not stopped, nitroglycerin can be reused at intervals of 3 minutes. and no more than 3 times (due to the danger of a sharp drop in blood pressure).

Planned drug therapy for angina pectoris includes taking antianginal (anti-ischemic) drugs that reduce the oxygen demand of the heart muscle: long-acting nitrates (pentaerythrityl tetranitrate, Isosorbide dinitrate, etc.), beta-blockers (anaprilin, oxprenolol, etc.), molsidomine, calcium channel blockers (verapamil, nifedipine), trimetazidine, etc.

In the treatment of angina pectoris, it is advisable to use anti-sclerotic drugs (statin group - lovastatin, simvastatin), antioxidants (tocopherol), antiplatelet agents (acetylsalicylic acid). According to indications, prevention and treatment of conduction and rhythm disorders is carried out; for angina pectoris of a high functional class, surgical revascularization of the myocardium is performed: balloon angioplasty, coronary artery bypass grafting.

Prognosis and prevention

Angina pectoris is a chronic disabling heart pathology. As angina progresses, the risk of myocardial infarction or death is high. Systematic treatment and secondary prevention help control the course of angina, improve the prognosis and maintain ability to work while limiting physical and emotional stress.

For effective prevention of angina pectoris, it is necessary to eliminate risk factors: reducing excess weight, controlling blood pressure, optimizing diet and lifestyle, etc. As a secondary prevention with an already established diagnosis of angina pectoris, it is necessary to avoid anxiety and physical effort, take prophylactic nitroglycerin before exercise, exercise prevention of atherosclerosis, treatment of concomitant pathologies (diabetes mellitus, gastrointestinal diseases). Accurate adherence to recommendations for the treatment of angina pectoris, taking long-acting nitrates and follow-up monitoring by a cardiologist allows you to achieve a state of long-term remission.

Angina pectoris or “angina pectoris” is a sharp pain or discomfort in the chest area caused by a lack of blood supply to a certain area of the heart. Angina pectoris is the leading symptom of coronary heart disease (CHD), which develops as a result of narrowing or blockage of the heart vessels.

Subjective sensations of patients with angina pectoris can be described as squeezing or pressing pain behind the sternum, often radiating (radiating) to the shoulder, arm, neck or jaw.

Typically, the pain lasts less than 5 minutes and goes away with appropriate medication or rest. However, various patients experienced angina attacks lasting from 30 seconds to 30 minutes.

What causes angina attacks?

As already noted, acute episodes occur in cases where the oxygen needs of the heart muscle are not met by the blood flow. Angina attacks occur after physical exertion, emotional stress, sudden hypothermia or overheating of the body, after eating heavy or spicy food, or drinking alcohol. In all of the above cases, the work of the heart increases, and accordingly the lack of oxygen is felt more acutely. A painful effect occurs.

Do angina attacks mean an impending heart attack?

First of all, it is necessary to understand that an attack of angina is not a heart attack; it is the result of only a temporary lack of oxygen in the working heart muscle.

Unlike angina, with a heart attack, irreversible changes occur in the heart tissue due to the complete cessation of blood supply to this area. Chest pain during a heart attack is more severe, lasts longer and does not go away after rest or taking nitroglycerin under the tongue. During a heart attack, nausea, severe weakness and sweating are also observed.

It should be remembered that in cases where angina episodes become longer, occur more frequently and occur even during rest, the risk of developing a heart attack is quite high.

Can any chest pain be considered angina?

Certainly not. Not all chest pain and not even all pain in the heart area are signs of angina. For example, if the pain lasts less than 30 to 40 seconds and goes away after taking a deep breath, changing position, or drinking a sip of water, you shouldn't worry about angina.

How is angina diagnosed?

Typically, your doctor will diagnose angina by finding out the nature of your symptoms and the circumstances in which they occur. To exclude concomitant diseases, a series of medical tests are performed, including an electrocardiogram (ECG) at rest and after exercise, a stress test and blood pressure measurement.

What is the treatment for angina?

For successful treatment of angina, attention should first be paid to reducing the risk factors that cause cardiovascular disorders. Risk factors include: high blood pressure, high blood cholesterol, excess weight, smoking. The doctor will prescribe you the necessary medications to normalize your blood pressure, advise you on the right diet and the necessary physical exercises.

For decades, nitrates have been the first choice in the treatment and prevention of angina. Currently, trinitrates, dinitrates and mononitrates are used. The mechanism of their action is dilatation (expansion) of the blood vessels of the heart, an increase in the flow of oxygen to the heart muscle and a decrease in the tension of the myocardial wall. When prescribing nitrate, the doctor must consult you about the side effects caused by these drugs. Undesirable effects of nitrates include headache, facial flushing, drop in blood pressure, dizziness and the development of tolerance (the body's insensitivity to a certain dose of the drug).

In addition to nitrates, beta blockers are used in the treatment of angina, which reduce the frequency and strength of heart contractions, and calcium channel blockers, which prevent vasospasm.

Can people with angina pectoris exercise?

Yes, definitely. However, when developing a schedule and intensity of physical activity, you should consult your doctor. Exercise will help you raise your pain threshold, reduce stress, improve oxygen supply to your heart and control your weight. Doctors advise gradually increasing physical activity, starting with small ones. You can start with a 5 minute daily walk and after a couple of months increase the time to 1/2 or 1 hour. Sudden overloads must be avoided.

What is the difference between stable and unstable angina?

It is necessary to distinguish the difference between stable angina (effort angina) and unstable angina (rest angina).

Angina attacks usually recur with predictable regularity. The patient can predict his condition by noting that attacks usually appear after stress or physical exertion. All this characterizes stable angina or exertional angina - the most common type of disease.

However, in some cases, angina can have an unpredictable course. This manifests itself in unexpectedly severe or frequently recurring attacks of chest pain that occur with minimal physical activity or even at rest. This form of angina is called unstable or resting angina and requires particularly careful treatment.

The term unstable angina is also used in the event of all the symptoms of a heart attack, which, however, are not confirmed by clinical tests and in which there is no damage to the heart muscle.

Prevention of angina

The first line of defense against the development of angina pectoris includes the following measures: physical activity, eating healthy foods, moderation in diet, reducing the amount of alcohol consumed, and quitting smoking.

Angina pectoris is characterized by a pronounced clinical picture and a long development process; in the old days it was better known as “angina pectoris.” The disease is characterized by specific symptoms that allow a faster and more accurate diagnosis of the pathology. When patients follow medical recommendations, stable angina is characterized by a favorable course.

Angina pectoris (AS) has been known to mankind for many centuries and was first described by the English physician William Heberden. The disease is characterized by the appearance of chest pain, which in typical cases stops 10-15 minutes after its onset. An important feature of angina is the relief of an attack by taking nitroglycerin. Sometimes painful sensations are not relieved by nitrates.

The likelihood of developing angina depends largely on age. Wikipedia notes that “at 45-54 years old, the incidence of angina is about 2-5%, while at 65-74 years old it is 10-20%.”

The increase in predisposing factors leads to the annual appearance in European countries of an average of 30,000 new patients with angina pectoris. To determine the disease, various research methods are used, but most often it is electrocardiography and Holter monitoring.

Video: What is angina?

Classification

There are various classifications of angina that were developed more than 30 years ago. Some are compiled with the aim of more accurately distributing the disease along the course, others are developed taking into account clinical characteristics.

1979 classification presented by WHO:

Angina at rest, also known as spontaneous and variant. It distinguishes a rare type of Prinzmetal's angina.
Angina pectoris. It can be primary, progressive and stable. The latter differs according to functional classes.

Angina pectoris is a separate item in the clinical classification of 1984, which considers all forms of coronary artery disease. According to this classification, angina pectoris can be:

Stable, which, depending on the course, may have I-IV FC.
Unstable, further divided into new-onset, progressive, pre-infarction, Prinzmetal.

by developmental acuity (class I, II, III);
according to the conditions of occurrence (class A, B, C).
by the availability of therapeutic measures provided during its occurrence (1, 2, 3).

Causes

The occurrence of angina is associated with disruption of the blood circulation process in the coronary arteries of the heart, which leads to a lack of oxygen and nutrients necessary for the myocardium. Acute coronary insufficiency occurs for various reasons, but most often due to atherosclerosis of the coronary arteries. The more the atherosclerotic plaque blocks the lumen of the vessel, the more the blood flow is disrupted and the more pronounced the myocardial ischemia.

In the development of pathology, the size of the vessel affected by atherosclerosis is of considerable importance. If a large artery of the heart is involved in the pathological process, then a larger area of the myocardium is exposed to a lack of oxygen. Involvement of a small part of the capillary network in the pathological process leads to less severe disease.

During ischemia in the myocardium, the redox mechanisms of action are disrupted, which is why many different metabolites accumulate in the muscle (in particular, acetic acid, as well as pyruvic, lactic, and phosphoric acid).

Video: Coronary heart disease and angina: mechanism, localization of pain and cause of myocardial infarction

Risk factors

Many bad habits, as well as an unhealthy lifestyle, can contribute to the development of angina. Also, when certain risk factors are identified in patients with KS, the progression of the disease increases noticeably. Therefore, cardiologists are engaged in identifying predisposing factors, after which the patient is explained the principles of their elimination.

Today, there are several groups of risk factors that are involved in the development of angina:

Unmodified factors (irresistible) - these include gender, age and heredity. Looking at such factors, it turns out that men aged 50-55 years are more likely to suffer from angina pectoris, while after menopause in women the risk of developing KS increases.
Modified factors (overcome) - constitute a large group in which some factors influence the formation of others. For example, consuming fatty foods increases body weight, which increases the risk of angina. This group of risk factors includes:

hyperlipidemia;
obesity;
physical inactivity;
smoking;
arterial hypertension;
psycho-emotional experiences;
increased blood viscosity.

Correcting harmful factors and establishing a lifestyle as close to healthy as possible makes it possible to strengthen the cardiovascular system and, in some cases, avoid the development of angina.

Kinds

In clinical practice, particular importance is attached to such clinical forms of the disease as stable and unstable angina. There are differences in the development of these two pathologies. Also, stable SC is divided into functional classes.

Stable angina

The disease mainly manifests itself during physical activity. According to the severity of painful sensations, four functional classes of angina are distinguished:

1 FC - pain or shortness of breath occurs against the background of significant physical activity in the form of long running or lifting weights.
2 FC - everyday physical activity is somewhat reduced, which is why when running short distances or climbing several flights of stairs, painful sensations appear in the chest.
3 FC - tolerance to physical activity is reduced. Moving either one flight or a short distance begins to cause breathing difficulties and chest discomfort.

4 FC - even minor physical stress causes an attack of KS, so pain and shortness of breath may appear after a few steps.

The presented functional classes serve as a unique indicator of the degree of narrowing of the coronary arteries. The worse the blood flow in the vessels, the more severe the patient’s condition and the higher the FC. Bicycle ergometry is used in hospitals to determine functional class.

Unstable angina

The development of an attack of KS is not associated with the patient’s physical activity. Pain and shortness of breath can occur at any time, which is why the disease is defined as unstable. The manifestation of the disease is characterized by severe painful sensations, which are often accompanied by dizziness. Due to the high risk of transition of unstable angina to myocardial infarction, patients must be examined even with a single attack.

Diagnostics

The capabilities of modern medicine make it possible in most cases to determine the type of disease and establish the clinical form. For this purpose, various research methods are used, starting with laboratory tests and ending with instrumental methods. But first of all, the patient is interviewed, examined and auscultated to listen to the heart, which makes it possible to present a more or less complete clinical picture.

Clinic

A characteristic symptom of angina is chest pain. It was through its frequent detection in patients with angina pectoris that the disease was previously defined as “angina pectoris.”

Pain behind the sternum often feels like pressing, burning, squeezing. Its localization is in the region of the heart, and its area of distribution is approximately the size of the patient’s fist or palm. Pain can be transmitted to other parts of the body, namely the shoulder blade, left arm, lower jaw.

The pain may radiate to the epigastric region, contributing to the appearance of heartburn, nausea or discomfort in the form of colic. Pain is not so often localized in the head, which makes it difficult to immediately make an accurate diagnosis.

Angina pectoris is manifested by attacks that are relatively short-lived, lasting approximately 10-15 minutes. There are predisposing factors that contribute to the development of angina pectoris even with apparent well-being. This primarily applies to:

physical activity;
eating a large amount of food;
emotional overstrain;
staying in a cold room;
increased blood pressure.

With such factors affecting the myocardium, more oxygen is required, which is why the heart muscle begins to experience oxygen starvation. If the spasm or blockage of the vessel is small, then after the influence of the predisposing factor ceases, blood circulation is restored and the pain goes away. That is why the appearance of angina is often associated with physical activity or other external circumstances.

Instrumental examination methods

To clarify the diagnosis, laboratory and instrumental research methods are used. Also, with their help, the cause of the disease is established, as a result of which it will be possible to prescribe effective treatment.

Lab tests consist of conducting a clinical blood test and determining biochemical indicators of damage to the heart muscle. If necessary, a glucose tolerance test is performed or the concentration of thyroid hormones is determined.

Patients with cardiovascular pathology must do electrocardiography. With its help, concomitant pathologies in the form of arrhythmia and post-infarction state can be determined. Also, a number of pathologies such as left ventricular hypertrophy are clearly visible on the ECG. Depending on the indications and condition of the patient, an ECG is performed in a calm state and after physical activity. In the latter case, bicycle ergometry or treadmill test is used. For this purpose, special equipment is used, offered in hospitals and medical centers.

ECG monitoring using the Holter method Compared to stress tests, it is less informative, but at the same time it makes it possible to diagnose myocardial infarction in almost 15% of patients with angina pectoris, which is practically not detected on a regular ECG. This diagnostic method is often used to determine vasospastic angina, attacks of which are difficult to detect.

Echocardiography at rest is done for the purpose of differential diagnosis, that is, to confirm or, conversely, exclude the presence of various heart diseases. If necessary, the contractile function of the ventricles is assessed and the size of the heart cavities is determined. In some cases, standard echocardiography is supplemented with stress echocardiography. For this purpose, pharmacological or physical activity is used.

In exceptional cases, that is, only when indicated, it is carried out coronary angiography. This is an invasive technique, often prescribed to patients who have had a history of cardiac arrest or other research methods have not been able to determine the cause of the disease.

Treatment

First aid for angina

When KS occurs for the first time, you must immediately call an ambulance. If the patient has previously had seizures, then the services of a medical team should be used if:

a prolonged attack that could not be stopped with nitroglycerin or medications previously prescribed by a doctor;
the clinic worsens due to the appearance of severe weakness, heavy breathing, vomiting, etc.;
The chest pain reappeared after it had temporarily subsided.

While waiting for an ambulance, you should perform a number of actions:

The patient should be calmed and seated comfortably, with his legs down.
Half or a whole aspirin tablet is placed under the tongue.
If nitroglycerin is not available, you can take nitrolingual or use isoket spray.
Nitroglycerin can be taken again at intervals of three minutes, and aerosol medications - at one minute.
You can take medications no more than three times.

After stopping an attack of angina, the doctor prescribes basic treatment, the implementation of which pursues the following goals:

Remove unwanted manifestations or at least reduce their severity.
Prevent the development of such a serious complication as myocardial infarction.
Improve the patient's quality of life.

To achieve the presented goals, various treatment tactics are used: medication, surgery, auxiliary.

Drug therapy

Based on the use of drugs from various pharmacological groups. With their help, the condition of the circulatory system of the heart improves, biochemical blood parameters are corrected, and the severity of clinical signs decreases.

The main groups of drugs from which medications are selected for patients with angina pectoris:

Antiplatelet agents are prescribed almost for life, since they prevent blood clots by thinning the blood. In the absence of gastrointestinal diseases, patients are recommended to take acetylsalicylic acid, and if there are contraindications to it, clopidogrel, which is just as effective, but more expensive and with fewer contraindications.
Beta-blockers help cope with anginal attacks, since their mechanism of action is aimed at reducing oxygen consumption by the heart muscle. The most commonly used are bisoprolol and metoprolol. But at the same time they cause a number of side effects in the form of bradycardia, cold hands and feet, general weakness, etc.
Calcium channel blockers are quite effective in eliminating antianginal attacks caused by angina pectoris. Can be combined with beta blockers. From this group, verapamil and nifedipine are most often used.
Nitrates - in the treatment of angina pectoris, drugs from this group are used that have a short or prolonged effect. It is very important not to overdose on medications so as not to cause orthostatic hypotension, so they are used only for medical purposes.

Video: Angina symptoms and types. Treatment and nutrition for angina pectoris

Surgery

There are three types of surgical intervention that are most often used today to eliminate malignant angina.

Coronary artery bypass surgery is performed to restore normal blood flow in the heart arteries.
Balloon angioplasty - a technique that allows you to expand stenotic vessels through the use of a special balloon inserted through a catheter.
Stenting of the coronary arteries - during the process, stents are installed in the narrowed arteries, which do not allow them to collapse again. It is most often performed immediately after balloon angioplasty.

Before each type of treatment, coronary angiography is required, which allows you to accurately determine the location of narrowing in the coronary artery system. The surgical method of treatment is selected on an individual basis, taking into account the available indications.

Complications

Long-term angina is dangerous because cardiomyocytes gradually begin to die in the area of the heart muscle affected by ischemia. The result is necrosis, also known as myocardial infarction. Therefore, it is extremely important to start treatment for KS on time so that the circulatory system of the heart is restored as quickly as possible.

If angina attacks occur frequently, the patient's quality of life deteriorates significantly. It becomes difficult to perform usual physical work. It may be difficult to stay in transport for a long time. In severe cases, attacks of KS provoke the development of arrhythmia.

Prognosis and prevention

The prognostic conclusion for angina pectoris largely depends on the severity and duration of attacks. With their rare occurrence and relatively normal quality of life of the patient, the prognosis is favorable. If chest pain appears frequently or occurs like unstable angina, then they speak of a malignant course of the disease.

To improve the prognosis, as well as to prevent angina pectoris, you should aim not only to take medications, but also to follow other medical recommendations. In particular, it is required:

modify lifestyle;
stop smoking;
observe dietary nutrition;
control body weight;
carry out acceptable physical activity.
treat concomitant diseases;

Video: How to protect the heart and blood vessels? Prevention of cardiovascular diseases