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Angina pectoris

Angina pectoris is a form of ischemic heart disease characterized by paroxysmal pain in the heart area after acute myocardial infarction. Distinguish stenocardia of tension arising at physical or emotional loads, and stenocardia of rest, arising out of physical effort, more often at night. In addition to the pain behind the sternum, there are sensations of suffocation, pallor, skin, pulse fluctuations, sensations of interruptions in the work of the heart. May cause the development of heart failure and myocardial infarction.

As a manifestation of coronary artery disease, angina occurs in almost 50% of patients, being the most frequent form of ischemic heart disease. The prevalence of angina is higher among men - 5-20% (compared to 1-15% among women), with age its frequency increases dramatically. Angina due to specific symptoms is also known as "angina pectoris" or coronary heart disease.

The development of angina pectoris is provoked by an acute deficiency of coronary blood flow, at which an imbalance develops between the need for cardiomyotics in the supply of oxygen and its satisfaction. Violation of the perfusion of the heart muscle leads to its ischemia. As a result of ischemia, oxidative processes in the myocardium are disrupted: there is an excessive accumulation of under-oxidized metabolites (lactic, coal, pyruvic, phosphoric and other acids), ion equilibrium is impaired, ATP synthesis is weakened. These processes cause diastolic and then systolic dysfunction of the myocardium, electrophysiological disturbances (ST segment and T wave changes on the ECG) and, ultimately, the development of the pain reaction. The sequence of changes occurring in the myocardium is called the "ischemic cascade", which is based on the violation of perfusion and changes in metabolism in the heart muscle, and the developmental stage of angina is the conditional stage.

Oxygen deficiency is particularly acute during emotional or physical stress: for this reason, angina attacks occur more often with increased heart function (during physical activity, stress). Unlike acute myocardial infarction, in which irreversible changes develop in the cardiac muscle, coronary artery disorder is transient in angina pectoris. However, if myocardial hypoxia exceeds the threshold of its survival, angina may develop into a myocardial infarction.

Causes and risk factors for angina pectoris

The leading cause of angina, as well as coronary heart disease, is the atherosclerosis-induced narrowing of the coronary vessels. Angina attacks develop with a narrowing of the lumen of the coronary arteries by 50-70%. The more pronounced atherosclerotic stenosis, the more severe angina occurs. The severity of angina also depends on the extent and location of stenosis, on the number of affected arteries. The pathogenesis of angina pectoris is often mixed, and with atherosclerotic obstruction, there may be processes of thrombus formation and spasm of the coronary arteries.

Sometimes angina develops only as a result of angiospasm without arteriosclerosis. Primary pathology of the gastrointestinal tract (diaphragmatic hernia, cholelithiasis, etc.), as well as infectious and allergic diseases, syphilitic and rheumatoid vascular lesions (aortitis, periarteritis, vasculitis, endarteritis) can develop a reflex cardiac spasm caused by a violation of the higher nervous regulation of the coronary arteries heart - the so-called reflex angina.

The development, progression and manifestation of angina is affected by modifiable (removable) and unmodified (unrecoverable) risk factors.

Unmodified angina risk factors include sex, age and heredity. It has already been noted that men are most at risk of angina pectoris. This trend prevails up to 50-55 years, that is, before the onset of menopausal changes in the female body, when the production of estrogens, female sex hormones, that protect the heart and coronary vessels decreases. After 55 years, angina occurs in persons of both sexes with approximately the condition. Often, angina is observed in direct relatives of patients suffering from coronary artery disease or who underwent myocardial infarction.

At changed risk factors for angina, a person has the ability to remove or exclude them from his life. Often, these factors are closely interrelated, and reducing the negative impact of one elimination of the rest. So, reduction of fats in consumed food leads to cholesterol, body weight and blood pressure. Among the eliminable risk factors for angina pectoris include:


In 96% of patients with angina pectoris, an increase in cholesterol and other lipid fractions with atherogenic action (triglycerides, low density lipoproteins) is detected, which leads to the deposition of cholesterol in arteries feeding the myocardium. The increase in the lipid spectrum, in turn, enhances the processes of thrombosis in the vessels.


Usually occurs in individuals who consume high-calorie foods with excessive amounts of animal fats, cholesterol and carbohydrates. Patients with angina pectoris need to limit cholesterol in food up to 300 mg, table salt - up to 5 g, increase in the intake of dietary fiber - more than 30 g.


Insufficient physical activity predisposes to the development of obesity and the violation of lipid metabolism. The impact of several factors at the same time (hypercholesterolemia, obesity, hypodynamia) plays a decisive role in the occurrence of angina pectoris and its progression.


Smoking cigarettes increases the concentration of carboxyhemoglobin in the blood - a combination of carbon monoxide and hemoglobin, which causes oxygen starvation of cells, primarily cardiomyocytes, arterial spasm, increased blood pressure. In the presence of atherosclerosis, smoking contributes to the early manifestation of angina and increases the risk of developing acute myocardial infarction.

Arterial hypertension

Often accompanies the course of IHD and contributes to the progression of angina pectoris. With arterial hypertension, because of the increase in systolic blood pressure, myocardial stress increases and its need for oxygen is increased.

Anemia and intoxication

These conditions are accompanied by a decrease in the delivery of oxygen to the heart muscle and provoke angina attacks, both in the background of coronary atherosclerosis, and in its absence.


In the presence of diabetes, the risk of IHD and angina increases twofold. Diabetics with a 10-year experience of the disease suffer from severe atherosclerosis and have a worse prognosis in the case of angina and myocardial infarction.

Increase in the relative viscosity of blood

It promotes the processes of thrombus formation in the place of development of atherosclerotic plaque, increases the risk of coronary thrombosis and the development of dangerous complications of coronary artery disease and angina.

Psychoemotional stress

The heart under stress works under conditions of increased stress: angiospasm develops, blood pressure rises, myocardial oxygen supply and nutrients deteriorate. Therefore, stress is a powerful factor provoking angina, myocardial infarction, sudden coronary death.Among the risk factors for angina also include immune reactions, endothelial dysfunction, increased heart rate, premature menopause, and the intake of hormonal contraceptives in women, etc.The combination of 2 or more factors, even moderately expressed, increases the overall risk of developing angina pectoris. The presence of risk factors should be taken into account when determining treatment tactics and secondary prevention of angina pectoris.

Classification of angina pectoris

1. Stenocardia tension - occurs in the form of transient attacks of chest pain caused by emotional or physical stress, increasing the metabolic needs of the myocardium (tachycardia, increased blood pressure). Usually the pains disappear at rest or are stopped by the intake of nitroglycerin. The angina of the stress includes:

The first occurrence of angina pectoris - lasting up to 1 month. from the first manifestation. Can have a different course and prognosis: regress, go to stable or progressive angina.

Stable angina - lasting more than 1 month. According to the ability of the patient to transfer physical loads is divided into functional classes:

I class - good tolerance of usual physical exertion; the development of attacks of angina is caused by excessive loads, performed long and intensely;
II class - normal physical activity is somewhat limited; the occurrence of angina attacks is provoked by walking on level ground more than 500 m, climbing the stairs more than 1 floor. The development of an attack of angina is affected by cold weather, wind, emotional arousal, the first hours after sleep.
III class - usual physical activity is sharply limited; Attacks of angina pectoris are caused by walking at the usual pace over level ground for 100-200 m, climbing the stairs to the 1st floor.
IV class - angina develops with minimal physical activity, walking less than 100 m, among sleep, at rest.
Progressing (unstable) angina pectoris is an increase in the severity, duration and frequency of seizures in response to a patient's usual load.

2. Spontaneous (special, vasospastic) angina pectoris - caused by a sudden spasm of the coronary arteries. Angina pectoris develops only at rest, at night or early in the morning. Spontaneous angina, accompanied by the rise of the ST segment, is called variant, or Prinzmetal angina.

Progressing, as well as some variants of spontaneous and first-time angina pectoris combined into the concept of "unstable angina".

Symptoms of stenocardia

A typical symptom of angina pectoris is the pain behind the breastbone, rarely to the left of the sternum (in the projection of the heart). Pain sensations can be compressive, pressing, burning, sometimes - cutting, pulling, drilling. Pain intensity can be from tolerant to very pronounced, causing patients to moan and scream, to experience fear of near death.

The pain radiates mainly to the left arm and shoulder, the lower jaw, under the left scapula, into the epigastric region; in atypical cases - in the right half of the trunk, legs. Irradiation of pain with angina is caused by 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 often occurs at the time of walking, climbing the stairs, effort, stress, may occur at night. The attack of pain lasts from 1 to 15-20 minutes. Factors facilitating an attack of angina pectoris are the intake of nitroglycerin, standing or sitting.

During an attack the patient experiences shortage of air, tries to stop and stand still, presses his hand to his chest, turns pale; The face takes a painful expression, the upper limbs become cold and numb. In the beginning, the pulse becomes more frequent, then it shrinks, it is possible to develop arrhythmia, more often extrasystole, and an increase in blood pressure.

A prolonged attack of angina may develop into a myocardial infarction. Long-term complications of angina are cardiosclerosis and chronic heart failure.

Diagnosis of angina pectoris
When recognizing stenocardia, patient complaints, character, localization, irradiation, duration of pain, conditions of their occurrence and factors of arrest of an attack are taken into account. Laboratory diagnostics includes a study in the blood of total cholesterol, AST and ALT, high and low density lipoproteins, triglycerides, lactate dehydrogenase, creatine kinase, glucose, coagulogram and blood electrolytes. Particular diagnostic significance is the definition of cardiac troponins I and T - markers, indicative of damage to the myocardium. The detection of these myocardial proteins suggests a microinfarction or a myocardial infarction that occurred and helps prevent the development of postinfarction angina.

ECG, taken at the height of an attack of angina, reveals a decrease in the ST-interval, the presence of a negative T wave in the thoracic leads, conduction and rhythm disturbances. Daily ECG monitoring allows to fix ischemic changes or their absence with each attack of angina pectoris, heart rate, arrhythmia. Increasing heart rate before the attack allows thinking about angina pectoris, normal heart rate - about spontaneous angina. Echocardiography with angina identifies local ischemic changes and violations of myocardial contractility.

Velgoergometry (VEM) is a test showing which maximal load the patient can tolerate without the risk of developing ischemia. The load is set by means of an exercise bike before reaching the submaximal heart rate with the simultaneous recording of the ECG. With a negative sample, submaximal heart rate is reached in 10-12 minutes. in the absence of clinical and ECG-manifestations of ischemia. Positive is a test, accompanied by a stroke of angina at the time of loading, or by an offset of the ST segment by 1 or more millimeters. The detection of angina pectoris is also possible by inducing controlled transient ischemia of the myocardium with the help of functional (transesophageal atrial stimulation) or pharmacological (isoproterenol, test with dipyridamole) load tests.

Myocardial scintigraphy is performed to visualize the perfusion of the cardiac muscle and to identify focal changes in it. The radioactive preparation of thallium is actively absorbed by viable cardiomyocytes, and in the case of angina accompanied by coronary sclerosis, focal zones of myocardial perfusion are detected. Diagnostic coronary angiography is performed to assess the localization, extent and prevalence of arterial heart disease, which allows to determine the choice of the method of treatment (conservative or surgical).

Treatment of angina pectoris

It is aimed at stopping, as well as preventing attacks and complications of angina pectoris. The first-aid preparation for angina attacks is nitroglycerin (in a piece of sugar keep in the mouth until it is completely resorbed). Pain relief usually comes in 1-2 minutes. If the attack does not stop, nitroglycerin can be used again at intervals of 3 minutes. and no more than 3 times (in view of the danger of a sharp drop in blood pressure).

Planned medical therapy for angina includes the use of antianginal (antiischemic) drugs that reduce the need for cardiac muscle in oxygen: long-acting nitrates (pentaerythritol tetranitrate, isosorbide dinitrate, etc.), b-adrenoblockers (anaprilina, oxprenolol, etc.), molsidomine, calcium channel blockers (verapamil, nifedipine), trimetazidine and others;

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

Prognosis and prevention of angina pectoris
Angina pectoris is a chronic invalidating heart pathology. With the progression of angina, the risk of developing a myocardial infarction or death is high. Systematic treatment and secondary prevention contribute to monitoring the course of angina pectoris, improving prognosis and maintaining ability to work while limiting physical and emotional stress.

Effective prophylaxis of angina pectoris requires the elimination of risk factors: reducing excess weight, controlling blood pressure, optimizing diet and lifestyle, etc. As a secondary prevention in the already established diagnosis of angina, it is necessary to avoid disturbances and physical efforts, prophylactically take nitroglycerin before exercise, exercise prevention of atherosclerosis, to conduct concomitant pathologies (diabetes, GI diseases). Accurate adherence to the recommendations for the treatment of angina pectoris, the use of prolonged nitrates and dispensary control of the cardiologist allow reaching a state of long-term remission.