Angina pectoris classification, the main causes, characteristic symptoms, methods

The heart muscle pumps blood throughout the body. Thanks to her, they receive nutrition and large internal organs, and bones, and fatty tissue, and even hair follicles located on the entire surface of the body. Every cell needs timely delivery of nutrients and oxygen, and cleansing of harmful metabolic products. Let’s not forget, all this is necessary for the heart itself.

For its own needs, the heart receives blood from the aorta. This is the largest vessel in the body into which the left ventricle releases oxygen-rich arterial blood. Two small vessels originate from the base of the aorta, which branch into a network of other arteries that feed the myocardium.

In a healthy person, the heart is fully supplied with blood, moreover, when the load on the myocardium increases, its blood supply also increases. At any moment, the body receives as much oxygen necessary for the “extraction” of energy as it needs.

Things are completely different with angina pectoris. With this disease, atherosclerosis develops in the walls of the coronary arteries – fatty plaques form. They are formed due to the fact that under the inner shell of arteries penetrate molecules of cholesterol and other lipids with high molecular weight.

Fat deposits increase in size, the lumen of the arteries narrows, and this violates the nutrition of the myocardium. The result is ischemia, oxygen starvation of the areas of the heart to which the vessels narrowed by plaques are directed. First of all, the signs of ischemia appear with exertion, exertion – this is why the disease in question is called angina pectoris.

When the heart feels an increased need for oxygen, and the coronary vessels cannot provide its sufficient supply, under-oxidized metabolic products accumulate in the myocardium, which have an irritating effect on the nerve endings of the heart.

Each person is familiar with a peculiar burning sensation and constriction in the working muscles, which occurs with a suddenly strong and prolonged load on them. About the same thing happens with the heart during an attack of angina pectoris.

Causes of Angina Pectoris

By virtue of its continuous work, the heart is one of the most intensively supplied with blood organs. Blood feeds the heart muscle through the coronary (coronary) arteries branching directly from the aorta, the main and largest vessel in the body.

The reason why the blood enters the myocardium in insufficient volume during exertion, leading to an attack of angina pectoris, is most often atherosclerosis – narrowing of the coronary arteries (in more than 90% of cases), when the atherosclerotic plaque and calcium deposits formed in its walls overlap .

When the diameter of the lumen of the artery turns out to be 50% or more overlapped, this is accompanied by symptoms of coronary disease even with light physical exertion and emotional arousal.

The origin of the disease is much less often due to other reasons, such as:

  • malformations of the aorta;
  • severe form of anemia;
  • hypertrophic cardiomyopathy, in which the volume of the heart and its mass increase sharply, so that the vessels are not able to provide the myocardium with food in the proper amount; coronary spasm.

Pathological factors, along with physical and psychoemotional stress:

  1. Eating in excess.
  2. A sharp temperature difference (for example, a contrast shower).
  3. Change in weather conditions (pressure drop in the atmosphere), etc.

If the work of the myocardium is enhanced, and its blood supply does not keep up with the increased pace, a number of pathological changes develop in the heart. Other risk factors:

  • elderly age;
  • genetic predisposition;
  • smoking and alcohol abuse;
  • arterial hypertension;
  • high cholesterol;
  • sedentary lifestyle;
  • diabetes;
  • obesity;
  • in women, a deficiency of estrogen hormones in the absence of replacement therapy during menopause;
  • hormonal contraceptive use;
  • thrombosis;
  • atrial fibrillation;
  • damage to coronary arteries during radiation therapy, etc.

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Functional classification of angina pectoris of the Canadian Cardiovascular Society. The classification was proposed in 1976 and then was supplemented with information on exercise tolerance according to bicycle ergometric testing data obtained at the All-Russian Scientific Center for Medical Sciences.

Classification is of great importance, as it allows you to assess the severity of angina pectoris. According to the Canadian classification, 4 classes of stable angina pectoris are distinguished (as amended by the VKSC RAMS).

Everyday, habitual physical activity, such as walking or climbing stairs, does not cause an angina attack. An attack of angina pectoris develops as a result of intense, or fast, or prolonged exercise.

Tolerance to a standardized bicycle ergometric test is high: the amount of mastered load (W) is not less than 750 kgm / min (125 W); double product (DP), reflecting the need for oxygen (DP = HR / Blood pressure syst. / 100), not less than 278.

A slight restriction on daily activities, normal physical activity. Attacks of angina pectoris occur when walking on level ground at an average pace (80-100 steps / min) for a distance of more than 500 m, when climbing stairs more than on the 1st floor.

The likelihood of an attack of angina pectoris increases with emotional arousal, physical exertion, after eating, in cold or windy weather, or for several hours after waking up.

W = 450-660 kgm / min (75-100 W). DP = 216-277.

A significant limitation of normal physical activity. Attacks of angina pectoris occur when walking at a normal pace in a flat place at a distance of 100-500 m, when climbing one floor.

W = 300 kgm / min (50 W). DP = 151-215.

Minimum domestic and emotional stress causes angina attacks, patients are not able to perform any physical activity without a sore throat. Angina pectoris occurs when walking on level ground at a distance of less than 100 m.

Characterized by the appearance of angina attacks at rest, as well as during sleep, when moving to a horizontal position.

Attacks of angina pectoris alone, as well as attacks of tension, are caused by an increase in myocardial oxygen demand (increased blood pressure, tachycardia, increased venous blood flow to the heart when moving to a horizontal position), rare attacks of resting angina pectoris are not an obligatory criterion of class IV.

W = 150 kgm / min (25 W). DP = 150.

It should be emphasized that in patients with 4 functional class of angina pectoris, anginal pain at rest is often observed. The use of modern methods of studying cardiohemodynamics revealed the relativity of this “rest”. It was established that before a pain attack occurring at rest, there is an increase in blood pressure, an increase in heart rate, which, of course, contributes to an increase in myocardial oxygen demand.

Sometimes this is due to emotional factors that create an increased load on the myocardium and require an increase in coronary blood flow, despite the state of physical rest. Strengthening the heart (increased blood pressure, increased heart rate) can be recorded even during sleep and cause an attack of angina pectoris in a dream.

In some cases, the strengthening of the heart during sleep is explained by dreams (performing in a dream a lot of physical activity, for example, you have to run away from pursuers, etc.)

Most often, an angina attack occurs in the REM sleep phase (phase B). It is during this phase of sleep that rapid movements of the eyeballs are observed, heart rate, breathing become more frequent, blood pressure increases – all these factors increase the myocardial oxygen demand and lead to the development of ischemia.

Thus, we can assume that angina pectoris that occurs at rest due to the indicated pathogenetic features is actually an angina pectoris, however, such patients have a very low threshold for angina pectoris.

Of course, this variant of angina pectoris occurs in patients with severe stenosing atherosclerotic lesions of the coronary arteries, while the reserves of coronary blood flow are almost exhausted, and there is a pronounced mismatch between the oxygen demand of the myocardium and the delivery of blood and oxygen to the myocardium.

The classification of angina pectoris is quite detailed. This helps to correctly diagnose and determine the exact therapeutic regimen.

And this is important to achieve a stable remission. So, first of all, the disease is divided into 3 forms:

  1. First appeared: when no more than 30 days have passed from the moment of the first attack of pain. This is a very dangerous condition, because it often becomes the first “bell” before myocardial infarction, when the death of the myocardial site occurs. This form of the disease can independently pass (regress) or go into a more difficult process – stable angina pectoris.
  2. Stable It is characterized by an >At the very beginning of the attack, patients feel a slight discomfort in the chest area, which develops into severe pain.
    Pain spreads to the area of ​​the heart, scapula, left arm. Often she gives to the neck or jaw. Pain can have a different nature:

The total duration of the acute stage of an attack rarely exceeds 5 minutes. The main symptom disappears as soon as a person stops doing exercise or calms down.

Many patients take Nitroglycerin to get rid of an attack. Additional symptoms accompany pain:

  • weakness (occurs abruptly);
  • shortness of breath, difficulty breathing;
  • heart rate acceleration;
  • arrhythmia;
  • increase or decrease in blood pressure.

The rest of the time, a person practically does not notice the presence of angina pectoris. Occasionally, other symptoms may torment him: excessive pallor, frequent urination, causeless thirst.

Sometimes the attack is accompanied by symptoms from the gastrointestinal tract. It can be nausea, upset stools, or vomiting. Many people themselves are diagnosed with angina pectoris, although they actually suffer from a different disease. Similar pain sensations arise with pathologies of the digestive system, namely with damage to the esophagus or stomach ulcer.

The respiratory system also often makes itself felt with the help of pain behind the sternum. Most often, they appear in the acute course of pneumonia or pleurisy. Discomfort on the left can be caused by other diseases, for example, osteochondrosis or shingles.

Remember that in most cases with exertional angina, shortness of breath occurs, and stress exhausts and tires a person. If these symptoms are absent, you should go through a diagnosis and look for the cause of the pain in other body systems.

Diagnostics

The use of special instrumental research methods. For the diagnosis of myocardial ischemia, including exertional angina, the following methods are used:

  • ECG recording during an attack;
  • ECG recording at rest;
  • load ECG tests (VEM, treadmill test, NPES);
  • stress echocardiography;
  • Holter ECG monitoring;
  • myocardial scintigraphy;
  • isotopic ventriculography;
  • positron emission tomography;
  • Magnetic resonance imaging;
  • coronary arteriography.

When choosing a research methodology, the clinical picture of coronary heart disease, indications and contraindications to the technique, its cost, as well as information content, sensitivity and specificity of the technique are taken into account. The sensitivity of the method for detecting or verifying coronary heart disease is the percentage of truly positive results in the presence of coronary heart disease; specificity – the percentage of truly negative results in the absence of IHD.

Registration of an ECG during an attack of angina pectoris is of great diagnostic importance and is often altered. However, it is not always possible to record an ECG during angina pectoris, because the attack of pain does not last long, the patient stops the load, stops, takes nitroglycerin.

ECG changes during an angina attack are caused by ischemia and myocardial damage. An attack of angina pectoris is accompanied by a short-term, transient decrease in blood supply to individual sections of the myocardium and, consequently, their temporary hypoxia with metabolic impairment.

As a result of these disturbances, the bioelectric processes in the myocardium change, and above all, the myocardial repolarization, which leads to a change in the polarity, amplitude and shape of the T wave. More pronounced and prolonged (but reversible) ischemic changes lead to myocardial dystrophy and are referred to as ischemic injuries, which affects ECG in the form of an ST segment shift above or below the isoline.

The most characteristic changes are observed in those ECG leads, the positive electrodes of which are located directly above the ischemic zone.

Changes in the T wave depend on the location of the site of ischemia. As you know, the earliest and most pronounced ischemic changes develop in the subendocardial zone. Subendocardial ischemia is manifested by a high pointed T wave, the base of which can be somewhat enlarged (“high coronary T wave”).

With localization of ischemia in the subepicardial zone, as well as with transmural and intramural ischemia, a negative symmetrical T wave (“negative coronary T wave”) appears. In the leads reflecting the area of ​​the heart opposite to the area of ​​ischemia, reciprocal changes are observed.

During an attack of angina pectoris, some patients may have smoothed or biphasic teeth with an initial positive or negative phase (+/– or – / +), they are usually caused by changes at the border of the ischemic and intact zones. In typical cases, during an attack of angina pectoris, the interval is shifted downward from the isoline and the negative T wave in the leads corresponding to the ischemic focus.

An ECG at rest in patients with stable angina pectoris remains unchanged in 50% of patients. In the interictal period, the ECG may remain normal, however, characteristic changes in the ST segment and T wave are quite often observed.

Changes in the ST segment consist in its displacement downward from the isoline by 1 mm or more, which is caused by subendocardial myocardial damage due to a decrease in blood circulation. Exercise stress ECG tests are used to detect latent coronary insufficiency, assess coronary blood flow reserves, and for differential diagnosis of coronary heart disease.

Stress tests provoke myocardial ischemia by increasing myocardial oxygen demand (bicycle ergometry, treadmill test, transesophageal electrocardiostimulation, dobutamine test) or due to a decrease in oxygen delivery to the myocardium (tests with chimes, adenosine).

Criteria for a positive bicycle ergometry test, indicating the presence of IHD:

  • development during a VEM of a typical angina pectoris attack;
  • decrease in the ST interval according to the “ischemic” type (mainly horizontal or oblique depression of the ST segment by 1 mm or more, primarily in the leads V4, V5, V6, ie in the anterior lateral precardial leads; slow oblique shift of the ST interval with the location ischemic point below the contour by 1 mm or more);
  • rise of the ST interval above the contour by more than 1 mm;
  • the occurrence of various pronounced ventricular arrhythmias with moderate load (less than 70% of maximum heart rate);
  • the appearance of an asthma attack;
  • drop in blood pressure by 25-30% of the initial level.

The most reliable sign of transient myocardial ischemia is a horizontal or oblique depression of the ST segment by 1 mm or more. The probability of a diagnosis of coronary heart disease reaches 90% if during exercise the depression of the ST interval of the ischemic type reaches 2 mm or more, especially if accompanied by a typical attack of angina pectoris.

Stress echocardiography is a method of recording violations of local myocardial contractility of the left ventricle using two-dimensional echocardiography under load. The method is widespread. This is due to the fact that quite often VEM, treadmill test, NPVs are uninformative in the diagnosis of coronary heart disease.

In this situation, stress echocardiography can be a method to verify coronary artery disease. The possibilities of stress echocardiography in the diagnosis of coronary heart disease are currently increasing, which is explained by an improvement in the resolution of two-dimensional echocardiography and the introduction of computer-based image analysis methods.

Stress echocardiography can be very informative with an initially altered electrocardiogram (signs of left ventricular myocardial hypertrophy, disturbance of intraventricular conduction, electrolyte disturbances, the effect of certain drugs – cardiac glycosides, antiarrhythmic drugs, etc.). In these cases, stress echocardiography reveals local impairment of contractility due to myocardial ischemia.

Depending on the applied load, the following types of stress tests of stress echocardiography are distinguished:

  • dynamic physical activity (treadmill test, VEM in a sitting position, VEM in a horizontal position);
  • electrical stimulation of the heart (NPES);
  • pharmacological tests (dobutamine, dipyridamole, arbugamine, adenosine);
  • combined samples (dipyridamole + dobutamine, dipyridamole + NPES).

Criteria for a positive test for stress echocardiography with physical activity (i.e. indicating the presence of coronary heart disease). Violation of local myocardial contractility at a height of submaximal load, sometimes with a load of lower intensity (depending on the functional class of angina pectoris).

Differential diagnostics

As mentioned above, in the diagnostic criteria for angina pectoris, one of the most important aspects of the diagnosis of this disease is a thorough assessment of pain in the heart. However, there are a large number of causes and diseases that can cause pain in the region of the heart and chest and which need to be differentiated from angina pectoris and other forms of coronary artery disease.

The causes of pain in the heart and chest can be divided into the following groups.

  1. Diseases of the cardiovascular system.
    • Coronary heart disease (includes forms that cause pain in the heart; various forms of angina pectoris, myocardial infarction).
    • Inflammatory diseases (myocarditis, pericarditis, endocarditis, aortitis).
    • Heart defects, mitral valve prolapse, abnormalities of the coronary arteries.
    • Idiopathic cardiomyopathies.
    • Arterial hypertension.
    • Aortic aneurysm.
    • Pulmonary embolism.
    • Tumors of the heart.
    • Cardiopsychoneurosis.
    • Alcoholic cardiopathy.
  2. Systemic vasculitis and systemic connective tissue diseases.
  3. Diseases of the bronchopulmonary system, pleura and mediastinal organs.
  4. Diseases of the abdominal cavity and diaphragm.
  5. Menopausal cardiopathy.
  6. Diseases of the spine, anterior chest wall, shoulder girdle.

Differential diagnosis of stable angina and other diseases of the cardiovascular system. Various diseases of the cardiovascular system are accompanied by pain in the heart. First of all, stable angina pectoris should be distinguished from other forms of angina pectoris and myocardial infarction.

This can be done using the diagnostic criteria for various forms of angina pectoris and myocardial infarction, described further in the relevant chapters.

Myocardial infarction differs from angina pectoris in significantly greater intensity and duration of pain in the region of the heart, inefficiency of taking nitroglycerin, characteristic electrocardiographic signs (the presence of a Q wave – a sign of necrosis, a dome-shaped elevation of the ST interval with a subsequent decrease and the formation of a negative coronary T wave), the presence of resorption-necrotic syndrome (including increased blood levels of cardiospecific enzymes – KFK-MV, LDH 1, troponin).

Inflammatory heart diseases are almost always accompanied by cardialgia, which is sometimes difficult to distinguish from angina pectoris. Diagnostic criteria for myocarditis, pericarditis, infectious endocarditis are described in the relevant chapters.

It should be emphasized here that myocarditis is characterized by a connection between the appearance of cardialgia and other unpleasant sensations:

  • in the area of ​​the heart with a viral infection;
  • persistent (often aching, less often – stitching) pain in the heart (usually in the apex);
  • nonspecific ECG changes (mainly a decrease in the amplitude of the T wave, sometimes a negative but asymmetric T wave);
  • lengthening of the PQ interval, various degrees of atrioventricular block and cardiac arrhythmias; positive effect of anti-inflammatory therapy.

The main clinical symptoms of fibrinous pericarditis are persistent stitching or constricting pains in the heart area (mainly to the left of the sternum in the III – IV intercostal space), aggravated by breathing, tilting the head back, pressing in place of pain, pericardial friction noise (heard in the area of ​​absolute dullness heart), characteristic ECG changes in the form of a concordant shift of the ST interval up.

Exudative pericarditis is manifested mainly by shortness of breath, widening of the borders of the heart in all directions, detection of fluid in the pericardial cavity during echocardiography, low voltage ECG.

In the diagnosis of endocarditis, an important role belongs to the assessment of auscultatory symptoms (changes in the timbre of systolic murmur, the appearance of diastolic murmur), echocardiographic findings (signs of valve damage, vegetation), the appearance of thromboembolic syndrome, and fever. Aortitis has a diverse etiology, but most often it is a syphilitic aortitis.

In this case, there is a lesion of the coronary arteries, sometimes with a significant narrowing of their lumen. In patients with syphilitic aortitis, there may be a fairly pronounced angina pectoris. The nature of the pain may not differ significantly from angina pectoris of atherosclerotic origin.

The characteristic features of syphilitic aortitis that help to recognize it are: the presence of x-ray and echocardiographic symptoms of thoracic aortic aneurysm, auscultatory signs of aortic valve insufficiency, positive serological reactions to syphilis.

Heart defects can be accompanied by pain in the heart, however, these pains almost never have typical features. Most often, pains in the region of the heart are stitching, do not have a clear connection with the load (when the patient is stressed, mainly shortness of breath worries), they can be constant. Heart defects have a corresponding auscultatory picture and are verified using phonocardiography and echocardiography.

Cardialgia can also occur with idiopathic cardiomyopathies. However, it should be emphasized that pain in the region of the heart is most characteristic of hypertrophic cardiomyopathy (sometimes it is the dominant, and sometimes the only complaint) and is rarely observed with dilated and obstructive cardiomyopathy (with these types of cardiomyopathy, shortness of breath and other manifestations of heart failure dominate).

Pain with idiopathic cardiomyopathies usually does not meet the criteria of classical angina pectoris, although in some cases cardialgia is associated with physical activity, but without a clear stopping effect of nitroglycerin.

The diagnosis of idiopathic cardiomyopathy should take into account mainly the young age of patients, cardiomegaly, progressive heart failure, the presence of a variety of arrhythmias, the absence of signs of atherosclerosis and atherogenic dyslipidemia, typical echocardiographic signs.

Arterial hypertension is often accompanied by pain in the heart. It should also be noted that arterial hypertension is a risk factor for coronary heart disease. A characteristic feature of cardialgia in arterial hypertension is a clear connection between the appearance of pain in the region of the heart and an increase in blood pressure – hemodynamic pain, as defined by M.S. Kushakovsky.

This is usually prolonged aching pain or a feeling of heaviness in the heart. In middle-aged and elderly people, pain in the heart region due to coronary heart disease should be excluded or confirmed. Ambulatory ECG monitoring, radioisotope scintigraphy, stress echocardiography, and stress ECG tests (depending on blood pressure, but, of course, not at the height of an acute increase in blood pressure) can be used to diagnose coronary heart disease in people with arterial hypertension.

In addition, with the development of coronary heart disease in a patient with arterial hypertension, pain in the region of the heart becomes typical for angina pectoris. With a stratified aortic aneurysm, intense pain behind the sternum, in the back or in the epigastric region is characteristic, the pain then subsides, then sharply intensifies.

There is a need for differential diagnosis primarily with myocardial infarction, often with angina pectoris. Differential diagnosis of angina pectoris and pulmonary embolism (pulmonary embolism) is usually not very difficult. M. Zlochevsky (1978) identifies three types of pain in pulmonary embolism:

  1. Sore throat (more characteristic of thromboembolism of large branches or the main trunk of the pulmonary artery);
  2. Pulmonary pleural (with the development of pulmonary infarction involving pleura);
  3. Mixed.

Pain with pulmonary embolism is intense, localized behind the sternum, appears suddenly (without regard to physical activity), accompanied by shortness of breath, often hemoptysis.

In the diagnosis of pulmonary embolism, ECG changes are of great importance (sudden deviations of the electrical axis of the heart to the right, the appearance of high pointed P waves in leads II, III, AVF, V1-2, the appearance of syndrome SI, QIII, the shift of the STIII interval upward from the contour), X-ray data lung studies, fever, drop in blood pressure.

Heart tumors are a rare pathology. Cardiac tumors are primary benign (myxoma, rhabdomyoma, fibroma, lipoma, papillary fibroelastoma – come from endocardium, hemangioma, teratoma), primary malignant (angiosarcoma, rhabdomyosarcoma, fibrosarcoma) and secondary malignant (metastasis).

The most characteristic clinical manifestations of heart tumors are congestive heart failure, heart rhythm and conduction disturbances, syncope attacks (especially when changing the position of the body), embolic syndrome, involvement of the pericardium in the pathological process (usually exudative pericarditis), pain in the heart area.

Cardialgia appears, as a rule, when a pericardium is involved in the pathological process. Pain in the area of ​​the heart increases with inspiration, is vague, but usually constant. The noise of pericardial friction is often heard. These clinical features make it relatively easy to conduct differential diagnosis of angina pectoris and cardialgia with a heart tumor.

Echocardiography also plays an important role in differential diagnosis. The need for differential diagnosis of angina pectoris and neurocirculatory dystonia (NDC) is very rare, and we can say that the topic is of little relevance. This is explained by the fact that NDC is a disease of young people (mainly young men, adolescents, young women and men under the age of 30).

Help with an attack

A prolonged attack of angina pectoris can lead to myocardial infarction. In the case of a mild attack of angina pectoris, it resolves on its own within a few minutes. If the attack is strong and difficult, it is necessary to call an ambulance. Prior to this, emergency measures can be taken to help alleviate the patient’s condition before the doctor arrives.

With angina pectoris, first of all, you need to stop physical activity and calm down. Simple emergency measures will help improve the patient’s condition:

    Help the patient take a comfortable position.

The patient needs to be put or planted as he sees fit. A lying position is recommended, but in such a way that the head is slightly raised.

  • Provide fresh air. The patient needs to unbutton his collar, belt, open the window, so as to relieve shortness of breath.
  • Give Nitroglycerin.

    Nitroglycerin is one of the main drugs for heart attacks. It allows you to provide oxygen to the myocardium, reduce blood pressure and relieve even a severe attack of angina pectoris.

    In the event that nitroglycerin had no effect, you need to call a doctor, but do not increase the dosage of the drug.

    Give a sedative.

    During an attack of angina pectoris, a person may begin to panic, there is a fear for his life. To reduce anxiety, you can give a mild sedative or Corvalol. Even if urgent measures helped relieve the attack, you must consult a doctor for advice and examination.

    It is urgent to call an ambulance if the attack lasts for 15 minutes or more, as well as if new symptoms have joined.

    It is also worth remembering what should not be done with an attack of angina pectoris:

    • You can not give the patient nitroglycerin or take it yourself if there is no certainty that the attack is associated with the work of the heart. Nitroglycerin has a strong effect on the body, significantly lowers blood pressure, leads to dizziness, so you can’t take it for no reason.
    • It is also dangerous to take nitroglycerin in large doses. If it does not work, you need to urgently call a doctor, but taking more than 4 tablets of nitroglycerin can be dangerous.
    • With an onset of angina pectoris, you can go out into the fresh air, but in no case should you smoke or take alcohol.

    Treatment

    IHD is a chronic progressive disease. Treatment for stable angina pectoris includes diet, smoking cessation, correction of other risk factors, rational physical activity, medication and surgery.

    In the treatment of angina pectoris, different groups of drugs are used, often in combinations with each other, taking into account concomitant diseases of the heart and other organs. Self-medication in this case can cause complications and side effects. Therefore, therapy should be prescribed by a cardiologist, and the diagnosis should be confirmed by additional diagnostic studies.

    Often, patients are prescribed antianginal drugs without in-depth diagnosis, based only on complaints of pain in the heart. This is wrong, as the pain may be associated with another disease. Taking extra medications is economically unprofitable and may harm the patient’s health.

    The standard treatment for angina pectoris includes two large groups of drugs: improving prognosis and preventing the onset of symptoms.

    Medication

    The main goal of treating angina pectoris is to reduce the severity of symptoms and prevent ischemia, or at least reduce its degree. If an acute attack occurs, nitroglycerin should be taken under the tongue. If a person has a high risk of developing coronary heart disease or is already diagnosed with this disease, the doctor will prescribe him a regular intake of drugs that may belong to different groups.

    They inhibit platelet aggregation. Each drug in this group reduces the risk of complications of ischemia, but the best effect is usually achieved with the appointment of several drugs. If there is a contraindication to any medicine, the patient should take another drug. Beta-blockers reduce the manifestations of angina pectoris.

    In addition, they are better than other drugs to prevent sudden death and heart attack. They have a blocking effect on sympathetic stimulation of the heart, reduce the heart rate, systolic blood pressure, cardiac output and myocardial contractility.

    All this contributes to a lower oxygen demand of the myocardium, thereby a person becomes more resistant to physical exertion. These same drugs increase the threshold for ventricular fibrillation. Most patients tolerate such drugs fairly well.

    They are also available. The dose is selected by a gradual increase. This happens until side effects or bradycardia appear. If the patient cannot take drugs of this group, he is prescribed calcium channel blockers, which have a negative chronotropic effect.

    Long-acting nitrates. They are taken orally, they can also act through the skin. Their use is due if the use of the maximum dose of beta-blockers does not bring the desired result, that is, the manifestations of angina pectoris still persist. If these manifestations can be foreseen, nitrates are prescribed in order to prevent this.

    Ointments with nitroglycerin are often replaced with plasters with nitroglycerin, as this is more convenient and practical. Patches promote slow release of the drug, which contributes to a prolonged effect. After gluing the patch, physical activity is transferred during the day.

    Tolerance to drugs of this group is formed more often when the concentration of the drug is constantly observed in the blood plasma.

    Calcium channel blockers. They are used when nitrates do not help or the patient does not tolerate them.

    Preparations of this group are especially effective for spasm of coronary arteries and hypertension. Drugs differ in their effects. For example, dihydropyridine drugs do not have a chronotropic effect, but differ in their inotropic negative effect.

    Dihydropyridines with a short action can cause reflex tachycardia. They also contribute to an increase in mortality. They can not treat stable angina pectoris. Long-acting dihydropyridines are more commonly used with beta-blockers.

    Nitroglycerine. It is a powerful vasodilator and smooth muscle relaxant.

    The main effect extends to the peripheral vascular bed, venous depot and coronary vessels. Sublingually, this drug is prescribed in order to stop an acute attack or to prevent it before exercise. Relief occurs after approximately two minutes, and complete relief occurs after five minutes.

    The duration of the effect lasts half an hour. Reception of nitroglycerin can be repeated in five minutes if at first the necessary effect is not reached. This can be done three times. The patient should always carry the drug with him so that it can be quickly applied at the right time.

    Tablets should be stored in a container that is tightly closed. It is desirable that it is glass and does not transmit light. This will help preserve its properties. It must be remembered that this medicine loses its effectiveness quite quickly, so it needs to be kept in small quantities and often replaced.

    Timely diagnosis will help to avoid the transition of angina to a more severe form, one of which is progressive angina pectoris. By carefully monitoring your health, you will be able to avoid serious complications, and a healthy lifestyle will prevent the occurrence of angina pectoris.

    Remember, our heart is a very sensitive and functional organ. If the work in it is disrupted, the whole organism suffers, therefore you should not allow yourself to be careless about our life motor.

    Surgery

    When determining the tactics of surgical treatment of stable angina, it is necessary to take into account a number of factors: the number of affected coronary arteries, ejection fraction of the left ventricle, and the presence of concomitant diabetes. So, with one – two-vessel lesion with a normal ejection fraction of the left ventricle, myocardial revascularization with percutaneous transluminal coronary angioplasty and stenting usually begin.

    In the presence of two to three vascular lesions and a decrease in the ejection fraction of the left ventricle of less than 45% or the presence of concomitant diabetes, it is more advisable to perform coronary artery bypass grafting (see also Atherosclerosis of coronary arteries).

      Percutaneous angioplasty (balloon dilatation) is the expansion of a portion of the coronary artery narrowed by an atherosclerotic process with a miniature balloon under high pressure during visual inspection during angiography.

    The success of the procedure is achieved in 95% of cases. Complications are possible during angioplasty: mortality is 0,2% for a single vascular lesion and 0,5% for a multivascular lesion, MI occurs in 1% of cases, the need for coronary artery bypass grafting appears in 1% of cases; late complications include restenosis (in 35–40% of patients within 6 months after dilatation), as well as the appearance of angina pectoris (in 25% of patients within 6–12 months).

  • In parallel with the expansion of the lumen of the coronary artery, stenting has recently been used – implantation at the site of narrowing of stents (the thinnest wire frames that prevent restenosis).
  • Coronary bypass surgery – the creation of an anastomosis between the aorta (or internal thoracic artery) and the coronary artery below (distal to) the site of narrowing to restore effective myocardial blood supply. As a graft, a section of the saphenous vein of the femur, the left and right internal thoracic arteries, the right gastro-omental gland artery, and the lower epigastric artery are used.
  • Indications for coronary bypass surgery (recommendations of the European Society of Cardiology; 1997):

    • Left ventricular ejection fraction less than 30%.
    • Damage to the trunk of the left coronary artery.
    • The only unaffected coronary artery.
    • Left ventricular dysfunction in combination with a three-vascular lesion, especially with damage to the anterior interventricular branch of the left coronary artery in the proximal section.

    During coronary bypass surgery, complications are also possible – MI in 4–5% of cases (up to 10%). Mortality is 1% for a single vascular lesion and 4–5% for a multivascular lesion. Late complications of coronary artery bypass grafting include restenosis.

    When using arterial grafts, shunts remain open in 90% of patients for 10 years. Within 3 years, angina pectoris resumes in 25% of patients.

    Possible consequences and complications of the disease

    According to statistical studies, angina pectoris quite often transforms into more complex forms of coronary heart disease, especially when it comes to the first occurring or unstable form of the disease. In clinical practice, the following complications of the disease are most often diagnosed:

    • myocardial infarction (necrosis of a part of the heart muscle against a background of chronic or acute coronary circulation disorder);
    • sudden cardiac arrest;
    • heart rhythm disturbances;
    • chronic heart failure.

    The aggravating moments that provoke the rapid development of complications in patients with angina pectoris are young age, the presence of endocrine disorders in patients, in particular diabetes mellitus, obesity, high blood pressure, food flaws, progressive coronary atherosclerosis and much more.

    To live without knowing what angina pectoris and its consequences are, a person needs to take care of his body in his young years. Only in this way can he avoid serious complications from the cardiovascular system in old age.

    Prognosis and prevention

    To prevent this disease, it is necessary to observe a number of measures and rules to improve the quality of life:

    1. Monitor weight, follow a hypocholesterol diet:
      • reduce the intake of fatty, salty foods;
      • refuse flour, sweet, spicy, strong tea and coffee;
      • increase consumption of fresh vegetables, fruits and fish.
    2. To refuse from bad habits.
    3. Attend physiotherapy exercises.
    4. To live an active lifestyle.
    5. Do not skip taking medications prescribed by your doctor.

    The prognosis for patients with stable angina pectoris depends on the functional class of the disease. So, with III-IV FC, the risk of developing myocardial infarction is high, but despite this, subject to the recommendations of the doctor and the correct regimen, patients can live from 20 years or more.

    The problem of coronary heart disease has been well studied. Effective methods of therapy and diagnosis were found, and high-quality drugs for treatment were developed. Thanks to this, the disease no longer carries such a threat to life as before.

    However, if you suddenly felt pain behind the sternum, you should not delay with going to the doctor, because there are a number of other diseases with a similar clinical picture. Be healthy!
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    Svetlana Borszavich

    General practitioner, cardiologist, with active work in therapy, gastroenterology, cardiology, rheumatology, immunology with allergology.
    Fluent in general clinical methods for the diagnosis and treatment of heart disease, as well as electrocardiography, echocardiography, monitoring of cholera on an ECG and daily monitoring of blood pressure.
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