IBS clinic diagnostics treatment. Cardiac ischemia

Coronary heart disease (CHD)- this is a myocardial pathology caused by a relative deficiency of oxygen in the coronary bloodstream. This deficiency can be associated both with an absolute decrease in the efficiency of blood flow (for example, with atherosclerotic narrowing of the coronary arteries), and with a relative increase in the myocardial oxygen demand, for example, with heavy physical activity, extreme anxiety, with an increase in the intensity of tissue metabolism due to thyrotoxicosis, etc. d. However, as a result of all these reasons, hypoxic changes develop in the myocardium, first reversible, then organic (irreversible). IHD includes diseases such as angina pectoris, myocardial infarction and their intermediate forms.

Atherosclerosis ranks first among the causes of mortality and disability in the developed countries of the world. More than 95% of all people over the age of 60 have vascular atherosclerosis. More than a million people suffer from myocardial infarction every year in the United States.

Etiology. One of the main causes of coronary heart disease is atherosclerosis, i.e., excessive deposition of lipids in the inner lining (intima) of the coronary arteries. It has been established that the atherosclerotic process begins already at 20-30 years of age (stage of lipid streaks and spots), and then continues at different rates depending on the so-called risk factors. Risk factors are not the causes of IHD, but its necessary prerequisites.

Pathological data show that 20% of people aged 26-30 years already have atherosclerosis of the coronary arteries.

The most important risk factor is high levels of cholesterol in the blood, which “trigger” the atherosclerotic process. With hypercholesterolemia above 260 mg% (due to abuse of fatty foods or hereditary predisposition), IHD progresses steadily.

It has been established that cholesterol and fatty acids have a direct damaging effect on the vessel wall (atherogenic effect), which “pushes” the atherosclerotic process. Overeating before bed is especially harmful. In some individuals, hypercholesterolemia is hereditary, and in them complicated ischemic heart disease (for example, myocardial infarction) occurs already in young years, which is explained by increased synthesis of cholesterol and atherogenic low-density lipoproteins, and decreased synthesis of protective high-density lipoproteins.

Hypercholesterolemia is maintained by insufficient physical activity (hypodynamia), so typical for modern urban residents, as well as chronic nervous tension and fatigue. It has been established that in physically inactive people the incidence of myocardial infarction increases by 3 times.

The next serious risk factor for coronary heart disease is obesity. Body weight that exceeds the norm by 30% or more already limits a person’s physical activity, creates an increased load on the cardiovascular system, and contributes to hypoventilation of the lungs (due to limited excursion of the diaphragm). All this provokes ischemic heart disease. It has been proven that overeating is harmful even in childhood.

The most important risk factors for coronary heart disease include diabetes mellitus and high blood pressure. In diabetes, tissue acidosis occurs and microcirculation deteriorates. It has been established that in Akita Prefecture (Japan), where residents consume about 25 g of salt per day, hypertension, complicating coronary artery disease, is sharply increasing.

Note that in old age, the listed risk factors are usually summed up, which sharply intensifies the atherosclerotic process. IHD is observed much more often (2-3.6 times) in men; In women, estrogens have a certain protective effect.

A combination of risk factors (for example, hypercholesterolemia, arterial hypertension and smoking) greatly increases the risk of myocardial infarction.
Most researchers include smoking (more than 10 cigarettes per day), alcohol abuse, and excessive consumption of tea and coffee as risk factors. It has been established that alcohol has a direct toxic effect on the myocardium, increases blood clotting, blood pressure, cholesterol and adrenaline levels, causes tissue acidosis and hyperglycemia, and often a deficiency of dietary proteins occurs with alcoholism.

With a high degree of atherosclerosis, there is a sharp thickening of the wall of the coronary arteries, parietal thrombosis in the area of ​​atheromatous plaques, and deposition of calcium salts; sometimes the plaque circumferentially covers the coronary artery, reducing its lumen to the thickness of a hair. Of course, these changes make it difficult for the arteries to dilate; which is necessary during physical or emotional stress, and therefore oxygen starvation (ischemia) of the myocardium occurs.

The reserves of the coronary circulation are large, so atherosclerotic vasoconstriction, even by 50%, does not yet manifest itself clinically; neither the patient nor the doctor yet suspects that the process of coronary artery disease has already gone far, and only when the coronary lumen is narrowed by 75% do symptoms of angina pectoris and changes in ECG data appear .

IHD is most common in Scandinavia, the USA, and Western Europe; it is very rare in developing and semi-colonial countries of Africa, Latin America, and Southeast Asia. It mainly affects people who do mental work.

The clinical manifestation of fairly deep, but short-term (and therefore reversible) myocardial ischemia is angina. The main symptom of angina is pain in the heart area.

According to the clinical course, angina pectoris is distinguished between exertional and resting. Pain during exertional angina is provoked by physical activity, most often localized behind the sternum, sometimes slightly to the left, it has a pressing or squeezing nature of varying intensity, most often the pain begins gradually, then intensifies. At the time of the attack, patients try to maintain a motionless position, are afraid to take a deep breath, in some cases there is pallor of the skin due to spasm of blood vessels, skin, and increased sweating. Sometimes there are burning pains, they resemble heartburn, accompanied by tightness in the chest, stiffness in the throat, neck, and a feeling of suffocation. Irradiation of pain into the arms is typical, most often to the left along its inner surface to the little finger. Very often the pain radiates to the left shoulder blade, neck, and lower jaw.

At the beginning of an attack of angina, there may be a feeling of numbness in the left arm, a feeling that goosebumps are crawling throughout the body. The pain can be “shooting” or squeezing. Some patients experience the urge to urinate and defecate. Sometimes nausea, vomiting, dizziness, and trembling throughout the body begin. Usually the attack lasts 5-10 minutes, less often - up to 30 minutes. All these are very important differential diagnostic symptoms.

During an attack, the pulse slows down or speeds up, and blood pressure usually rises. The boundaries of the heart remain unchanged by percussion, heart sounds are often muffled. In some cases, extrasystoles may appear during an attack, and very rarely an alternating pulse.
In most cases, the attack is stopped quickly, 1-2 minutes after taking validol or nitroglycerin, which is also a differential diagnostic test.

After an attack, patients feel weak and tired for some time, and the pallor of the skin gives way to hyperemia.
Cooling increases the flow of adrenaline from the adrenal glands into the blood. In cold weather, patients often have to stop. Usually the attack begins while walking, passes when you stop, and then resumes again.

The main electrocardiographic signs of angina are displacement of the ST segment, changes in the T wave - its flattening, negativity or increase (“giant” T wave). It is characteristic that in all these cases the T wave is isosceles. If a decrease in the ST segment and a negative T wave persist after an attack, then chronic coronary insufficiency can be assumed.

It has been established that the most valuable for the early diagnosis of coronary insufficiency is an electrocardiographic test with dosed physical activity, less valuable is coronary angiography - a method of probing the aortic mouth with the introduction of a radiopaque substance into the coronary arteries. The peripheral blood picture and biochemical tests do not change.

Elderly and senile people very often develop a painless form of angina, manifested by shortness of breath or significant circulatory disorder; sometimes a painful attack occurs against the background of paroxysmal tachycardia or atrial fibrillation.

Angina at rest is manifested by paroxysmal anginal pain that occurs with minimal physical activity (for example, turning in bed), with the slightest excitement, sometimes at night.

Very close to angina at rest is this form of IBO as a pre-infarction state. It is characterized by profound insufficiency of coronary circulation and, as a rule, ends with myocardial infarction if the patient does not have time to receive adequate treatment.

Chest pain in the pre-infarction state has the same properties as with angina pectoris, however, painful attacks become constantly progressive, they become more frequent (up to 20-30 times a day), occur at night, their duration increases to 20-30 minutes, new irradiation zones. A very characteristic sign is the poor effect of nitroglycerin; sometimes it is possible to relieve pain only after taking 20-30 tablets of nitroglycerin or sustacamite. Therefore, diagnosis of a pre-infarction condition is based on careful questioning of the patient, analysis of complaints and anamnesis.

There are also atypical variants of the pre-infarction state: asthenic (the patient has weakness, dizziness, insomnia, and pain is not expressed), asthmatic (shortness of breath increases), abdominal (pain is localized in the epigastric zone), arrhythmic, when the leading symptom is extrasystole, an attack of tachycardia , heart block, etc. It is easy to notice that these options correspond to the options for acute myocardial infarction, which often ends (without treatment) in the pre-infarction state.

Among the reasons that cause the transition from angina to a pre-infarction state are nervous and mental overload, conflicts in the family and at work, drinking alcohol, smoking, etc. The ECG is characterized by a decrease in the height of the T waves in the chest leads (up to negative), moderate pronounced horizontal or arcuate displacements of the ST segment in the same leads. Unlike myocardial infarction, these changes are unstable, they normalize within 1-2 weeks (with adequate treatment of the patient).

No laboratory changes (blood changes, biochemical and enzymatic reactions) are observed in the pre-infarction state.

Myocardial infarction is the most dangerous manifestation of IHD. In 20-25% of all cases, acute myocardial infarction leads to death, and in 60-70% of cases - in the first 2 hours of the disease. Let us recall that in 20% of all cases of myocardial infarction, thromboembolic complications, persistent blockades and arrhythmias, and cardiac aneurysm are observed.

A classic description of the symptoms of acute myocardial infarction was given in 1909 by Russian doctors V.P. Obraztsov and N.D. Strazhesko. They identified 3 main clinical variants of the disease: anginal, asthmatic and gastralgic.

For the anginal variant, the leading symptom is chest pain, as with angina pectoris, only more severe (“morphine”), sometimes tearing in nature, it does not disappear with rest and is not relieved by nitroglycerin.

A thorough analysis of the properties of pain will, in most cases, allow the paramedic to recognize myocardial infarction in the anginal variant, even before taking an electrocardiogram. It has been proven that the irradiation of pain itself does not have much informative value, although the favorite zone of irradiation of anginal pain is the left arm (sometimes only the hand), the left shoulder blade, and, less often, the neck, teeth, and tongue. However, every 4th case of myocardial infarction is atypical or asymptomatic.

The gastralgic (abdominal) variant of myocardial infarction is characterized by dyspeptic disorders: heartburn, nausea, vomiting, dysphagia and “searing” pain in the epigastric region. Somewhat more often, this option is observed with damage to the posterior diaphragmatic zone of the left ventricle. It is characteristic that the abdomen is usually soft, there is no irritation of the peritoneum or stool disorders.

Dyspeptic disorders are also observed in the anginal variant of myocardial infarction: pain in the epigastric region, flatulence, hiccups, they are explained by irritation of the splanchnic and sympathetic nerves and the release of biogenic amines - histamine, serotonin, bradykinin, etc.

Acute ulcers of the stomach and intestines, often with bleeding, during myocardial infarction are caused by arterial hypotenia and shock. Patients may also experience reflex paresis of the gastrointestinal tract.

In the asthmatic version of myocardial infarction, the leading symptom is acute circulatory failure, manifested by cyanosis, cold sweat, severe shortness of breath, and a drop in blood pressure.

Listening to the heart during myocardial infarction reveals dullness of sounds, sometimes systolic murmur, various arrhythmias, and sometimes pericardial friction murmur. On percussion, the boundaries of the heart are often expanded. Sometimes a patient with myocardial infarction experiences a sudden decrease in heart rate to 60-40 per minute, which usually indicates complete atrioventricular block or bigeminy; this symptom should alert you.

Due to the fact that the clinical symptoms of myocardial infarction are not always convincing, the electrocardiographic method of research becomes crucial in diagnosis.

The earliest electrocardiographic symptom - a convex elevation of the ST segment in the area corresponding to myocardial damage - is recorded already in the first hour of a heart attack. Somewhat later, a deep and wide Q wave is formed, reflecting necrosis of the heart muscle.

There is also a decrease in the amplitude of the R waves (“dip”) in the areas corresponding to the infarction. Posterobasal myocardial infarction is not easy to recognize even with the help of electrocardiography - there are no “direct” infarct changes in any of the generally accepted leads, only in leads V1, V2 “mirror” ECG changes are noted - an increase in the R and T waves.

We emphasize the mandatory registration of an ECG in cases of suspected myocardial infarction. Statistics convince us that 25% of all cases of acute myocardial infarction are not diagnosed on time, because either the ECG is not recorded or it is assessed incorrectly.

According to the electrocardiographic picture, an acute stage of myocardial infarction is distinguished, which lasts 5-7 days, a subacute stage (5-7 weeks) and a chronic (scar) stage, which practically lasts a lifetime.

Quite typical for myocardial infarction is a moderate increase in body temperature (up to 37.5 ° C) from the 2nd to the 5-8th day. From the 1st to the 7-10th day, neutrophilic leukocytosis is observed in the blood (up to 9000-12,000 per μl), a moderate acceleration of ESR from the 2nd to the 20-25th day, and various changes in the biochemical spectrum of the blood. In cardiology clinics, the diagnosis of myocardial infarction can also be confirmed by assessing the level of creatine phosphokinase, lactate dehydrogenase and its isoenzymes.

Myocardial infarction is dangerous due to its complications, the most typical being cardiogenic shock and cardiac arrhythmias. It has been established that shock during myocardial infarction is caused by both excruciating pain and overstimulation of the cells of the central nervous system, and a decrease in myocardial contractility due to the presence of an area of ​​necrosis and edema of neighboring zones. The main feature of cardiogenic shock is deterioration of microcirculation in vital organs: brain, heart, kidneys, liver.

Based on an analysis of hundreds of cases of acute myocardial infarction, it was established that systolic hypotension below 100 mm Hg. Art. for more than 4 hours sharply worsens the prognosis of the disease. A serious complication of myocardial infarction is pulmonary edema due to left ventricular weakness. Early symptoms of pulmonary edema are increasing pallor, cyanosis, wheezing in the lungs, and then bubbling breathing, the release of foamy fluid from the mouth.

Severe cardiac arrhythmias occur in 40% or more of all cases of myocardial infarction; they are caused by necrosis or edema of the cardiac conduction system, as well as disruption of extracardiac nervous and humoral regulation (“symptomatic storm”). Extrasystole is usually observed, there may be attacks of atrial fibrillation or flutter; various conduction disorders. The most dangerous symptoms are group and early ventricular extrasystoles. Detailed diagnosis of arrhythmias is possible only with the help of electrocardiography. In 20% of all cases of myocardial infarction, cardiac arrest (asystole) is observed, in 8-10% - ventricular fibrillation. In 12-20% of all cases, thromboembolic complications are observed - infarctions of the lungs, kidneys, and brain.

This pathology is caused by a decrease or cessation of blood supply to the myocardium as a result of occlusive damage to the coronary arteries of the heart. In the vast majority of cases, the cause is stenosing atherosclerosis of the coronary arteries - a particular form of general atherosclerosis. Much less often, ischemic heart disease is caused by heart injuries, metabolic disorders, and coronary thromboembolism. As a rule, atherosclerosis affects the proximal parts of large, subepicardially located coronary arteries. In this case, the lesion is segmental in nature and distal to the site of occlusion the vascular bed retains satisfactory or good patency. A decrease in coronary perfusion leads to tissue acidosis in the myocardium and causes anginal syndrome. As ischemic cardiosclerosis develops, myocardial contractility decreases and the oxygen demand of the heart muscle increases sharply. Physical exercise tolerance decreases. Failure of the Na+ - K+ pump leads to increased Ca2+ activity, distortion of repolarization, electrical heterogeneity of the myocardium and, consequently, to various forms of rhythm disturbances. With complete occlusion of the coronary artery with insufficient collateral circulation, acute myocardial infarction (AMI) is formed, as a result of which part of the heart muscle is turned off from the pumping function. Extensive transmural infarctions cause cardiogenic shock, rupture of the heart muscle, ventricular fibrillation and, as a result, rapid sudden death. In some cases, stable angina passes into AMI through the stage of pre-infarction or so-called unstable angina.

Clinic for Coronary Heart Disease

The main clinical symptom of the disease is angina. In other cases, shortness of breath prevails. Anginal pain occurs in the form of attacks and is localized behind the sternum, less often in the epigastric region. The pain is provoked by physical activity, lasts 3-5 minutes and goes away with rest. Characterized by rapid pain relief by taking nitroglycerin. Irradiation of pain to the upper extremities, left shoulder blade, and neck is typical. The occurrence of chest pain at rest indicates a worsening of the course of coronary artery disease, since this can be a consequence of myocardial oxygen deficiency only as a result of a slight slowdown in the speed of blood flow. In uncomplicated ischemic heart disease, the physical picture is poor. Against the background of stable angina, a more severe form of coronary heart disease may develop - unstable angina. It is manifested by a sharp exacerbation of habitual angina, prolongation of anginal attacks and their greater resistance to nitroglycerin. This form of angina in its outcome can lead to AMI. Clinical manifestations of AMI depend on the extent of myocardial damage. However, the most typical are acute, prolonged chest pain that is not relieved by nitroglycerin, arrhythmias, a drop in hemodynamics and symptoms of heart failure (cardiogenic shock). The appearance of a pathological III tone, rough systolic murmur indicates dysfunction of the papillary muscle or separation of the chordae from the mitral valve leaflet. In rare cases, the cause of the murmur may be a rupture of the interventricular septum.

Diagnosis of coronary heart disease

The earliest sign of ischemic heart disease is prolongation of the diastolic relaxation phase of the myocardium on echocardiography. With stable angina, the ECG may reveal various rhythm and conduction disturbances. Many patients have an unremarkable ECG at rest. Therefore, the picture of IHD is revealed only with daily electrocardiographic monitoring. Under load conditions (bicycle ergometry, increasing transesophageal electrical stimulation of the left atrium), a decrease in coronary reserve is noted: an increase in the S-T interval in standard leads by at least 1 mm, in the chest leads by more than 2 mm. On the ECG in patients with unstable angina, similar changes are detected at rest. However, they are expressed much more roughly (focal ischemia). In the case of transmural AMI, a deep Q wave is detected in the leads corresponding to the infarction zone. Transmural AMI is also accompanied by a significant decrease in the R wave until its complete disappearance (QT complex).

The most typical method of topical diagnosis of coronary occlusions is selective coronary angiography. It identifies the affected arteries, the degree of their narrowing, and the nature of the collateral circulation. All this allows us to predict the further course of the pathology and, accordingly, select patients for surgical treatment.
There are 4 degrees of coronary artery stenosis:
I - moderate narrowing of the lumen of the vessel (up to 50%);
II - pronounced narrowing (from 50 to 75%);
III - sharp narrowing (from 75 to 90%);
IV - complete occlusion of the vessel.
Left ventriculography reveals areas of myocardial hypokinesia and is necessary for a comprehensive assessment when establishing indications for surgery. Radionuclide diagnostics based on 201T1, which accumulates in the functioning myocardium, makes it possible to determine the localization and extent of scarred myocardium. In case of AMI, it is rational to use “tTs, which accumulates in necrotic areas of the myocardium, creating here a focus of increased radioactivity (“hot spot”) in the first 24-28 hours after the development of the disease. In AMI, indicators of increased enzymatic activity (AST, ALT, CPK) have diagnostic value , cardiac LDH), an increase in leukocytosis in the blood.Vectorcardiography has a fairly high information content.

Coronary heart disease (CHD)– organic and functional damage to the myocardium caused by a lack or cessation of blood supply to the heart muscle (ischemia). IHD can manifest itself in acute (myocardial infarction, cardiac arrest) and chronic (angina pectoris, post-infarction cardiosclerosis, heart failure) conditions. Clinical signs of IHD are determined by the specific form of the disease. IHD is the most common cause of sudden death in the world, including in people of working age.

ICD-10

I20-I25

General information

It is a serious problem of modern cardiology and medicine in general. In Russia, about 700 thousand deaths caused by various forms of IHD are recorded annually; in the world, mortality from IHD is about 70%. Coronary heart disease mostly affects men of active age (55 to 64 years), leading to disability or sudden death.

The development of coronary heart disease is based on an imbalance between the need of the heart muscle for blood supply and the actual coronary blood flow. This imbalance can develop due to a sharply increased need of the myocardium for blood supply, but its insufficient implementation, or with normal need, but a sharp decrease in coronary circulation. The deficiency of myocardial blood supply is especially pronounced in cases where coronary blood flow is reduced, and the need of the heart muscle for blood flow increases sharply. Insufficient blood supply to the tissues of the heart, their oxygen starvation is manifested in various forms of coronary heart disease. The group of IHD includes acutely developing and chronic conditions of myocardial ischemia, accompanied by subsequent changes: dystrophy, necrosis, sclerosis. These conditions in cardiology are considered, among other things, as independent nosological units.

Causes and risk factors

The vast majority (97-98%) of clinical cases of coronary artery disease are caused by atherosclerosis of the coronary arteries of varying severity: from slight narrowing of the lumen by atherosclerotic plaque to complete vascular occlusion. With 75% coronary stenosis, heart muscle cells react to the lack of oxygen, and patients develop angina pectoris.

Other causes of IHD are thromboembolism or spasm of the coronary arteries, which usually develop against the background of an existing atherosclerotic lesion. Cardiospasm aggravates the obstruction of the coronary vessels and causes manifestations of coronary heart disease.

Factors contributing to the occurrence of IHD include:

• hyperlipedemia

Promotes the development of atherosclerosis and increases the risk of coronary heart disease by 2-5 times. The most dangerous in terms of the risk of coronary heart disease are hyperlipidemia types IIa, IIb, III, IV, as well as a decrease in the content of alpha-lipoproteins.

Arterial hypertension increases the likelihood of developing coronary artery disease by 2-6 times. In patients with systolic blood pressure = 180 mmHg. Art. and higher, coronary heart disease occurs up to 8 times more often than in hypotensive patients and people with normal blood pressure.

• smoking

According to various data, cigarette smoking increases the incidence of coronary artery disease by 1.5-6 times. Mortality from coronary heart disease among men 35-64 years old who smoke 20-30 cigarettes daily is 2 times higher than among non-smokers of the same age category.

• physical inactivity and obesity

Physically inactive people are 3 times more likely to develop coronary artery disease than people who lead an active lifestyle. When physical inactivity is combined with excess body weight, this risk increases significantly.

• impaired carbohydrate tolerance

• angina pectoris (stress):

1. stable (with determination of functional class I, II, III or IV);
2. unstable: new-onset, progressive, early postoperative or post-infarction angina;

• spontaneous angina (syn. special, variant, vasospastic, Prinzmetal's angina)

3. Painless form of myocardial ischemia.

• large-focal (transmural, Q-infarction);
• small-focal (not Q-infarction);

6. Cardiac conduction and rhythm disorders(form).

7. Heart failure(form and stages).

In cardiology, there is the concept of “acute coronary syndrome”, which combines various forms of coronary heart disease: unstable angina, myocardial infarction (with and without Q-wave). Sometimes sudden coronary death caused by ischemic heart disease is also included in this group.

Symptoms of IHD

Clinical manifestations of IHD are determined by the specific form of the disease (see myocardial infarction, angina pectoris). In general, coronary heart disease has a wave-like course: periods of stable normal health alternate with episodes of exacerbation of ischemia. About 1/3 of patients, especially with silent myocardial ischemia, do not feel the presence of coronary artery disease at all. The progression of coronary heart disease can develop slowly over decades; at the same time, the forms of the disease, and therefore the symptoms, may change.

Common manifestations of IHD include chest pain associated with physical activity or stress, pain in the back, arm, and lower jaw; shortness of breath, increased heartbeat or a feeling of irregularities; weakness, nausea, dizziness, clouding of consciousness and fainting, excessive sweating. Often, IHD is detected already at the stage of development of chronic heart failure with the appearance of edema in the lower extremities, severe shortness of breath, forcing the patient to take a forced sitting position.

The listed symptoms of coronary heart disease usually do not occur simultaneously; with a certain form of the disease, a predominance of certain manifestations of ischemia is observed.

Precursors of primary cardiac arrest in coronary heart disease can be paroxysmal sensations of discomfort in the chest, fear of death, and psycho-emotional lability. In case of sudden coronary death, the patient loses consciousness, breathing stops, there is no pulse in the main arteries (femoral, carotid), heart sounds cannot be heard, the pupils dilate, and the skin becomes a pale grayish tint. Cases of primary cardiac arrest account for up to 60% of deaths from coronary artery disease, mainly in the prehospital stage.

Complications

Hemodynamic disturbances in the heart muscle and its ischemic damage cause numerous morpho-functional changes that determine the forms and prognosis of IHD. The result of myocardial ischemia is the following mechanisms of decompensation:

• insufficiency of energy metabolism of myocardial cells – cardiomyocytes;
• “stunned” and “sleeping” (or hibernating) myocardium – forms of impaired contractility of the left ventricle in patients with coronary artery disease, which are transient in nature;
• development of diffuse atherosclerotic and focal post-infarction cardiosclerosis - a decrease in the number of functioning cardiomyocytes and the development of connective tissue in their place;
• violation of systolic and diastolic myocardial functions;
• disorder of the functions of excitability, conductivity, automaticity and contractility of the myocardium.

The listed morpho-functional changes in the myocardium in coronary artery disease lead to the development of a persistent decrease in coronary circulation, i.e., heart failure.

Diagnostics

Diagnosis of coronary artery disease is carried out by cardiologists in a cardiology hospital or dispensary using specific instrumental techniques. When interviewing the patient, complaints and the presence of symptoms characteristic of coronary heart disease are clarified. Upon examination, the presence of edema, cyanosis of the skin, heart murmurs, and rhythm disturbances are determined.

Laboratory diagnostic tests involve the study of specific enzymes that increase during unstable angina and heart attack (creatine phosphokinase (during the first 4-8 hours), troponin-I (on days 7-10), troponin-T (on days 10-14), aminotransferase , lactate dehydrogenase, myoglobin (on the first day)). These intracellular protein enzymes, when cardiomyocytes are destroyed, are released into the blood (resorption-necrotizing syndrome). A study of the level of total cholesterol, low (atherogenic) and high (antiatherogenic) density lipoproteins, triglycerides, blood sugar, ALT and AST (nonspecific markers of cytolysis) is also carried out.

The most important method for diagnosing cardiac diseases, including coronary heart disease, is an ECG - recording the electrical activity of the heart, which makes it possible to detect disturbances in the normal functioning of the myocardium. EchoCG is a cardiac ultrasound method that allows you to visualize the size of the heart, the condition of the cavities and valves, and evaluate myocardial contractility and acoustic noise. In some cases, in case of coronary artery disease, stress echocardiography is performed - ultrasound diagnostics using dosed physical activity, recording myocardial ischemia.

Functional stress testing is widely used in the diagnosis of coronary heart disease. They are used to identify the early stages of coronary artery disease, when disorders cannot yet be determined at rest. Walking, climbing stairs, exercise on exercise machines (an exercise bike, a treadmill), accompanied by ECG recording of heart function indicators, are used as stress tests. The limited use of functional tests in some cases is caused by the inability of patients to perform the required amount of load.

Treatment of coronary artery disease

The treatment tactics for various clinical forms of coronary heart disease have their own characteristics. However, it is possible to identify the main directions used for the treatment of coronary artery disease:

• non-drug therapy;
• drug therapy;
• performing surgical revascularization of the myocardium (coronary artery bypass grafting);
• use of endovascular techniques (coronary angioplasty).

Non-drug therapy includes measures to correct lifestyle and nutrition. For various manifestations of coronary artery disease, a limitation of the activity regime is indicated, since during physical activity the myocardial need for blood supply and oxygen increases. Failure to satisfy this need of the heart muscle actually causes manifestations of IHD. Therefore, in any form of coronary heart disease, the patient’s activity regimen is limited, followed by a gradual expansion during rehabilitation.

The diet for coronary artery disease involves limiting the intake of water and salt with food to reduce the load on the heart muscle. In order to slow the progression of atherosclerosis and combat obesity, a low-fat diet is also prescribed. The following food groups are limited and, if possible, excluded: fats of animal origin (butter, lard, fatty meat), smoked and fried foods, quickly absorbed carbohydrates (baked goods, chocolate, cakes, candies). To maintain a normal weight, it is necessary to maintain a balance between energy consumed and energy expended. If it is necessary to lose weight, the deficit between consumed and expended energy reserves should be at least 300 kC daily, taking into account that a person spends about 2000-2500 kC per day during normal physical activity.

Drug therapy for ischemic heart disease is prescribed according to the “A-B-C” formula: antiplatelet agents, β-blockers and cholesterol-lowering drugs. In the absence of contraindications, it is possible to prescribe nitrates, diuretics, antiarrhythmic drugs, etc. The lack of effect of drug therapy for coronary heart disease and the threat of myocardial infarction are an indication for consultation with a cardiac surgeon to resolve the issue of surgical treatment.

Surgical revascularization of the myocardium (coronary artery bypass grafting - CABG) is resorted to in order to restore blood supply to the ischemic area (revascularization) in case of resistance to pharmacological therapy (for example, with stable angina pectoris of class III and IV). The essence of the CABG method is to create an autovenous anastomosis between the aorta and the affected artery of the heart below the area of ​​its narrowing or occlusion. This creates a bypass vascular bed that delivers blood to the site of myocardial ischemia. CABG operations can be performed using cardiopulmonary bypass or on a beating heart. Minimally invasive surgical techniques for ischemic heart disease include percutaneous transluminal coronary angioplasty (PTCA) – balloon “expansion” of a stenotic vessel with subsequent implantation of a stent frame that holds the vessel lumen sufficient for blood flow.

Prognosis and prevention

Determining the prognosis for ischemic heart disease depends on the interrelation of various factors. The combination of coronary heart disease and arterial hypertension, severe lipid metabolism disorders and diabetes mellitus has an unfavorable effect on the prognosis. Treatment can only slow down the steady progression of IHD, but not stop its development.

The most effective prevention of IHD is to reduce the adverse effects of threat factors: avoiding alcohol and smoking, psycho-emotional stress, maintaining optimal body weight, exercising, controlling blood pressure, and a healthy diet.

So you went to the clinic. On this site, find the list of doctors, their experience and, in addition, a telephone number for visiting. It’s a good idea to read the opinions of visitors who received advice. Everyone would like to be advised by a scientist. Pay attention to bad reviews to avoid being overlooked. The quality of services in each clinic depends on the quality of training of doctors and also on the level of equipment installed in the clinic. Not every medical institution can boast of the latest set of department equipment. It’s a good idea to find out if the clinic has a professor or other specialist of the highest class.

Last week of the “Start the Year with Health!” campaign

According to the World Health Organization, of the ten leading causes of mortality in the world, coronary heart disease (CHD) is in second place - approximately two and a half million victims per year, and stroke and other cerebrovascular diseases are in 6th place and amounts to approximately one and a half million . It is easier to prevent a disease than to treat it!

St. Catherine's Clinic dedicated this section specifically to heart disease. We hope that this information will be interesting and useful to you, because it is important for yourself to understand that only you can control the situation and the state of your health! Don't remain indifferent to your problems!

Hypertonic disease ( essential arterial hypertension) is the most common disease in the world. Every third person in the world is hypertensive. The disease is characterized by a persistent increase in blood pressure above 140 to 90 mmHg. Art. and is manifested by disorders of the function of the brain, heart, kidneys and retina.

Stroke is one of the most common and serious complications of hypertension and is associated with acute cerebrovascular accident and impaired brain function.

Johann Sebastian Bach, Franklin Roosevelt, Walter Scott, Frederico Fellini, Lenin, Stalin, Andrei Mironov - this is not a complete list of those who died from stroke.

There is a misconception that a slight increase in blood pressure levels is acceptable in older people. However, this opinion is incorrect. Even with an increase in pressure of 10 mm Hg. the risk of stroke increases 7 times!

Considering the high prevalence of the disease, we recommend that you periodically measure your blood pressure level even if it exceeds 140/90 mm Hg. See a doctor, even if it is asymptomatic. Identified hypertensive patients are just the tip of the iceberg; the majority of patients - about two thirds - do not even suspect that they suffer from this terrible disease.

There are individuals predisposed to developing arterial hypertension. First of all, these are people who consume excessive amounts of table salt or are obese. Heredity also plays a big role - even if one of the parents suffers from this disease, children also have a high chance of developing arterial hypertension.

What to do if you find your blood pressure is 140/90 mm Hg. or higher? Firstly, you should immediately inform your doctor about this or contact us at the St. Catherine Cardiology Clinic. There are also several simple recommendations that will help lower blood pressure:

1. Following the DASH diet. Limit the consumption of table salt to 5 g per day. Daily consumption of foods containing calcium, magnesium and microelements (low-fat cottage cheese, yogurt, bran, dried apricots, raisins, bananas, seafood). The corrective effect on blood pressure of certain products (tonic drinks) is known - weak Hibiscus rose tea, weak green tea, freshly squeezed beet juice or chokeberry. Do not abuse large amounts of liquid (up to 1-1.5 l/day).
2. Adequate physical activity. A regimen of motor and training activity is required. Only kinetic types of training are acceptable (without excessive effort). The recommended duration of training is at least 30 minutes a day, at least 5 days a week. Remember, regular exercise reduces blood pressure by an average of 3.5/3.2 mmHg.
3. Reducing excess body weight. Even with a normal weight-height ratio, it is necessary to remember to control the size of the waist, which in circumference should not exceed 110 cm for men, and 88 cm for women. Reducing excess body weight by 5 kg allows you to reduce blood pressure by an average of 4.4 /3.6 mmHg
4. Systematic blood pressure monitoring. It is advisable to monitor it in the morning immediately after you wake up, without getting out of bed (the so-called basal blood pressure).

If your attending physician nevertheless recommended antihypertensive drug therapy, you should strictly follow it, since modern ideas for the treatment of hypertension imply daily medication. Today in the arsenal of a cardiologist there are many medications that are safe even for long-term use. The attending physician will try to select the most suitable medications for you, which will effectively and reliably lower blood pressure and prevent the development of serious complications such as stroke or myocardial infarction.

Coronary heart disease (CHD) is a chronic disease caused by insufficient blood supply to the heart muscle or, in other words, its ischemia. In the vast majority (97-98%) of cases, IHD is a consequence of atherosclerosis of the arteries of the heart, that is, narrowing of their lumen due to the so-called atherosclerotic plaques formed during atherosclerosis on the inner walls of the arteries.

In this case, the course of the disease can be different, and therefore there are several main clinical forms of IHD. These are angina pectoris, myocardial infarction and the so-called post-infarction cardiosclerosis, which is a direct consequence of a myocardial infarction. These forms of the disease occur in patients both isolated and in combination, including with various complications and consequences. These include heart failure, that is, a decrease in the pumping function of the heart muscle, heart rhythm disturbances or arrhythmias, fraught with the same heart failure, and sometimes sudden cardiac arrest, and some other complications.

This variety of manifestations of the disease determines the wide range of therapeutic and preventive measures used in the treatment of coronary heart disease. Today, the most accurate and diagnostically valuable method for verifying ischemic heart disease is coronary angiography. This procedure is an X-ray examination of the blood vessels of the heart. The prognosis and ability of patients to work depend on the frequency of exacerbations of coronary heart disease, as well as on the nature and persistence of dysfunction of the heart (and other organs) resulting from complications of the disease.

Timely diagnosis and proper treatment is the surest way to resist cardiovascular diseases. There is no spare life - you need to save this one!

Polish-American Heart Clinics

A limited liability company named Polish-American Heart Clinics was founded in 2000 by experienced cardiologists and cardiac surgeons from Poland and the United States. Our main goal is to build modern networks of Polish-American Heart Clinics. Currently, the Polish-American Heart Clinics have 20 branches in Poland, which provide highly specialized medical services in the scope of diagnosis and treatment of cardiovascular diseases.

All departments of the Polish-American Heart Clinics maintain 24-hour duty for patients with various types of acute coronary syndrome, including acute myocardial infarction.

Our achievement is to reduce the mortality rate due to heart attack from 30 to 3% in Poland.

In 2011, Polish-American Clinics established a new Cardiovascular Center in Poland with a hybrid operating room where an interdisciplinary cardiac surgery-cardiology team can perform innovative surgeries. The Cardiovascular Center specializes in videoscope operating techniques - minimally invasive cardiac surgery.

Polish-American Heart Clinics have the ability to receive patients from all over the world in medical facilities in Poland, providing a wide range of medical services. We also offer our patients specialized medical transport by ambulance to our Clinics and complete rehabilitation after medical treatment in the Ustron Spa.

Results and effectiveness of treatment at the Polish-American Heart Clinics (PACS):

The survival rate of patients one year after the onset of acute coronary syndrome (ACS) in medical institutions of the Polish-American Heart Clinics is:

In the case of myocardial infarction with ST segment elevation, the most dangerous for the patient (i.e., a fragment of the electrocardiogram) - 88.9%,

In case of myocardial infarction without ST segment elevation - 90.6%,

In the case of unstable angina - 95.7%.

If we compare these data with the European results collected in the ACS-2 registry - data from the European Heart Association) - in PAX they are better:

Non-ST segment elevation myocardial infarction PAX 90.6% compared to 88.9% - European figure

Unstable angina PAX 95.7% compared to 94.7% - European figure.

The 3-year survival rate of PAX patients with acute coronary syndrome is higher than in a comparable group of patients included in the international GRACE (Global Registry of Acute Coronary Events) registry by approximately 7%. 87% according to PAKS compared to 80% according to the GRACE registry.

Unique advantages of Polish-American heart clinics.

1. Concentration of diagnostics, cardiology, cardiac surgery and vascular surgery in one medical center - the complexity of diagnosis and treatment of cardiovascular diseases in one center for the client!

CONSULTATIONS AND NON-INVASIVE EXAMINATIONS

• cardiological, cardiac surgery and vascular surgery consultations
• non-invasive examinations: ECG at rest and after exercise, cardiac ultrasound, Holter,
• control and programming of stimulators and cardioverter-defibrillators

MEDICAL IMAGING

· CT scan

Magnetic resonance

HEALING PROCEDURES

Differential diagnosis of cor pulmonale.

The presence of cor pulmonale is especially important to establish in elderly patients, when there is a high probability of sclerotic changes in the heart, especially if for many years they have been bothered by a cough with sputum production (chronic bronchitis) and there are obvious clinical manifestations of right ventricular failure. Determination of the blood gas composition is most informative if it is necessary to determine which of the ventricles (right or left) is the root cause of heart disease, since severe arterial hypoxemia, hypercapnia and acidosis rarely occur with left heart failure, unless pulmonary edema develops simultaneously.

Additional confirmation of the diagnosis of pulmonary heart disease is provided by radiographic and ECG signs of enlargement of the right ventricle. Sometimes, if cor pulmonale is suspected, right heart catheterization is required. When this test is performed, it typically reveals pulmonary hypertension, normal left atrial pressure (pulmonary wedge pressure), and classic hemodynamic signs of right ventricular failure.

Enlargement of the right ventricle is characterized by the presence of a cardiac impulse along the left border of the sternum and a fourth heart sound arising in the hypertrophied ventricle. Concomitant pulmonary hypertension is suspected in cases where a cardiac impulse is detected in the second left intercostal space near the sternum, an unusually loud 2nd component of the second heart sound is heard in the same area, and sometimes in the presence of a murmur of pulmonary valve insufficiency. With the development of right ventricular failure, these signs are often accompanied by an additional heart sound, causing the occurrence of a gallop rhythm of the right ventricle. Hydrothorax rarely occurs even after the onset of overt right ventricular failure. Persistent arrhythmias, such as atrial fibrillation or flutter, are also rare, but transient arrhythmias usually occur in cases of severe hypoxia when respiratory alkalosis occurs due to mechanical hyperventilation. The diagnostic value of electrocardiography for cor pulmonale depends on the severity of changes in the lungs and ventilation disorders (Table 191-3). This is most valuable in cases of pulmonary vascular disease or interstitial tissue damage (especially in cases where they are not accompanied by exacerbation of respiratory diseases), or in cases of alveolar hypoventilation in normal lungs. On the contrary, with cor pulmonale, which developed secondary to chronic bronchitis and emphysema, increased airiness of the lungs and the episodic nature of pulmonary hypertension and right ventricular overload, diagnostic signs of right ventricular hypertrophy are rare. And even if the enlargement of the right ventricle due to chronic bronchitis and emphysema is quite pronounced, as happens during exacerbations during an upper respiratory tract infection, ECG signs may be inconclusive as a result of rotation and displacement of the heart, an increase in the distance between the electrodes and the surface of the heart, and the predominance of dilatation over hypertrophy with enlarged heart. Thus, a reliable diagnosis of right ventricular enlargement can be made in 30% of patients with chronic bronchitis and emphysema, in whom right ventricular hypertrophy is revealed at autopsy, while such a diagnosis can be easily and reliably established in the vast majority of patients with cor pulmonale caused by lung pathologies other than chronic bronchitis and emphysema. With this in mind, the following seem to be more reliable criteria for right ventricular hypertrophy in a patient with chronic bronchitis and emphysema: S1Q3 type, deviation of the electrical axis of the heart more than 110°, S1, S2, S3 type, R/S ratio in lead V6 Table 191-3. ECG signs of chronic pulmonary heart disease

1. Chronic obstructive pulmonary diseases (probable, but not diagnostic signs of enlargement of the right ventricle)" a) "P-pulmonale" (in leads II, III, aVF) b) deviation of the heart axis to the right more than 110° c) R/S ratio c V6 >>>

Kyiv City Heart Center

Pavel Glebov | 12/21/2014

My wife is a foreigner, I am writing at her request an appeal:

Anyone who needs heart surgery - go to the Heart Institute.

You have something in your country that you can be proud of and be sure that everything will be done professionally, plus excellent conditions and equipment. Moreover, compared to Western clinics, it is also budget-friendly. It is clear that everything is learned by comparison, but still, this is a heart operation, not appendicitis, and consumables, a priori, cannot be cheap.

Special thanks to Boris Todurov - a modern and smart leader, and most importantly - a Cardiac Surgeon with a capital C

Kalinichenko S.A. | 07/22/2014

"Heart Clinic" - cardiac center in Yekaterinburg

hclinic.ru/, which provides comprehensive information about their activities.

Human health weakens every year, and the risk of cardiovascular diseases after the age of 35 is constantly increasing. A timely examination of the heart allows one to detect a possible pathology, and then take measures to neutralize it.

Cardiology in Yekaterinburg is represented by several large medical centers, the main goal of which is to identify cardiovascular diseases in patients. Similar centers include the Cardiac Center “Heart Clinic”, which in its work uses the latest technologies and diagnostic methods to obtain more reliable information. The effectiveness of further treatment of the patient depends on the quality of the data obtained as a result of heart diagnosis. In the “heart clinic”, the following are used for qualitative examination: biochemical blood test, computed tomography of the heart. ultrasound of the heart. You can get detailed information on each of the departments of the cardiocenter on the website.

It is worth highlighting computed tomography separately. The “heart clinic” has the most modern device in the entire Sverdlovsk region. With its help, you can get the most accurate diagnosis and see the smallest changes in the vessels. Thanks to the high quality of the results obtained, it is possible to ultimately select the optimal course of treatment.

Hclinic.ru/ provides a full list of services, which include appointments with a cardiologist, computed tomography scans, ultrasound, comprehensive examination, laboratory tests, and rehabilitation programs for patients. For a rough overview, this information is important, but first of all you need to visit a doctor to select the appropriate type of examination. You can also make an appointment through the cardiocenter website.

The main thing to remember is that a person has only one health! And you need to constantly take care of it and check it periodically.

Clinic and treatment of pulmonary heart disease in phthisiopulmonary patients

A.K. Ivanov, K.G. Tyarasova

The problem of cor pulmonale (CP) in patients with tuberculosis of the respiratory system is of great interest to this day, although back in 1819 R. Laennec identified sharp hypertrophy and dilatation of the right ventricle in a woman who died from tuberculosis and pulmonary emphysema with symptoms of severe respiratory failure. In recent years, mortality from drugs in respiratory tuberculosis has increased, which is associated with an increase in common and progressive forms of tuberculosis in the structure of morbidity, as well as with an increase in the number of patients with chronic tuberculosis that developed due to multidrug resistance of mycobacterial strains.

The definition proposed by V.P. is most consistent with ideas about drugs. Silvestrov (1991), according to which “by drugs we should understand the entire complex of hemodynamic disorders (primarily secondary pulmonary hypertension), which develops as a result of diseases of the bronchopulmonary apparatus and manifests itself at the final stage as irreversible morphological changes in the right ventricle of the heart with the development of progressive circulatory failure.”

The clinic uses the classification of cor pulmonale B.E. Votchala (1964) (Table 1). From the perspective of modern research in the field of pathogenesis of drugs in patients with respiratory tuberculosis, it should be noted that pulmonary tuberculosis with its unique pathogenetic mechanisms of development, spread through the vascular bed, bronchial tree, lymphatic vessels and contact pathways can be presented in several sections of this classification. The basis still remains the temporal characteristic of the process, and pulmonary tuberculosis, as a rule, leads to chronic LS; subacute formation of LS is less often determined in acute specific processes (miliary tuberculosis, caseous pneumonia). Spontaneous pneumothorax as a complication of pulmonary tuberculosis (due to its rapid development over time) can lead to the development of acute pulmonary tuberculosis.

The main mechanism in the pathogenesis of LS is pulmonary hypertension (PH). Pressure in the pulmonary circulation (PCC) is considered increased if it exceeds normal values ​​(systolic 30 mm Hg, diastolic 8-9 mm Hg).

Classification of pulmonary hypertension in chronic nonspecific lung diseases (CNLD) N.G. Paleeva (1990) complements the classification of B.E. Votchala and significantly helps in the early diagnosis of drugs.

In stage I of pulmonary hypertension (transient), an increase in pulmonary arterial pressure occurs during physical activity, exacerbation of the inflammatory process in the lungs, or increased bronchial obstruction.

Stage II (stable) is characterized by PH at rest and without exacerbation of bronchopulmonary pathology. These two stages of PH correspond to the state of drug compensation.

Stage III PH is characterized by persistent PH, which is accompanied by circulatory failure.

Pulmonary Heart Clinic

The drug clinical picture consists of symptoms caused by respiratory tuberculosis, as well as signs of pulmonary and heart failure.

Compensated cor pulmonale

The clinical picture of compensated cor pulmonale includes signs that are present in the stage of stable pulmonary hypertension. However, some of the symptoms, according to experts, may be present in patients already in the stage of transient PH. The main diagnostic criterion is physical activity, tolerance to which changes in patients already with transient PH.

Dyspnea, which appears with significant physical effort in patients with transient PH and with minor exertion in the stage of stable PH. The intensity of shortness of breath depends on food intake, weather conditions, cooling, and especially the presence of cough. The sensation of shortness of breath is usually not proportional to arterial hypoxemia or hypercapnia, or the level of pressure in the pulmonary artery. Measured physical labor with a gradual increase in load may not cause increased shortness of breath. At the same time, any stress that requires a rapid increase in the volume of ventilation is accompanied by a significant increase in shortness of breath. Many patients, without complaining of shortness of breath, unconsciously limit physical activity. In these cases, a targeted interview with the patient is necessary to determine exercise tolerance.

Patients prefer a horizontal body position. In this case, the diaphragm takes a greater part in intrathoracic hemodynamics, which facilitates the breathing process.

Pain in the heart area (pulmonary angina pectoris Katcha), which does not have a typical clinical characteristic. Pain appears mainly during physical exertion. Nitroglycerin is ineffective in this case, but aminophylline helps. In addition, patients also feel palpitations and “interruptions” in the heart during physical activity. However, ECG signs of arrhythmia are not found in them. This complex of cardiac symptoms is explained by several reasons: myocardial hypoxia, infectious-toxic damage to the myocardium, and in some cases it is a pulmonary reflex.

An objective examination of the patient reveals cyanosis. The severity of cyanosis is emphasized during physical activity. In the compensation stage, cyanosis is rich, dark earthy, “warm” (warm hands). Blueness in patients with drugs is caused by respiratory failure and occurs when blood oxygen saturation decreases, hypoxemia is less than 85%. It should be noted that in the stage of stable PH, cyanosis of the tongue is noticeable, the so-called “rabbit (or frog) emphysematic eyes” are expressed due to the expansion and increase in the number of conjunctival vessels.

The chest is characterized by changes characteristic of emphysema (increase in the epigastric angle, increase in anteroposterior size, etc.). The supraclavicular fossae bulge sharply, and more often sink due to pneumosclerotic changes and pleural adhesions. Upon percussion, a boxy percussion sound is determined; on auscultation: weakened vesicular breathing, often dry rales. Importance is given to the quiet “squeaking” sound in the small bronchi, which is easier to detect after light physical activity.

In the stage of transient PH, heart sounds are muffled, especially in the “lying” position. Strengthening of the second tone above the pulmonary artery can rarely be heard (due to inflated lungs). Often by palpation, rarely by eye, pulsation of the right ventricle can be noted in the epigastric region, palpable under the xiphoid process to the left and up.

In cases of pleuropericardial adhesions and severe emphysema, the heart is “removed” from the anterior chest wall.

In some patients, even at rest, there is a tendency for the heart rate to increase slightly - 78-84 beats per minute.

In the stage of stable PH, pulsation in the epigastric region is determined visually in most cases. An accent of the second tone of the suprapulmonary artery is observed infrequently. I.B. Lichtsier (1976) describes an auscultatory phenomenon that occurs in approximately half of patients with LS - an increase in the first tone, and often a flapping first sound at the site of auscultation of the tricuspid valve. The distance of the pulmonary artery from the chest wall is caused by a clockwise rotation of the heart during right ventricular hypertrophy. This can also explain the loud first sound above the tricuspid valve. Most patients at this stage have tachycardia, reaching 84-90 beats per minute at rest. Sometimes, at the site of listening to the pulmonary artery, a soft, blowing diastolic murmur can be detected - Grahamstill murmur, which is caused by diastolic regurgitation with relative insufficiency of the pulmonary artery valves.

Decompensated cor pulmonale

This is the inability of the hypertrophied right ventricle to maintain its flow rate at a level adequate to the amount of venous blood flow to it.

Decompensated LS is characterized by several clinical course options:

1. Respiratory, in which the leading signs are shortness of breath, suffocation, cyanosis, wheezing in the lungs, and cough.

2. Cerebral, when as a result of chronic hypoxia and hypercapnia, increased permeability of cerebral vessels is formed, small perivascular hemorrhages, cerebral edema are formed and encephalopathy develops (S. Todorov and S. Georgiev, 1972). This is manifested by increased excitability, aggressiveness, euphoria up to psychosis; and also vice versa - depression, drowsiness, lethargy, apathy: dizziness, persistent and intense headaches in the morning. In severe cases, there may be episodes of loss of consciousness and convulsions. With severe decompensation of drugs, a decrease in intelligence was noted. These cerebral disorders to the same extent and with the same frequency are not observed in cardiac decompensation of another origin (not due to drugs).

3. Anginous, occurring as “pulmonary angina pectoris”. Patients, even at rest, are sometimes bothered by severe and almost always prolonged pain in the heart area without the typical irradiation to the left arm and neck. Hypertensive crises in the pulmonary artery are considered prognostically unfavorable. In this case, the pain is combined with suffocation.

4. Abdominal variant, manifested by excruciating pain in the epigastric region, nausea, vomiting, up to the development of peptic ulcer. These disorders are associated with hypoxia, which reduces the stability of the gastric mucosa, while hypercapnia increases the secretion of hydrochloric acid.

5. Collaptoid, with periods of severe pallor, weakness, feelings of horror, cold extremities, profuse cold sweat on the face, drop in blood pressure, “thread-like” pulse, severe tachycardia. It is noted that the addition of even short-term collaptoid states to the clinical picture of drugs is a prognostically unfavorable sign.

Circulatory failure in decompensated LS develops predominantly of the right ventricular type. Congestion is determined in the systemic circulation. One of the early symptoms is liver enlargement and pain on palpation. The positive symptom of Plesh is significant - swelling of the neck veins when pressing with the palm of the hand on the enlarged liver. Swelling of the neck veins is better detected during a prolonged cough, while facial cyanosis increases.

T.Ya. Ilyina et al. (1992) noted that in a state of subcompensation of drugs, in doubtful cases, one can ascertain the cyanosis of the nasolabial triangle, chin, and ears after the patient with tuberculosis bends his torso down. In addition, the authors observed a combination of cyanosis with telangiectasia in patients with decompensated LS.

The appearance of skin and conjunctival hemorrhages several days before death in some patients with decompensated LS has been described.

Peripheral edema is an important indicator of decompensation of drugs. At first they are transient, appearing towards the end of the day or during an exacerbation of the bronchopulmonary process, which indicates the initial stages of drug decompensation. Subsequently, swelling becomes permanent and widespread. However, pronounced edematous syndrome in patients with pulmonary tuberculosis complicated by drugs almost never occurs. It is believed that “dry decompensation” develops, which is explained by increased excretion of sodium ions by the kidneys due to hypoxemia and changes in protein fractions of blood serum.

Examination of the chest and lungs in patients with decompensated LS reveals changes corresponding to pronounced emphysema and pneumosclerosis of varying degrees. However, the chest is not always emphysematous due to pronounced pleural adhesions. Almost all patients, in addition to quiet dry rales, have fine bubbling wet rales. They depend, I.B. believed. Lichtsier (1976), from bronchiolitis, but in some cases with the development of total heart failure, the role of some congestion in the lungs cannot be completely excluded. Respiratory rate up to 30-40 per minute at rest.

The heart, despite pulmonary emphysema, is determined by percussion to be enlarged in most cases, but not in all. The establishment of “normal” boundaries of the heart in case of emphysema already indicates its expansion. However, in 20-25% of cases, the borders of the heart are quite difficult to determine by percussion. The pulsation of the right ventricle in the epigastric region is almost always visible, and upon palpation it is possible to feel a push from the wall of the right ventricle. Heart sounds at the apex are muffled, sometimes the first sound is bifurcated, and there may be a flapping first sound above the tricuspid valve. The emphasis of the second tone on the pulmonary artery is heard more often than with compensated LS. A Grahamstill noise may be heard. Tachycardia is very constant, arrhythmias are rare. Blood pressure is often low.

Laboratory and instrumental methods for diagnosing cor pulmonale

Hemogram indicators in patients with compensated drugs are determined by the underlying disease, that is, the form and phase of the tuberculosis process in the lungs.

In patients with decompensated drugs, due to severe hypoxia, compensatory erythrocytosis and normal ESR values ​​are possible (even with exacerbation of the pulmonary process) due to increased blood viscosity.

Electrocardiography

Quantitative signs of right ventricular (RV) hypertrophy are: R/S ratio in lead VI >= 1.0; R/S ratio in lead V6<= 2,0; зубцы RV1 >= 7 mm and SV5-6 >= 7 mm, the sum of teeth RV1 + SV5-6 >= 10.5 mm (N.B. Zhuravleva, 1990). Severe right ventricular hypertrophy gradually causes an increase in the RV1-2 and SV5-6 waves and can lead to the appearance of a complex of qRV1 and rSV6 (“R” - type of changes).

In the “S” type of right ventricular hypertrophy, the limb leads have deep terminal S waves in leads I, II, III, and aVF, while in lead aVR the terminal R wave increases significantly and may become the main wave of the ventricular complex.

Radiation diagnostics

Echocardiography. The most informative criteria according to echocardiography (EchoCG) should be considered an increase in the thickness of the pancreatic wall (more than 3.5 mm), an increase in the size of its cavity (N = 1.5-2.3 cm), a decrease in the ejection fraction and stroke index.

The value of the pancreatic ejection fraction is determined using the method of radionuclide ventriculography. In response to exercise, the RV ejection fraction decreases, and the degree of its decrease correlates with the level of LH.

Recently, the possibility of using magnetic resonance imaging in the diagnosis of PH has been proven. In addition, there are calculated methods for determining pressure in the pulmonary artery (by phlebogram, rheogram, etc.) that are also based on the L. Burstin method and are justified.

There are signs of hypertrophy of the right heart and signs of pulmonary hypertension. The right ventricle, when enlarged, does not change the shadow of the heart in the frontal position, but reduces the retrosternal space, which is determined on a lateral radiograph. With a significant increase, the pancreas becomes edge-forming along the right contour. Then it pushes the right atrium upward and posteriorly, which is visualized on the lateral radiograph by the narrowing of the retrocardial space. Yu.V. Kulachkovsky (1981) considers an enlarged cone of the pulmonary artery to include the “pseudomitral” heart among the criteria for RV hypertrophy. Signs of PH should be considered:

1) violation of the “gradual” decrease in the lumen of blood vessels from the center to the periphery - “amputation” of the roots;

2) expansion of the pulmonary artery trunk more than 15 mm;

3) violation of the 1:1 ratio (intermediate artery: intermediate bronchus).

The information content of the x-ray method can be increased by calculating the Moore index. This is the percentage of the diameter of the pulmonary artery arch to half the diameter of the chest. These dimensions are determined by direct radiographs at the level of the right dome of the diaphragm. In healthy people aged 16-18 years, the index is 28; 19-21 years old - 28.5; 22-50 years old - 30.

An increase in the index indicates pulmonary hypertension.

Study of external respiration function in patients with cor pulmonale

Impaired external respiration function (ERF) is the basis for the formation of drugs. Changes in respiratory function indicators give an idea of ​​the severity of drugs. The following characteristics of the FVD are considered the most informative:

total lung capacity (TLC); vital capacity of the lungs (VC); residual lung volume (RLV); functional residual capacity (FRC).

In patients with pulmonary tuberculosis, restrictive type changes in respiratory function are observed, developing as a result of pneumosclerosis and pleural adhesions. This leads to a decrease in VC and TEL.

With LS in the stage of compensation: TLC decreases with a significant disruption of its structure, a decrease in VC and an increase in TBL reflects the presence of partial respiratory failure.

In the stage of decompensation: a significant decrease in vital capacity, an increase in total volume, signs of “total” respiratory failure.

V.A. Yakovlev and I.G. Kurenkova (1996) noted that in the stage of compensated HP, the indicators of bronchial patency were important, and in the case of decompensation of HP, the indicators of the blood gas composition were important.

Treatment of cor pulmonale in patients with respiratory tuberculosis

Therapeutic measures for drugs in patients with tuberculosis are complex therapy, including a number of basic positions:

1) treatment of the underlying pathology (tuberculosis);

2) lowering blood pressure in the ICC and improving hemodynamics in the ICC;

3) improvement of the function of the bronchial tree;

4) influence on the rheological properties of blood;

5) prevention of hypoxic myocardial dystrophy.

I. Treatment of the underlying disease

Treatment of tuberculosis in patients with drugs is anti-tuberculosis therapy that is adequate to the process.

However, a number of anti-tuberculosis drugs (GINK, streptomycin, PAS groups) negatively affect the altered muscle tissue of the heart, and also (rifampicin, pyrazinamide, thioacetozone) create an additional toxic factor that aggravates the existing tension in the blood coagulation system in patients with tuberculosis, therefore, adequate chemotherapy should be reasonable and with elements of sparing. Therefore, it is advisable to use a chemotherapy regimen with fractional doses of drugs, intermittent regimens, if necessary, with a slight decrease in the daily dose of the tuberculostatic agent.

II. Therapy aimed at reducing pressure in the ICC

Therapy aimed at reducing pressure in the ICC occupies an extremely important place in the complex of therapeutic measures for cor pulmonale.

Medicines from several groups are used for this purpose. It is imperative to take into account the patient’s systemic blood pressure.

1. Arteriovenous-type vasodilators include ganglion blockers and alpha-adrenergic blockers.

Ganglion blockers deposit blood in the venous part of the systemic circulation. They are recommended for use in acute drugs, a sharp increase in pressure in the ICB, and with high or normal (but not low) systemic blood pressure. The preferred route of administration is intravenous under the control of systemic blood pressure:

a) Pentamine 0.5-1% solution intramuscularly 3 times a day.

b) Gangleron 1.0-2.0 1.5% solution 3 times a day intramuscularly.

c) Benzohexonium 0.1 2-3 times orally or 2.5% solution 0.5-1.0 subcutaneously, intramuscularly or inhaled.

Side effects cannot be ruled out with long-term use of ganglion blockers: dry mouth, atonic constipation, bladder atony, nausea, impaired accommodation.

Alpha adrenergic blockers:

a) Phentolamine hydrochloride 0.05 3-4 times orally after meals.

b) Prazosin, which is prescribed orally, the dose is selected individually, the first dose should not exceed 0.5 mg. The effect of the drug develops after several weeks.

The use of ganglion blockers and alpha-adrenergic receptor blockers involves the possibility of orthostatic collapse.

2. Venous type vasodilators - nitrates, Sidnopharm (Corvaton).

The use of prolonged nitrates is indicated for patients with drugs with tuberculosis, since a good effect of reducing pressure in the ICC has been noted, especially with long-term use. The combined use of nitrates and cardiac glycosides in patients with decompensated drugs is justified. A positive shift in hemodynamic parameters (decrease in pressure in the pulmonary artery, decrease in wall and myocardial tension, decrease in platelet aggregation) was noted when taking Sidnopharma in patients with pulmonary tuberculosis with drugs. In addition, patients tolerate the drug well. The average daily dose is 3 mg in three doses.

3. Arterial-type vasodilators, which include calcium antagonists (verapamil, nifedipine). Arteriodilatators reduce the “afterload” of the heart, which for the right ventricle is the vascular resistance of the ICC. It has been experimentally confirmed that drugs of this group have a pulmonary vasodilating effect. At the same time, calcium antagonists reduce platelet aggregation, increase myocardial resistance to hypoxia, and have a slight anti-inflammatory effect. These drugs are preferable for long-term use in cases of combination of pulmonary and systemic arterial hypertension.

4. Vasodilators of other groups. When using rauwolfia preparations, the best effect was observed in combination with aminophylline, given that rauwolfia can cause bronchospasm.

To reduce pressure in the MCC T.Ya. Ilyina (1992) recommends the use of antispasmodics - a 2% solution of papaverine, or a 2% solution of no-shpa 2.0-4.0 ml intravenously or intramuscularly, as well as a 1% solution of nicotinic acid 1.0 ml 1-2 times per day intramuscularly, or with 500 mg of ascorbic acid per 250.0 ml - 5% glucose solution with 5-6 units of insulin intravenously.

5. Diuretic drugs. In patients with drugs with pulmonary tuberculosis with chronic intoxication and disorders of the coagulation system, the rheological properties of the blood are significantly changed (DIC stages 1 and 2). Therefore, the prescription of diuretics becomes possible only with the introduction of additional fluid or as symptomatic therapy in a preterminal situation. Diuretics are prescribed for circulatory failure complicating drugs. At initial manifestations of right ventricular failure, the use of aldosterone antagonists (aldoctone, spironolactone, veroshpiron) with their moderate diuretic effect and potassium-sparing effect is indicated. Carbonic anhydrase inhibitors (diacarb, fonurite) are more effective in preventing edema than in treating it. Saluretics (hypothiazide, furosemide, brinaldix) are used with great caution so as not to cause thickening of sputum, impaired mucociliary clearance, or deterioration of pulmonary ventilation due to dehydration.

6. Inhibitors of angiotensin-pleural enzyme (ACE) synthesis: captopril, enalapril.

The results of studies of the effect of ACE inhibitors on pulmonary hemodynamics are controversial. Captopril did not in all cases reduce the pressure in the ICB, while peripheral resistance and systemic blood pressure decreased. On the other hand, the hypotensive effect of captopril in the ICC is observed in patients with severe hypoxemia or when combined with oxygen therapy.

Cardiac glycosides occupy a special place in the treatment of drugs. The question of the advisability of their use in drug therapy is currently being discussed. The range of judgments includes opinions from the complete exclusion of cardiac glycosides from drug therapy to their mandatory inclusion in the complex of drug treatment measures. Considering the positive results of glycoside therapy of drugs for tuberculosis obtained by many authors, options for the possible use of cardiac glycosides should be discussed.

Treatment of decompensated drugs begins with intravenous administration of cardiac glycosides (corglicon 0.06% - 1.0 ml per day, strophanthin 0.05% - 0.5 ml per day); later they switch to small doses of tablet drugs (isolanide, celanide) - 1-1/2 tablets per day. For dynamic monitoring, an ECG is performed, since the therapeutic dose of cardiac glycosides in patients with LS is close to toxic. Patients with pulmonary tuberculosis complicated by drugs tolerate small doses of intravenous glycosides satisfactorily; a good effect was noted when using cardiac glycosides in drops (the dose is selected individually).

An important place in the treatment of drugs belongs to oxygen therapy, which normalizes pulmonary and systemic hemodynamics and restores the sensitivity of the cell receptor apparatus to drugs. At the initial manifestations of drugs or for the purpose of its prevention, use a humidified 40-60% mixture of oxygen and air with a high flow rate (up to 6-9 l/min). In case of drug decompensation and severe respiratory failure, the patient is given oxygen at a concentration of 28-34% through a catheter or mask at a rate of 1-4 l/min.

In severe clinical situations, long-term (nighttime) low-flow oxygenation is indicated. The duration of the procedure, according to various authors, is 15-17 hours a day, 1-2 l/min with a nasal mask or cannula. In patients with tuberculosis T.Ya. Ilyina (1992) recommends 24-35% oxygen concentration for long-term oxygenation. Patients with nonspecific pulmonary pathology complicated by drugs with decompensation are treated with higher concentrations of oxygen. In all cases, oxygen must be humidified. It is strictly not recommended for patients with decompensated drugs to inhale 100% oxygen; this can lead to depression of the respiratory center and the development of hypercapnic coma.

The use of hyperbaric oxygenation will give good results in patients with compensated HP, negative results in patients with decompensated HP. Probably, the following should be considered promising: plasmapheresis, lymphocytapheresis, erythrocytapheresis, hemosorption.

III. Improving the function of the bronchial tree

In order to improve the function of the bronchial tree, the following groups of drugs are used: bronchodilators; drugs that restore mucociliary clearance; hormonal drugs; antibiotics and sulfonamides.

Bronchodilators are divided into three groups according to their mechanism of action:

1. Adrenolytics (salbutamol, terbutaline, Berotec, Saventol), which quickly relieve bronchospasm, have a preventive antiallergic effect, and at the same time reduce pressure in the ICB. Convenient form - inhalers with a metering device. The prolonged tablet drug spiropent also stimulates ciliary function and is well tolerated by patients with rhythm disturbances and circulatory failure. Cardiotoxic side effects are more often noted when using non-selective beta-stimulants (isadrin, alupent), therefore they are used less frequently in patients with pulmonary tuberculosis with drugs. When beta2-stimulants (salbutamol) are prescribed in large doses, resistance or a reverse effect may occur.

2. Anticholinergics (atrovent, troventol) are practically free of the side effects of atropine and therefore are very effective in patients with tuberculosis.

3. Methylxanthines (theophylline group), the mechanism of therapeutic action of which is the blockade of adenosine receptors. In addition to the bronchodilator effect, theophylline reduces pressure in the ICB and improves mucociliary clearance. Most effective when administered intravenously. In patients with tuberculosis and drugs, it is advisable to use prolonged methylxanthines (theolong, euphylong, teopek, teodele, etc.). Side effects of methylxanthines can include gastrointestinal dysfunction and epileptiform seizures. For concomitant diseases of the kidneys and liver in old age, the dose of methylxanthines is reduced by half.

Recently, combined bronchodilators have been developed: Eudur (theophylline and terbutaline), Berodual (Berotec + Atrovent).

Drugs that restore mucociliary clearance.

Mucociliary clearance has a great influence on bronchial patency, pulmonary ventilation and, ultimately, on the hemodynamics of the lungs in patients with tuberculosis. Products that improve mucus formation and stimulate the formation of surfactant (bromhexine group) are considered promising. High viscosity of sputum is an indication for the prescription of mucolytics - potassium iodide 3%; essential oils (preferably inhalations). The use of alkalis in inhalations is effective.

In cases where it is necessary to reduce a painful cough, you can use non-narcotic antitussives - Glauvent, Libexin, Tusuprex. A.G. Khomenko et al. (1991) used prostaglandin E2 (prostenon) with good results to eliminate bronchial obstruction in tuberculosis patients with concomitant COLD.

Nonspecific antibacterial therapy in patients with tuberculosis is effective in reducing the inflammatory reaction not only in the lung tissue, but also in the bronchial tree. It is used in short-term courses, taking into account the drug sensitivity of the flora. However, it is necessary to pay attention to the possibility of developing side effects of the antibiotic itself: dysbacteriosis, immunity disorders, allergic reactions.

Glucocorticoids are used to treat nonspecific inflammation in patients with drugs. According to T.Ya. Ilyin (1992), glucocorticoids in patients with tuberculosis with drugs promote the resorption of inflammation in the lung tissue, the mucous membrane of the tracheo-bronchial tree, relieve bronchospasm, ventilation disorders, improve alveolar ventilation, reduce hypoxemia and pressure in the ICB. A certain advantage is their ability to eliminate refractoriness to cardiac glycosides and diuretics, usually used in patients with drugs. It is recommended to minimize the side effects of glucocorticoids by using short courses and rational doses of the drug. For drugs and refractory circulatory failure, it is advisable to take 15 mg of prednisolone per day for 7 days with rapid (within 3 days) withdrawal of the drug. Prednisolone can be used, starting with 25-30 mg per day with a dose reduction of 5 mg after 3-4 days. For decompensated drugs, glucocorticoids with a more pronounced diuretic effect (dexamethasone, polcortolone) are preferred. For broncho-obstructive syndrome, it is better to use glucocorticoids in the form of aerosols.

IV. Changes in the rheological properties of blood

Cardiac ischemia

INTRODUCTION

Coronary heart disease is the main problem in the clinic of internal diseases; in WHO materials it is characterized as an epidemic of the twentieth century. The basis for this was the increasing incidence of coronary heart disease in people in various age groups, the high percentage of disability, and the fact that it is one of the leading causes of mortality.

Currently, coronary heart disease in all countries of the world is regarded as an independent disease and is included in<Международную статистическую классификацию болезней, травм и причин смерти>. The study of coronary heart disease has a history of almost two centuries. To date, a huge amount of factual material has been accumulated indicating its polymorphism. This made it possible to distinguish several forms of coronary heart disease and several variants of its course. The main attention is drawn to myocardial infarction - the most severe and common acute form of coronary heart disease. Significantly less described in the literature are forms of coronary heart disease that occur chronically - these are atherosclerotic cardiosclerosis, chronic cardiac aneurysm, angina pectoris. At the same time, atherosclerotic cardiosclerosis, as a cause of mortality among diseases of the circulatory system, including among forms of coronary heart disease, is in first place.

Coronary heart disease has become notorious, becoming almost epidemic in modern society.

Coronary heart disease is the most important problem of modern healthcare. For a variety of reasons, it is one of the leading causes of death among the population of industrialized countries. It strikes able-bodied men (more than women) unexpectedly, in the midst of vigorous activity. Those who do not die often become disabled.

Coronary heart disease is understood as a pathological condition that develops when there is a violation of the correspondence between the need for blood supply to the heart and its actual implementation. This discrepancy can occur when the myocardial blood supply remains at a certain level, but the need for it has sharply increased, or when the need remains, but the blood supply has decreased. The discrepancy is especially pronounced in cases of decreased blood supply and an increasing need for blood flow from the myocardium.

The life of society and the preservation of public health have repeatedly posed new problems for medical science. Most often these are different<болезни века>, which attracted the attention of not only doctors: cholera and plague, tuberculosis and rheumatism. They were usually characterized by prevalence, difficulty of diagnosis and treatment, and tragic consequences. The development of civilization and the successes of medical science have pushed these diseases into the background.

Currently, one of the most pressing problems is undoubtedly coronary heart disease. The criteria for angina pectoris were first proposed by the English physician W. Heberden in 1772. Even 90 years ago, doctors rarely encountered this pathology and usually described it as casuistry. Only in 1910 V.P. Obraztsov and N.D. Strazhesko in Russia, and in 1911 Herrik in the United States of America gave a classic description of the clinical picture of myocardial infarction. Now myocardial infarction is known not only to doctors, but also to the general population. This is explained by the fact that every year it occurs more and more often.

Coronary insufficiency occurs as a result of a lack of oxygen supply to the heart tissue. Insufficient oxygen supply to the myocardium can result from various reasons.

Until the 80s of the 19th century, the prevailing opinion was that the main and only cause of angina pectoris (angina) was sclerosis of the coronary arteries. This was explained by the one-sided study of this issue and its main morphological direction.

By the beginning of the twentieth century, thanks to the accumulated factual material, domestic clinicians pointed to the neurogenic nature of angina pectoris (angina pectoris), although the frequent combination of spasms of the coronary arteries with their sclerosis was not excluded (E.M. Tareev, 1958; F.I. Karamyshev, 1962 ; A.L. Myasnikov, 1963; I.K. Shvatsoboya, 1970, etc.). This concept continues to this day.

In 1957, a group of experts on the study of atherosclerosis at the World Health Organization proposed the term<ишемическая болезнь сердца>to denote an acute or chronic heart disease that occurs as a result of a decrease or cessation of blood supply to the myocardium due to a pathological process in the coronary artery system. This term was adopted by WHO in 1962 and included the following forms:

1) angina pectoris;

2) myocardial infarction (old or fresh);

3) intermediate forms;

4) coronary heart disease without pain:

a) asymptomatic form,

b) atherosclerotic cardiosclerosis.

In March 1979, WHO adopted a new classification of coronary heart disease, which distinguishes five forms of coronary heart disease:

1) primary circulatory arrest;

2) angina pectoris;

3) myocardial infarction;

4) heart failure;

5) arrhythmias.

ANATOMICAL AND PHYSIOLOGICAL FEATURES BLOOD SUPPLY TO THE MYOCARDIAL

The blood supply to the heart is carried out through two main vessels - the right and left coronary arteries, starting from the aorta immediately above the semilunar valves. The left coronary artery begins from the left posterior sinus of Vilsalva, goes down to the anterior longitudinal groove, leaving the pulmonary artery to the right, and to the left the left atrium and the appendage surrounded by fatty tissue, which usually covers it. It is a wide but short trunk, usually no more than 10-11 mm long. The left coronary artery is divided into two, three, in rare cases, four arteries, of which the anterior descending and circumflex branches, or arteries, are of greatest importance for pathology.

The anterior descending artery is a direct continuation of the left coronary artery. Along the anterior longitudinal cardiac groove it is directed to the region of the apex of the heart, usually reaches it, sometimes bends over it and passes to the posterior surface of the heart. Several smaller lateral branches depart from the descending artery at an acute angle, which are directed along the anterior surface of the left ventricle and can reach the obtuse edge; in addition, numerous septal branches depart from it, piercing the myocardium and branching in the anterior 2/3 of the interventricular septum. The lateral branches supply the anterior wall of the left ventricle and give branches to the anterior papillary muscle of the left ventricle. The superior septal artery gives off a branch to the anterior wall of the right ventricle and sometimes to the anterior papillary muscle of the right ventricle.

Throughout its entire length, the anterior descending branch lies on the myocardium, sometimes plunging into it to form muscle bridges 1-2 cm long. Throughout the rest of its length, its anterior surface is covered with fatty tissue of the epicardium.

The circumflex branch of the left coronary artery usually departs from the latter at the very beginning (the first 0.5-2 cm) at an angle close to a straight line, passes in the transverse groove, reaches the obtuse edge of the heart, goes around it, passes to the posterior wall of the left ventricle, sometimes reaches posterior interventricular groove and in the form of the posterior descending artery goes to the apex. Numerous branches extend from it to the anterior and posterior papillary muscles, the anterior and posterior walls of the left ventricle. One of the arteries supplying the sinoauricular node also departs from it.

The first hepatic artery begins in the anterior sinus of Vilsalva. First, it is located deep in the adipose tissue to the right of the pulmonary artery, bends around the heart along the right atrioventricular groove, passes to the posterior wall, reaches the posterior longitudinal groove, and then, in the form of a posterior descending branch, descends to the apex of the heart.

The artery gives 1-2 branches to the anterior wall of the right ventricle, partially to the anterior part of the septum, both papillary muscles of the right ventricle, the posterior wall of the right ventricle and the posterior part of the interventricular septum; a second branch also departs from it to the sinoauricular node.

There are three main types of blood supply to the myocardium: middle, left and right. This division is based mainly on variations in the blood supply to the posterior or diaphragmatic surface of the heart, since the blood supply to the anterior and lateral sections is quite stable and is not subject to significant deviations.

With the average type, all three main coronary arteries are well developed and fairly evenly developed. The blood supply to the entire left ventricle, including both papillary muscles, and the anterior 1/2 and 2/3 of the interventricular septum is carried out through the left coronary artery system. The right ventricle, including both right papillary muscles and the posterior 1/2-1/3 of the septum, receives blood from the right coronary artery. This appears to be the most common type of blood supply to the heart.

In the left type, the blood supply to the entire left ventricle and, in addition, to the entire septum and partially to the posterior wall of the right ventricle is carried out due to the developed circumflex branch of the left coronary artery, which reaches the posterior longitudinal sulcus and ends here in the form of the posterior descending artery, giving some branches to the posterior surface of the right ventricle.

The right type is observed with weak development of the circumflex branch, which either ends before reaching the obtuse margin or passes into the coronary artery of the obtuse margin without extending to the posterior surface of the left ventricle. In such cases, the right coronary artery, after the origin of the posterior descending artery, usually gives several more branches to the posterior wall of the left ventricle. In this case, the entire right ventricle, the posterior wall of the left ventricle, the posterior left papillary muscle and partly the apex of the heart receive blood from the right coronary arteriole.

The blood supply to the myocardium is carried out directly:

a) capillaries lying between the muscle fibers, entwining them and receiving blood from the coronary artery system through the arterioles;

b) a rich network of myocardial sinusoids;

c) Viessant-Tebesius vessels.

Outflow occurs through veins that collect in the coronary sinus.

Intercoronary anastomoses play an important role in coronary circulation, especially in pathological conditions. There are, firstly, anastomoses between different arteries (intercoronary or intercoronary, for example, between the right and branches of the left coronary artery, the circumflex and anterior descending arteries), and secondly, colliterals that connect the branches of the same artery and create both would be bypass paths, for example, between the branches of the anterior descending branch, extending from it at different levels.

There are more anastomoses in the hearts of people suffering from coronary artery disease, so closure of one of the coronary arteries is not always accompanied by necrosis in the myocardium. In normal hearts, anastomoses are found only in 10-20% of cases, and of small diameter. However, their number and magnitude increase not only with coronary atherosclerosis, but also with valvular heart defects. Age and gender by themselves do not have any effect on the presence and degree of development of anastomoses.

In a healthy heart, communication between the basins of various arteries occurs mainly through small-diameter arteries - arterioles and prearterioles - and the existing network of anastomoses cannot always ensure the filling of the basin of one of the arteries when a contrast mass is introduced into another. Under pathological conditions with coronary atherosclerosis, especially stenotic atherosclerosis, or after thrombosis, the network of anastomoses increases sharply and, what is especially important, their caliber becomes much larger. They are found between branches of the 4th-5th order.

ETIOLOGY AND PATHOGENESIS OF IHD

The adequacy of the coronary blood supply to the metabolic demands of the myocardium is determined by three main factors: the amount of coronary blood flow, the composition of arterial blood (primarily the degree of its oxygenation) and the myocardial oxygen demand. In turn, each of these factors depends on a number of conditions. Thus, the magnitude of coronary blood flow is determined by the level of blood pressure in the aorta and the resistance of the coronary vessels.

The blood may be less rich in oxygen, for example due to anemia. Myocardial oxygen demand can increase sharply with a significant increase in blood pressure during physical activity.

An imbalance between myocardial oxygen demand and its delivery leads to myocardial ischemia, and in more severe cases, to ischemic necrosis.

During myocardial infarction, some part of the myocardium becomes necrotic, the localization and size of which are largely determined by local factors.

The most common cause that determines the development of coronary heart disease is atherosclerosis of the coronary vessels. Atherosclerosis acts as the main cause of the development of coronary heart disease and myocardial infarction, for example, with occlusion of the coronary artery. It also plays a leading role in the most common mechanism of development of large-focal myocardial infarction - coronary artery thrombosis, which, according to modern concepts, develops both due to local changes in the intima of blood vessels, and in connection with an increased tendency to thrombus formation in general, which is observed with atherosclerosis.

Against the background of partial occlusion of the coronary artery, any cause that leads to an increase in myocardial oxygen demand can be a provoking or resolving factor. Such reasons may include, for example, physical and psycho-emotional stress, hypertensive crisis.

The functional capacity of atherosclerotic changed coronary arteries is significantly reduced not only due to a mechanical factor - narrowing of their lumen. They largely lose their adaptive capabilities, in particular to adequate expansion when blood pressure decreases or arterial hypokymia.

Serious importance in the pathogenesis of IHD is attached to the functional aspect, in particular to spasm of the coronary arteries.

The etiological factor in myocardial infarction may include septic endocarditis (embolism of the coronary arteries with thrombotic masses), systemic vascular lesions involving the coronary arteries, dissecting aortic aneurysms with compression of the mouths of the coronary arteries, and some other processes. They are rare, accounting for less than 1% of cases of acute myocardial infarction.

Of no small importance in the pathogenesis of coronary heart disease is the change in the activity of the sympatho-adrenol system. Excitation of the latter leads to increased release and accumulation of catecholamines (norepinephrine and adrenaline) in the myocardium, which, by changing the metabolism in the heart muscle, increase the heart's need for oxygen and contribute to the occurrence of acute myocardial hypoxia up to its necrosis.

In coronary vessels not affected by atherosclerosis, only excessive accumulation of catecholamines can lead to myocardial hypoxia. In the case of sclerosis of the coronary arteries, when their ability to expand is limited, hypoxia can occur with a slight excess of catecholamines.

An excess of catecholamines causes disturbances in both metabolic processes and electrolyte balance, which contributes to the development of necrotic and degenerative changes in the myocardium. Myocardial infarction is considered as a result of metabolic disorders in the heart muscle due to changes in the composition of electrolytes, hormones, toxic metabolic products, hypoxia, etc. These reasons are closely intertwined with each other.

Social issues are also of great importance in the pathogenesis of coronary heart disease.

WHO statistics indicate an extreme incidence of coronary heart disease in all countries of the world. The incidence and mortality from ischemic heart disease increases with age. When studying coronary insufficiency, a predominance of males was found, especially at the age of 55-59 years.

On March 13, 1979, WHO adopted a classification that distinguishes the following five classes, or forms, of IHD:

2. Angina pectoris

2.1. Angina pectoris

2.1.1. Newly emerging

2.1.2. Stable

2.1.3. Progressive

2.2. Angina at rest (synonym - spontaneous angina)

2.2.1. A special form of angina

3. Myocardial infarction

3.1. Acute myocardial infarction

3.1.1. Definite

3.1.2. Possible

4. Heart failure

5. Arrhythmias.

WHO expert definitions provide clarifications for each of the named classes of IHD.

1. Primary circulatory arrest

Primary circulatory arrest is a sudden failure presumed to be associated with electrical instability of the myocardium if there are no signs to make another diagnosis. Most often, sudden death is associated with the development of ventricular fibrillation. Deaths occurring in the early phase of verified myocardial infarction are not included in this class and should be considered as deaths from myocardial infarction.

If resuscitation measures were not carried out or were not effective, then primary circulatory arrest is classified as sudden death, which serves as the acute final manifestation of coronary artery disease. The diagnosis of primary circulatory arrest as a manifestation of coronary artery disease is greatly facilitated if there is a history of indications of angina pectoris or myocardial infarction. If death occurs without witnesses, the diagnosis of primary circulatory arrest remains presumptive, since death could have occurred from other causes.

2. Angina pectoris

Angina is divided into exertional and spontaneous angina.

2.1. Angina pectoris

Angina pectoris is characterized by transient attacks of pain caused by physical activity or other factors leading to an increase in myocardial oxygen demand. As a rule, the pain quickly disappears with rest or when taking nitroglycerin under the tongue. Angina pectoris is divided into three forms:

2.1.1. Angina pectoris, which occurs for the first time - duration of existence is less than a month.

New-onset angina is not homogeneous. It may be a harbinger or the first manifestation of acute myocardial infarction, may develop into stable angina or disappear (regressive angina). The prognosis is uncertain. Term<нестабильная стенокардия>many authors identify with the concept<предынфарктное состояние>, with which we cannot agree.

2.1.2. Stable exertional angina - existing for more than one month.

Stable (resistant) angina is characterized by a stereotypical reaction of the patient to the same load.

Angina is considered stable if it is observed in the patient for at least one month. In most patients, angina pectoris can be stable for many years. The prognosis is more favorable than with unstable angina.

2.1.3. Progressive angina pectoris is a sudden increase in the frequency, severity and duration of attacks of chest pain in response to stress, which previously caused pain of a familiar nature.

In patients with progressive angina, the usual pattern of pain changes. Angina attacks begin to occur in response to less stress, and the pain itself becomes more frequent, more intense and longer lasting. The addition of attacks of resting angina to attacks of exertional angina often indicates a progressive course of the disease. The prognosis is worse in those patients in whom changes during the disease are accompanied by changes in the final part of the ventricular ECG complex, which may indicate a pre-infarction state.

2.2. Spontaneous angina

Spontaneous angina is characterized by attacks of chest pain that occur without any apparent connection with factors leading to an increase in myocardial oxygen demand. The pain in these cases is usually longer and more intense than with angina pectoris. The pain is worse than the action of nitroglycerin. Enzyme activity does not increase. The ECG often shows slight transient ST segment depression or changes in T wave configuration.

Attacks of spontaneous angina can occur as a result of a primary decrease in blood flow in a certain area of ​​the coronary bed, that is, vasospasm.

Spontaneous angina can exist as an isolated syndrome or be combined with exertional angina. The frequency, duration and intensity of pain may vary from patient to patient. Sometimes attacks of chest pain may resemble myocardial infarction in duration, but the characteristic changes in ECG and enzyme activity are absent.

2.2.1. In some cases of spontaneous angina, a transient elevation of the segment is observed during attacks. This form is known as a special form of angina, which is also known as Prinzmetal's angina.

3. Myocardial infarction

3.1. Acute myocardial infarction

The clinical diagnosis of acute myocardial infarction is usually based on history, ECG changes, and serum enzyme activity tests.

A typical history is considered to be the presence of a severe and prolonged attack of chest pain. Sometimes the history is atypical, and arrhythmias and heart failure often come to the fore.

ECG changes during myocardial infarction include the formation of a pathological, persistent Q or QS wave, as well as electrocardiographic signs of damage that have characteristic dynamics over the course of one day. In these cases, the diagnosis of acute myocardial infarction can be made without additional data.

The characteristic dynamics of changes in the activity of serum enzymes or an initial increase in activity followed by a subsequent decrease should be considered pathognomonic for myocardial infarction. Increased activity of cardiac-specific isoenzymes is also a pathognomonic sign of myocardial infarction. If there is an initial increase in enzyme activity without a subsequent decline or the dynamics of enzyme activity has not been established, then the enzymatic picture is not pathognomonic for myocardial infarction.

3.1.1. Definite myocardial infarction. The diagnosis of definite myocardial infarction is made in the presence of pathognomonic ECG changes and pathognomonic changes in enzyme activity. However, the analysis may be atypical. In the presence of pathognomonic ECG changes, a definite myocardial infarction can be designated as transmural. If, in the absence of the Q wave or QS complexes, changes in the ST segment, E wave and typical changes in enzyme activity develop dynamically, the infarction is designated as non-transmural, or subendocardial.

3.1.2. Possible myocardial infarction. A diagnosis of possible myocardial infarction is made if non-pathognomonic changes in the ECG dynamics persist for more than a day, and enzyme changes are not of a typical nature or are completely absent; the medical history may be typical or atypical. These signs fit into the clinical picture of acute focal myocardial dystrophy, a diagnosis that is accepted in most domestic clinics.

Sometimes, during the period of recovery from acute myocardial infarction, patients complain of chest pain, which is combined with ECG changes, but enzyme activity does not increase. In such a case, Dressler's syndrome can be diagnosed, and in some patients - a relapse or expansion of the myocardial infarction zone. Additional research methods help clarify the diagnosis.

3.2. Previous myocardial infarction

Post-myocardial infarction is usually diagnosed on the basis of pathognomonic ECG changes in the absence of a typical history or enzymatic changes characteristic of acute myocardial infarction.

This diagnosis is completely equivalent to the diagnosis of post-infarction (focal) cardiosclerosis accepted in Russia. In patients who have previously suffered a myocardial infarction, signs of chronic cardiac aneurysm are periodically detected. If the ECG shows no signs of a previous myocardial infarction, the diagnosis of post-infarction cardiosclerosis can be made based on typical ECG changes and enzymatic changes in the past. The absence of electrocardiographic signs of a scar at the time of the study is not sufficient reason to reject the diagnosis of post-infarction cardiosclerosis.

4. HEART FAILURE IN IHD

This term to designate a separate form of IHD is not accepted in Russia, since heart failure in IHD can be based on various causes: acute myocardial infarction, post-infarction cardiosclerosis, cardiac aneurysm, as well as severe rhythm disturbances in atherosclerotic cardiosclerosis. If patients do not have clinical or electrocardiographic signs of CAD (subject to exclusion of all other causes of heart failure), the diagnosis of CAD remains doubtful.

5. ARRHYTHMIAS

We can talk about the arrhythmic variant of IHD only in cases where arrhythmias are the only symptom of IHD. In such cases, the diagnosis of coronary artery disease remains presumptive until selective coronary angiography is performed, which reveals obstructive lesions of the coronary bed.

In most patients, arrhythmias are combined with other clinical manifestations of coronary artery disease, which makes the diagnosis easier. Arrhythmias in coronary artery disease are often a symptom of atherosclerotic cardiosclerosis, especially in the presence of angina or heart failure. However, isolated rhythm and conduction disturbances are not pathognomonic signs of cardiosclerosis. The diagnosis of atherosclerotic cardiosclerosis in the absence of both arrhythmias and heart failure remains questionable.

CLINICAL PICTURE OF ANGINA IN IHD

Angina may be the only manifestation of coronary artery disease - cardiosclerosis (diffuse atherosclerotic or focal post-infarction), chronic cardiac aneurysm.

Many patients who first consulted a doctor about angina pectoris, without knowing it, had previously suffered a myocardial infarction (according to ECG data), and in some patients arrhythmia or heart failure is detected as a manifestation of coronary artery disease.

More often, patients are diagnosed with exertional angina, which occurs in response to physical or emotional stress and can be provoked by other conditions accompanied by tachycardia and increased blood pressure.

Resting angina, which occurs in the absence of obvious provoking factors, but upon closer examination turns out to be heterogeneous in origin, deserves special consideration.

Angina pectoris

Recognizing angina pectoris is a reliable way to diagnose coronary artery disease, and assessing the frequency and severity of angina attacks and their dependence on the level of physical activity allows us to assess the functional state of the coronary circulation and myocardium. Already at the outpatient stage of examining the patient, relying only on a detailed questioning about the patient’s complaints and anamnesis, without resorting to complex and expensive research methods, 60% of patients can be correctly diagnosed with IHD.

An attack of angina pectoris can manifest itself in various forms, but when analyzing the patient’s complaints and questioning, it is important to be able to identify the features that are fundamental to the diagnosis. Those features of an angina attack that are not obligatory components of the anginal syndrome, but their presence can confirm the diagnosis, may also have important diagnostic significance. And finally, features of pain sensations that are not characteristic of myocardial ischemia can be identified and help exclude the diagnosis of angina pectoris.

The nature of pain deserves special consideration. Patients describe an attack of angina as a cutting, pressing pain, as if burning the heart, squeezing the throat. However, often an anginal attack is perceived by patients not as obvious pain, but as an inexpressible discomfort, which can be characterized as heaviness, compression, tightness, compression or dull pain. If the doctor limits himself in such cases to asking whether the patient is experiencing chest pain, this important symptom may go unnoticed. Sometimes a patient with obvious angina may deny the presence of pain, which leads to a diagnostic error.

The retrosternal localization of pain with irradiation to the left shoulder and arm is the most typical. In most cases, the pain begins inside the chest behind the sternum and from there spreads in all directions. The pain often begins behind the upper part of the sternum rather than the lower part. Less commonly, it begins on the left near the sternum, in the epigastrium, in the area of ​​the left scapula or left shoulder.

The irradiation of anginal pain to the shoulder blade, neck, face, jaw, teeth, as well as to the right shoulder and right shoulder blade is well known. Rare cases of pain radiating to the left half of the lower back and the left side of the abdomen, and to the lower extremities have been described. The more severe the angina attack, the wider the area of ​​pain irradiation may be.

Although radiating pain is an important sign of angina, its presence is not necessary to make a diagnosis.

The patient's gesture is important, which can sometimes tell the doctor more than a verbal description of pain in the chest.

A reliable sign of an anginal attack is the symptom<сжатого кулака>when the patient places his fist or palm, or two palms, on his sternum to describe his sensations. If the patient is not inclined to gesture, the doctor may ask the patient to indicate the location of the pain with a gesture.

The intensity and duration of anginal pain varies markedly in different patients. They are not strictly dependent on the number of affected arteries of the heart and the degree of their damage. However, in the same patient with a stable course of the disease, angina attacks are quite comparable to each other.

The duration of an anginal attack during angina is almost always more than one minute and usually less than 15 minutes. More often an attack of angina lasts 2-5 minutes and less often lasts up to 10 minutes. The attack will be shorter and less intense if the patient immediately stops the exercise and takes nitroglycerin. Thus, if an attack of angina is caused by physical stress, its duration and intensity depend to a certain extent on the patient’s behavior. If an angina attack occurs in response to emotional stress, when the patient is unable to control the situation, the attack may be protracted and more intense than in response to physical activity.

If the patient does not take nitroglycerin, the painful attack may be prolonged. A painful attack lasting more than 15 minutes requires medical intervention. In some cases, a prolonged attack of angina may immediately precede the occurrence of acute myocardial infarction.

Pain during angina pectoris increases gradually in the form of successive, increasingly intensifying attacks of burning and compression. Having reached its climax, which is always approximately the same in intensity for a given patient, the pain quickly disappears. The duration of the period of increase in pain always significantly exceeds the duration of the period of its disappearance.

Pain, the duration of which is calculated in seconds (less than one minute), as a rule, is of non-cardiac origin. In most cases, prolonged attacks of pain that last many hours, if myocardial infarction has not developed, are not associated with damage to the large coronary arteries and have a different origin.

The most important sign of angina pectoris is the appearance of retrosternal discomfort during physical activity and the cessation of pain 1-2 minutes after the load is reduced.

In the classic description of the anginal syndrome, very short and expressive, made by Theberden more than 200 years ago, attention is drawn to the clear connection between the appearance of anginal pain and physical stress (walking uphill, especially after eating) and their disappearance when the load is stopped.

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.

Thus, the connection between the occurrence of pain and physical activity is one of the most important signs of classic angina pectoris. If pain does not occur at the height of the load, but some time after its completion, this is not typical for angina pectoris. Pain that regularly appears after exercise or after a hard day marked by physical and emotional stress is almost never associated with cardiac ischemia. An anginal attack is typically provoked in the cold or in a cold wind, which is especially often observed in the morning when leaving the house. Cooling the face stimulates vasoregulatory reflexes aimed at maintaining body temperature. These reflexes cause vasoconstriction and systemic arterial hypertension, thereby increasing myocardial oxygen consumption, which provokes an attack of angina.

In patients with changes in the psychoemotional state, angina attacks may occur with a lesser degree of damage to the coronary arteries. The frequency of angina attacks largely depends on how often the circumstances that provoke the pain are repeated. If the patient avoids exposure to factors that provoke anginal pain, then angina attacks occur less frequently. Of course, not everything is determined by the patient’s behavior. The more pronounced the pathology of the coronary arteries, the lower the threshold for pain in response to provoking factors.

An attack of angina is usually relieved by nitroglycerin. Under its influence, sensations of chest discomfort disappear completely or partially. This is an important, but not mandatory sign for diagnosis.

Another important sign of anginal syndrome is that the attack is stopped more quickly when the patient is sitting or standing. During a typical attack of angina, patients avoid lying down. In the supine position, the volume of the left ventricle and the tension of the myocardial wall increase, which leads to an increase in intraventricular pressure and an increase in oxygen consumption by the myocardium. In a sitting or standing position, the myocardial oxygen demand decreases. Autonomic symptoms can sometimes accompany an attack of angina. In these cases, there is increased breathing, pale skin, dry mouth, increased blood pressure, extrasystole, tachycardia, and the urge to urinate.

The severity of vegetative symptoms cannot serve as a criterion for the severity of anginal syndrome, since the vegetative coloring of an attack is also characteristic of cardialgia of various origins. Some authors even believe that the more severe the degree of coronary insufficiency, the more stingy the patient is with external manifestations during an attack of angina.

ANGINA AT REST

The manifestation of attacks of angina at rest in a patient who previously suffered only from exertional angina marks a transition to a more severe phase of the disease. In patients with angina at rest, who usually have severe stenosing coronary atherosclerosis, compensatory mechanisms for maintaining coronary blood supply are disrupted. As the disease progresses, a period comes when minimal stress is required for an angina attack to occur (low-tension angina) and, finally, attacks begin to occur in conditions of physical rest (in bed, in sleep, etc.). Angina at rest, joining exertional angina, is usually combined with it. During the day, such a patient experiences attacks of angina pectoris associated with walking or other physical activity, and at night attacks of angina pectoris at rest may occur.

In some patients, attacks of resting angina may occur as a result of a primary decrease in blood flow through a large coronary artery, as a consequence of an increase in its vasomotor tone (i.e., as a result of vasospasm). In a number of patients in this group, attacks of angina at rest can be combined with a relatively high tolerance to physical activity, and sometimes they can be isolated, that is, observed in the absence of attacks of angina pectoris.

The factors that provoke attacks of angina at rest are diverse. In most cases, the onset of an attack is preceded by conditions that increase the myocardial oxygen demand. The cause of an attack of angina at rest may be a transistor increase in blood pressure or an attack of paroxysmal tachycardia.

Attacks of angina at rest often occur at night during sleep. The patient wakes up from the feeling that someone is preventing him from breathing, or due to pain in the heart area. Sometimes the patient reports that in the dream he had to perform heavy physical activity (lifting weights, running fast).

The intensity and duration of pain with angina at rest is much greater than with angina on exertion. Attacks may be accompanied by fear of death and pronounced vegetative reactions. These attacks force patients to wake up, sit up in bed, and take nitroglycerin. An attack of angina occurs during the so-called rapid phase of sleep. More often, angina attacks of this origin occur in the early morning hours. The administration of beta-blockers to such patients appears to be effective.

In a number of patients, angina at rest occurs due to left ventricular failure, which intensifies in the horizontal position of the patient. In the supine position of the patient, the volume of the left ventricle increases, which leads to an increase in myocardial tension. This increases the myocardium's need for oxygen. This type of angina usually occurs in patients with a marked decrease in myocardial function.

In the pathogenesis of nocturnal angina attacks in these patients, water-electrolyte balance disorders are of particular importance.

The administration of diuretics and cardiac glycosides can have a good therapeutic effect in this type of angina, helping to prevent attacks. The attack itself can be stopped by the patient moving to a sitting position, as well as by taking nitroglycerin, which, being a powerful, fast-acting vasodilator, promotes blood redistribution and unloading of the pulmonary circulation.

SPECIAL FORM OF ANGINA

A number of patients may have a special form of angina (variant angina, Prinzmetal type angina). Named after the clinician who was one of the first to describe it as an independent form of angina in 1959.

A special form of angina (Prinzmetal type) is characterized by attacks of anginal pain that occur at rest, which are accompanied by transient electrocardiographic signs of damage to the subepicardial parts of the myocardium.

In the pathogenesis of Prinzmetal's angina, the periodically occurring spasm of the coronary arteries of the heart is of decisive importance. Angiospasm can occur in patients with both unchanged and slightly changed coronary arteries, and with a widespread stenotic process in the coronary arteries.

The anatomical state of the coronary bed largely determines the nature of clinical manifestations in a particular form of angina. We can distinguish three groups of patients with a special form of angina (Prinzmetal type), in whom spasm occurs:

1) in a normal or slightly changed coronary artery;

2) in a single coronary artery affected by atherosclerosis;

3) against the background of widespread atherosclerosis of the coronary arteries.

The nature and location of chest pain differs little from the pain associated with ordinary angina. An attack usually occurs at rest or during the patient’s normal physical activity. In approximately half of patients, Prinzmetal's angina develops without warning. One of the signs of a special form of angina is the cyclical nature of pain.

A special form of angina pectoris often occurs in the form of series consisting of 2-5 painful attacks, which follow one after another at intervals of 2-3 to 10-15 minutes. In some patients, attacks may have a shorter or longer duration. The maximum duration of an attack can reach 45 minutes. A prolonged attack of a special form of angina is usually regarded by doctors as a threatening myocardial infarction and serves as a basis for hospitalization. The period of pain increase in a special form of angina is approximately equal to the period of its disappearance, whereas in ordinary angina the first period is noticeably longer than the second.

The most important diagnostic sign of Prinzmetal's angina is the elevation of the ST segment of the ECG at the time of a painful attack, which indicates ischemia of not only the subendocardial, but also the subepicardial layer of the myocardium. The severity of ECG changes varies from a slight upward shift of the ST segment by 2 mm to a sharp rise of 20-30 mm, as a result of which the ECG curve becomes monophasic. ST segment elevation is recorded more often within 10-20 minutes, after which it reaches the isoelectric level.

A special form of angina does not include prolonged elevations of the ST segment, which are one of the phases in the evolution of the electrocardiographic picture of acute myocardial infarction.

Depending on the location of the spasm in the coronary artery, in some patients a sign of a special form of angina may be transient depression of the ST segment, which requires special evidence in each individual case. At the time of the attack, other less specific ECG changes of a transient nature are also possible, in particular - an increase in the voltage of the waves and the widening of the R wave, the transient appearance of the Q wave and a short-term sharpening of the T wave. In approximately half of patients with a special form of angina, various transient disturbances of heart rhythm are recorded: extrasystole , paroxysmal tachycardia.

Cases of clinical death caused by ventricular fibrillation have been described. ECG changes more often correspond to the anterior localization of myocardial damage, less often lesions of the posteroinferior or lateral are detected.

In most patients, the localization of ECG changes corresponds to the localization of the coronary arteries supplying blood to this area of ​​the myocardium. This pattern is especially clear when one coronary artery is affected. Between attacks, the ECG may be normal or altered.

The resting ECG outside an attack is normal, as a rule, in patients with unchanged or slightly changed coronary arteries. ECG abnormalities in the interictal period are detected more often, the greater the prevalence of coronary arteriosclerosis. With stenosis of several branches of the coronary arteries, resting ECG changes are found in 90% of patients.

A patient suffering from a special form of angina can tolerate physical activity well and feel healthy throughout the day. The results of an electrocardiographic exercise test may be negative. Good tolerance to physical activity and a negative bicycle ergometer test do not provide grounds to exclude the diagnosis of a special form of angina, but suggest that the patient’s coronary arteries are either unchanged or have a single local stenosis.

In the diagnosis of a special form of angina, urgent registration of an ECG immediately at the time of an attack of resting angina is of great importance. Identification of specific ECG changes provides important prerequisites for the diagnosis of angina pectoris of this form. In patients with typical attacks of Prinzmetal's angina, accompanied by characteristic ECG changes, transient elevations of the ST segment may be observed, not accompanied by pain.

Not every attack of chest pain with a special form of angina is a manifestation of the underlying disease. Registration of a daily ECG in these cases has differential diagnostic value. In patients with multiple spontaneous attacks of Prinzmetal's angina during the day, most attacks may not be accompanied by pain, but are manifested only by transient ischemic ECG changes. Diagnosis of a special form of angina is of great practical importance, as it allows the application of pathogenetic treatment and determination of the prognosis. The appearance of attacks of a special form of angina pectoris against the background of angina pectoris has an unfavorable prognostic value.

Prinzmetal's angina, which develops against the background of severe damage to the coronary arteries, often leads to the development of myocardial infarction or death associated with severe cardiac arrhythmias, in particular, paroxysmal ventricular tachycardia.

Patients with a special form of angina require inpatient monitoring and treatment. Relapses of a particular form of angina have an unfavorable prognostic value.