A patient suffering from chronic ischemic heart disease. I25 Chronic ischemic heart disease. Symptoms of chronic ischemic heart disease

Ischemic (coronary) heart disease (CHD) due to atherosclerosis coronary arteries, is the leading cause of disability and death among the working-age population worldwide. In Russia, the prevalence cardiovascular disease and coronary artery disease is growing, and in terms of mortality from them, our country is one of the first places in the world, which necessitates the use of modern and effective methods of their treatment and prevention by doctors. Among the population of Russia, a high prevalence of the main risk factors for the development of coronary artery disease remains, of which smoking, arterial hypertension, and hypercholesterolemia are of the greatest importance.

Atherosclerosis is main reason development of IHD. It proceeds secretly for a long time until it leads to complications such as myocardial infarction, cerebral stroke, sudden death, or to the appearance of angina pectoris, chronic cerebrovascular insufficiency, and intermittent claudication. Atherosclerosis leads to gradual local stenosis of the coronary, cerebral and other arteries due to the formation and growth of atherosclerotic plaques in them. In addition, such factors as endothelial dysfunction, regional spasms, microcirculation disorders, as well as the presence of a primary inflammatory process in the vascular wall such as possible factor formation of thrombosis. An imbalance of vasodilatory and vasoconstrictor stimuli can also significantly change the state of coronary artery tone, creating an additional dynamic stenosis to the already existing fixed one.

The development of stable angina can be predictable, for example, in the presence of factors that cause an increase in myocardial oxygen demand, such as physical or emotional stress (stress).

Patients with angina pectoris, including those who have already had a myocardial infarction, constitute the largest group patients with coronary artery disease. This explains the interest of practitioners in the proper management of patients with angina pectoris and the choice best practices treatment.

Clinical forms of coronary artery disease. IHD manifests itself in many clinical forms: chronic stable angina, unstable (progressive) angina, asymptomatic coronary artery disease, vasospastic angina, myocardial infarction, heart failure, sudden death. Transient myocardial ischemia, usually resulting from narrowing of the coronary arteries and increased oxygen demand, is the main mechanism for the onset of stable angina.

Chronic stable angina is usually divided into 4 functional classes according to the severity of symptoms (Canadian classification).

The main goals of treatment are to improve the patient's quality of life by reducing the frequency of angina attacks, preventing acute myocardial infarction, and improving survival. Successful antianginal treatment is considered in the case of complete or almost complete elimination of angina attacks and the return of the patient to normal activity (angina pectoris is not higher than functional class I, when pain attacks occur only with significant stress) and with minimal side effects of therapy.

In the treatment of chronic coronary artery disease, 3 main groups of drugs are used: β-blockers, calcium antagonists, organic nitrates, which significantly reduce the number of angina attacks, reduce the need for nitroglycerin, increase exercise tolerance and improve the quality of life of patients.

However, practitioners are still reluctant to prescribe new effective drugs in sufficient doses. In addition, in the presence of a large selection of modern antianginal and anti-ischemic drugs, obsolete, insufficiently effective ones should be excluded. A frank conversation with the patient, an explanation of the cause of the disease and its complications, the need for additional non-invasive and invasive methods research.

According to the results of the ATP-survey study (Angina Treatment Patterns), in Russia, when choosing antianginal drugs with a hemodynamic mechanism of action in monotherapy mode, preference is given to nitrates (11.9%), then b-blockers (7.8%) and calcium antagonists (2 .7%).

β-blockers are the drugs of first choice for the treatment of patients with angina, especially in patients who have had myocardial infarction, as they lead to a decrease in mortality and the incidence of re-infarction. The drugs of this group have been used in the treatment of patients with coronary artery disease for more than 40 years.

β-blockers cause an antianginal effect by reducing myocardial oxygen demand (due to a decrease in heart rate, lowering blood pressure and myocardial contractility), increasing oxygen delivery to the myocardium (due to increased collateral blood flow, its redistribution in favor of ischemic layers of the myocardium - subendocardium ), antiarrhythmic and antiaggregatory action, reducing the accumulation of calcium in ischemic cardiomyocytes.

Indications for the use of β-blockers are the presence of angina pectoris, angina pectoris with concomitant arterial hypertension, concomitant heart failure, "silent" myocardial ischemia, myocardial ischemia with concomitant arrhythmias. In the absence of direct contraindications, β-blockers are prescribed to all patients with coronary artery disease, especially after myocardial infarction. The goal of therapy is to improve distant forecast a patient with IBS.

Among β-blockers propranolol (80-320 mg/day), atenolol (25-100 mg/day), metoprolol (50-200 mg/day), carvedilol (25-50 mg/day), bisoprolol (5 - 20 mg/day), nebivolol (5 mg/day). Drugs with cardioselectivity (atenolol, metoprolol, betaxolol) have a predominantly blocking effect on β 1 -adrenergic receptors.

One of the most widely used cardioselective drugs is atenolol (tenormin). The initial dose is 50 mg / day. In the future, it can be increased to 200 mg / day. The drug is prescribed once in the morning. With severe renal impairment, the daily dose should be reduced.

Another cardioselective β-blocker is metoprolol (Betaloc). Its daily dose averages 100-300 mg, the drug is prescribed in 2 doses, since the β-blocking effect can be traced up to 12 hours. At present, prolonged metoprolol preparations - betalok ZOK, metocard, the duration of the effect of which reaches 24 hours.

Bisoprolol (Concor) in comparison with atenolol and metoprolol has a more pronounced cardioselectivity (in therapeutic doses it blocks only β 1 -adrenergic receptors) and a longer duration of action. It is used once a day at a dose of 2.5-20 mg.

Carvedilol (Dilatrend) has a combined non-selective β-, α 1 -blocking and antioxidant effect. The drug blocks both β 1 - and β 2 -adrenergic receptors, without its own sympathomimetic activity. Due to the blockade of α 1 -adrenergic receptors located in the smooth muscle cells of the vascular wall, carvedilol causes pronounced vasodilation. Thus, it combines β-adrenergic blocking and vasodilatory activity, which is mainly due to its antianginal and anti-ischemic effect, which persists with long-term use. Carvedilol also has hypotensive action and inhibits the proliferation of smooth muscle cells, which plays a proatherogenic role. The drug is able to reduce the viscosity of blood plasma, aggregation of red blood cells and platelets. In patients with impaired left ventricular (LV) function or circulatory failure, carvedilol favorably affects hemodynamic parameters (reduces pre- and afterload), increases ejection fraction and reduces LV size. Thus, the appointment of carvedilol is indicated primarily for patients with coronary heart disease, myocardial infarction, with heart failure, since in this group of patients its ability to significantly improve the prognosis of the disease and increase life expectancy has been proven. When comparing carvedilol (mean daily dose 20.5 mg) and atenolol (mean daily dose 25.9 mg), it was shown that both drugs, administered 2 times a day, are equally effective in the treatment of patients with stable exertional angina. One of the guidelines for the adequacy of the used dose of β-blockers is the reduction in heart rate at rest to 55-60 beats / min. In some cases, in patients with severe angina, resting heart rate may be reduced to less than 50 beats / min.

Nebivolol (nebilet) is a new selective β 1 -blocker that also stimulates the synthesis of nitric oxide (NO). The drug causes hemodynamic unloading of the heart: reduces blood pressure, pre- and afterload, increases cardiac output increases peripheral blood flow. Nebivolol is a b-blocker with unique properties, which lie in the ability of the drug to participate in the process of synthesis of the relaxing factor (NO) by endothelial cells. This property gives the drug an additional vasodilating effect. The drug is used primarily in patients with arterial hypertension with angina attacks.

Celiprolol (200-600 mg/day), a third-generation β-blocker, differs from other β-blockers in its high selectivity, moderate stimulation of β2-adrenergic receptors, direct vasodilatory effect on blood vessels, modulation of nitric oxide release from endothelial cells, and the absence of adverse metabolic effects . The drug is recommended for patients with coronary artery disease with chronic obstructive pulmonary disease, dyslipidemia, diabetes mellitus, peripheral vascular disease caused by tobacco smoking. Celiprolol (200-600 mg/day), atenolol (50-100 mg/day), propranolol (80-320 mg/day) have comparable antianginal efficacy and equally increase exercise tolerance in patients with stable exertional angina.

β-blockers should be given preference, appointing patients with coronary artery disease in the presence of a clear relationship between physical activity and the development of an angina attack, with concomitant arterial hypertension; the presence of rhythm disturbances (supraventricular or ventricular arrhythmias), with myocardial infarction myocardium, expressed state of anxiety. Most of the adverse effects of β-blockers are associated with the blockade of β 2 receptors. The need to control the appointment of β-blockers and the side effects that occur (bradycardia, hypotension, bronchospasm, increased signs of heart failure, heart block, sick sinus syndrome, fatigue, insomnia) lead to the fact that the doctor does not always use these drugs. The main medical errors in the appointment of β-blockers are the use of small doses of drugs, their appointment less often than necessary, and the abolition of drugs when heart rate at rest is less than 60 beats / min. It should also be borne in mind the possibility of developing a withdrawal syndrome, and therefore β-blockers must be canceled gradually.

Calcium channel blockers (calcium antagonists). The main point of application of drugs of this group at the cell level are slow calcium channels, through which calcium ions pass into the smooth muscle cells of blood vessels and the heart. In the presence of calcium ions, actin and myosin interact, providing contractility of the myocardium and smooth muscle cells. In addition, calcium channels are involved in the generation of pacemaker activity of the cells of the sinus node and the conduction of an impulse along the atrioventricular node.

It has been established that the vasodilating effect caused by calcium antagonists is carried out not only through a direct effect on smooth muscle vascular wall, but also indirectly, through potentiation of the release of nitric oxide from the vascular endothelium. This phenomenon has been described for most dihydropyridines and isradipine, and to a lesser extent for nifedipine and non-hydropyridine drugs. For long-term treatment of angina from dihydropyridine derivatives, it is recommended to use only prolonged dosage forms or long-acting generation of calcium antagonists. Calcium channel blockers are powerful vasodilators, they reduce myocardial oxygen demand, dilate the coronary arteries. The drugs can be used for vasospastic angina, concomitant obstructive lung diseases. An additional indication for the appointment of calcium antagonists are Raynaud's syndrome, as well as (for phenylalkylamines - verapamil and benzodiazepines - diltiazem) atrial fibrillation, supraventricular tachycardia, hypertrophic cardiomyopathy. Of the calcium antagonists in the treatment of coronary artery disease, the following are used: nifedipine of immediate action 30-60 mg / day (10-20 mg 3 times) or prolonged action (30-180 mg once); verapamil immediate action (80-160 mg 3 times a day); or prolonged action (120-480 mg once); diltiazem immediate action (30-60 mg 4 times a day) or prolonged action (120-300 mg / day once); long-acting drugs amlodipine (5-10 mg / day once), lacidipine (2-4 mg / day).

Activation of the sympathoadrenal system by dihydropyridines (nifedipine, amlodipine) is currently regarded as an undesirable phenomenon and is considered the main cause of some increase in mortality in patients with coronary artery disease when taking short-acting dihydropyridines for unstable angina, acute myocardial infarction and, apparently, with their long-term use by patients with stable angina pectoris . In this regard, it is currently recommended to use retard and prolonged forms of dihydropyridines. They do not have fundamental differences in the nature of the pharmacodynamic action with short-acting drugs. Due to the gradual absorption, they are deprived of a number side effects associated with sympathetic activation, so characteristic of short-acting dihydropyridines.

In recent years, data have appeared indicating the possibility of slowing down the damage to the vascular wall with the help of calcium antagonists, especially in the early stages of atherosclerosis.

Amlodipine (norvasc, amlovas, normodipine) is a third-generation calcium antagonist from the group of dihydropyridines. Amlodipine dilates peripheral vessels, reduces afterload of the heart. Due to the fact that the drug does not cause reflex tachycardia (since there is no activation of the sympathoadrenal system), energy consumption and myocardial oxygen demand are reduced. The drug expands the coronary arteries and enhances the supply of oxygen to the myocardium. Antianginal effect (reducing the frequency and duration of angina attacks, daily requirement in nitroglycerin), increased exercise tolerance, improved systolic and diastolic function of the heart in the absence of a depressant effect on the sinus and atrioventricular node and other elements of the cardiac conduction system put the drug in one of the first places in the treatment of angina pectoris.

Lacidipine is a third-generation calcium antagonist drug with high lipophilicity, interaction with the cell membrane, and independence of tissue effects from its concentration. These factors are leading in the mechanism of anti-atherosclerotic action. Lacidipine has a positive effect on the endothelium, inhibits the formation of adhesion molecules, the proliferation of smooth muscle cells and platelet aggregation. In addition, the drug is able to inhibit peroxidation of low-density lipoproteins, i.e., it can affect one of the early stages of plaque formation.

In the European study of the effect of lacidipine on atherosclerosis (European Lacidipine Study on Atherosclerosis, ELSA), the carotid intima-media thickness was compared in 2334 patients with arterial hypertension during 4 years of therapy with lacidipine or atenolol. In the patients included in the study, the carotid arteries were initially normal and/or altered. Treatment with lacidipine was accompanied by a significantly more pronounced decrease in the thickness of the "intima-media" in comparison with atenolol, both at the level of the bifurcation and the common carotid artery. During treatment with lacidipine compared with atenolol, the increase in the number of atherosclerotic plaques in patients was 18% less, and the number of patients in whom the number of plaques decreased was 31% more.

Thus, calcium antagonists, along with pronounced antianginal (anti-ischemic) properties, can have an additional anti-atherogenic effect (stabilization of the plasma membrane, which prevents the penetration of free cholesterol into the vessel wall), which allows them to be prescribed more often to patients with stable angina pectoris with damage to arteries of different localization. Currently, calcium antagonists are considered second-line drugs in patients with exertional angina, following β-blockers. As monotherapy, they can achieve the same pronounced antianginal effect as β-blockers. The undoubted advantage of β-blockers over calcium antagonists is their ability to reduce mortality in patients with myocardial infarction. Studies of the use of calcium antagonists after myocardial infarction have shown that the greatest effect is achieved in individuals without severe left ventricular dysfunction, suffering from arterial hypertension, who have had myocardial infarction without a Q wave.

Thus, the undoubted advantage of calcium antagonists is wide range pharmacological effects aimed at eliminating the manifestations of coronary insufficiency: antianginal, hypotensive, antiarrhythmic. Therapy with these drugs also favorably affects the course of atherosclerosis.

organic nitrates. The anti-ischemic effect of nitrates is based on a significant change in hemodynamic parameters: a decrease in pre- and afterload of the left ventricle, a decrease in vascular resistance, including coronary arteries, a decrease in blood pressure, etc. The main indications for taking nitrates are angina pectoris of exertion and rest in patients with IHD (also in in order to prevent them), attacks of vasospastic angina pectoris, attacks of angina pectoris, accompanied by manifestations of left ventricular failure.

Sublingual nitroglycerin (0.3-0.6 mg) or nitroglycerin aerosol (nitromint 0.4 mg) are intended for the relief of acute angina attacks due to the rapid onset of action. If nitroglycerin is poorly tolerated, nitrosorbide, molsidomine, or the calcium antagonist nifedipine can be used to relieve an angina attack, chewing or sucking tablets when taken under the tongue.

Organic nitrates (drugs of isosorbide dinitrate or isosorbide-5-mononitrate) are used to prevent angina attacks. These drugs provide long-term hemodynamic unloading of the heart, improve blood supply to ischemic areas and increase physical performance. They are tried to be prescribed before physical exertion that causes angina pectoris. Of the drugs with proven efficacy, the most studied are kardiket (20, 40, 60 and 120 mg/day), nitrosorbide (40-80 mg/day), olicard retard (40 mg/day), monomac (20-80 mg/day ), Mono Mac Depot (50 and 100 mg/day), Efox Long (50 mg/day), Mono Cinque Retard (50 mg/day). Patients with stable angina pectoris I-II FC may intermittent administration of nitrates before situations that can cause an angina attack. Patients with a more severe course of angina pectoris III-IV FC nitrates should be prescribed regularly; in such patients, one should strive to maintain the effect throughout the day. With angina pectoris IV FC (when angina attacks can occur at night), nitrates should be prescribed in such a way as to ensure an effect throughout the day.

Nitrate-like drugs include molsidomine (Corvaton, Sydnopharm, Dilasid), a drug that is different from nitrates in terms of chemical structure, but no different from them in terms of the mechanism of action. The drug reduces vascular wall tension, improves collateral circulation in the myocardium, and has antiaggregatory properties. Comparable doses of isosorbide dinitrate and corvatone are 10 mg and 2 mg, respectively. The effect of Korvaton appears after 15-20 minutes, the duration of action is from 1 to 6 hours (average 4 hours). Corvaton retard 8 mg is taken 1-2 times a day, since the effect of the drug lasts more than 12 hours.

The weak side of nitrates is the development of tolerance to them, especially with prolonged use, and side effects that make it difficult to use them (headache, palpitations, dizziness) caused by reflex sinus tachycardia. Transdermal forms of nitrates in the form of ointments, patches and discs, due to the difficulty of their dosing and the development of tolerance to them, have not been found. wide application. It is also not known whether nitrates improve the prognosis of a patient with stable angina with long-term use, making it questionable whether they are useful in the absence of angina (myocardial ischemia).

When prescribing drugs with a hemodynamic mechanism of action to elderly patients, the following rules should be observed: start treatment with lower doses, carefully monitor unwanted effects and always consider changing the drug if it is poorly tolerated and does not work well.

Combination Therapy. Combined therapy with antianginal drugs in patients with stable angina pectoris III-IV FC is carried out according to the following indications: the impossibility of selecting effective monotherapy; the need to enhance the effect of ongoing monotherapy (for example, during a period of increased physical activity of the patient); correction of adverse hemodynamic changes (for example, tachycardia caused by nitrates or calcium antagonists from the group of dihydropyridines); with a combination of angina pectoris with arterial hypertension or cardiac arrhythmias that are not compensated in cases of monotherapy; in case of intolerance to patients of conventional doses of drugs in monotherapy, while small doses of drugs can be combined to achieve the desired effect.

The synergy of the mechanisms of action of different classes of antianginal drugs is the basis for assessing the prospects of their combinations. When treating a patient with stable angina, doctors often use various combinations of antianginal agents (β-blockers, nitrates, calcium antagonists). In the absence of the effect of monotherapy, combination therapy is often prescribed (nitrates and β-blockers; β-blockers and calcium antagonists, etc.).

The results of the ATP-survey study (a review of the treatment of stable angina pectoris) showed that in Russia 76% of patients receive combination therapy with hemodynamically active drugs, while in more than 40% of cases - a combination of nitrates and b-blockers. However, their additive effects have not been confirmed in all studies. The guidelines of the European Society of Cardiology (1997) indicate that if one antianginal drug is ineffective, it is better to first evaluate the effect of another, and only then use the combination. The results of pharmacologically controlled studies do not confirm that combination therapy with a b-blocker and a calcium antagonist is accompanied by a positive additive and synergistic effect in the majority of patients with coronary artery disease. Prescribing 2 or 3 drugs in combination is not always more effective than therapy with one drug in an optimally selected dose. We must not forget that the use of several drugs significantly increases the risk of adverse events associated with effects on hemodynamics.

The modern approach to the combination therapy of patients with stable angina pectoris implies the advantage of combining antianginal drugs with multidirectional action: hemodynamic and cytoprotective.

The main disadvantages of the domestic pharmacotherapy of stable angina pectoris include the often erroneous, according to modern concepts, choice of a group of antianginal drugs (nitrates are usually prescribed (in 80%)), the frequent use of clinically insignificant dosages and the unjustified prescription of combination therapy with a large number of antianginal drugs.

metabolic agents. Trimetazidine (preductal) causes inhibition of fatty acid oxidation (by blocking the enzyme 3-ketoacyl-coenzyme A-thiolase) and stimulates pyruvate oxidation, i.e., switches myocardial energy metabolism to glucose utilization. The drug protects myocardial cells from the adverse effects of ischemia, while reducing intracellular acidosis, metabolic disorders and damage to cell membranes. A single dose of trimetazidine is not able to stop or prevent the onset of an angina attack. Its effects are observed mainly during combination therapy with other antianginal drugs or during course treatment. Preductal is effective and well tolerated, especially in high risk groups for coronary events such as diabetics, the elderly, and those with left ventricular dysfunction.

The combination of preductal with propranolol was significantly more effective than the combination of this β-blocker with nitrate. Trimetazidine (preductal 60 mg/day), preductal MB (70 mg/day) have an anti-ischemic effect, but more often they are used in combination with the main hemodynamic antianginal drugs.

In Russia, a multicenter, simple, blind, randomized, placebo-controlled, parallel-group study of TACT (Trimetazidin in patients with Angina in Combination Therapy) was conducted, covering 177 patients with angina pectoris II-III FC, partially stopped by nitrates and β-blockers in order to evaluate the effectiveness of preductal in combination therapy with nitrates or β-blockers. Evaluation of the effectiveness of treatment was carried out according to the following criteria: time to 1 mm ST segment depression during exercise tests, time of onset of angina pectoris, increase in exercise duration. It was found that preductal significantly increased these indicators. There are a number of clinical situations in which trimetazidine, apparently, can be the drug of choice in elderly patients, with circulatory failure of ischemic origin, sick sinus syndrome, with intolerance to antianginal drugs of the main classes, as well as with restrictions or contraindications to their appointment. .

Among the drugs with antianginal properties are amiodarone and other "metabolic" drugs (ranolazine, L-arginine), as well as ACE inhibitors, selective heart rate inhibitors (ivabradine, procolaran). They are used mainly as adjuvant therapy, prescribed in addition to the main antianginal drugs.

The problem of drug treatment of patients with coronary artery disease is the lack of adherence of patients to the chosen therapy and their insufficient willingness to consistently change their lifestyle. With drug treatment, proper regular contact between the doctor and the patient is necessary, informing the patient about the nature of the disease and the benefits of prescribed drugs to improve the prognosis. Trying to influence the prognosis of the life of patients with the help of drug therapy, the doctor must be sure that the drugs prescribed by him are actually taken by the patient, and in appropriate doses and according to the recommended treatment regimen.

Surgery. With the ineffectiveness of drug therapy, surgical methods of treatment (myocardial revascularization procedures) are used, which include: percutaneous transluminal coronary angioplasty, implantation of coronary stents, coronary artery bypass surgery. In patients with coronary artery disease, it is important to determine the individual risk based on clinical and instrumental parameters, which depends on the respective clinical stage illness and treatment. Thus, the maximum efficiency of coronary artery bypass grafting was noted in patients with the highest preoperative risk of developing cardiovascular complications (with severe angina pectoris and ischemia, extensive lesions of the coronary arteries, and LV dysfunction). With a low risk of developing complications of coronary artery disease (lesion of one artery, absence or slightly pronounced ischemia, normal function LV) surgical revascularization is usually not indicated until the failure of medical therapy or coronary angioplasty has been established. When considering the use of coronary angioplasty or coronary artery bypass grafting for the treatment of patients with lesions of multiple coronary arteries, the choice of method depends on the anatomical features of the coronary bed, LV function, the need to achieve complete myocardial revascularization and patient preferences.

Thus, with the current methods of combating cardiovascular diseases (table), it is important for a doctor to be aware of the latest advances in medicine and make the right choice of treatment method.

For literature inquiries, please contact the editor.

D. M. Aronov, doctor medical sciences, Professor V. P. Lupanov, Doctor of Medical Sciences, State Research Center for Preventive Medicine of the Ministry of Health of the Russian Federation, Institute of Clinical Cardiology named after A.I. A. L. Myasnikov Russian Cardiological Research and Production Complex of the Ministry of Health of the Russian Federation, Moscow

IHD is a serious problem facing many people. Stress, malnutrition, too high a rhythm of life in big cities - all this contributes to the development of coronary artery disease.

Chronic ischemia develops with a small supply of oxygen to the myocardium through the arteries, which are clogged with cholesterol plaques. There is insufficient blood supply to various parts of the heart. IBS is subdivided as:

• acute;
• chronic.

Causes of chronic ischemic heart disease

All doctors consider atherosclerosis to be the main cause of heart disease. It is manifested by the presence of protein and fatty deposits inside the vessels, which narrow the lumen of the artery by more than 70% and do not allow blood to pass to the heart in the required volume.

The risk of atherosclerosis increases in the presence of the following factors:

• High Cholesterol: There is an imbalance between good and bad cholesterol called dyslipidemia. All this is due to unhealthy nutrition: the predominance of fatty foods and quickly digestible carbohydrates.
• Age: if the formation of atherosclerosis in CIHD can begin at a young age, over the years this process only worsens, forming irreversible changes on the walls of blood vessels. The critical age is considered to be from 50 to 65 years.
• Hypodynamia: weak physical activity, unwillingness to play sports with moderate loads.
• concomitant diseases: Such diseases are diabetes mellitus, in which the elasticity of blood vessels is lost; obesity puts even more strain on the heart and other organs; hypothyroidism - insufficient production of thyroid hormones.
• Hypertension: increases the load on the blood vessels.
• Heredity: there is a predisposition associated with heart disease.
• Gender: men are more likely to suffer; in women, chronic ischemia is associated with menopause.
• Stress: a recognized fact that aggravates the work of the whole organism.

Important: Atherosclerosis of the arteries can occur due to aggression or anxiety. It is better not to conflict with others, to be calm, to restrain your emotions.

Also to the reasons chronic ischemia can be attributed to a violation of blood microcirculation in the myocardium and its high coagulability. The latter reason increases the risk of blood clots.

Chronic forms of coronary artery disease

Chronic ischemic heart disease manifests itself in the following chronic forms of coronary artery disease, which exist as independent diseases:

• Angina: subdivided into stable and unstable. Stable exertional angina is characterized by chest pain with increasing physical and emotional stress, which subsides with their decrease. Unstable angina does not depend on the activity of the body, it occurs suddenly and for a longer time. It can turn into a heart attack.
• Focal ischemic myocardial dystrophy: occurs with ischemia lasting more than 20 minutes.
• Myocardial infarction: characterized by the death of a section of the heart muscle due to an acute violation of the blood supply.
• Cardiosclerosis: a disease of the heart characterized by the replacement of connective tissue, scar tissue of the heart muscle, resulting in deformity of the heart valve.
• Arrhythmia: Manifested as a heart rhythm disorder: too fast or too slow, irregular heartbeat.
• Heart failure: manifested in the inability of the heart to pump the amount of blood necessary for normal operation the whole organism. To replenish the required volume, pumping occurs when high pressure which further wears out the heart.
• Sudden death: complete cessation of the activity of the heart. Accompanied by loss of consciousness, dilated pupils, disappearance of the pulse.

Symptoms of chronic ischemic heart disease

The chronic form of coronary artery disease is characterized by an increase in symptoms. At first they appear rarely and quickly disappear. Over time, the heart wears out, multiple side diseases join this, and the manifestation of symptoms intensifies. They become more frequent and last longer.

Main symptoms:

• Pain in the region of the heart is pressing, squeezing, burning with varying frequency. Lasts from 30 seconds to 15 minutes. At the beginning of the development of the disease, it is quickly removed with nitroglycerin tablets.
• Atypical pains can be manifested by dizziness, heartburn, pain in the epigastric region, numbness of the hand.
• Shortness of breath and swelling of the legs: due to the lack of oxygen supplied through the blood to the organs, including the lungs, there is strained breathing.
• An irregular heart rhythm manifests itself either as tachycardia - a rapid heartbeat, or as bradycardia - a slow heartbeat. Often there is an arrhythmia - an irregular beat, sometimes fast, sometimes slow.
• Tiredness and fatigue typical signs for all diseases of the heart, the patient feels sudden fatigue, weakness in the legs.
• Attacks of anxiety and fears for no apparent reason. Another typical symptom for patients suffering from ischemia of the heart.

Treatment

The treatment of coronary artery disease is based on the elimination of the risk factor and pain relief. Treatment is divided into the following types:

• medication;
• non-drug;
• surgical.

Medical treatment

To date, there is no such drug that could reverse the disease of chronic ischemia. With the right treatment, it is possible to slow down the development of the disease.

Cholesterol-lowering drugs (statins). Aimed at lowering cholesterol levels and reducing risks for the work of the heart. affect lipid metabolism. Drugs of this pharmacological group: Atorvastatin, Lovastatin, Pravastatin.

Blood thinners. Drugs that affect blood clotting, contribute to its thinning, slow down platelet aggregation. When giving such drugs, it is necessary to control the INR indicator so that the patient does not experience internal bleeding. Antiplatelet drugs and anticoagulants include: Aspirin, Warfarin, Plavix, Heparin.

Blockers. The most common remedy prescribed for HIBS. Slows down the heartbeat, it becomes less need for oxygen and blood supply. These drugs are contraindicated in bronchial asthma. The drugs in this group include: Biprolol, Visken, Atenolol.

Nitrates. They affect smooth muscles in the walls of blood vessels, help to increase the lumen, which relieves chronic ischemia. Dinisorb, Isoket - drugs of this group.

Calcium channel blockers. These drugs reduce the frequency of seizures and improve exercise tolerance. Side effects are often severe headaches. Drugs belonging to this group: Verapamil, Nifedipine, Amlodipine.

Diuretics. Assign to remove fluid from the body, help lower blood pressure. This reduces the workload on the heart. Diuretics include: Furosemide, Hypotheazid.

Non-drug treatment

Non-drug treatment of chronic ischemia is based on changing the lifestyle and quality of life, the need to minimize the causes that affect further development chronic ischemic heart disease:

• adherence to a healthy diet: do not eat fatty, fried, smoked foods, try to give up salt;
• give up bad habits: alcohol, smoking;
• increased physical activity, reasonable hardening, the fight against excess weight.

Surgical treatments

They should be aimed at increasing the lumen of the arteries, which are closed by atherosclerotic plaques. This method is used only when drug therapy fails. There are several ways to restore the lumen:

• Stenting: A stent, a metal tube, is inserted into an artery to restore the lumen. The operation is performed by inserting a stent through a vein.
• Coronary artery bypass grafting: this type of operation was performed earlier than stenting. The operation is based on the introduction of a shunt (bypass) to supply blood to the heart. Bypass surgery is a more complicated operation, done under general anesthesia. This operation is preferable for the elderly over 65 years old, for diabetics, for hypertensive patients.

It is very difficult to achieve success in the treatment of chronic coronary artery disease. It is impossible to completely get rid of the disease, but you can reduce symptoms, improve the quality of life by following all the prescriptions of doctors and changing your lifestyle.

Good day, dear readers!

In today's article, we will consider with you such a disease as coronary heart disease (CHD), as well as its symptoms, causes, classification, diagnosis, treatment, folk remedies and prevention of CHD. So…

What is ischemic heart disease?

Ischemic disease heart (IHD)- a pathological condition that is characterized by insufficient blood supply, and, accordingly, oxygen to the heart muscle (myocardium).

Synonyms for IHD– Coronary heart disease (CHD).

The main and most common cause of coronary artery disease is the appearance and development of atherosclerotic plaques in the coronary arteries, which narrow and sometimes block blood vessels, which disrupts normal blood flow in them.

Now let's move on to the development of the IHD itself.

The heart, as we all know, is the "motor" of a person, one of the main functions of which is to pump blood throughout the body. However, just like a car engine, without enough fuel, the heart stops functioning properly and may stop.

The function of fuel in the human body is performed by blood. Blood delivers oxygen, nutrients and other substances necessary for normal functioning and life to all organs and parts of the body of a living organism.

The blood supply to the myocardium (heart muscle) occurs with the help of 2 coronary vessels that depart from the aorta. Coronary vessels, dividing into a large number of small vessels, go around the entire heart muscle, feeding each part of it.

If there is a decrease in the lumen or blockage of one of the branches of the coronary vessels, that part of the heart muscle remains without nutrition and oxygen, the development of coronary heart disease, or as it is also called, coronary heart disease (CHD) begins. The larger the artery is blocked, the worse consequences illness.

The onset of the disease usually manifests itself in the form of chest pain during intense physical exertion (running and others), but over time, if no action is taken, pain and other signs of coronary artery disease begin to haunt a person even during rest. Some signs of coronary artery disease are also - shortness of breath, swelling, dizziness.

Of course, the above model of the development of coronary heart disease is very superficial, but it reflects the very essence of the pathology.

IHD - ICD

ICD-10: I20-I25;
ICD-9: 410-414.

The first signs of IBS are:

• Elevated blood sugar;
• Elevated cholesterol;

The main signs of IHD, depending on the form of the disease, are:

• angina pectoris- characterized by pressing pain behind the sternum (capable of radiating to the left side of the neck, left shoulder blade or arm), shortness of breath during physical exertion (fast walking, running, climbing stairs) or emotional stress (stress), increased blood pressure,;
• Arrhythmic form- accompanied by shortness of breath, cardiac asthma, pulmonary edema;
• - a person develops a seizure severe pain behind the sternum, which is not removed by conventional painkillers;
• Asymptomatic form- the person does not have any obvious signs indicating the development of coronary artery disease.
• , malaise;
• Edema, predominantly;
• , blurred consciousness;
• , sometimes with seizures ;
• Strong sweating;
• Feelings of fear, anxiety, panic;
• If you take nitroglycerin during pain attacks, the pain subsides.

The main and most common cause of the development of IHD is, the mechanism of which we spoke about at the beginning of the article, in the paragraph "Development of IHD". In short, the essence lies in the presence of atherosclerotic plaques in the coronary blood vessels, narrowing or completely blocking the access of blood to one or another part of the heart muscle (myocardium).

Among the others causes of coronary artery disease can be distinguished:

• Eating - fast foods, lemonade, alcoholic products, etc .;
• Hyperlipidemia (elevated levels of lipids and lipoproteins in the blood);
• Thrombosis and thromboembolism of the coronary arteries;
• Spasms of the coronary arteries;
• Dysfunction of the endothelium (inner wall of blood vessels);
• Increased activity of the blood coagulation system;
• Damage to blood vessels - herpes virus, cytomegalovirus, chlamydia;
• Hormonal imbalance (with the onset of menopause, and other conditions);
• Metabolic disorders;
• hereditary factor.

An increased risk of developing coronary artery disease is in the following people:

• Age - the older the person, the higher the risk of developing coronary artery disease;
• Bad habits - smoking, alcohol, drugs;
• Poor quality food;
• Sedentary lifestyle;
• Exposure to frequent;
• Male gender;

IHD classification

Classification of IHD occurs in the form:
1. :
- Angina pectoris:
— — Primary;
— — Stable, indicating the functional class
- Unstable angina (Braunwald classification)
- Vasospastic angina;
2. Arrhythmic form (characterized by a violation of the heart rhythm);
3. Myocardial infarction;
4. Postinfarction cardiosclerosis;
5. Heart failure;
6. Sudden coronary death (primary cardiac arrest):
- Sudden coronary death with successful resuscitation;
- Sudden coronary death with a fatal outcome;
7. Asymptomatic form of coronary artery disease.

IHD diagnostics

Diagnosis of coronary heart disease is carried out using the following examination methods:

• Anamnesis;
• Physical research;
• Echocardiography (EchoECG);
• Angiography and CT angiography of the coronary arteries;

How to treat coronary heart disease? IHD treatment is carried out only after a thorough diagnosis of the disease and determination of its form, because. It is on the form of IHD that the method of therapy and the means necessary for it depend.

Treatment for coronary heart disease usually includes following methods therapy:

1. Limitation of physical activity;
2. Drug treatment:
2.1. Antiatherosclerotic therapy;
2.2. Supportive care;
3. Diet;
4. Surgical treatment.

1. Limitation of physical activity

As you and I already know, dear readers, the main point of IHD is insufficient blood supply to the heart. Due to the insufficient amount of blood, of course, the heart does not receive enough oxygen, along with various substances necessary for its normal functioning and life. At the same time, you need to understand that during physical exertion on the body, the load on the heart muscle also increases in parallel, which at one time wants to receive an additional portion of blood and oxygen. Naturally, because with coronary artery disease, the blood is not enough, then under load this insufficiency becomes even more critical, which contributes to the deterioration of the course of the disease in the form of enhanced symptoms, up to a sudden cardiac arrest.

Physical activity is necessary, but already at the stage of rehabilitation after the acute stage of the disease, and only as prescribed by the attending physician.

2. Drug treatment (drugs for coronary artery disease)

Important! Before using drugs, be sure to consult your doctor!

2.1. Antiatherosclerotic therapy

AT recent times, for the treatment of coronary artery disease, many doctors use the following 3 groups of drugs - antiplatelet agents, β-blockers and hypocholesterolemic (cholesterol-lowering) drugs:

Antiplatelet agents. By preventing the aggregation of red blood cells and platelets, antiplatelet agents minimize their sticking and settling on inner walls blood vessels (endothelium), improve blood flow.

Among the antiplatelet agents, the following drugs can be distinguished: acetylsalicylic acid (Aspirin, Acecardol, Thrombol), Clopidogrel.

β-blockers. Beta-blockers help to lower the heart rate (HR), which reduces the load on the heart. In addition, with a decrease in heart rate, oxygen consumption also decreases, due to the lack of which, coronary heart disease mainly develops. Doctors note that with the regular use of β-blockers, the quality and life expectancy of the patient improves, because. this group of drugs stop many symptoms of coronary artery disease. However, you should be aware that contraindications to taking β-blockers are the presence of such concomitant diseases, like -, pulmonary pathologies and chronic obstructive pulmonary disease (COPD).

Among β-blockers, the following drugs can be distinguished: bisoprolol (Biprol, Kordinorm, Niperten), carvedilol (Dilatrend, Coriol, (Talliton), metoprolol (Betaloc, Vasocardin, Metocard", "Egilok").

Statins and fibrates- hypocholesterolemic (cholesterol-lowering) drugs. These groups of drugs lower the amount of "bad" cholesterol in the blood, reduce the number of atherosclerotic plaques on the walls of blood vessels, and also prevent the appearance of new plaques. The combined use of statins and fibrates is the most effective way to combat cholesterol deposits.

Fibrates increase the amount of high density lipoproteins (HDL), which actually counteract low density lipoproteins (LDL), and as you and I know, it is LDL that forms atherosclerotic plaques. In addition, fibrates are used in the treatment of dyslipidemia (IIa, IIb, III, IV, V), lower triglyceride levels and, most importantly, minimize the percentage of deaths from coronary artery disease.

Among the fibrates, the following drugs can be distinguished - "Fenofibrate".

Statins, unlike fibrates, have a direct effect on LDL, lowering its amount in the blood.

Among statins, the following drugs can be distinguished - Atorvastin, Lovastatin, Rosuvastin, Simvastatin.

The level of cholesterol in the blood in IHD should be - 2.5 mmol / l.

2.2. Supportive care

Nitrates. They are used to reduce the preload on the work of the heart by expanding the blood vessels of the venous bed and depositing blood, which stops one of the main symptoms of coronary heart disease - angina pectoris, which manifests itself in the form of shortness of breath, heaviness and pressing pain behind the chest. Especially for the relief of severe attacks of angina pectoris, intravenous drip of nitroglycerin has recently been successfully used.

Among the nitrates, the following drugs can be distinguished: "Nitroglycerin", "Isosorbide mononitrate".

Contraindications to the use of nitrates are - below 100/60 mm Hg. Art. Side effects include lowering blood pressure.

Anticoagulants. They prevent the formation of blood clots, slow down the development of existing blood clots, and inhibit the formation of fibrin threads.

Among the anticoagulants, the following drugs can be distinguished: "Heparin".

Diuretics (diuretics). Contribute accelerated withdrawal from the body of excess fluid, due to a decrease in the volume of circulating blood, thereby reducing the load on the heart muscle. Among diuretics, 2 groups of drugs can be distinguished - loop and thiazide.

Loop diuretics are used in emergency situations when fluid from the body needs to be removed as quickly as possible. Group loop diuretics reduce the reabsorption of Na +, K +, Cl- in the thick part of the loop of Henle.

Among the loop diuretics, the following drugs can be distinguished - Furosemide.

Thiazide diuretics reduce the reabsorption of Na +, Cl - in the thick part of the loop of Henle and the initial section of the distal tubule of the nephron, as well as the reabsorption of urine, and remain in the body. Thiazide diuretics, in the presence of hypertension, minimize the development of IHD complications from the cardiovascular system.

Among thiazide diuretics, the following drugs can be distinguished - "Hypothiazide", "Indapamide".

Antiarrhythmic drugs. Contribute to the normalization of the heart rate (HR), which improves respiratory function, facilitates the course of coronary artery disease.

Among the antiarrhythmic drugs, the following drugs can be distinguished: Aymalin, Amiodarone, Lidocaine, Novocainamide.

Angiotensin-converting enzyme (ACE) inhibitors. ACE inhibitors, by blocking the conversion of angiotensin II from angiotensin I, prevent spasms of blood vessels. ACE inhibitors also normalize, protect the heart and kidneys from pathological processes.

Among the ACE inhibitors, the following drugs can be distinguished: Captopril, Lisinopril, Enalapril.

Sedative drugs. They are used as a means of calming the nervous system, when emotional experiences and stress are the cause of an increase in heart rate.

Among the sedative drugs can be identified: "Valerian", "Persen", "Tenoten".

The diet for IHD is aimed at reducing the load on the heart muscle (myocardium). To do this, limit the amount of water and salt in the diet. Also, products that contribute to the development of atherosclerosis are excluded from the daily diet, which can be found in the article -.

Of the main points of the diet for IHD, we can distinguish:

• Calorie content of food - by 10-15%, and with obesity by 20% less than your daily diet;
• The amount of fat - no more than 60-80 g / day;
• The amount of proteins - no more than 1.5 g per 1 kg of human body weight / day;
• The amount of carbohydrates - no more than 350-400 g / day;
• The amount of table salt - no more than 8 g / day.

What not to eat with coronary artery disease

• Fatty, fried, smoked, spicy and salty foods - sausages, sausages, ham, fatty dairy products, mayonnaises, sauces, ketchups, etc.;
• Animal fats, which are found in large quantities in lard, fatty meats (pork, domestic duck, goose, carp and others), butter, margarine;
• High-calorie foods, as well as foods rich in easily digestible carbohydrates - chocolate, cakes, pastry, sweets, marshmallows, marmalade, jams and jams.

What can you eat with coronary artery disease

• Food of animal origin - low-fat meats (low-fat chicken, turkey, fish), low-fat cottage cheese, egg white;
• Cereals - buckwheat, oatmeal;
• Vegetables and fruits - mostly green vegetables and orange fruits;
• Bakery products - rye or bran bread;
• Drinking - mineral water, low-fat milk or kefir, unsweetened tea, and juices.

In addition, the diet for coronary artery disease should also be aimed at eliminating excessive amounts of extra pounds() if present.

For the treatment of coronary heart disease, M.I. Pevzner developed a therapeutic nutrition system - diet No. 10s (table No. 10s)

Ascorbic acid also contributes to the rapid breakdown of "bad" cholesterol and its removal from the body.

Horseradish, carrots and honey. Grate the horseradish root so that it comes out 2 tbsp. spoons and fill it with a glass of boiled water. After, mix the horseradish infusion with 1 glass of freshly squeezed carrot juice and 1 glass of honey, mix everything thoroughly. You need to drink the remedy for 1 tbsp. spoon, 3 times a day, 60 minutes before meals.

Ischemic 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 as acute (myocardial infarction, cardiac arrest) and chronic (angina pectoris, postinfarction cardiosclerosis, heart failure) conditions. Clinical signs of coronary artery disease are determined by the specific form of the disease. IHD is the world's most common cause of sudden death, including among people of working age.

ICD-10

I20-I25

General information

It is the most serious problem of modern cardiology and medicine in general. About 700,000 deaths caused by various forms of coronary artery disease are recorded in Russia every year; in the world, mortality from coronary artery disease is about 70%. Coronary heart disease mostly affects men of active age (from 55 to 64 years), leading to disability or sudden death.

The development of coronary artery 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 for blood supply to the myocardium, but its insufficient implementation, or with a normal need, but a sharp decrease coronary circulation. The deficiency of myocardial blood supply is especially pronounced in cases where the coronary blood flow is reduced, and the need of the heart muscle for blood flow increases dramatically. Insufficient blood supply heart tissues, their oxygen starvation is manifested by various forms of coronary heart disease. The IHD group includes acutely developing and chronically occurring states of myocardial ischemia, accompanied by its 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%) clinical cases IHD is caused by atherosclerosis of the coronary arteries varying degrees severity: from a slight narrowing of the lumen by an atherosclerotic plaque to complete vascular occlusion. At 75% coronary stenosis, the heart muscle cells respond to a lack of oxygen, and patients develop exertional angina.

Other causes of coronary artery disease are thromboembolism or spasm of the coronary arteries, usually developing against the background of an already existing atherosclerotic lesion. Cardiospasm exacerbates the obstruction of the coronary vessels and causes manifestations of coronary heart disease.

Factors contributing to the occurrence of IHD include:

• hyperlipidemia

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 artery 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 mm Hg. Art. and above, coronary heart disease occurs up to 8 times more often than in hypotensive patients and people with normal level blood pressure.

• smoking

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

• hypodynamia and obesity

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

• intolerance to carbohydrates

• angina pectoris (load):

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

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

3. Painless form of myocardial ischemia.

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

6. Disorders of cardiac conduction and rhythm(the 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 this group also includes sudden coronary death caused by coronary artery disease.

Symptoms of coronary artery disease

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

Common manifestations of coronary artery disease include retrosternal pain associated with physical exertion or stress, pain in the back, arm, mandible; shortness of breath, palpitations, or a feeling of interruption; weakness, nausea, dizziness, clouding of consciousness and fainting, excessive sweating. Often, coronary artery disease 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, there is a predominance of certain manifestations of ischemia.

Harbingers of primary cardiac arrest in coronary heart disease can serve as paroxysmal sensations of discomfort behind the sternum, fear of death, psycho-emotional lability. With sudden coronary death, the patient loses consciousness, breathing stops, there is no pulse on the main arteries (femoral, carotid), heart sounds are not audible, the pupils dilate, the skin becomes pale grayish. Cases of primary cardiac arrest account for up to 60% of deaths from coronary artery disease, mainly at the prehospital stage.

Complications

Hemodynamic disorders in the heart muscle and its ischemic damage cause numerous morphological and functional changes that determine the forms and prognosis of coronary artery disease. The result of myocardial ischemia are 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;
• 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 functions of the myocardium;
• disorder of the functions of excitability, conduction, automatism and contractility of the myocardium.

The listed morphological and functional changes in the myocardium in IHD 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 cardiological hospital or dispensary using specific instrumental techniques. When questioning the patient, complaints and the presence of symptoms characteristic of coronary heart disease are clarified. Examination reveals edema, cyanosis skin, heart murmurs, rhythm disturbances.

Laboratory diagnostic tests involve the study of specific enzymes that increase with 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 are released into the blood during the destruction of cardiomyocytes (resorption-necrotic syndrome). Also, 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 carried out.

The most important diagnostic method cardiac diseases, including coronary heart disease, is an ECG - registration of the electrical activity of the heart, which makes it possible to detect violations of the normal operation of the myocardium. EchoCG - a method of ultrasound of the heart allows you to visualize the size of the heart, the state of the cavities and valves, assess myocardial contractility, acoustic noise. In some cases, with IHD, stress echocardiography is performed - ultrasound diagnostics using dosed physical activity, which registers myocardial ischemia.

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

IHD treatment

The tactics of treating various clinical forms of coronary heart disease has its own characteristics. Nevertheless, it is possible to identify the main directions used for the treatment of IHD:

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

Non-drug therapy includes measures to correct lifestyle and nutrition. With various manifestations of coronary artery disease, a restriction of the activity regimen is shown, since during physical activity there is an increase in myocardial demand for blood supply and oxygen. Dissatisfaction with this need of the heart muscle actually causes manifestations of coronary artery disease. Therefore, in any form of coronary heart disease, the patient's activity mode is limited, followed by its gradual expansion during rehabilitation.

The diet for coronary heart 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 fight obesity, a low-fat diet is also prescribed. The following food groups are limited, and, if possible, excluded: animal fats (butter, lard, fatty meat), smoked and fried foods, quickly absorbed carbohydrates (baking pastries, chocolate, cakes, sweets). To maintain a normal weight, it is necessary to maintain a balance between consumed and expended energy. If it is necessary to reduce 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 IHD is prescribed according to the formula "A-B-C": antiplatelet agents, β-blockers and hypocholesterolemic drugs. In the absence of contraindications, it is possible to prescribe nitrates, diuretics, antiarrhythmic drugs, etc. The lack of effect from ongoing drug therapy for coronary heart disease and the threat of myocardial infarction are an indication for a consultation with a cardiac surgeon to resolve the issue of surgical treatment.

Surgical myocardial revascularization (coronary bypass grafting - CABG) is used to restore the blood supply to the ischemic area (revascularization) in case of resistance to conduction. pharmacological therapy(for example, with stable angina III and IV FC). The essence of the CABG method is the imposition of an autovenous anastomosis between the aorta and the affected artery of the heart below the site 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. To minimally invasive surgical techniques with IHD, percutaneous transluminal coronary angioplasty (PTCA) is a balloon "expansion" of a stenotic vessel with subsequent implantation of a frame-stent that holds the vessel lumen sufficient for blood flow.

Cardiac ischemia (IHD) remains one of the most common diseases among people over 40 years old (in men of this age in large European cities it is 4-6%) and the most common (up to 50%) cause of death from cardiac pathology.

Pathogenesis. The development of coronary artery disease is based on a discrepancy between the need of the heart muscle for oxygen and its delivery by blood, which is due to a violation of coronary blood flow. IHD as a nosological form is a narrower concept than coronary insufficiency, which can be caused by various diseases that occur with damage to the coronary vessels (systemic vasculitis, rheumatism, syphilis, etc.). The most studied pathogenetic mechanisms of coronary artery disease include: sclerosis of the coronary vessels, vasospasm and impaired blood clotting with the formation of platelet aggregants, usually in the area of ​​sclerotic plaque.

Despite the frequent (in almost 95% of patients) association of coronary artery disease with coronary sclerosis, they cannot be equated, since atherosclerosis is a pathomorphological process, while coronary artery disease is a nosological form that has various variants of clinical manifestations. The role of coronary angiospasm in the pathogenesis of IHD is beyond doubt, and in some forms of angina pectoris (Prinzmetal's form, variant angina), this mechanism is decisive. The fact that severe angina pectoris can develop with little changed vessels is obviously due to early damage to the receptor apparatus of the coronary arteries and their "paradoxical" response to increased myocardial oxygen demand.

The third mechanism is the formation of unstable thrombi, usually in the area of ​​the sclerotic plaque. At the same time, prostacyclin and prostaglandin E2 are produced in the intima of the vessels - active vascular dilators: their antagonist is thromboxane, which is produced by platelets. Depending on the direction in which the dynamic balance changes, a spasm or expansion of the coronary vessels occurs. The three main mechanisms of CHD pathogenesis (atherosclerotic plaque, spasm, platelet aggregants) are closely related to each other and, as it has now become known, to the composition of blood lipids. Thus, the most "atherogenic" lipids are low and very low density lipoproteins (LDL and VLDL), which affect both the formation of sclerotic plaques and the formation of blood clots; great importance attached to the composition of the protein fraction of lipoproteins - apolipoproteins. It has been established that an increase in the content of apoprotein B and a significant predominance of its content over apoprotein AI (B. A I> 1.7) indicates the possibility of developing severe angina pectoris. There is no doubt about the importance of the characteristics of the metabolism of the heart muscle in each individual patient, since the intensity of metabolic processes can compensate for the insufficiency of coronary blood flow for a certain time, and the violation of metabolic processes, on the contrary, exacerbates the final effect of coronary insufficiency. Obviously, the peculiarity of metabolism explains the fact that the severity of clinical manifestations of coronary artery disease in individual patients may be different, despite the same degree of narrowing of the coronary vessels, which was established in them with contrast angiography.

In addition to the described pathogenetic mechanisms, the role of which in the origin of IHD can be considered established, the so-called risk factors are of considerable importance, in the presence of which the risk of IHD for a person increases significantly.

Currently, more than 200 risk factors for CHD have been identified, of which the most significant in terms of distribution and significance of the impact on individual pathogenetic mechanisms of CHD are:

1) violation of lipid metabolism - among patients with coronary artery disease, dyslipidemia of type II and III (according to Fredrickson) is common, in which β- and pre-β-lipoproteins predominate in the blood serum;

2) arterial hypertension;

3) sedentary lifestyle;

4) obesity. The combination of several risk factors in one person significantly increases the risk of coronary artery disease and, as a rule, aggravates its course.

Structural changes characteristic of IHD are pathomorphological - sclerotic plaques, often with thrombotic overlays, are usually located in the proximal coronary vessel. The most frequently affected are: the anterior interventricular branch of the left coronary artery (60%), the right coronary artery (40%) and the circumflex branch of the left coronary artery (24.3%). The narrowing of one large coronary branch by 70% or 2 by 50%, as a rule, is accompanied by the development of severe coronary disease. At the same time, angiospastic reactions can also develop in the absence of severe stenosing changes in the vessels, especially if it concerns a large arterial trunk, for example, the left coronary artery.

The progression of coronary heart disease is associated with the appearance of new atheromatous plaques, ulceration, rupture and hemorrhage in already formed plaques, deepening of the disorder of the blood coagulation system with the formation of blood clots. The manifestation of these processes is closely related to the severity and combination of several risk factors in one patient. Exacerbation of the disease, as a rule, is provoked by physical activity and psycho-emotional excesses, which cause activation of the sympathetic-adrenal system, an increase in the load on the heart and an increase in the histotoxic effect of catecholamines.

Clinical classification ischemic heart disease (synonym"coronary heart disease" - WHO, 1962) was adopted by WHO in 1985 and includes the following clinical variants:

1. Sudden coronary death (primary cardiac arrest). Death that occurs suddenly or within 6 hours and has no other cause than the assumption of electrical instability due to a violation of the coronary blood flow.

2. Angina pectoris is a clinical variant of coronary artery disease, characterized by an attack of retrosternal pain, which is based on a transient discrepancy between the coronary blood flow and myocardial oxygen demand and the resulting metabolic disorders in the myocardium. The equivalent of pain in angina pectoris can sometimes be paroxysmal shortness of breath, rhythm disturbances, or changes in the ECG (painless form of coronary artery disease).

2.1. Angina pectoris. It manifests itself as typical anginal attacks, the occurrence of which is associated with physical stress (often walking) or other moments that cause increased myocardial oxygen demand (emotional stress, increased blood pressure, drug tachycardia etc.). Attacks are easily stopped by nitroglycerin and rest.

2.1.1. First time angina pectoris. Within one month from the onset of seizures. It has different outcomes: it can progress (end with the development of acute myocardial infarction), form into a stable or regress.

2.1.2. Stable exertional angina. Attacks of pain continue for more than a month. They arise for a certain physical activity and are relatively of the same type in duration, localization, color of pain and are stopped by a certain dose of nitroglycerin. The diagnosis of this type of angina should include the determination of the functional class of exercise tolerance.

2.1.3. Progressive angina pectoris. Attacks of pain for 4 weeks without apparent reason occur more often, with less physical activity than before, become longer, change their character, localization or irradiation and stop overdose nitroglycerin. The same type of angina pectoris includes post-infarction angina pectoris, in which anginal pain occurs and recurs in the early (during the first month) periods after the development of acute myocardial infarction.

2.2. Spontaneous (special, variant, Prinzmetal) angina pectoris. Attacks occur more often in the early morning hours, before the patient has risen from bed. They are more severe than ordinary angina pectoris. Often (but not always) combined with angina pectoris. The frequent association of seizures with spasm of a large coronary vessel has been proven. On the ECG during an attack, an increase in the ST segment is noted. There are indications that 30 - 50% of patients with spontaneous angina develop myocardial infarction in the next 3-4 months.

For the first time, progressive, post-infarction and spontaneous angina pectoris, which pose a risk of possible development of myocardial infarction, are united by the concept of unstable angina. The term "unstable angina", if it is included in the clinical diagnosis, requires a mandatory specific indication of the type of angina pectoris in this patient.

Diagnosis examples: a) ischemic heart disease, exertional angina, FC III;

b) IHD - unstable (progressive) angina pectoris.

3. Myocardial infarction, which can be macrofocal or transmural (Q wave infarction) and small focal (intramural, subendocardial, non-Q wave infarction). Clinical options are varied, the diagnosis is confirmed ECG changes mi and laboratory (primarily enzymatic) indicators. The diagnosis of myocardial infarction is made within 8 weeks from the moment of the attack.

4. Postinfarction cardiosclerosis. The diagnosis is established 8 weeks after myocardial infarction in the presence of post-MI changes in the ECG, EchoCG, or on the basis of clinical, ECG and laboratory confirmation of a heart attack in the past, if there are currently no post-MI changes on the ECG.

5. Violations of the heart rhythm. They are regarded as a manifestation of coronary artery disease if they are combined with other forms of coronary insufficiency: angina pectoris, myocardial infarction, "coronary signs" on the ECG, the results of coronary angiography, confirming the narrowing of the coronary arteries.

6. Heart failure. Most often it is a consequence of post-infarction cardiosclerosis, especially after a macrofocal (transmural) infarction. As a rule, it is combined with rhythm disturbance and angina pectoris. In the absence of these symptoms, the diagnosis of coronary heart disease as a cause of decompensation is always doubtful.

Symptoms and treatment of chronic coronary heart disease

Ischemic heart disease is a progressive disease. According to statistics, about two thirds of the world's population has symptoms of chronic coronary heart disease, and one third dies from this disease. Therefore, the topic "symptoms and treatment of chronic coronary heart disease" is extremely relevant and needs to be considered.

Symptoms of chronic coronary heart disease

On the early stage development of coronary heart disease, lipids are incorporated in the intima, forming atherosclerotic plaques surrounded by fibrous tissue. The disease is accompanied by a gradual narrowing and decrease in the lumen of the coronary arteries, and consequently, a decrease in the blood supply to the myocardium.

In some cases, in ischemic heart disease, fibrous tissue contains calcium deposits. At a later stage, a symptom of chronic coronary heart disease is tissue rupture over the plaque, its ulceration. A platelet clot forms over the damaged plaque, giving rise to a thrombus, a further decrease in the lumen of the arteries, and myocardial infarction. As the coronary arteries narrow, there is a discrepancy between myocardial oxygen demand and the possibilities of its delivery. As a result, angina attacks occur.

At the onset of coronary heart disease, spasm of the coronary arteries predominates, accompanied by symptoms of chronic coronary heart disease during exercise (angina pectoris) or at rest (angina pectoris). Subsequently, myocardial infarction occurs very often.

Chronic ischemic heart disease can be limited or diffuse. Obturation of the lumen of the arteries leads to focal myocardial ischemia, which can be reversible or irreversible (myocardial infarction). The most important symptom coronary heart disease are retrosternal pain, angina pectoris.

Diagnosis of symptoms of chronic coronary heart disease

Patients are concerned about attacks of retrosternal pain, which stop after taking nitroglycerin; rhythm disturbance, palpitations. Clinical symptoms of chronic coronary heart disease are highly variable. According to the classification of the New York Heart Association (NYHA), the severity of retrosternal pain and the course of chronic coronary heart disease are divided into four classes.

Class I - there are no distinct symptoms of the disease;

P class - the appearance of angina pectoris after heavy physical exertion;

Class III - the appearance of angina pectoris after light physical exertion;

Class IV - angina pectoris at rest.

Patients assigned to class I-II do not experience severe angina attacks, the disease does not prevent them from leading a normal life (stable angina pectoris). In the case of an increase in the class of chronic coronary heart disease over a short period of time, there is reason to talk about progressive angina pectoris, which significantly worsens the prognosis. Late-stage coronary artery disease occurs at rest and becomes refractory to current medical treatment (unstable angina). The prognosis at this stage of the disease worsens significantly, there is a risk of a heart attack or sudden death. In a significant proportion of patients, the disease does not develop according to the above classes, but can immediately manifest itself as a heart attack or sudden death. Sometimes asymptomatic myocardial ischemia is observed, then the disease is recognized only at a late stage.

Important information for the treatment of chronic coronary heart disease is provided by an electrocardiogram obtained at rest and during dosed exercise on a bicycle ergometer. Analysis of the electrocardiogram allows you to determine the severity and localization (foci) of myocardial ischemia, the degree of conduction disturbance, the nature of the arrhythmia.

Of great importance in chronic coronary heart disease is also a color Doppler ultrasound and echocardiographic study. It allows you to determine changes in myocardial contractility. By the nature of the movements of the walls of the ventricles of the heart, it is possible to identify the focus and prevalence of myocardial ischemia in the zones of hypokinesia, akinesia or dyskinesia in the zone supplied by the narrowed branch of the coronary artery. The slowdown in the rate of movement of the walls of the ventricle during myocardial contraction is called hypokinesia, the absence of movement of the ventricular wall is called akinesia. With an aneurysm of the heart, at the time of contraction of the unaffected myocardium, the scar-modified area protrudes (dyskinesia).

Echocardiographic study allows you to determine the systolic, end-diastolic and residual volumes of the left ventricle, ejection fraction, minute volume and cardiac index and other hemodynamic parameters. Magnetic resonance imaging provides the most accurate information about the state of the coronary circulation in coronary heart disease.

To clarify the degree and localization of the narrowing of the coronary arteries, the state of peripheral and collateral circulation in the heart muscle, selective coronary angiography, including cinematography, is performed. This is important for determining the location and extent of the narrowing before and during surgery.

Radionuclide studies make it possible to clarify the extent of the focus of myocardial damage by the degree of accumulation of the nuclide in the myocardium.

Progressive segmental narrowing of the coronary arteries inevitably leads to myocardial infarction. The fate of the patient depends on the extent and localization of the infarction, the degree of dysfunction of the heart and internal organs.

Treatment of chronic coronary heart disease

Surgical treatment of chronic coronary heart disease is indicated for stenosis of the main trunk of the left coronary artery by 75%, with stenosis of 2-3 branches of the artery and clinical manifestations according to NYHA class III-IV, a decrease in left ventricular ejection fraction of less than 50% .

An urgent indication for myocardial revascularization is an unstable "pre-infarction angina" that is not amenable to conservative treatment, as well as a pronounced stenosis of the left coronary artery, stenosis of the proximal section of the anterior interventricular branch of the left coronary artery, since their blockage is accompanied by extensive myocardial infarction. With stable angina, amenable to drug treatment, surgery for chronic coronary heart disease is performed in a planned manner. The result of the operation is the restoration of coronary circulation, in 80-90% of patients after the operation the phenomena of angina pectoris disappear, the risk of myocardial infarction sharply decreases.

The main method of surgical treatment of chronic coronary heart disease in the case of atherosclerotic lesions of the coronary arteries is coronary artery bypass grafting (bypass). The operation consists in creating one or more anastomoses between the ascending aorta and the coronary artery and its branches distal to the site of occlusion. A section of the vein of the leg (v. saphena magna) is used as a shunt. In 1964, V. I. Kolesov for the first time made an anastomosis between the internal thoracic and coronary arteries below its narrowing (coronary-mammary anastomosis). This operation, for certain indications, is performed in a number of institutions. Currently, mobilized sections of arteries (a. thoracica in-terna, a. epigastrica, etc.) are often used for angioplasty.

In a number of indicators, angioplasty using an artery in chronic coronary heart disease is superior to coronary artery bypass grafting using a vein segment. Prerequisites for successful myocardial revascularization are:

1) stenosis of the coronary arteries (50% or more) with good patency of their peripheral parts;

2) sufficient diameter (not less than 1 mm) of the peripheral section of the coronary arteries;

3) preservation of myocardial contractility ("living" myocardium) beyond arterial stenosis.

In recent years, with the development of endovascular X-ray surgery for the treatment of chronic coronary heart disease in the case of narrowing of the coronary vessels, their dilatation using special probes with balloons, which are inserted into the lumen of the artery, began to be used. Filling the balloon with a contrast agent, stretching the narrowed segment of the lumen of the artery and restoring its patency is achieved. The success achieved with dilatation can be fixed by the installation of a stent.

The choice of treatment for coronary heart disease depends on the nature of coronary artery disease and the patient's condition according to the NYHA class. Attempts are being made to destroy the atherosclerotic plaque with a laser beam. With the development of a pre-infarction state in a patient due to thrombosis of a narrowed coronary artery, emergency coronary angiography is performed to detect the localization of a thrombus. Then, streptokinase is injected through the catheter into the coronary artery to the site of its blockage. In this way, they achieve recanalization of the coronary artery, reducing the zone of coronary heart disease. Subsequently, coronary artery bypass grafting is performed in a planned manner.

CARDIAC ISCHEMIA

Cardiac ischemia (ischemic heart disease) – acute or chronic lesion heart, caused by a decrease or cessation of blood delivery to the myocardium due to the atherosclerotic process in the coronary arteries, which upsets the balance between coronary blood flow and myocardial oxygen demand.

Risk factors for coronary artery disease are:

1) male gender (men get coronary artery disease earlier and more often than women);

2) age (the risk of coronary artery disease increases with age, especially after 40 years);

3) hereditary predisposition (the presence of coronary artery disease, hypertension and their complications in parents under the age of 55);

4) dysproteinemia: hypercholesterolemia (fasting total cholesterol level 250 mg / dl or 6.5 mmol / l or more), hypertriglyceridemia (blood triglyceride level 200 mg / dl or 2.3 mmol / l or more), hypoalphacholesterolemia (34 mg /dl or 0.9 mmol/l) or a combination thereof;

5) arterial hypertension: blood pressure level 160/95 mm Hg. Art. and above or the presence arterial hypertension in history in persons taking antihypertensive drugs at the time of the examination, regardless of the recorded level of blood pressure;

6) overweight body (determined by the Quetelet index). With normal body weight, the Quetelet index does not exceed 20-25;

7) with obesity I-II Art. Quetelet index more than 25, but less than 30;

8) with obesity III Art. Quetelet index over 30;

9) smoking (regular smoking according to at least one cigarette a day)

10) physical inactivity (low physical activity) - work more than half of the working time while sitting and inactive leisure (walking, playing sports, working in the garden, etc. less than 10 hours a week);

11) increased level of psycho-emotional stress (stress coronary profile);

diabetes;

12) hyperuricemia.

The main risk factors for coronary artery disease are currently arterial hypertension, hypercholesterolemia, smoking ("big three").

The main etiological factors of IHD are as follows.

1. Atherosclerosis of the coronary arteries.

In 95% of patients with IHD, atherosclerotic lesions are found in the coronary arteries, mainly in the proximal sections (A. M. Vikhert, E. I. Chazov, 1971). The anterior interventricular branch of the left coronary artery is most often affected, less often the right coronary artery, then the circumflex branch of the left coronary artery.

2. Spasm of the coronary arteries.

Currently, the role of coronary spasm in the development of coronary artery disease has been proven using selective coronary angiography. In most patients with coronary artery disease, spasm of the coronary arteries occurs against the background of atherosclerosis. Atherosclerosis perverts the reactivity of the coronary arteries, they become hypersensitive to environmental factors.

Main pathophysiological mechanism IHD is the discrepancy between myocardial oxygen demand and the ability of coronary blood flow to meet these needs.

The development of this discrepancy is facilitated by the following main pathogenetic mechanisms of coronary artery disease, which should be taken into account in the treatment of patients.

1. Organic obstruction of the coronary artery by an atherosclerotic process.

The mechanism of the resulting sharp restriction of coronary blood flow is due to infiltration of the wall with atherogenic lipoproteins, the development of fibrosis, the formation of an atherosclerotic plaque and stenosis of the artery, and the formation of a thrombus in the coronary artery.

2. Dynamic obstruction of the coronary arteries - is characterized by the development of coronary spasm against the background of atherosclerotically altered arteries. In this situation, the degree of narrowing of the lumen depends on both the degree of organic damage and the severity of the spasm (the concept of "dynamic stenosis"). Under the influence of spasm, stenosis of the coronary arteries can increase to a critical value - 75%, which leads to the development of angina pectoris.

The coronary arteries have dual innervation: parasympathetic and sympathetic. Fibers from the cardiac plexuses containing mixed cholinergic and adrenergic nerve endings approach the coronary arteries.

When the cholinergic nerves are stimulated, the coronary arteries expand. The sympathetic nervous system exerts both a vasoconstrictive and dilatatory effect on the coronary arteries through alpha and beta adrenoreceptors.

In the development of coronary spasm, along with sympathetic nervous system and other neurotransmitters also take part in its mediators. It has been established that there are nerves in the blood vessels that do not belong to either the adrenergic or cholinergic systems. Mediators of these nerve endings are substance P, neurotensin.

In the development of coronary spasm, metabolites of arachidonic acid are also important - PgF2a (prostaglandin F2a), leukotrienes LTC4 and LTD4, serotonin (I. S. Lambich, S. P. Stozhinich, 1990).

In the coronary arteries, serotonin is released from platelet aggregates (Cotner, 1983) and causes vasoconstriction as follows (Vanhoute, 1984):

1) activates serotonergic receptors in vascular smooth muscle cells;

2) increases the vasoconstrictor response to other neurohumoral mediators (norepinephrine, angiotensin II);

3) activates postsynaptic alpha-1-adrenergic receptors;

4) promotes the release of norepinephrine from the depot of adrenergic nerve endings.

3. Decrease in the adequacy of the expansion of the coronary arteries under the influence of local metabolic factors with an increase in myocardial oxygen demand.

The most important role in the regulation of coronary blood flow is played by local metabolic factors. An increase in myocardial oxygen demand causes dilation of the coronary arteries. With a decrease in coronary blood flow, a drop in oxygen partial pressure, myocardial metabolism changes, switches to an anaerobic pathway, vasodilatory metabolites (adenosine, lactic acid, inosine, hypoxanthine) accumulate in the myocardium, which dilate the coronary arteries. Dilatation of the coronary arteries improves blood flow and normalizes the supply of oxygen to the myocardium.

In coronary artery disease, coronary arteries altered by the atherosclerotic process cannot adequately expand in accordance with the increased myocardial oxygen demand, which leads to the development of ischemia.

4. The role of endothelial factors.

The endothelium produces substances that have vasoconstrictive and procoagulant effects, as well as substances that have vasodilating and anticoagulant effects. Normally, there is a dynamic balance between these two groups of substances.

Procoagulant substances produced by the endothelium: tissue thromboplastin, von Willebrand factor, collagen, platelet activating factor. These biologically active compounds promote platelet aggregation and increase blood clotting. In addition, endothelins (ET) are produced in the endothelium.

Endothelins is a family of vasoconstrictor factors (ET-1, ET-2, ET-3) encoded by three different genes. The process of endothelin formation includes several stages. Endothelin also stimulates platelet aggregation. Receptors for endothelin are found in the atria, lungs, glomeruli of the kidneys, vessels of the kidneys, and the brain. The endothelium also produces vasodilators: prostaglandin prostacyclin and endothelial relaxing factor.

Prostacyclin was discovered in 1976 by Moncada. The main source of prostacyclin in the heart is the coronary arteries, it is produced mainly by the endothelium and to a lesser extent by smooth muscle cells.

Prostacyclin PgI2 has the following properties:

1) a pronounced vasodilating effect, including coronary dilating; it is carried out through the activation of the adenylate cyclase - cAMP system;

2) inhibits platelet aggregation;

3) cardioprotective action (limits the area of ​​myocardial infarction in its early stage);

4) reduces the loss of energy-rich nucleotides in the ischemic myocardium and prevents the accumulation of lactate and pyruvate in it;

5) reduces the accumulation of lipids in the vascular wall and thus exhibits an anti-atherosclerotic effect.

The prostacyclin-synthesizing ability of the endothelium of the coronary arteries altered by the atherosclerotic process is significantly reduced, which contributes to the development of coronary artery disease.

Endothelial relaxing (vasodilating) factor (ERF) is a nitric oxide (NO), formed in endothelial cells as a result of the metabolism of the amino acid L-arginine under the action of the enzyme NO-synthetase.

ERF activates soluble guanylate cyclase, which leads to the accumulation of cyclic guanosine monophosphate (cGMP) in the smooth muscle cell. In turn, cGMP activates cGMP-dependent protein kinase, which promotes dephosphorylation of myosin chains and relaxation of smooth muscle fibers.

Like prostacyclin, endothelial relaxing factor is a potent antiplatelet agent.

Normally, endothelial cells carry out a constant basal secretion of ERF, which prevents vasospasm.

In ischemic heart disease, hypercholesterolemia, arterial hypertension, thrombosis, under the influence of smoking, the dynamic balance between endothelial vasodilator and antiplatelet factors, on the one hand, and vasoconstrictor and proaggregant factors, on the other, is disturbed. The second group of factors in IHD and the above conditions begins to prevail and contributes to the development of coronary spasm, increased platelet aggregation.

5. Increased platelet aggregation.

In IHD, there is an increase in platelet aggregation and the appearance of microaggregates in the branches of the coronary arteries, which leads to impaired microcirculation and aggravation of myocardial ischemia. An increase in platelet aggregation is due to an increase in platelet production of thromboxane (which is also a powerful vasoconstrictor), hyperproduction of procoagulant factors.

Normally, there is a dynamic balance between thromboxane (a proaggregant and a vasoconstrictor) and prostacyclin (an antiplatelet agent and a vasodilator). With IHD, this balance is disturbed, thromboxane activity increases, which creates conditions for the formation of platelet aggregates in the coronary circulation system and coronary spasm.

6. Increased myocardial oxygen demand.

In coronary artery disease, there is a discrepancy between the possibilities of coronary blood flow and increased myocardial oxygen demand. This leads to the following.

2) emotional stress(at the same time, there is a release and entry into the blood of a large amount of catecholamines, which contributes to spasm of the coronary arteries, hypercoagulation; hypercatecholaminemia also has a cardiotoxic effect);

3) a decrease in myocardial contractility (in this case, end-diastolic pressure increases, the volume of the left ventricle increases, and myocardial oxygen demand increases).

7. Development of the phenomenon of "intercoronary steal".

In IHD patients with stenosing coronary atherosclerosis and developed collaterals during exercise, as a result of vasodilation, blood flow increases in unaffected coronary arteries, which is accompanied by a decrease in blood flow in the affected artery distal to the stenosis and the development of myocardial ischemia.

8. Insufficiency of collateral circulation.

The development of collaterals partially compensates for disorders of the coronary circulation in patients with coronary artery disease associated with stenosis of the coronary arteries. However, with a pronounced increase in myocardial oxygen demand, collaterals do not adequately compensate for the lack of blood supply, which contributes to myocardial ischemia. Insufficiency of coronary collateral blood flow may also be due to insufficient expression in vascular smooth muscle cells and cardiomyocytes of proto-oncogenes that control cell growth, division, and differentiation.

9. Increasing the activity of lipid peroxidation.

With IHD, the activity of lipid peroxidation increases, which contributes to increased platelet aggregation. Products of lipid peroxidation aggravate myocardial ischemia.

10. Activation of the lipoxygenase pathway of arachidonic acid metabolism.

With coronary heart disease, the activity of the enzyme 5-lipoxygenase significantly increases in the coronary arteries, under its influence leukotrienes are formed from arachidonic acid, which have a narrowing effect on the coronary arteries.

11. Violation of the production of enkephalins and endorphins.

Enkephalins and endorphins are endogenous opioid peptides. They have analgesic and anti-stress effects, reduce myocardial ischemia and protect it from the damaging effects of excess catecholamines. With IHD, the production of enkephalins and endorphins is reduced, which contributes to the development and progression of myocardial ischemia.

Working classification of coronary artery disease (V. S. Gasilin, A. P. Golikov, I. L. Klocheva, A. I. Martynov, I. V. Martynov, A. S. Melentiev, V. G. Popov, B. A. Sidorenko, A V. Sumarokov, 1986).

I. Angina.

1. Angina pectoris:

1) first appeared;

2) stable (indicating the functional class from I to IV);

3) progressive: slowly progressive, rapidly progressive (unstable).

2. Vasospastic (variant).

II. Acute focal myocardial dystrophy.

III. Myocardial infarction.

1) small focal primary;

2) small-focal repeated.

4. Subendocardial.

IV. Cardiosclerosis.

1. Postinfarction focal.

2. Diffuse small focal.

V. Heart rhythm disturbances.

VI. Painless form of coronary artery disease.

VII. Sudden coronary death.

Acute forms of coronary artery disease include myocardial infarction, forms of unstable angina pectoris, acute focal dystrophy; to chronic forms of coronary artery disease - cardiosclerosis, stable angina pectoris, cardiac arrhythmias, painless form of coronary artery disease.

1. Angina pectoris:

1) first-time angina pectoris;

2) stable angina pectoris with indication of the functional class (I-IV);

3) progressive angina pectoris.

2. Spontaneous angina.

V. Cardiac arrhythmias (indicating the form).

VI. Heart failure (indicating the form and stage).

CHRONIC ISCHEMIC HEART DISEASE

Chronic ischemic heart disease (CHD) includes forms of the disease that occur chronically: stable angina pectoris, diffuse (atherosclerotic) and postinfarction cardiosclerosis.

The main cause of the development of the disease is atherosclerosis of the coronary arteries. Significantly less often, angina attacks occur with unchanged coronary arteries. Among the factors contributing to the development of the disease, one should include functional overload of the heart, the histotoxic effect of catecholamines, changes in the coagulation and anticoagulation systems of the blood, insufficient development of collateral circulation.

The development of chronic coronary artery disease is based on coronary insufficiency, the result of an imbalance between myocardial oxygen demand and the possibility of its delivery with blood. With insufficient access of oxygen to the myocardium, its ischemia occurs. The pathogenesis of ischemia is different in altered and unchanged coronary arteries.

Arterial spasm acts as the main mechanism for the occurrence of coronary insufficiency in morphologically unchanged vessels. Spasm is caused by disorders of neurohumoral regulatory mechanisms, currently understudied. The development of coronary insufficiency is promoted by nervous and (or) physical stress, which causes an increase in the activity of the sympathetic-adrenal system. Due to the increased production of catecholamines by the adrenal glands and postganglionic endings of the sympathetic nerves, an excess of these biologically active substances accumulates in the myocardium. active substances. Strengthening the work of the heart, in turn, increases the demand for oxygen in the myocardium. The activation of the blood coagulation system, as well as the inhibition of its fibrinolytic activity and changes in platelet function, observed under the influence of increased activity of the sympathetic-adrenal system, exacerbate coronary insufficiency and myocardial ischemia.

With atherosclerosis of the coronary arteries, the discrepancy between myocardial oxygen needs and the possibilities of coronary circulation is clearly manifested during physical activity (increased heart function, increased activity of the sympathetic-adrenal system). The severity of coronary insufficiency is exacerbated by insufficiency of collateral vessels, as well as extravascular effects on the coronary arteries. Such influences include the compressive effect of the myocardium on small coronary arteries in the systole phase, as well as an increase in intramyocardial pressure due to contractile myocardial insufficiency developing during an angina attack and an increase in end-diastolic volume and pressure in the left ventricle.

Acute coronary insufficiency, manifested by an attack of angina pectoris, can turn on compensatory mechanisms that prevent the development of myocardial ischemia. Such mechanisms are the disclosure of existing and the formation of new intercoronary anastomoses, an increase in the extraction of oxygen by the myocardium from arterial blood. With the depletion of this "coronary reserve", myocardial ischemia during an angina attack becomes more pronounced.

In addition to an attack of angina pectoris, myocardial ischemia is manifested by various ectopic arrhythmias, as well as the gradual development of atherosclerotic cardiosclerosis. In cardiosclerosis, the replacement of muscle fibers with connective tissue gradually leads to a decrease in the contractile function of the myocardium and the development of heart failure.

ANGINA

Angina pectoris is the main manifestation of chronic coronary artery disease, but can also occur as a syndrome in other diseases ( aortic defects severe anemia). In this regard, the term "angina pectoris", unless the disease that caused it is specifically indicated as a synonym for the concept of coronary artery disease. As noted, the main cause of the development of angina pectoris is atherosclerosis of the coronary arteries, much less often - dysregulation of unchanged coronary arteries.

Clinical picture

The main manifestation of angina pectoris is a characteristic pain attack. AT classic description angina pectoris is characterized as an attack-like pressing sensation in the sternum that occurs with physical effort, increasing in severity and prevalence.

Usually the pain is accompanied by a feeling of discomfort in the chest, radiating to the left shoulder or both arms, to the neck, jaw, teeth; it may be accompanied by a feeling of fear, which causes patients to freeze in a motionless position. Pain quickly disappears after taking nitroglycerin or eliminating physical tension(stopping while walking, elimination of other conditions and factors that provoked an attack: emotional stress, cold, food intake).

Depending on the circumstance in which the pain occurred, there are angina pectoris and rest. The appearance of pain syndrome in typical angina pectoris depends on the level of physical activity. According to the accepted classification of the Canadian Society of Cardiology, according to the ability to perform physical activity in patients with angina pectoris, 4 functional classes are distinguished:

I - functional class - ordinary physical activity does not cause angina pectoris. Angina pectoris appears with an unusually large, rapidly performed load.

II - functional class - slight limitation of physical activity. Angina pectoris is caused by ordinary walking over a distance of more than 500 m or climbing stairs to the 1st floor, uphill, walking after eating, in the wind, in the cold; angina pectoris is also possible under the influence of emotional stress.

III - functional class - severe limitation of physical activity. Angina pectoris occurs during normal walking at a distance of 100–200 m. Rare attacks of rest angina are possible.

IV - functional class - the inability to perform any physical work without discomfort. There are typical attacks of rest angina pectoris.

As special cases of angina pectoris, angina pectoris can be distinguished with excitement and smoking.

To rest angina it is customary to attribute attacks of pain that occur during complete rest, mainly in a dream.

The so-called variant angina pectoris (Prinzmetal's angina pectoris) should be especially highlighted: angina attacks of rest, usually at night, occurring without previous angina pectoris. Unlike ordinary angina attacks, they are accompanied by a significant rise in the ST segment on the ECG at the time of pain. Using coronary angiography, it was shown that variant angina pectoris is caused by spasm of sclerosed or unchanged coronary arteries. This variant of IHD is referred to as unstable angina (an intermediate form of IHD).

The main clinical symptom - an attack of angina pectoris - is not pathognomonic only for coronary artery disease. In this regard, the diagnosis of angina pectoris as a form of chronic coronary artery disease can only be made taking into account all the data obtained at various stages of the patient's examination.

At the same time, the clinical picture of angina pectoris in IHD has its own characteristics, which are found during a diagnostic search.

Based on the complaints of patients, it is possible to identify:

a) typically occurring angina pectoris;

b) other manifestations of chronic ischemic heart disease (rhythm disturbances, heart failure);

c) IHD risk factors;

d) atypical cardiac pain and their assessment taking into account age, gender, risk factors for NBS and concomitant diseases;

e) the effectiveness and nature of the ongoing drug therapy;

e) other diseases manifested by angina pectoris.

All complaints are evaluated taking into account the age, gender, constitution, psycho-emotional background and behavior of the patient, so often already at the first communication with the patient, one can reject or verify the correctness of the preliminary diagnosis of coronary artery disease. So, with classic complaints during last year and the absence of cardiovascular disease in the past in a 50-60-year-old man, chronic coronary artery disease can be diagnosed with very highly likely. Nevertheless, a detailed diagnosis indicating the clinical variant of the disease and the severity of coronary artery and myocardial damage can only be made after completing the entire basic diagnostic search scheme, and in some situations (described below) after an additional examination.

Sometimes it is difficult to distinguish between angina pectoris and various pain cardiac and extracardiac origin. Features of pain various diseases described in textbooks and manuals. It should only be emphasized that stable angina pectoris is characterized by a constant, identical nature of pain during each attack, and its appearance is clearly associated with certain circumstances. With neurocirculatory dystonia and a number of other diseases of the cardiovascular system, the patient notes the diverse nature of pain, their different localization, and the absence of any regularity in their occurrence. In a patient with angina pectoris, even in the presence of other pains (caused, for example, by lesions of the spine), it is usually possible to isolate characteristic "ischemic" pains.

Simultaneously with complaints of pain in the region of the heart, the patient may present complaints due to a violation of the heart rhythm and circulatory failure outside of an angina attack. This allows a preliminary assessment of the severity of atherosclerotic or post-infarction cardiosclerosis and makes the diagnosis of coronary artery disease more likely. The correct diagnosis is facilitated by the identification of risk factors for coronary artery disease.

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

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

In some cases, there is no typical localization of pain, pain occurs only in those places where they usually radiate. Since the pain syndrome in angina pectoris can proceed atypically, with any complaints of pain in the chest, arms, back, neck, lower jaw, epigastric region (even in young men), you should find out if these pains do not correspond to the patterns of occurrence and disappearance pain syndrome in angina pectoris. In such cases, with the exception of localization, the pain retains all other features of "typical" angina pectoris (the cause of occurrence, the duration of the attack, the effect of nitroglycerin or stopping when walking, etc.).

According to subjective signs, the effectiveness of taking nitroglycerin is evaluated (with the disappearance of pain after 5 minutes and later, the effect is very doubtful) and other medications previously taken by the patient (important not only for diagnosis, but also for building an individual treatment plan in the future).

An objective examination of the patient is not very informative for diagnosis. Physical examination may not reveal any abnormalities (with recent onset angina). You should actively look for symptoms of diseases (heart defects, anemia, etc.), which may be accompanied by angina pectoris.

Important for diagnosis is non-cardiac localization of atherosclerosis: aorta (accent of II tone, systolic murmur on the aorta), lower extremities (a sharp weakening of the pulsation of the arteries); symptoms of left ventricular hypertrophy with normal blood pressure and the absence of any diseases of the cardiovascular system.

Instrumental and laboratory studies to diagnose chronic coronary artery disease and evaluate angina pectoris as its manifestation.

Electrocardiography - leading method of instrumental diagnosis of chronic coronary artery disease. In doing so, the following provisions must be taken into account.

1. ST segment depression (possibly combined with a coronary T wave) is a confirmation of the preliminary diagnosis of chronic coronary artery disease. However, there are no ECG changes that are absolutely specific for chronic coronary artery disease; a coronary T wave may be a manifestation of a previously transferred small-focal infarction (negative laboratory results indicating a resorption-necrotic syndrome must be taken into account).

2. The presence of coronary artery disease can be confirmed by identifying characteristic ECG signs during an attack and their rapid disappearance (within several hours, up to a day). For verification of coronary artery disease, 24-hour Holter ECG monitoring is used (Holter monitoring).

3. In the majority of patients with angina pectoris who have not undergone MI, the ECG outside the attack is not changed, and during an attack, changes do not occur in all patients.

4. "Cicatricial" changes detected on the ECG, if available characteristic pains in the heart are an important argument in favor of the diagnosis of coronary artery disease.

5. To detect signs of myocardial ischemia, when they are absent on an ECG taken at rest, as well as to assess the state of the coronary reserve (severity of coronary insufficiency), exercise tests are performed.

Among the various stress tests, the most common are tests with physical activity on a bicycle ergometer or a treadmill (treadmill).

Indications for bicycle ergometry for the diagnosis of coronary artery disease are:

a) atypical pain syndrome;

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

c) no ECG changes in case of suspected coronary artery disease.

The sample is considered positive if, at the time of loading, the following is noted:

a) the occurrence of an attack of angina pectoris;

b) the appearance of severe shortness of breath, suffocation;

c) decrease in blood pressure;

d) decrease in the SR segment of the "ischemic type" by 1 mm or more;

e) elevation of the ST segment by 1 mm or more.

The main contraindications to exercise testing are:

a) acute myocardial infarction;

b) frequent attacks of angina pectoris and rest;

c) heart failure;

d) prognostically unfavorable violations of the heart rhythm and conduction;

e) thromboembolic complications;

e) severe forms arterial hypertension;

g) acute infectious diseases.

If necessary (the impossibility of performing bicycle ergometry or its technical implementation, detraining of patients), an increase in the work of the heart is achieved using the test of frequent atrial stimulation (the pacemaker electrode is inserted into the right atrium; the invasive nature of the study sharply limits the scope of the test) or the test of frequent transesophageal stimulation (the method is non-traumatic, widespread).

6. For ECG diagnosis of coronary artery disease, various pharmacological stress tests are also used using drugs that can affect the coronary bed and functional state myocardium. So, for ECG diagnostics of the vasospastic form of IHD, tests with ergometrine or dipyridamole are used.

pharmacological tests with propranolol, potassium chloride are carried out in cases where there are initial changes in the final part of the ventricular complex on the ECG, if necessary, differential diagnosis between coronary artery disease and NCD. These tests are not critical for the diagnosis of coronary artery disease. The changes detected on the ECG are always evaluated taking into account other data from the examination of the patient.

Ultrasound procedure heart should be carried out in all patients suffering from angina pectoris. It allows you to evaluate the contractility of the myocardium, to determine the size of its cavities. So, when a heart disease, obstructive cardiomyopathy is detected, the diagnosis of chronic coronary artery disease becomes unlikely; in the elderly, a combination of these diseases is possible.

A number of instrumental methods of research, carried out in the generally accepted manner in a patient with suspected IHD, allows us to identify non-cardiac signs of atherosclerosis of the aorta (chest x-ray) and vessels of the lower extremities (rheovasography) and obtain an indirect argument confirming IHD.

Laboratory studies (clinical and biochemical blood tests) allow:

a) identify hyperlipidemia - a risk factor for coronary artery disease;

b) exclude the manifestation of resorption-necrotic syndrome and, in the presence of changes in the ECG and a prolonged attack of angina pectoris, reject the diagnosis of myocardial infarction.

In some cases, additional studies are carried out.

1. Coronary ventriculography allows to establish the degree and prevalence of atherosclerotic narrowing of the coronary arteries and the state of collateral blood flow.

2. Selective coronary angiography is performed :

1) for the diagnosis of coronary artery disease in unclear cases, mainly in young and middle-aged people, in whom labor recommendations largely depend on the diagnosis;

2) with undoubted coronary artery disease to resolve the issue of surgical treatment.

Given the invasive nature and complexity of the study, coronary angiography is often performed not for diagnostic purposes, but when deciding on coronary artery bypass grafting and percutaneous transluminal coronary angioplasty (PTCA) in patients with undoubted CAD.

It should be noted that a “normal” coronary angiogram only indicates the absence of a significant narrowing of the main coronary arteries and their branches, while changes in small arteries may remain undetected.

Carrying out these methods is possible only in specialized hospitals and according to certain indications.

ATHEROSCLEROTIC AND POST-INFARCTION CARDIOSCLEROSIS

Cardiosclerosis is a common form of chronic coronary artery disease.

There are 2 variants of it.

1) ischemic (atherosclerotic), developing slowly, with diffuse damage to the heart muscle;

2) post-necrotic (post-infarction) - in the form of a large focus of myocardial fibrosis at the site of former necrosis; a transitional, or mixed, variant, in which, against the background of a slow diffuse development of connective tissue, large fibrous foci periodically form after repeated myocardial infarctions.

Atherosclerotic and postinfarction cardiosclerosis can be manifested by rhythm disturbances and congestive heart failure. It is suggested that this form of chronic coronary artery disease also include chronic aneurysm of the heart.

Sometimes cardiosclerosis occurs without obvious clinical manifestations. The presence of coronary artery disease can also be suspected by changes in the ECG taken for random reasons.

In clinical terms, there are forms that are combined with angina pectoris and proceed without pain (only with rhythm disturbances and (or) signs of heart failure). On the early stages development of coronary artery disease in painless forms there is no clear subjective symptoms. Such forms proceed as if imperceptibly, and the first suspicions of coronary artery disease appear only during a physical examination, and often during deciphering the ECG. This must be taken into account when conducting each of the three stages of a diagnostic search.

Complaints of the patient, especially the elderly, indicating a violation of the heart rhythm (palpitations, interruptions in the work of the heart, a rare pulse, etc.), and manifestations of heart failure (shortness of breath, swelling of the lower extremities, heaviness in the right hypochondrium, etc.) without indication on past cardiovascular diseases should lead the doctor to the idea of ​​chronic coronary artery disease. The assumption becomes more reliable if the patient is disturbed, in addition, by pains in the heart of an angina pectoris, or, upon questioning, it is possible to obtain information about their equivalents (feeling of tightness in the chest, burning sensation).

When questioning a patient who has had a myocardial infarction, it is necessary to find out about possible heart rhythm disturbances, shortness of breath, episodes of suffocation (manifestations of postinfarction cardiosclerosis), even if he himself does not remember this.

It is possible to assume the presence of atherosclerotic cardiosclerosis in a patient with complaints of non-cardiac manifestations of atherosclerosis (intermittent claudication, memory loss, etc.) and non-specific complaints (decreased performance, general weakness).

It is necessary to establish, especially in young and middle-aged people, past illnesses, which may be accompanied by symptoms of heart failure and heart rhythm disturbances (myocarditis, heart defects, etc.). If they are present, the probability of coronary artery disease is significantly reduced, but the examination along the intended path of diagnostic search should be carried out at subsequent stages.

The objective of the physical examination of patients is to identify:

a) symptoms of heart failure in the pulmonary and systemic circulation;

b) chronic heart aneurysm;

c) rhythm disturbances;

d) non-cardiac localizations of atherosclerosis.

Signs of heart failure - shortness of breath, liver enlargement, tachycardia, edema - can be detected in a patient, especially the elderly, who did not present relevant complaints.

Pulsation in the precordial region, especially with indications of a previous myocardial infarction, makes it possible to suspect an aneurysm of the left ventricle. Heart rhythm disturbances may be first detected at this stage of the diagnostic search.

The presence of persistent atrial fibrillation in the absence of angina first of all requires the exclusion of rheumatic heart disease (active search for direct and indirect objective signs of malformation at this and subsequent stages of the examination), even if this diagnosis has never been made in the past.

Identification of such physical signs as left ventricular hypertrophy in a patient who does not suffer from any heart disease and hypertension, the accent of the II tone over the aorta with normal blood pressure and a decrease in pulsation in the vessels of the lower extremities, makes the proposed diagnosis of coronary artery disease extremely important.

In a laboratory diagnostic search, it is possible to detect:

a) rhythm and conduction disturbances;

b) initial manifestations heart failure;

c) chronic aneurysm of the heart;

d) symptoms of atherosclerosis.

The solution of this problem is facilitated by general clinical studies (ECG, x-ray examination organs of the chest, rheovasography of the lower extremities, biochemical blood tests). If at this stage the diagnosis of chronic coronary artery disease is not possible, then additional studies are carried out.

Electrocardiogram allows you to detect violations of the heart rhythm and conduction. In the absence of other diseases leading to similar manifestations, one should think about chronic coronary artery disease.

An ECG may reveal signs of left ventricular hypertrophy in a patient without hypertension and heart disease. In this case, the diagnosis of atherosclerotic cardiosclerosis can be made without its other manifestations, if the possibility of cardiomyopathy is excluded with the help of ultrasound.

Signs of a heart aneurysm can be detected on the ECG (clarify its presence by additional methods). Signs of cicatricial changes on the ECG make it possible to diagnose postinfarction cardiosclerosis even without its other obvious manifestations.

X-ray examination of the chest organs helps to identify signs of atherosclerosis of the aorta, an increase in the left ventricle, a decrease in the contractile function of the myocardium of the left ventricle (these changes are of diagnostic value only in combination with other signs of chronic coronary artery disease). important diagnostic sign IHD are radiographic symptoms of left ventricular aneurysm.

In the elderly x-ray examination can help identify heart disease that is not physically clearly manifested (verification of the diagnosis according to ultrasound of the heart).

Ultrasound examination of the heart is carried out for all patients with chronic coronary artery disease, its information content increases in the following cases:

1) if the diagnosis is unclear: to exclude idiopathic cardiomyopathy, valvular defects and other heart diseases;

2) with an established diagnosis of coronary artery disease - to exclude chronic aneurysm of the heart and postinfarction mitral insufficiency;

3) as an additional method for assessing the severity of myocardial damage (assessment of contractile function, degree of hypertrophy and dilatation of the heart chambers);

4) to resolve the issue of conducting percutaneous transluminal coronary angiography (PTCA) or coronary artery bypass grafting (CABG).

Biochemical blood test should be performed to detect lipid disorders, especially types of hyperlipidemias characteristic of atherosclerosis. It does not play a decisive role in diagnosis.

The following are considered additional instrumental methods research: ventriculography, radionuclide diagnostic methods.

Ventriculography is performed to identify and clarify the nature of chronic aneurysms of the heart (as a rule, during the preparation of the patient for plastic surgery for an aneurysm).

Radionuclide methods diagnostics are indicated for postinfarction cardiosclerosis in doubtful cases (to detect changes in the myocardium, it is used, which does not accumulate in scar areas).

Diagnosis of chronic ischemic heart disease

When making a diagnosis, the main and additional diagnostic criteria are taken into account. The main criteria are:

1) typical attacks of angina pectoris of exertion and rest (history, observation);

2) reliable indications of myocardial infarction (history, signs of chronic aneurysm of the heart, signs of cicatricial changes on the ECG);

3) positive results of exercise tests (veloergometry, frequent atrial pacing);

4) positive results of coronary ventriculography (coronary artery stenosis, chronic heart aneurysm);

5) identification of zones of postinfarction cardiosclerosis using cardiac scintigraphy.

Additional diagnostic criteria consider:

1) signs of circulatory failure;

2) violations of the heart rhythm and conduction (in the absence of other diseases that cause these phenomena).

The formulation of a detailed clinical diagnosis takes into account:

1) clinical variant of chronic coronary artery disease (often one patient has a combination of two or even three variants). With angina pectoris, its functional class is indicated;

2) the nature of rhythm and conduction disturbances, as well as the state of blood circulation;

3) main localizations of atherosclerosis; the absence of coronary atherosclerosis (the presence of convincing evidence according to coronary angiography) is necessarily reflected in the diagnosis.

Therapy for chronic coronary artery disease is determined by many factors. The main areas of treatment are:

1) treatment of hypertension, atherosclerosis and diabetes mellitus;

2) treatment of diseases that cause reflex angina;

3) proper antianginal therapy;

4) treatment of cardiac rhythm and conduction disorders, as well as congestive insufficiency blood circulation;

5) anticoagulant and antiplatelet therapy.

Treatment also includes diet therapy, adherence to a certain regimen, and drugs. Restricted diet shown easily digestible carbohydrates, the predominance of unsaturated fats, a sufficient amount of protein and vitamins. The energy value diet should strictly correspond to the energy needs of the body. It is necessary to limit the use of table salt with concomitant hypertension and signs of heart failure.

The patient's regimen should provide for limiting emotional and physical stress. Dosed physical activity is determined by the doctor individually for each patient.

Treatment of coronary artery disease with medicines It is aimed at balancing the myocardial oxygen demand and its delivery to the myocardium.

From various drugs best effect possess nitrates, B-blockers and calcium antagonists. Nitrates have a venodilating effect, which leads to the deposition of blood in the venous system and a decrease in blood flow to the heart. This, in turn, leads to a decrease in the volume and tension of the left ventricle and a decrease in myocardial oxygen demand. A decrease in oxygen demand leads to a redistribution of coronary blood flow in favor of ischemic areas of the myocardium.

Among the nitrates, the derivatives of isosorbide dinitrate and mononitrate are currently most widely used.

Preparations of isosorbide-5-mononitrate - monomak, isomonat, mononit and others - are used in tablets and have a significant (up to 12 hours) duration of action.

Preparations of isosorbide dinitrate (nitrosorbide, cardiquet, isoket, isodinite, isomak, etc.) are available in various dosage forms (tablets, aerosols, ointments) and have different durations of action (from 1 to 12 hours).

The preparations of prolonged nitrates have not lost their significance either. As prolonged nitrates, Sustak-mite (2.6 mg) and Sustak-Forte (6.4 mg) are used 1-2 tablets with an interval of 4-5 hours, nitrong (6.5 mg) 1-2 tablets every other day. 7-8 hours Trinitrolong is prescribed orally and in plates for applications on the oral mucosa to prevent angina attacks.

An attack of angina pectoris should be stopped by sublingual administration of nitroglycerin (in a tablet of 0.5 mg), the peak of the drug's action is 3-5 minutes.

If one tablet does not stop the attack, then you should repeat the reception. The duration of the drug action is 20 minutes.

In addition, other dosage forms of nitroglycerin are also used: buccal forms (trinitrolong plates are applied to the gum mucosa); aerosols of nitroglycerin or isosorbide dinitrate (inhaled through the mouth).

With poor tolerance to nitrates, you can prescribe a tablet of molsidomine (Corvaton) at a dose of 2 mg. If necessary, narcotic analgesics are administered to stop a protracted attack.

In the interictal period, drug therapy is selected taking into account the individual characteristics of the patient and the functional class of angina pectoris. As a rule, one of the drugs of the three main groups of prolonged dinitrates or mononitrates, B-blockers, calcium channel blockers is prescribed. As you know, B-blockers interfere with the action of catecholamines on the myocardium, resulting in a decrease in heart rate and a decrease in myocardial oxygen demand. In their antianginal action, most B-blockers in adequate doses differ little from each other, however, with an initial tendency to bradycardia, the use of drugs with the so-called internal sympathetic activity is indicated, due to which bradycardia does not develop (oxprenolol, pindolol - non-selective B-blockers and acebutalol, talinolol - selective blockers).

Non-selective B-blockers, such as propranolol, are widely used. Treatment begins with relatively small doses (40-60 mg / day), if necessary, the dose is increased to 80-160 mg / day. However, propranolol, in addition to the lack of selectivity, has another drawback - it is a short-acting drug and it must be taken 3-4 times a day (in order to maintain a sufficient concentration of the drug in the blood and antianginal effect). Selective B-blockers (metoprolol, atenolol, betaxolol, acebutolol) are much more effective. The dose of metoprolol is 100-200 mg / day, atenolol - 100-200 mg / day, acebutolol - 400-600 mg / day, betaxolol - 20-40 mg / day. All drugs have a prolonged action and can be taken 1-2 times a day (especially betaxolol). A very promising B-selective adrenoblocker with vasodilating action is carvedilol. In the absence of the effect of B-blockers or long-acting nitrates, calcium antagonists are prescribed, the most effective is isoptin-240 (daily dose 120-480 mg) and diltiazem (240-360 mg / day).

It is mandatory to constantly take antiplatelet agents - acetylsalicylic acid at a dose of 125-160 mg.

With functional class II angina pectoris, it is desirable to avoid the appointment of permanent therapy. For patients of this group, it is preferable to take the drug before the expected physical activity (buccal forms of nitroglycerin, and if it is poorly tolerated, calcium antagonists with antianginal activity - isoptin, diltiazem, etc.).

With prolonged physical exertion, it is advisable to prescribe prolonged forms of nitroglycerin in the form of an ointment rubbed into the skin (up to 6 hours) or a patch applied to the skin (up to 24 hours).

With prolonged use of nitrates (regardless of the form of the drug), tolerance to them may develop. The best way to avoid tolerance - apply nitrates intermittently (a significant decrease in the concentration of nitrates in the blood within 12 hours is sufficient to restore the sensitivity of specific receptors to nitrates).

Drug therapy of patients suffering from coronary atherosclerosis and high content blood cholesterol, especially low-density lipoprotein, should include regular use of statins - lovastatin or simvastatin. Permanent reception of these lipid-lowering drugs increases the survival rate of patients with coronary artery disease.

Currently, cytoprotective "protection" of the myocardium, which leads to an increase in myocardial resistance to ischemia, is very promising. The drug trimetazidine (preductal) affects the optimization of energy metabolism in the mitochondria of myocardiocytes, thereby providing their "protection". Preductal is prescribed at 60 mg / day for 2-3 months. It reduces the frequency and intensity of anginal attacks.

However, there is a group of patients for whom drug therapy is not enough; they should be advised surgical treatment - PTCA or CABG.

It is dangerous to remain without surgical treatment for the following groups of patients:

1) with damage to the main trunk of the left coronary artery;

2) with a three-vessel lesion of the main main coronary arteries;

3) with damage to two coronary arteries, one of which is the anterior interventricular branch of the left coronary artery.

With drug treatment, the prognosis in these patients is worse than with surgical treatment due to the high risk of MI and sudden death.

Patients with unstable angina need urgent hospitalization in cardiology department, and if a pre-infarction condition is suspected - in the intensive care unit.

Of the antianginal agents, nitrates are prescribed, including intravenous infusions of a solution of nitroglycerin, and sometimes calcium antagonists (diltiazem infusions: 25 mg for 5 minutes, and then a long-term infusion at a rate of 5 mg / h).

Currently, in the treatment of postinfarction cardiosclerosis, ACE inhibitors (Capoten, Enap) are used under the control of blood pressure. These drugs are especially effective when there are signs of heart failure.

Sometimes, in the treatment of coronary artery disease, drugs from other groups are used, in particular amiodarone (cordarone), a drug that is similar in mechanism to B-blockers. Especially justified is the use of cordarone in the presence of ventricular arrhythmias. Kordaron is prescribed at 600–800 mg/day for 2–4 weeks, and then the dose is reduced (maintenance therapy period) to 200–400 mg/day.

Drug therapy is carried out more intensively during periods of increased frequency and intensification of angina attacks, and upon reaching the effect and in cases of remission of the disease, the doses of drugs are gradually reduced to the minimum effective (sufficient to prevent angina attacks).

AT without fail carry out the treatment of arterial hypertension, cardiac arrhythmias, heart failure according to the rules set forth in the relevant sections.

The prognosis should always be evaluated with caution, as chronic course the disease can suddenly worsen, be complicated by the development of MI, sometimes by sudden death.

Primary prevention is reduced to the prevention of atherosclerosis.

Secondary prevention should be aimed at conducting rational anti-atherosclerotic therapy, adequate treatment pain syndrome, rhythm disturbances and heart failure.