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The main cause of coronary heart disease. Coronary heart disease. Causes: how coronary heart disease occurs

Cardiac ischemia or IHD - one of the most common and serious cardiac ailments, characterized by unpredictability and severity of manifestations. The victims of this disease most often are men of active age - 45 years and older.

Disability or sudden death is a very likely outcome with IHD. In our country alone, about 700 thousand deaths caused by various forms of ischemia are recorded annually. Globally, the mortality rate from this disease is almost 70%. That's why regular monitoring is so important!

Blood test for ischemia


Tests for cardiac ischemia


Diagnostics of ischemic heart disease in "MedicCity"

The development of coronary artery disease is provoked by an imbalance between the myocardial need for blood supply and the actual coronary blood flow.

The main reason for insufficient blood supply and oxygen starvation of the heart muscle is narrowing of the coronary arteries due to (atherosclerotic plaques in the lumen of blood vessels), atherothrombosis and (or) spasm.

The pathological process can affect either one or several arteries at once (multivascular lesion). Significant narrowing of the coronary arteries impedes the normal delivery of blood to the myocardial fibers and causes pain in the heart.

Without proper treatment and medical supervision, coronary ischemic heart disease, caused by a lack of oxygen and nutrients, can lead to cardiac arrest and sudden cardiac death.

Factors contributing to the development of ischemic heart disease

The main causes of the development of coronary heart disease can be identified:

  • (increases the likelihood of developing ischemia by 2-6 times);
  • smoking (in tobacco addicts, the risk of developing coronary heart disease is 1.5-6 times higher than in non-smokers);
  • disturbance of lipid and lipoprotein metabolism (promotes the development and increases the risk of ischemia by 2-5 times);
  • physical inactivity and obesity (obese, inactive people get sick at least 3 times more often than thin and athletic people);
  • disorders of carbohydrate metabolism (with diabetes of both types, the threat of coronary heart disease increases by 2-4 times).

Risk factors also include family history, being of the stronger sex, and old age. When two or more of the listed positions are combined, the risk of developing IHD increases significantly.


ECG for cardiac ischemia


ABPM in the diagnosis of ischemia


ECHO-CG for ischemic heart disease

Detection of myocardial ischemia

Symptoms of coronary heart disease can be either pronounced or subtle.

Among the most characteristic symptoms of IHD are the following:

  • Pressing pain and burning behind the sternum and in the heart area during physical activity;
  • shortness of breath on exertion.

But sometimes IHD does not reveal itself until myocardial infarction! In this case, the classic symptoms of coronary heart disease may be noticed too late.

Classification of coronary heart disease

Depending on the symptoms, the following main forms of the disease are distinguished:

Coronary death . Symptoms develop rapidly: loss of consciousness, pupils are dilated and do not respond to light. No pulse, no breathing.

Post-infarction cardiosclerosis . Among the characteristic signs: heart rhythm disturbances, acute manifestations (attack of suffocation - “cardiac asthma”, pulmonary edema) and chronic (swelling of the legs, shortness of breath). The patient complains of a feeling of lack of air, shortness of breath, and swelling of his legs and feet.

Acute coronary syndrome. New-onset angina, progressive angina, myocardial infarction, etc.

Myocardial infarction . Often severe pressing and burning pain behind the sternum, radiating to the jaw, left shoulder blade and arm. Lasts up to half an hour or more, does not go away when taking nitroglycerin under the tongue. The patient also develops cold sweats, blood pressure decreases, weakness, vomiting and fear of death may appear.

Angina pectoris . A person complains of chest pain - squeezing, squeezing, burning behind the sternum during physical activity and sometimes at rest. Possible symptoms of angina include pain in the neck, left shoulder blade, lower jaw or left arm. The pain is usually short-lived.

Angina is one of the most striking manifestations of coronary heart disease. Self-treatment of angina pectoris with folk remedies is unacceptable! Only a doctor, based on his professional experience and diagnostic techniques, can draw conclusions about a person’s condition and the necessary treatment measures!


Ultrasound of the heart for angina pectoris


Ultrasound of the heart in "MedicCity"


Blood tests for ischemic heart disease

If angina pectoris occurs for the first time, if angina attacks begin to occur more often, last longer and manifest themselves more strongly, we are talking about acute coronary syndrome and a high risk of developing myocardial infarction. Such patients should be urgently hospitalized by ambulance to a hospital, where coronary angiography will be performed on an emergency basis and blood flow in the arteries of the heart will be restored, which will avoid the occurrence of myocardial infarction and, as a consequence, disability.

Silent myocardial ischemia

IHD may not be accompanied by pain. This ischemia is called silent ischemia.

The manifestation of the disease in the case of silent myocardial ischemia is often immediate or sudden coronary death. Therefore, it is very important to be regularly examined by a cardiologist, especially for people at risk (diabetics, hypertension, smokers, obese people, the elderly, etc.).

Such hidden ischemia can be detected using some instrumental techniques, for example, treadmill). It is during a stress test that changes specific to IHD are especially pronounced.

Diagnosis of coronary heart disease

The success of preventive and therapeutic measures depends on the timely detection of the disease and correct diagnosis.

Of course, the initial stage of diagnosing IHD is the collection and analysis of the patient’s complaints. This is followed by an examination, during which the cardiologist measures the patient’s blood pressure, visually assesses his condition (degree of swelling, skin tone, sweating, behavioral characteristics, etc.), listens to his heart with a stethoscope for murmurs, rhythm disturbances, etc.

  • clinical and biochemical blood tests;
  • blood test for markers of myocardial infarction;
  • coronary angiography (x-ray contrast examination of the coronary arteries).


Ultrasound of the heart for ischemic heart disease


Diagnostics of ischemic heart disease in "MedicCity"


ABPM in IHD

Treatment of coronary heart disease. Prevention

The success of treating coronary heart disease depends on many factors. Thus, a combination of ischemia with and can significantly aggravate the situation. Whereas the patient’s commitment to a healthy lifestyle and focus on recovery can be a huge help to the doctor and his chosen treatment regimen.

The treatment strategy for coronary artery disease for each individual patient is individual and is determined by the attending physician based on the results of studies and tests. However, we can list the main types of treatment for coronary heart disease used in modern cardiology.

As a rule, patients with coronary artery disease are prescribed:

1. Non-drug therapy , which includes the maximum possible elimination of the threats of coronary artery disease (detection and treatment of concomitant diseases, diet, adherence to work and rest, weight loss, blood pressure control, feasible physical activity, lifestyle changes).

2. Pharmacotherapy (depending on the form of ischemia, the following may be prescribed: aspirin, nitroglycerin, nitrates, calcium antagonists, statins and/or other cholesterol-lowering medications, beta-blockers, angiotensin-converting enzyme inhibitors, trimetazidine, etc.).

3. Surgery . The most common operations for coronary artery disease today are endovascular techniques (stenting of the coronary vessels of the heart and angioplasty), as well as myocardial revascularization (coronary artery bypass grafting).

During operations of the first type, a catheter is inserted into the artery, through which a super-thin conductor is passed with a deflated air balloon and a folded stent - a tube made of the finest medical wire. The balloon is inflated as soon as it reaches the point of narrowing of the lumen - this is necessary to expand the walls of the artery, then the stent is straightened. Next, the balloon is deflated and removed along with the catheter, and the expanded stent remains in the artery, preventing its re-narrowing and ensuring normal blood flow. Coronary artery bypass grafting is a method in which the surgeon bypasses blocked coronary vessels using a graft - a vein taken from the patient's arm or leg. The operation is performed for very serious reasons, since it is performed on an open heart.

As for preventing the disease, the most effective prevention of coronary heart disease, as well as most CVDs, are blood pressure control, a healthy diet, maintaining physical fitness, and quitting tobacco.

Diagnostics and treatment at MedicCity is the right choice for every person who cares about their health! Our team knows how to help you maintain good health for many years! We use equipment from leading manufacturers and carry out all necessary types of diagnostics and other organs and systems with high quality.

Coronary heart disease has taken a leading place in the list of major medical problems of the 21st century. Pathology has become the leading cause of death among the population in many countries of the world, including developed European ones. A certain downward trend in the popularity of IHD was observed in the United States at the end of the last century, but in general, the spread of the disease is observed among people of different ages and genders.


Coronary heart disease (CHD) is a general concept that combines acute and chronic pathological processes with similar pathogenesis. The key role in the formation of coronary artery disease is attributed to the disruption of coronary circulation, as a result of which the metabolic metabolism in the heart muscle changes. In other words, the myocardium requires more oxygen and nutrients than is supplied to it with the existing blood flow.

The course of IHD is divided into acute, in the form of myocardial infarction, and chronic, when the patient is bothered by periodic attacks of angina.

A special role in determining the type and nature of the course of IHD is given to modern diagnostic methods. The patient's complaints, objective examination, laboratory parameters and results of instrumental methods are taken into account. All this makes it possible to make an accurate diagnosis and subsequently prescribe effective treatment. Otherwise, an unfavorable prognosis is given.

Video: Coronary heart disease - causes, diagnosis, treatment

Classification of IHD

The disease is considered in various rubricators, classifiers and open databases. But the most commonly used is the International Classification of Diseases, 9th and 10th revision. According to ICD-10, IHD is listed under I20-I25 font, and in ICD-9 - under 410-414.

According to material from Wikipedia, the term “coronary heart disease” comes from Lat. morbus ischaemicus cordis from ancient Greek. ἴσχω - “delay, restrain” and αἷμα - “blood”.

In the IHD group, the following clinical forms are distinguished:

  1. Angina, which in turn is divided into unstable and stable, or exertional angina.
  2. Myocardial infarction (primary).
  3. Myocardial infarction (repeated).
  4. Previous myocardial infarction, manifested in post-infarction cardiosclerosis.
  5. Sudden coronary death, which may result in successful resuscitation and death.
  6. Heart failure.

When making a diagnosis, the clinical form of the disease must be indicated, for example: “IHD: stable angina pectoris class II.” Some clinical forms are considered in separate classifications, according to which the required designation is necessarily indicated in the final diagnosis.

Braunwald classification of unstable angina

A – there is an external cause that increases ischemia. Secondary unstable angina B – there is no external cause of angina. Primary unstable angina C – occurs within 2 weeks after myocardial infarction. Post-infarction angina
I – new onset, progressive angina, without angina at rest I.A. I.B. IC
II – angina at rest within a month, but not within the next 48 hours IIA IIB IIC
III – angina at rest in the near future IIIA IIIB IIIC

A – there is an external cause that increases ischemia. Secondary unstable angina B – there is no external cause of angina. Primary unstable angina C – occurs within 2 weeks after myocardial infarction. Post-infarction angina
I – new onset, progressive angina, without rest angina IA IB IC
II – angina at rest within a month, but not within the next 48 hours IIA IIB IIC
III – angina at rest in the next 48 hours IIIA IIIB IIIC

In addition to the above classification, in the group of unstable angina there are early post-infarction KS, progressive and new-onset, as well as Prinzmetal, or variant.

The classification of myocardial infarction is very comprehensive and is considered according to the stages of development, the scale and anatomy of the lesion, the localization of the necrotic focus, and the course of the disease. In addition, there are more modern classifications developed on the basis of general considerations of the European, American and world cardiological communities.

Causes of IHD

The development of the disease is directly related to the insufficient amount of oxygen supplied to the heart muscle. Due to oxygen starvation, the myocardium begins to lose the ability to perform its functions, and the larger the affected area, the more pronounced the clinical picture of the disease will be. In some cases, blood circulation in the coronary vessels stops so abruptly that an acute oxygen deficiency occurs with all the ensuing consequences

Why does blood flow in the coronary vessels stop? One or more pathological mechanisms may be involved:

  1. Atherosclerosis and thrombosis.
  2. Atherosclerosis of coronary vessels.
  3. Spasm of blood vessels.

There are also so-called extravascular etiological factors that contribute to the development of coronary artery disease. In some cases, risk factors that contribute to the manifestation of the clinical picture of a sluggish process play an important role.

Development factors

The key etiological factor in the development of IHD is atherosclerosis. With this pathology, a narrowing of the lumen of the coronary arteries is observed, which is why the needs of the myocardium for blood supply do not coincide with the real capabilities of the bloodstream.

With atherosclerosis, specific plaques are formed, which in some cases block the lumen of the vessel by 80%. Then myocardial infarction develops, or, as a “milder” option, angina pectoris.

The formation of an atherosclerotic plaque does not occur simultaneously. This may take months or even years. Initially, low-density lipoproteins are deposited on the walls of the coronary vessels, which gradually begin to affect the epithelium located nearby.

At the site of the lesion, platelets and other blood cells accumulate, which is why the lumen of the vessel is blocked by an increasingly protruding part of the plaque. If the pathological formation occupies up to 50% of the lumen of the vessel, then the clinical picture of the disease is sluggish or not expressed at all. Otherwise, IHD develops in one clinical form or another.

Each coronary artery supplies blood to a specific area of ​​the myocardium. The further the area of ​​the vessel affected by atherosclerosis is from its distal end, the more extensive ischemia or necrosis may be. If the mouth of the left coronary artery or the main trunk is involved in the pathological process, then the most severe ischemia of the heart muscle develops.

In addition to developmental factors lying inside the vessel, there are also extravasal causes. First of all, this is arterial hypertension, which most often provokes spasm of the coronary vessels. The formation of coronary artery disease is promoted by frequent and severe tachycardia, as well as myocardial hypertrophy. In the last two cases, the oxygen demand of the heart muscle increases sharply and when they are not met, ischemia develops.

Risk factors

Modern scientists and leading clinicians attach great importance to predisposing circumstances in the formation of coronary artery disease. Against their background, with the highest probability, a pathological condition can develop with all the ensuing consequences. The risk factors for ischemic heart disease are in many ways similar to those for atherosclerosis, which is associated with the direct participation of the atherosclerotic plaque in the partial or complete blocking of the lumen of the vessel.

Coronary heart disease is associated with many risk factors (RFs), so a unique classification was required to organize them for better understanding.

  1. Biological RF:
  • Men get sick more often than women.
  • In older people, atherosclerosis is more often determined, and therefore the likelihood of myocardial ischemia is higher.
  • Hereditary predispositions that contribute to the development of diabetes mellitus, hypertension, dyslipidemia, and therefore coronary artery disease.

2. Anatomical, physiological and metabolic risk factors:

  • Diabetes mellitus, mainly of the insulin-dependent type.
  • Overweight and obesity.
  • Arterial hypertension.
  • An increased amount of lipids in the blood (hyperlipidemia) or an imbalance in the percentage of different types of lipids (dyslipidemia).

3. Behavioral risk factors:

  • Poor nutrition.
  • Having bad habits, especially smoking and drinking alcohol.
  • Physical inactivity or excessive physical activity.

Muscular-elastic hyperplasia of the intimal arteries, including coronary arteries, is another possible risk factor for the occurrence of coronary heart disease, but today it is under study. Changes in vessels according to the type of hyperplasia are already detected among children, so there are assumptions about the contribution of such risk factors to the development of coronary artery disease at an older age. In addition, the role of the CDH13 gene and its mutation in the formation of ischemia is being studied, but so far this assumption has not been fully proven.

Types of IHD

In patients with coronary artery disease, the most common clinical forms are myocardial infarction and angina pectoris. Other varieties are not as common, and they are more difficult to diagnose. Based on this, the clinical picture and course of myocardial infarction, angina pectoris, sudden coronary death and post-infarction cardiosclerosis will be considered.

Myocardial infarction

Such a diagnosis can be established when there is myocardial necrosis confirmed by clinical, laboratory and instrumental methods. It can be small or large, but regardless of this, the patient should be sent to the intensive care unit as soon as possible.

  • Large-focal myocardial infarction is characterized by pathognomonic changes, which are determined on the ECG and during laboratory diagnostics. Particularly important is the increase in serum lactate dehydrogenase, creatine kinase and a number of other proteins.

Such enzymes indicate the activity of the redox reaction taking place in the body. If normally these components are found only in cells, then when they are destroyed, the proteins pass into the blood, so by their quantity one can indirectly judge the scale of necrosis.

  • Small-focal myocardial infarction is often tolerated by patients “on their feet,” since the clinical picture may not be expressed, and changes in the ECG and in tests are also not as critical as in the case of large-focal myocardial infarction.

Angina pectoris

The disease has a characteristic clinical sign - chest pain, which can arise from any stress (physical or emotional). The pain can be felt as a burning sensation, heaviness or severe discomfort, and often spreads along the nerve fibers to other parts of the body (scapula, lower jaw, left arm.

The duration of an angina attack is most often 1-10 minutes, much less often - up to half an hour.

Another feature characteristic of angina is pain relief with nitroglycerin, which practically does not help with myocardial infarction. Also, painful sensations can go away on their own if the emotional or physical irritant has been eliminated.

Characteristics of individual forms of angina pectoris:

  • New-onset angina is quite variable in its course, so it is not immediately possible to make an accurate diagnosis. This usually takes up to three months. During this period, the patient’s condition and the development of the disease, which can become progressive or stable, are monitored.
  • Stable angina is characterized by the occurrence of pain with a certain pattern. The severity of stable angina is determined by functional classes; the corresponding FC is necessarily indicated in the final diagnosis.
  • Progressive angina - the intensity of painful attacks increases quite quickly, while the patient's resistance to physical and emotional stress decreases. This form of angina is poorly controlled by nitroglycerin and in severe cases, the administration of narcotic analgesics may be required.

Angina pectoris occurs spontaneously and is not associated with any physical or emotional stimuli. This form of angina is often detected at rest, at night or in the morning. This pathology is defined as spontaneous angina.

Sudden coronary death

The second clinical designation is primary cardiac arrest. Its formation is associated with electrical instability of the myocardium. Such a diagnosis is made only if there is no confirmation by definition of another specific form of IHD. For example, the heart may stop due to myocardial infarction, and then the diagnosis indicates death from myocardial infarction.

A high risk of sudden coronary death is observed in those patients who have signs of narrowing of a large number of coronary vessels on coronary angiography. An unfavorable condition is considered to be dilatation of the left ventricle. The likelihood of developing sudden coronary death after a heart attack increases significantly. Also, any myocardial ischemia, including those without pronounced painful sensations, can be considered as a danger due to the sudden cessation of cardiac activity.

Post-infarction cardiosclerosis

In clinical practice, this disease is considered a complication of a previous myocardial infarction. It takes at least 2 months to make such a diagnosis. In some cases, post-infarction cardiosclerosis is considered as an independent disease, but for this the presence of angina pectoris, heart failure, etc. should not be confirmed. In addition, the ECG must show signs of focal or diffuse cardiosclerosis.

In relatively mild cases, patients experience interruptions in heart rhythm. The severe course of the disease is accompanied by shortness of breath, edema, heart pain, inability to bear the load, etc. The complexity of the pathology lies in the fact that there is a more or less noticeable progression of the process, which can only be stopped temporarily by well-chosen therapy.

Video: Types and forms of coronary heart disease

Diagnostics

Patients diagnosed with coronary heart disease are treated by a cardiologist, who during the initial appointment pays attention to clinical symptoms. The following characteristic complaints are distinguished with IHD:

  • Pain behind the sternum, which in most cases is associated with emotional and physical stress.
  • Improper functioning of the heart, which is accompanied by weakness and arrhythmia.
  • Swelling in the legs, indicating heart failure.
  • Feeling short of breath.

Anamnesis of the disease is of considerable importance during the examination. This is when the doctor asks clarifying questions about the nature of the pain, its duration, etc. The amount of physical activity that the patient can withstand relatively calmly is also important. For correct diagnosis, information must be obtained on the effectiveness of various pharmacological drugs, including nitroglycerin. Risk factors are further clarified.

All patients with suspected ischemic heart disease undergo electrocardiography. This indirect diagnostic method cannot accurately indicate how many cardiomyocytes have died, but it can be used to determine myocardial functions such as automaticity and conduction capacity.

The following signs of myocardial infarction are clearly visible on the ECG:

  • The appearance of a pathological Q wave, which in some leads is combined with a negative T wave.
  • In acute infarction, the ST segment rises high and appears as a “sailboat” or “cat’s back”.
  • With myocardial ischemia, ST segment depression is observed.
  • If there is a scar in the myocardium, the ECG shows a weak negative T wave and a pathological Q wave for two days or more.

An ECG is necessarily supplemented by an ultrasound of the heart. Using this modern research method, it is possible to assess in real time the condition of the heart muscle, how much the contractility of the heart has been affected by a heart attack, and whether there are any disturbances in the functioning of the valve apparatus. If necessary, echocardiography is combined with Doppler ultrasound, which allows assessing the possibilities of blood flow.

Laboratory research are relevant for diagnosing myocardial infarction, since various biochemical parameters change during the development of the pathological process. First of all, protein fractions are determined, which are normally found only inside the cell, and after the destruction of cardiomyocytes enter the blood. For example, in the first 8 hours after a heart attack, the level of creatine kinase increases, and in the first day - myoglobin. Up to 10 days, troponins are determined, the amount of lactate dehydrogenase and aminotransferase is also important.

When the structure of the myocardium is disrupted, a nonspecific reaction is observed in the form of an increase in the concentration of AST and ALT, erythrocyte sedimentation rate (ESR) and the appearance of neutrophilic leukocytosis.

In patients with coronary artery disease, the lipid profile must be examined. For this purpose, indicators such as total cholesterol, triglycerides, high and low density lipoproteins, apolipoproteins and the atherogenic index are determined.

Functional tests in combination with ECG registration, they allow one to assess the capabilities of the heart muscle under the influence of physical activity. This is extremely important for early diagnosis of the disease, since not all patients exhibit clinical changes at rest. A person can be stressed in a variety of ways. The most common is an exercise bike. A treadmill, walking on stairs, etc. are also often used.

Additional instrumental studies:

  • CT angiography (or angiography of the coronary vessels) is performed to obtain X-ray images of vessels contrasting with a special substance. The resulting images show blockage of the arteries, their occlusion, and the degree of patency is also assessed.
  • Monitoring using the Holter method consists of recording an ECG for a day or two, for which the patient carries a special device with him all the time. The study makes it possible to determine subtle and hidden changes in cardiac activity when a standard ECG cannot detect changes due to the rare occurrence of an attack.
  • Intraesophageal ECG - is performed in cases where no changes are recorded on the standard ECG, but there are clinical signs of the presence of additional foci of excitation. To conduct the study, an active electrode is inserted into the esophagus, which studies the electrical activity of the atria and atrioventricular node.

Treatment of coronary artery disease

Treatment tactics are based on the classification of coronary heart disease, since each clinical form has its own specific therapy method. Despite this, there are general guidelines for the management of patients with coronary artery disease, which are as follows:

  • Moderate physical stress is important in stabilizing patients with coronary artery disease, since the higher the physical activity, the greater the need for oxygen, and due to impaired blood supply to the heart muscle, this only aggravates the course of the disease by provoking new attacks. If the patient is recovering, then gradually physical activity increases.
  • Dietary nutrition should be as gentle as possible for the myocardium, therefore the amount of salt and the volume of water is reduced. When determining atherosclerosis, foods such as smoked meats, pickles, and animal fats are excluded from the diet. High-calorie and fatty foods are also not recommended for consumption. If the patient is obese, then they are especially careful about counting calories, since energy expenditure must be related to the energy supplied from food.

Drug therapy

US cardiologists proposed a treatment regimen under the abbreviation “A-B-C”. It is based on the use of drugs from three pharmacological groups: antiplatelet agents, beta-blockers, statins (considered cholesterol-lowering drugs). If a concomitant disease in the form of hypertension is determined, then medications are added to treat this pathology.

  • Antiplatelet agents - prevent the gluing of red blood cells and platelets, as well as their further adhesion to the inner wall of the vessel. As a result, blood rheology improves and the risk of developing blood clots is reduced. Of the drugs in this group, acecardol and aspirin are most often used, and clopidogrel is also prescribed.
  • Beta-blockers - according to the mechanism of action, they stimulate adrenergic receptors in myocardial cells, which leads to a decrease in cardiac contractility. This, in turn, has a beneficial effect on the condition and performance of the organ. Drugs from this group are contraindicated in some pulmonary diseases. Today, metoprolol, carvedilol, and bisoprolol are most often used.
  • Statins and fibrates are classified as anticholesterolemic medications because they help slow the growth of existing atherosclerotic plaques and prevent the formation of new ones. To some extent they can alleviate the severity of an attack of ischemic heart disease. From this group, lovastatin, simvastatin, rosuvastatin, and atorvastatin are most often prescribed. Fibrates, among which fenofibrate is the best known, can increase the level of high-density lipoproteins, which have antiatherogenic significance.

Depending on the indications and concomitant pathology, the patient may be prescribed nitrates (expand the venous bed and thereby relieve the load on the heart), anticoagulants (prevent the formation of blood clots), diuretics (loop or thiazide). Antiarrhythmic drugs in the form of amiodarone may also be prescribed to treat and prevent arrhythmia.

Video: What drugs are used to treat coronary heart disease (CHD)?

Natural lipid-lowering agents

In complex therapy, lipid-lowering agents such as aspirin and policosanol can be used. The latter name is a general term for long-chain alcohols that are produced from plant waxes. Today, they are often detected in various food additives.

When used, policosanol does not have a negative effect on coagulation, while it helps to increase the concentration of high-density lipoproteins and reduce the fraction of “harmful” low-density lipoproteins. Additionally, the substance has an antiplatelet effect.

Endovascular coronary angioplasty

It is an alternative to open surgery. It is used for various forms of coronary artery disease, even in the case of progression of the pathology and to prevent complications. This method combines coronary angioplasty and endovascular technologies, often represented by transluminal and transluminal instrumentation.

To dilate spasmodic vessels, which cause myocardial ischemia, stenting is most often used, and, less commonly, balloon angioplasty. All manipulations are performed under the control of coronary angiography and fluoroscopy. To introduce the required instruments, a large vessel is selected, mainly the femoral artery is preferred.

Video: Stenting of coronary arteries

Surgery

In some circumstances, coronary heart disease cannot be treated with medication. Then the option of surgical intervention is considered, in particular coronary artery bypass grafting. The purpose of this technique is to connect the coronary vessels to the aorta through an autograft (represented mainly by the great saphenous vein).

The main indications for surgery for ischemic heart disease:

  • multiple lesions of the coronary vessels;
  • determination of trunk stenosis in the area of ​​the left coronary vessel;
  • determination of ostial stenoses in the area of ​​the right or left coronary vessel;
  • stenosis of the anterior coronary vessel, which is not amenable to angioplasty.

Surgical treatment cannot be carried out when the patient has multiple lesions of the peripheral coronary vessels, located diffusely. Also considered a contraindication are low myocardial contractility, the presence of heart failure in the stage of decompensation and a post-infarction state that is no more than 4 months old.

Non-drug treatment

Conservative therapy, if necessary, can be supplemented with non-drug methods of influence, which also help improve the condition of the myocardium.

Basic non-drug treatment methods:

  • Hirudotherapy is known as leech treatment. The saliva of these creatures contains components with an antiplatelet effect, as a result of which blood clots are prevented. It is difficult to judge the effectiveness of the method, since it does not have approval from the field of evidence-based medicine.
  • Shock wave therapy of the heart - low power shock waves are used to implement the technique. Under their influence, new vessels begin to form in the myocardium, which significantly improves blood supply to the tissues. This is exactly what is necessary to reduce the ischemic area. The non-invasive method is most often used when conservative and surgical treatment is ineffective. According to some researchers, improvement in myocardial perfusion is observed in almost 60% of patients.
  • Enhanced external counterpulsation - the method of implementation is similar to internal counterpulsation. It refers to non-surgical methods and is based on the work of special air cuffs that are worn on the legs. Due to the sharp pumping of air from the cuffs during systole, the pressure in the vascular bed is reduced, which means the load on the heart is relieved. At the same time, during diastole, the bloodstream, on the contrary, is intensively filled with blood, which improves the condition of the myocardium. After extensive research in the USA, the method was approved and is now widely used in clinics.

Forecast

The conclusion on the development of the disease largely depends on the severity of the clinical picture and the severity of structural changes in the myocardium. In most cases, the prognosis is relatively poor because, regardless of treatment, it is impossible to reverse the disease. The only thing is that therapy helps to improve the patient’s well-being, make attacks less frequent, and in some cases it is possible to significantly improve the quality of life. Without treatment, the disease progresses very quickly and is fatal.

Coronary heart disease (or IHD) is a condition of complete or relative disruption of the blood supply to the heart muscle (myocardium) as a result of damage to the coronary arteries (blood vessels of the muscle layer).

Coronary heart disease is preceded by a decrease in blood supply (ischemia), causing myocardial damage. Due to decreased blood circulation, oxygen enters the myocardium in less quantity than necessary.

IHD is a fairly common phenomenon. According to the World Health Organization (WHO), the mortality rate from cardiovascular diseases is 32% worldwide. The mortality rate from heart and vascular diseases in Russia is 51%, of which 29% of deaths were from ischemic heart disease. This means that every year 29,000 people out of 100 thousand people die from coronary heart disease. In the European Union, mortality from coronary heart disease is recorded in 20% of cases (20,000 people out of 100 thousand), which is lower than in the Russian Federation.

With age, the risk of developing coronary artery disease increases. Coronary heart disease is observed in 30% of women, while the figure for the male population is 50%.

The root cause of coronary heart disease is:

  • coronary vessels (cholesterol plaques deposited on the walls of blood vessels);
  • spasm of coronary vessels;
  • hypertension (a manifestation of high blood pressure);
  • severe blood clotting.

There are risk factors that can provoke the condition of IHD. There are controllable factors (depending on the person) and uncontrollable factors (occurring against the will, they cannot be changed) that cause IHD.

Uncontrollable risk factors for IHD are:

  • male gender;
  • age (for men - from 45 years, for women - from 55);
  • heredity;
  • race (among the Negroid race the disease is less common).

Controllable risk factors for IHD include:

  • obesity;
  • hypothyroidism (lack of thyroid hormones);
  • hyperlipidemia (high levels of fats in the blood);
  • malnutrition;
  • smoking;
  • alcoholism;
  • sedentary lifestyle;
  • long-term use of hormonal drugs;
  • increased blood clotting;
  • prolonged stress state;
  • diabetes mellitus (CHD is observed in people who have had diabetes for more than 10 years).

The structure of the heart and its functions

To better understand such a pathology as coronary artery disease, let’s consider the structure of the heart. The average weight of a human heart is 300 grams. It performs a pumping function, driving blood through the vascular system, which allows the body to function fully.

The human heart is four-chambered, that is, it consists of 4 cavities. The cardiac septum vertically divides the organ into 2 compartments, containing 2 chambers. The cavities of the heart located at the top are the atria, and at the bottom are the ventricles.

The atria are separated from each other by the interatrial septum. Between the ventricles is the interventricular septum. Each atrium is connected to the corresponding ventricle through an opening. It closes and opens the cusp (valve) between the corresponding atrium and ventricle.

The valve located between the left atrium and the left ventricle is called bicuspid (or mitral), and the valve located between the right atrium and the right ventricle is called tricuspid (or tricuspid).
The chordae tendineae are also a component of the heart.

They control the heart valves through which blood flows. When contracting, they pull the valve along with them.
The heart contains papillary (papillary) muscles that help move blood in the right direction.

The cardiac conduction system (CCS) is the anatomical nodes, bundles and fibers of the heart responsible for electrical conductivity. The heart has a sinus node (sinoatrial), which is where the path of electrical impulses through the heart begins, causing it to function. The node is located in the right atrium, in its upper part. It is responsible for the formation of electrical impulses supplied to the organ and setting the correct rhythm of work.

A person has a cardiovascular system, which is divided into 2 circles of blood circulation: small and large. Heart contractions provoke the movement of blood in these circles. Blood movement occurs through diastole (a state of relaxed heart) and systole (contraction of the heart). When the muscles relax, blood fills the chambers, and when the muscles contract, it is pushed out by the muscles.

The superior and inferior vena cava flow into the right atrium. Deoxygenated blood comes from the body along them, then it goes from the right atrium to the right ventricle, then passes to the pulmonary trunk (it is a continuation of the right ventricle). The pulmonary trunk has a pulmonary valve, through which blood flows to the lungs (more precisely to their capillaries). There the blood is saturated with oxygen and returns to the left atrium.

Once oxygenated, the blood moves to the left atrium and then to the left ventricle. The ventricle sends blood through the aortic valve to the aorta of the left ventricle. Through it, blood flows to all tissues of the body, providing them with oxygen, then the deoxygenated blood returns to the right atrium and the blood circulation cycle repeats. Thus, the heart performs a pumping function in the cardiovascular system.

Between the ventricles and arteries there are semilunar valves that serve as an obstacle to the blood flow back.

The heart also needs oxygen, so the heart is nourished through the coronary circulation. Two coronary arteries (branches of the aorta) supply the myocardium with blood.

The structure of the heart wall consists of 3 layers:

  • pericardium (outer lining of the heart, separated from the epicardium);
  • epicardium (separated from the pericardium);
  • myocardium (middle muscle layer);
  • endocardium (inner epithelial layer).

Heart characteristics:

  • contractility (contracts, works like a pump);
  • automaticity (produces electrical impulses);
  • conductivity (conducts electrical impulses);
  • excitability (reacts to impulses).

Pathogenesis of IHD

The leading cause of the development of coronary artery disease is atherosclerosis of the coronary vessels. The condition of clogged blood vessels occurs when lipid and protein metabolism is disrupted. With this disorder, cholesterol is deposited on the walls of blood vessels, forming cholesterol plaques.

As a result of the settling of cholesterol plaques, the lumen in the blood vessels narrows. Over time, plaques grow in size and can completely block the vessel. The small lumen of the artery prevents the blood from providing the heart with sufficient oxygen and nutrients. As a result of a deficiency of useful oxygen, catecholamines are activated (they enter the blood and are a reaction to stressful situations or emotions). These include adrenaline (“stress hormone”), dopamine (“happiness hormone”), norepinephrine (“rage hormone”). Catecholamines increase the activity of the heart, as a result, the muscle layer needs even more oxygen. In this regard, the production of hormones increases and a vicious circle is obtained.

IHD according to ICD 10

According to the International Classification of Diseases, 10th revision, coronary heart disease (CHD) has codes I20-I25:

  • I20 - Angina pectoris (angina pectoris)
  • I21 - Acute myocardial infarction
  • I22 - Repeated myocardial infarction
  • I23 - Some current complications of acute myocardial infarction
  • I24 - Other forms of acute coronary heart disease
  • I25 - Chronic ischemic heart disease

Classification of IHD

Coronary heart disease manifests itself as an acute (cardiac arrest, heart failure, unstable angina, myocardial infarction) and chronic condition (heart failure, post-infarction cardiosclerosis, silent myocardial ischemia, angina).

The forms of IHD are described below:

  1. Sudden cardiac (coronary) death:
    • sudden cardiac death with successful resuscitation;
    • death.
  2. Angina includes:
    • stable angina;
    • microvascular angina (cardiac syndrome X);
    • Stable angina also includes spontaneous angina (vasospastic, Prinzmetal or variant). Disturbs a patient who is completely calm.
    • unstable angina. This includes the following types of angina:
        1. progressive;
        2. first appeared;
        3. early post-infarction;
        4. angina at rest (recurrent attacks).
  3. Myocardial infarction (heart attack) is divided into:
    • large-focal;
    • finely focal.
  4. Post-infarction cardiosclerosis (PICS)
  5. Asymptomatic myocardial ischemia
  6. Arrhythmia
  7. Heart failure

According to the modern classification, the forms of IHD include arrhythmia and heart failure, mentioned above.

Clinical forms of IHD

Below is a description of each type of coronary heart disease (CHD).

Sudden cardiac death

It is the most severe variant of the course of IHD. The precursor to instant cardiac arrest is loss of consciousness. Death may occur within an hour or 6 hours from the onset of symptoms. In this condition, a person can be resuscitated, otherwise death occurs.

Sometimes instant death occurs after drinking alcohol or excessive exercise. The onset of symptoms may occur unexpectedly, even if a person feels healthy.

Sudden death can occur due to primary ventricular fibrillation (abnormal heart rhythm), tachycardia (increased heart contractions), bradyarrhythmia (slow heart rate) and ventricular asystole (disappearance of the bioelectrical activity of the heart).

Most often, sudden coronary death occurs in people with myocardial infarction.

Angina pectoris

The condition of angina pectoris is characterized by severe sharp pain that occurs in the chest area. Often the pain “radiates” to the left arm, jaw, neck and abdomen. Such symptoms are observed for about 5-10 minutes. Symptoms of angina include shortness of breath, lightheadedness and severe fatigue.

Stable angina It is diagnosed more often than other types of coronary heart disease and makes itself felt after overeating, emotional stress or physical activity. Stable angina is treated with blood pressure stabilizing drugs.

Peculiarity microvascular angina The fact is that in the presence of shortness of breath, tachycardia and chest pain, there is no damage to the coronary vessels.

Unstable angina accompanied by chest pain as a result of rupture of an atherosclerotic plaque. This condition can cause myocardial infarction or death.

Progressive angina characterized by a rapid course with worsening symptoms. The progressive form may be a consequence of stable angina. This type of angina is characterized by vomiting, a feeling of suffocation and nausea.

Symptoms new-onset angina appear over a period of 4 weeks or more. Symptoms may occur during exercise, emotional distress, rest or sleep. After a few months, this type of angina may develop into another form of coronary artery disease.

Early post-infarction angina occurs after myocardial infarction and can recur. An angious (pressing, burning) attack can occur after a heart attack for a day or two weeks.

Variant angina(spontaneous, also called Prinzmetal's angina) is characterized by severe spasm of the coronary vessels. An attack can occur at rest at any time of the day, but is more often observed in the morning or at night.

Myocardial infarction

It is a life-threatening form of ischemic heart disease. During a heart attack, individual sections of the myocardium die. The scale and degree of muscle damage indicate a large-focal or small-focal infarction.

Large-focal covers almost the entire area of ​​the heart muscle and ends in death in 30% of cases.

Small focal infarction has a more favorable prognosis, but can develop into a large lesion of heart damage.

Due to prolonged deficiency of nutrients and oxygen, areas of the muscle layer die off within several hours. After a week, the affected layer begins to scar, and after a month or two, a scar appears instead of the lesion. In the vast majority of cases, after a heart attack the patient remains alive, but the consequences of the attack are irreversible. Post-infarction cardiosclerosis becomes a complication of myocardial infarction.

Post-infarction cardiosclerosis

This type is characterized by shortness of breath, fatigue and severe chest pain. This is due to impaired heart function due to scars after a heart attack, which interfere with the full functioning of the organ. A patient in a state of post-infarction cardiosclerosis requires maintenance therapy.

Asymptomatic myocardial ischemia

Also called silent or painless. The form is asymptomatic, which poses a threat to the patient’s life. It can be detected only by signs that appear after physical activity or after an ECG (electrocardiography). The prognosis for this type of IHD without treatment is unfavorable. The consequences of silent ischemia are myocardial infarction, death and angina attacks requiring hospitalization. The consequences make themselves felt within 2 and a half years after the diagnosis.

Arrhythmia

In a state of arrhythmia, there is a disturbance in the frequency and sequence of heart contractions, and the rhythm of the organ is disrupted. With arrhythmia, electrical conductivity and the formation of an electrical impulse are disrupted.

Sometimes arrhythmia is characterized by a normal heart rhythm, but impaired conduction is observed.

The cause of an abnormal heart rhythm may be:

  • myocardial infarction;
  • unstable angina;
  • heart failure;
  • cardiomyopathy (mechanical and electrical dysfunction of the myocardium);
  • taking medications;
  • smoking;
  • narcotic substances;
  • thyrotoxicosis (increased levels of thyroid hormones);
  • violation of water-electrolyte balance (excess or lack of water and electrolytes (ions with an electrical charge) in the body).

With arrhythmia, the patient feels a sinking heart, increased paroxysmal palpitations, suffocation, weakness and dizziness.

Heart failure

Manifestations of this pathology are stagnation in the circulatory system and a weakened ability of the myocardium to contract.

Heart failure is a common cause of death. The acute condition is dangerous due to complications such as pulmonary edema, organ hypoxia (oxygen starvation) and cardiogenic shock (critical left ventricular failure).

With heart failure, swelling, cyanosis of the nasolabial triangle (blue discoloration of the skin and mucous membranes) and nails, shortness of breath at rest, and fatigue are possible.

New forms of IHD

In medicine, the classification of coronary heart disease from the 70-80s of the last century is still used. But over time, other forms of IHD were discovered, which may in the future be included in the international classification of diseases.

Hibernating myocardium (sleeping)

After short-term or prolonged ischemia, changes occur in the heart that adversely affect the functioning of the organ. These changes can provoke various kinds of complications, without a reversible process, but dormant myocardium syndrome has reversible consequences. With adequate therapy, myocardial function and activity can be restored.

The preservation of the functions and vital activity of parts of the heart is due to a decrease in the contractile activity (“sleep”) of cardiomyocytes (muscle cells) during ischemia.

Stunned myocardium (stunned)

Unlike a heart attack, in which the complete death of heart cells occurs, during stagnation the cells remain intact and resume their vital functions. Stunned myocardium can recover from a couple of hours to several days and months. Normalization of blood flow restores heart function.

The difference between the hibernating (sleeping) myocardium and the stunned one is that in the hibernating myocardium during stimulation the contractile function increases, causing increased metabolism, while in the stunned myocardium this is not observed.

Ischemic preconditioning

This condition is called adaptation of the heart to ischemic attacks. The myocardium adapts to short-term periodic decreases in blood flow, then adapts to longer attacks.

According to information taken from the literature “The phenomenon of preconditioning today” by Dimitrios Kremastinos, such adaptation can protect against the development of heart attack and arrhythmia. But even if a heart attack occurs, in the presence of ischemic preconditioning, small areas of the myocardium are affected.
All the described forms can change from one to another.

Symptoms of IHD depend on the clinical form of the condition. The main symptoms of angina are:

  • pain behind the sternum (the nature of the pain is cutting, pressing, suffocating, burning);
  • pain radiating to the left arm, shoulder blade, abdomen, shoulder and lower jaw. Sometimes the right half of the body is involved;
  • attacks of pain lasting 1-10 minutes, longer ones (for 20 minutes) may indicate the transition of angina to a heart attack;
  • increased sweating;
  • feeling of lack of air;
  • pale skin;
  • cold, numb upper extremities;
  • dyspnea;
  • fatigue with light exertion.

Symptoms of myocardial infarction:

  • squeezing or burning pain behind the sternum;
  • pain lasts more than 20 minutes;
  • pain in the morning or at night;
  • pain radiating to the left arm, neck, shoulder, jaw and between the shoulder blades;
  • alternating pain intensity (increase, decrease);
  • pale skin;
  • cold sweat;
  • increased heart rate;
  • feeling of lack of air;
  • fear of death;
  • sudden cardiac arrest.

With an atypical course of a heart attack, the following symptoms of such types of heart attack may be observed:

  1. The abdominal form of a heart attack is characterized by the following symptoms:
    • hiccups;
    • nausea;
    • vomit;
    • flatulence;
    • abdominal pain;

    When palpating the abdomen, no pain is detected, which indicates a heart problem.

  2. The asthmatic form causes the following symptoms:
    • dry cough;
    • dyspnea.
  3. The painless form (occurs in the elderly and people with diabetes) provokes the following symptoms:
    • feeling of discomfort behind the sternum;
    • sleep disturbance;
    • depressed mood.
  4. Cerebral form, it is characterized by the following symptoms:
    • headache;
    • dizziness;
    • visual impairment;
    • nausea;
    • vomit;
    • clouding of consciousness.

Symptoms of post-infarction cardiosclerosis:

  • orthopnea (severe shortness of breath, forcing the patient to sit, because in a lying position the state of health worsens);
  • decreased tolerance to physical activity (poor endurance with symptoms characteristic of heart disease);
  • swelling;
  • depression;
  • possible weight loss;
  • decreased appetite;
  • fast fatiguability.

Symptoms of silent myocardial ischemia:

  • No symptoms. Can be detected during examination.

Symptoms of arrhythmia:

  • strong heartbeat;
  • sensations of heart sinking;
  • feeling of heart failure;
  • chest pain;
  • dizziness;
  • feeling of suffocation;
  • fainting;
  • lethargy, weakness;
  • cardiogenic shock.

Symptoms of acute heart failure:

  • heartache;
  • radiating pain in the shoulder blade, neck, elbow;
  • pale skin;
  • blueness of nails and skin in the area of ​​the nasolabial triangle;
  • severe shortness of breath;
  • cold sweat;
  • decreased blood pressure;
  • moist wheezing of the lungs;
  • increased heart rate;
  • swelling of the neck veins;
  • swelling;
  • ascites (accumulation of fluid in the abdominal cavity);
  • orthopnea;
  • pulmonary edema;
  • cough with foamy sputum (with blood).

Symptoms of chronic heart failure:

  • chest pain;
  • dyspnea;
  • increased fatigue;
  • dry cough;
  • cyanosis;
  • fast fatiguability;
  • weakness;
  • attacks of suffocation at night;
  • exercise intolerance.

Symptoms of IHD vary depending on the type.

Features of IHD in women

The period when the first symptoms of IHD appear in women is considered to be over 55 years of age. Symptoms of IHD are less pronounced than in men, which sometimes makes diagnosis difficult and is a negative factor for timely treatment. Among women, coronary heart disease is less common, because the female sex hormone (estrogen) prevents the appearance of atherosclerosis of the coronary vessels (sedimentation of cholesterol plaques in the vessel), which can cause the appearance of coronary artery disease.

However, during menopause in women, hormonal levels change and estrogen is produced less frequently, resulting in a higher risk of coronary heart disease.

Women's plasma contains antithrombin lll, which prevents blood clotting and therefore prevents the formation of blood clots that can clog blood vessels. In men after 40 years, antithrombin lll begins to decrease, but in women it does not, which also reduces their risk of developing coronary artery disease.

But women are at risk of premature coronary heart disease (CHD). This is due to heredity or the onset of early menopause.

In 88% of cases in women, the first manifestation is angina, and myocardial infarction occurs in 12%.

Features of IHD in men

Because men do not produce estrogen like women, they are more susceptible to coronary heart disease. In addition, according to statistics, men are more likely to drink alcohol, tobacco products (smoking 15 cigarettes a day provokes coronary artery disease), move little or, on the contrary, engage in excessive exercise, as a result, their risk of heart disease increases. The age of the first manifestations of IHD in men can be considered 45-55 years.

Men who frequently eat fatty foods are vulnerable to coronary heart disease because... cholesterol is deposited in the blood vessels, which subsequently leads to their blockage.

When diagnosing coronary artery disease, men more often undergo coronary angiography (examination of the arteries), since women tolerate this procedure less well, it can cause minor renal and vascular complications.

In men, the symptoms of the disease are more pronounced, unlike in women, which makes it possible to diagnose IHD in time and begin treatment. In addition, men tolerate surgery more easily and return to normal daily life faster.

When chest pain and shortness of breath appear, you first need to come to a therapist, he will examine, listen and give a referral to a cardiologist or neurologist, and they, in turn, will diagnose IHD based on the diagnostic results.

The cardiologist will listen to whether there are heart murmurs, ask what medications the patient is taking and whether relatives have heart disease. Then the patient is sent for examinations and tests.

Laboratory research

The patient must take a biochemical blood test. This analysis determines specific enzymes; their excess indicates the presence of heart pathologies, including coronary artery disease:

  • creatine kinase;
  • troponin-I;
  • troponin-T;
  • aminotransferase;
  • myoglobin;
  • lactate dehydrogenase.

These enzymes are released into the blood if cardiomyocytes (heart cells) are destroyed.

The study evaluates the level of cholesterol and glucose in the blood, as well as the content of sodium and potassium.

Additionally, blood is given for a general analysis, which allows you to find out the ratio and volume of leukocytes and red blood cells in the blood, the level of hemoglobin and the erythrocyte sedimentation rate. This analysis will not be informative in case of coronary artery disease, but it can detect anemia (anemia), and this disease complicates the course of coronary artery disease.

Instrumental research methods

Coronary angiography is a diagnostic procedure using a radiopaque contrast agent. Accurately determines the location and degree of narrowing of the vessel. The cardiologist alternately injects a radiocontrast agent into the left and right arteries using angiographic catheters. The substance fills the lumens of blood vessels along their entire length. Under X-ray, filled arteries display information about their internal structure and topography.

Intravascular ultrasound is an invasive examination method that uses an angiographic catheter (like a probe). Ultrasound helps identify cholesterol plaques in blood vessels. Before the procedure, the patient is injected with a substance that eliminates spasm for the duration of the examination and a probe is inserted, so that the ultrasound sensor is located inside the vessel. Diagnostics can be used in conjunction with vascular surgery. Contraindicated in people with complicated stenosis (narrowing of the canals) and occlusion (obstruction) of the coronary arteries. Intravascular ultrasound is rarely used due to the limited availability of equipment. On average, such a procedure will cost 40-100 thousand rubles.

Electrocardiography (ECG) is a procedure that allows you to record the electrical fields of the heart that arise during the functioning of the organ. Electrodes are attached to the patient's anterior chest wall and arm, recording the electrical potentials of the heart and displaying them with a graphic curve on the screen or on thermal paper. The result is an electrocardiogram with the biocurrents of the heart displayed on it.

Transesophageal pacing (TEPS) is a method of examining the heart by studying its electrical excitability and conductivity by sending impulses to the atria. A sensor is inserted into the patient's esophagus to record the organ's performance. TEE allows you to directly see pathologies, without additional interference created by the chest or when moving the sensor over the skin. There are contraindications for this procedure. It is prohibited for tumors of the esophagus, attacks of bronchial asthma, varicose veins of the esophagus, esophagitis (inflammation of the esophageal mucosa), strictures (compression of a hollow organ), diverticula (protrusions on the walls of hollow or tubular organs).

Holter (24-hour) ECG monitoring is a method of electrophysiological diagnostics of the heart and blood vessels, lasting for 24 hours or even more (up to 7 days). The patient is attached to the electrodes to the body and given a portable device - a recorder that records the patient's cardiac signals in everyday life. The electrode attachment sites are prepared before the procedure. The hair is shaved, the skin is disinfected and scarified (“polished”). This is necessary for recording quality. The patient must record all changes and conditions in a diary during the study.

CT angiography (computed tomographic angiography) is an examination aimed at assessing blood flow in the vessels through intravenous contrast enhancement with iodine-containing drugs. CT angiography creates a three-dimensional image of the cardiovascular system in the image. The advantage of CT is that the radiation dose is lower than with conventional X-rays. The patient is positioned on a mobile equipment table. Around the table there is a tomograph in the form of a ring, which examines the patient’s cardiovascular system.

Echocardiography is an ultrasound method that evaluates the condition of the soft tissues and valvular apparatus of the heart, the thickness of the walls of the organ, contractile activity and the volume of the chambers of the heart. Thanks to the sensor and monitor, the doctor sees the work of the heart in real time. There are no contraindications to echocardiography.

Myocardial scintigraphy is a method that involves the introduction of radioactive isotopes into the body, the radiation of which helps to obtain a two-dimensional image of the heart. The radioactive substance is injected intravenously. The active absorption of radionuclides by the tissues of the heart indicates their functioning, and the “emptiness” of areas without absorption indicates the death of myocardial tissue.

MRI (magnetic resonance imaging) of the heart is a safe diagnosis of the cardiovascular system. When exposed to a magnetic field, hydrogen atoms in the human body release energy, which makes it possible to take pictures in a three-dimensional projection. During the procedure, the patient does not receive radiation; magnets are used for examination. Like CT (computed tomography), MRI uses a mobile table and a tomograph. The difference between MRI and CT is that a CT scan exposes the person to radiation, while an MRI does not. MRI of the heart is also prescribed because this method better scans the soft tissues of the body, unlike CT, which better visualizes bone tissue.

Functional tests

Diagnosis of IHD is carried out through physical activity. Tests are used when it is difficult to detect IHD in the early stages or the behavior of the heart at rest.

For testing, they use treadmills (treadmill test), exercise bikes (bicycle ergometry) or observe the patient’s condition when he climbs stairs, does 30 climbs on a special platform for 5 minutes (step test) or walks. All loads are accompanied by ECG recording, which displays heart function indicators.

Differential diagnosis

Differential diagnosis through study and examination excludes diseases in the patient that do not match the symptoms or signs.

The patient may exhibit symptoms that are not typical for IHD, then we are talking about an atypical course of the disease. For differentiation, it is necessary to take tests, examine the gastrointestinal tract, lungs, nervous, heart and vascular, musculoskeletal systems in order to exclude diseases not related to coronary heart disease (CHD).

After the diagnosis is made, treatment for IHD is prescribed based on the diagnosis. Therapy necessarily includes following a diet, taking medications and lifestyle adjustments. For each form of coronary artery disease, different treatment methods and medications may be prescribed, but there are general principles used in the treatment of all forms of ischemic heart disease.

Drug treatment

If you have IHD, taking medications without consulting a doctor is prohibited!

Taking medications for IHD can be used according to the “A-B-C” formula, which implies the use of a triad of pharmacological agents, such as antiplatelet agents, Beta-blockers and cholesterol-lowering drugs in the treatment of IHD.

Antiplatelet agents are drugs that prevent the adhesion of blood cells (erythrocytes, leukocytes, platelets).

The doctor may prescribe the following antiplatelet drugs:

  • Clopidogrel;
  • Thrombopol;
  • Acecardole;
  • Aspirin.

Beta-blockers are pharmacological drugs that are prescribed for ischemic heart disease; they can reduce the heart rate, as a result of which the myocardium will need less oxygen. Research shows that these medications have a beneficial effect on heart function and life expectancy in people with coronary artery disease. These drugs are contraindicated for people with bronchial asthma or chronic obstructive pulmonary disease. The most popular beta blockers are:

  • Betalok Zok;
  • Dilatrend;
  • Coriol;
  • Biprol;
  • Concor;
  • Talliton;
  • Bisogamma;
  • Vasocardin;
  • Metocard;
  • Coronal;
  • Acrididol;
  • Egilok;
  • Niperten;
  • Cordinorm.

Hypocholesterolemic drugs (statins, fibrates) are drugs aimed at reducing cholesterol and triglycerides in the blood, which are prescribed for ischemic heart disease. They have a beneficial effect on life expectancy, and are a prevention of cholesterol plaques in blood vessels, and also reduce the growth rate of existing ones. Statins include:

  • Lovastatin;
  • Rosuvastatin;
  • Atorvastatin;
  • Simvastatin.

Fibrates for ischemic heart disease are used to treat metabolic pathologies; they work to reduce triglycerides and increase the HDL fraction (high-density lipoproteins, they reduce the risk of developing atherosclerosis). Fibrates include:

  • Fenofibrate;
  • Bezafibrate.

Nitrates are vasodilators. Possible side effects include headache and low blood pressure. They are used exclusively to eliminate the symptoms of angina pectoris and do not increase survival. Nitrates include:

  • Nitroglycerine;
  • Isosorbide mononitrate.

Anticoagulants are drugs that prevent increased blood clotting and the formation of blood clots. In the treatment of ischemic heart disease the following is used:

  • Heparin;
  • Warfarin.

Diuretics are diuretic drugs that help relieve swelling by accelerating the formation of urine and removing it from the body along with excess fluid; they are often prescribed for ischemic heart disease. Diuretics are:

  • Loop - reduce reabsorption (reverse absorption by the body) of water. Loop diuretics include, for example, Furasemide.
  • Thiazide - act to reduce urine reabsorption (reabsorption of water by the body from urine flowing through the renal tubules). Thiazide diuretics include hypothiazide and indapamide.

ACE inhibitors (angiotensin-converting enzyme) are drugs that reduce vascular spasm. The most popular ACE inhibitors are:

  • Enalapril;
  • Captopril;
  • Lisinopril;
  • Prestarium A.

Antiarrhythmic drugs are drugs that can correct abnormal heart rhythms and prolong the life of a patient with coronary artery disease. Amiodarone may be prescribed for these purposes.

Transluminal (endovascular) intervention for ischemic heart disease

This type of therapy includes coronary angioplasty. For ischemic heart disease, balloon angioplasty and stenting may be prescribed.

During balloon angioplasty, a special balloon is inserted into the patient through a large artery through a flexible catheter, which inflates inside the vessel, thereby expanding its walls for full blood flow. Sometimes, after such a procedure, a metal structure (stent) is installed into the lumen of the vessel; it maintains the normal lumen of the vessel. This is called stenting.

With transluminal intervention there are no cosmetic defects.

Surgery for ischemic heart disease

In certain cases, surgery is required.

Coronary artery bypass surgery is an operation to restore blood flow in the arteries of the heart. The essence of the operation is to bypass the site of narrowing of the vessel, introducing vascular prostheses (shunts) and restore normal blood circulation and heart function.

Non-drug treatment methods for ischemic heart disease

Hirudotherapy is a method of alternative medicine that uses leech saliva, which reduces human blood clotting.

Enhanced external counterpulsation is a treatment method for ischemic heart disease using air cuffs. Cuffs are placed on the patient's legs and at the moment of diastole (relaxation of the heart) they are filled with air, which exerts pressure and increases the filling of blood vessels. And during systole (contraction), air is sharply pumped out of the cuffs, which helps reduce the load on the heart. Inflation and deflation occurs synchronously with the rhythm of the heart.

Stem cell therapy is the introduction of cells that repair the heart. The procedure is designed for the fact that the cells entering the body will restore the structures of the myocardium, but sometimes they restore any other organs, because the process is uncontrollable. The method is experimental and is not yet widely used in the treatment of coronary artery disease.

Shock wave therapy is a short-term, remote effect of acoustic impulses on the heart, which causes therapeutic angiogenesis (stimulation for the formation of new vessels). New vessels will provide nutrition to the heart. Treatment of coronary artery disease in this way improves myocardial microcirculation.

Diet for coronary artery disease is often ignored by the patient, or it is not given as much attention as taking medications. However, diet is of great importance in the treatment of coronary heart disease.

When treating IHD, limit the consumption of table salt and water; such a ban will reduce the load on the myocardium and prevent swelling. Attention is focused on fat consumption. It is necessary to limit the use of:

  • animal fat (eg lard, pork, butter);
  • fried foods and smoked meats;
  • foods containing a lot of salt (eg salted fish);
  • high-calorie foods, especially fast carbohydrates (bakery, chocolate, sweets, cakes).

You should control the consumption of cholesterol contained in food, because it is the first “culprit” of vascular atherosclerosis, which leads to coronary artery disease.

Diet greatly affects the functioning of the heart and vascular system, therefore it is necessary to strictly adhere to the doctor’s recommendations for treatment of coronary artery disease to be effective.

Complications of IHD

The most severe complication of coronary artery disease is an attack of acute heart failure, leading to sudden cardiac death. With this condition, immediate death or its onset 6 hours after the onset of symptoms is possible.

Myocardial infarction is also a serious complication that can disrupt the function and structure of the heart, leading to death.

Forecast

The prognosis for the patient's life will depend on the form of IHD and concomitant diseases, but IHD is an incurable condition. If the patient suffers from coronary artery disease and arterial hypertension (persistent increase in blood pressure) or diabetes mellitus, then the prognosis for him is unfavorable, because Treatment of IHD will only slow down the progression of the disease, but will not stop it.
Patients who have been diagnosed with angina pectoris and a history of myocardial infarction are given a disability, which can be removed after repeated testing, but on the condition that the laboratory data are normal, otherwise the disability is extended until the end of life.

Since the main cause of coronary heart disease lies in the “clogging” of blood vessels with cholesterol plaques, preventive measures should be aimed at preventing fatty deposits that prevent blood from flowing fully through the vessels into the heart. The fight and prevention of coronary heart disease includes 2 types of prevention: primary and secondary. The primary one is carried out among healthy people who want to prevent the development of the disease, and the secondary one is aimed at preventing relapse of the disease or its rapid progression.

Primary prevention of coronary artery disease

To prevent the cardiovascular system from reaching such a dangerous state, you must:

  • Stop smoking and drinking alcohol.
  • Spend more time in the fresh air and enrich yourself with oxygen.
  • Limit consumption of fatty foods.
  • Visit a cardiologist if you experience suspicious chest pain. Your doctor may prescribe lipid-lowering drugs or statins for prevention. They normalize lipid metabolism and cholesterol levels.
  • Move more. Physical activity is always important for the prevention of various diseases, primarily the cardiovascular system.
  • Try to avoid stress.
  • Control body weight. The weight of an adult healthy person is always approximately the same level with slight fluctuations. Therefore, it is necessary to monitor body weight; its sharp increase or decrease may indicate illness.
  • Fight hypertension. Normalize high blood pressure.
  • Reduce excessive physical activity.
  • Get rid of excess weight.
  • Eat more seafood (except those that contain a lot of cholesterol), fresh vegetables and fruits.

Secondary prevention of coronary artery disease

To avoid complications of coronary heart disease, you must:

  • Adhere to all points of primary prevention.
  • Eliminate vascular spasms with medications.
  • Perform surgery if necessary.

Anyone with a condition such as coronary heart disease should have nitroglycerin in their first aid kit. It relieves pain immediately.

Video

Coronary heart disease (CHD) is a serious disease that can be fatal. Treatment should be selected by a specialist and be comprehensive.

From the article you will learn the features of coronary heart disease, types of the disease, risk factors, causes of development, danger of the pathology, symptoms, features of treatment and prevention.

What is IHD

Coronary heart disease (CHD) is a reversible (functional) or irreversible (organic) damage to the heart muscle due to insufficient blood supply to the organ or its complete absence. The essence is the pathology of the coronary arteries.

IHD is one of the most serious problems in cardiology and medicine in general, since for decades it has been the leading cause of death worldwide (more than 70% of all cases). In the EU, acute myocardial infarction and stroke account for up to 90% of all vascular and cardiac pathologies.

A characteristic sign of IHD is chest pain of various types.

The disease has a gender connotation. Men of working age suffer more. This is explained by some hormonal protection of the female body by sex hormones, which prevent the development of atherosclerosis. However, during menopause this barrier disappears, and the risk of developing IHD immediately increases. But still the ratio remains 50/30 in favor of men. In the Russian Federation, about 700,000 deaths are reported every year from various forms of cardiac ischemia. Of particular concern is the increase in sudden cardiac arrest against the background of apparent well-being.

The pathogenesis of the development of coronary disease is associated with an imbalance between the blood supply necessary for normal myocardial function and the actual blood flow in the coronaries. The causes of IHD can be very different, but the lack of blood flow is especially noticeable when the supply arteries are damaged by atherosclerosis against the background of a sharp increase in the heart’s need for proteins, fats, carbohydrates and oxygen supply that are vital for normal metabolism.

Types of disease

IHD, unlike other diseases, is a whole group of pathologies with a huge number of symptoms that correlate with the cause of the disease. Moreover, various types of coronary heart disease spontaneously change from one to another, which creates great difficulty in diagnosis and adequate therapy. In practice, there are two fundamentally different forms of IHD:

  • acute myocardial ischemia – the most common cause of fulminant death;
  • chronic ischemic heart disease, which is combined with arrhythmias and other negative symptoms that exist for a long period of time.

There is also a more complex, detailed classification of the disease.

Classification

It is quite difficult to specify individual nosological forms of cardiac ischemia, since the main cause is common, and the clinical manifestations are very different. WHO recommends systematizing IHD as follows:

  1. Primary cardiac arrest or immediate coronary death is an unpredictable pathological condition, probably due to electrical instability of the heart muscle, that occurs within 6 hours after a heart attack in front of witnesses. There are two outcomes - successful resuscitation measures or a lethal, uncontrollable scenario.
  2. Angina pectoris: stable (divided into functional classes - from I to IV) and unstable (occurring for the first time, after surgery, after a heart attack, steadily progressing) - another form of coronary artery disease.
  3. Cardiac ischemia without pain (diagnosed accidentally during an instrumental examination of the patient).
  4. Infarction: (large focal) and (local). The essence is tissue necrosis due to lack or insufficiency of nutrition and oxygen supply.
  5. Post-infarction cardiosclerosis, which develops against the background of replacement of muscle fibers with connective tissue, which impairs the contractility of the myocardium, is a form of chronic ischemic heart disease.
  6. NRS: arrhythmias, tachycardia, tachysystoles, bradycardia, extrasystoles, flicker, fibrillation - precursors of angina or heart attack.
  7. Heart failure: acute and chronic, from stage I to IV – the result of a malnutrition of the coronaries of the heart.
  8. Special forms of angina: X-syndrome, refractory, spontaneous angina (vasospastic, variant, Prinzmetal).

Causes and risk factors

Many reasons can cause the development of coronary heart disease, but in 90% of cases it is coronary atherosclerosis.

If the blood flow is limited by 75%, angina pectoris develops; with complete occlusion, cardiac arrest occurs. The causes of IHD can be cardiospasm, thromboembolism, spasm of the coronary arteries.

In addition to the causes, factors that provoke the disease play an important role in the occurrence of IHD, which are conventionally divided into two groups: eliminated or irreducible by any means. The latter include race, hereditary predisposition, and gender factor.

In Africa, there are many times fewer cases of cardiac ischemia in various forms than in the EU and the USA, for example. In a family where there have been cases of death of loved ones from a heart attack before the age of 55, the risk of a recurrence of the situation is significant.

Factors that can be addressed to stop the progression of coronary heart disease include:

  • constant overeating, excess weight, obesity of varying degrees;
  • an unbalanced diet with excess carbohydrates and fats is an atherogenic nutritional profile, common in central Russia, the north of the country, the Trans-Urals and the Far East.
  • physical inactivity (men under 40-50 years of age engaged in mental work are 5 times more likely to experience coronary artery disease, just like athletes who have completed sports activities;
  • abuse of cigarettes, alcoholic beverages (vascular disorders due to nicotine intoxication);
  • diabetes mellitus of both types (heart attack is the main cause of death for diabetics);
  • stress, mental, emotional stress: the heart works faster, the pressure in the blood vessels increases, and the delivery of oxygen and vitamins to the heart decreases;
  • arterial hypertension provokes ischemic heart disease - left ventricular hypertrophy against the background of hypertension is the most likely cause of death in cardiac ischemia;
  • changes in blood viscosity provoke thrombosis, blockage of the coronary arteries, and myocardial necrosis.

The combination of several background factors over time contributes to the emergence of the main causes of CAD.

Symptoms of IHD

Coronary heart disease has its own clinical manifestations, which are preceded by the first signs of the disease, to which patients usually pay little attention.

Such precursors of pathology include:

  • unpleasant sensations behind the sternum: tingling, a feeling of discomfort, transient minor pain, which is associated with exercise, fatigue, age, but is not regarded as a warning about pathology;
  • fatigue that becomes chronic. A person gets up not recovered during the night, in the morning he feels weak and unwell, but thinks that this is the norm: the weather, poor sleep, colds;
  • shortness of breath during exercise, disappearing after a short rest;
  • ischemic disease - can manifest itself as arrhythmia, sudden, short-term, without consequences, which I also consider to be the age-related norm due to overload with work and household chores;
  • precursors of IHD are attacks of lightheadedness, vertigo, and fainting;
  • signs of coronary heart disease - heartburn or abdominal cramps.

Any of these unpleasant symptoms, and even more so, their combination, is a reason to consult a cardiologist.

Nature of pain

With the development of coronary artery disease, it is worth paying attention not only to the signs of coronary artery disease, but also to the nature of chest pain, the cause of which is irritation of nerve ending receptors by toxins formed in the myocardium due to hypoxia of the heart muscle. Triggers for this situation can be stress or physical activity.

Heart pain that begins at rest only intensifies with exercise. Possible irradiation to the left arm, shoulder, shoulder blade, neck. The intensity of the attack varies from 30 seconds to 10 minutes. Cardiac pain is always relieved by Nitroglycerin.

Abdominal pain is rarely perceived as cardiac pain. But in men, the first signs usually give exactly this localization. Another feature of cardialgia is that it begins mainly in the morning.

Gender differences

Symptoms of coronary artery disease in men and women do not differ by gender, depending only on the form of ischemic heart disease: shortness of breath, arrhythmia, cardialgia - are characteristic of both sexes. But there are age-related gender characteristics.

In men, clinical manifestations are first detected after the age of 55, in women - after 65. The first clinical manifestations of IHD in men are AMI (acute myocardial infarction), in women - angina pectoris. Moreover, one of its varieties, form X, occurs only in women. Gender and age characteristics are associated with estrogen protection of the female body. In addition, women are more susceptible to hysteria, so they are more likely to experience panic attacks and cardiophobia. In other words, women require a more thorough diagnosis of pathology.

The main symptoms of coronary heart disease manifest themselves in 9 acute and chronic variants of the course of the disease. Each specific case has its own symptoms, presented in the table.

Symptom of IHDCharacteristics of clinical manifestations
Sudden cardiac arrest (coronary death)The person immediately loses consciousness, there are practically no warning signs, and chest discomfort, emotional lability, and fear of death are rarely noted. More often – spontaneous cessation of breathing.

In the absence of emergency assistance, including chest compressions and mechanical ventilation in a hospital setting, death occurs.

Heart attack (AMI)This form of IHD is characterized by severe pain localized directly behind the sternum (the heart area does not hurt), radiating to the jaw, teeth, wrist, and fingers. The nature of the pain is pressing or burning, the duration of the attack is more than 15 minutes. The reason is any load.

Nitroglycerin doesn't help. Hyperhidrosis occurs, weakness, blood pressure drops

Combination of heart attack with encephalopathy, pre-strokeThis situation causes shortness of breath, cough, dizziness, fainting, signs of speech impairment, abdominal pain, arrhythmia, swelling of the legs, ascites
Angina pectorisIt is characterized by unbearable pain, but unlike a heart attack, the attack is relieved by Nitroglycerin. There are no other symptoms.
Cardiosclerosis after a heart attackThe diagnosis is made one month after AMI. General signs:
  • dyspnea;
  • arrhythmia;
  • pasty legs;
  • weakness;
  • hyperhidrosis

There is a risk of recurrent heart attack; constant medical supervision is required

Heart rhythm disturbances of various originsA type of chronic course of IHD. Pulse rapid or slow, intermittent or freezing, feeling tired
CHF (heart failure)The main symptom is swelling in combination with rapid fatigue, shortness of breath, symptoms of the underlying pathology against which the deficiency arose
Special forms of coronary heart diseaseThis includes X-syndrome, vasospastic and refractory angina. Symptoms are identical to exertional angina, aggravated by spasm of peripheral vessels, unresponsive to conventional treatment
Silent cardiac ischemiaLatent, detected by chance during instrumental examination of the patient

Why is pathology dangerous?

No one has canceled the fact that IHD is the result of impaired nutrition and oxygen supply to the most important organ of the human body. Patients with coronary heart disease get used to their disease and cease to consider it dangerous to health. It is this kind of carelessness that leads to the most dangerous consequences.

The most insidious is called spontaneous cardiac arrest. Electrical lability of the heart muscle is a direct consequence of ischemic heart disease, often a latent form of the disease.

A person goes to bed in perfect order, but in the morning his breathing stops and his heart stops. It is difficult for the relatives to believe that the cause is myocardial ischemia, which has been present in the patient for many years. Symptoms of coronary artery disease were not recorded, but at autopsy a scar on the heart was clearly visualized.

Medical examination is a way to prevent such a risk, but an annual examination, valuable in diagnostic and preventive terms, is often ignored by people. The price to pay is coronary death.

Another danger is the development of acute myocardial infarction with tissue necrosis, development, and impaired myocardial contractility without the possibility of recovery. A fatal outcome is likely.

Heart failure in acute and chronic forms is no less dangerous. The heart ceases to perform proper functions, blood does not flow in sufficient quantities to the internal organs, which leads to their first functional and then organic deformation with loss of performance.

Complications

Coronary heart disease is always accompanied by impaired blood flow; for this reason, the disease is classified as a hemodynamic disorder, which causes many morphological and functional changes in the body. They determine the prognosis of IHD. The essence is decompensation of the pathological process:

  • at the first stage, there is a failure in the energy system of cardiocytes;
  • on the second, the contractility of the left ventricle is impaired (a transient process);
  • the third stage is the replacement of cardiac muscle cells with connective tissue;
  • fourth – change in the ability of the heart to contract and relax;
  • fifth – a disorder of automatism, a violation of the conduction system of the heart with the development of arrhythmias, flicker, fibrillation.

All stages are a sequential mechanism for the development of heart failure, the main complication of coronary artery disease that poses a threat to the patient’s life.

Diagnostics

An accurate diagnosis of coronary heart disease (CHD) is needed to determine the form of the disease and select appropriate therapy. The algorithm is standard:

  • collection of complaints, anamnesis, physical (auscultatory examination);
  • pulsometry, blood pressure measurement;
  • CBC, TAM, biochemistry are markers of the patient’s general condition (high ESR is a reason to suspect myocardial ischemia, especially in combination with leukocytosis);
  • blood testing for enzymes: CPK (creatine phosphokinase), ACaT (aspartate aminotransferase), ALT (alanine aminotransferase);
  • testing for troponins - protein components of cardiocytes (makes sense in the first hours of a developing heart attack);
  • test for electrolytes: potassium-sodium (cause of arrhythmias);
  • determination of blood lipid spectrum;
  • electrocardiography (ECG);
  • coronary angiography (CAG);
  • Holter;
  • functional tests: bicycle ergometry, six-minute walk test;
  • echocardiography;
  • chest x-ray.

The scope of research performed is the prerogative of the doctor. Sometimes diagnostics are reduced to a minimum in order to gain time for prescribing therapy.

Treatment of coronary artery disease

Today, for the treatment of coronary heart disease, the doctor, focusing on the form of the pathology, prescribes a set of therapeutic measures, which includes drug and non-drug therapy, and surgical methods for correcting the patient’s condition.

Non-drug treatment

Approaches to the treatment of coronary artery disease are different. An acute process requires emergency measures in the intensive care unit of a hospital. If the process is chronic, then treatment of coronary disease begins with limiting exercise and physical (motor activity). Walking – slow, climbing stairs – stopping if the symptoms of the disease are severe. With minimal symptoms, swimming, cycling, and walking short distances are recommended.

Simultaneously with the correction of physical activity, diet therapy is included. Atherosclerosis is the main cause of IHD, so balancing the diet is an extremely important task.

Excluded fatty, smoked, spicy, hot, salty foods, canned food, fast food, alcoholic drinks.

Additional non-drug methods of treating coronary heart disease include hydrotherapy, shock wave therapy, massage, acupuncture, and oxygen therapy.

All treatment methods are agreed with the doctor.

Drug therapy

Treatment of cardiac ischemia with medications involves the use of a whole range of medications that help normalize blood pressure, relieve cardialgia, control blood viscosity, and reduce cholesterol levels.

The dose of medication, the regimen, and the duration of course therapy are chosen by the doctor. Pharmacological therapy is the basis for preventing complications, sudden cardiac arrest, and maintaining quality of life.

Despite all the advances in pharmacology, there is still no means to completely get rid of atherosclerosis and its complications.

According to the mechanism of action, all drugs are divided into several groups, the main ones are presented in the table.

Drug groupMechanism of action
– symptomatic drugs that do not affect the cause and prognosis of the disease: Nitroglycerin, Nitrosorbide, Erinit. Isosorbide, Pectrol, MonocinqueRelieves pain: nitric oxide released when taken dilates blood vessels, ensuring blood flow to the heart, relieving pain.

Used for the prevention of stable angina. Possible addiction, drop in blood pressure: not recommended for patients with blood pressure below 110/70

– act directly on the heart muscle, affect the prognosis: Metoprolol, Bisoprolol, Carvedilol, Propranolol, Atenolol, NebivololThe effect is associated with the effect on cell receptors that reduce heart rate and strength.

Contraindicated for bronchial asthma and COPD, pulse less than 60 beats/minute, blood pressure less than 90/60

– first-line drugs for the treatment of hypertension are prescribed for CHF: Captopril, Enalapril, Perindopril, Lisinopril, Fosinopril, Ramipril – have a positive effect on the prognosis of coronary artery disease, reducing the percentage of mortality from heart attack, decompensation of CHFThe drugs remodel the chambers of the heart, reducing the degree of myocardial hypertrophy. Contraindicated in case of individual intolerance, bilateral renal artery stenosis, hyperkalemia, pregnancy and lactation. Can be replaced if necessary: ​​Valsartan, Telmisartan.
– Atorvastatin, Rosuvastatin, Simvastatin. Taking the drug for life, provided that the proper level of cholesterol and its fractions is achievedThey normalize lipid metabolism, removing the main cause of coronary artery disease - atherosclerotic plaques. Prescribed when total cholesterol levels are above 4.5 mmol/l.

Contraindicated in diseases of the liver, kidneys, myopathies, pregnancy, lactation, individual intolerance, children

, – recommended for all forms of ischemic heart disease: Clopidogrel, Thrombo Ass, Cardiomagnyl, AspirinPrevent the development of thrombosis, thrombophlebitis, control the viscosity of the blood coagulation system
– Verapamil, Diltiazem, Nifedipine, AmlodipineThe effect is achieved by influencing intracellular calcium channels and vasodilation. Drugs are contraindicated for hypotension, CHF
– Indapamide, Hypothiazide, Furosemide, Torasemide, TriampurRemove excess fluid from the body, reducing the load on the myocardium
: Panangin, Potassium Orotate, Asparkam, Cordarone, Lidocaine, Cardiac glycosidesThey stop heart rhythm disturbances, restoring metabolic processes and the conductivity of electrical impulses in the myocardium.

Contraindicated for thyroid diseases, heart blockades, pregnancy, lactation, intolerance to iodine preparations

Cytoprotectors – Trimetazidine, Mexicor, MildronateProtect the myocardium from hypoxia, balance metabolism

Angioplasty

Angioplasty is an endoinvasive technique for coronary artery disease that allows for coronary stenting. The insertion process is carried out through the femoral or brachial artery using a thin catheter with a balloon at the end. Under X-ray control, a stent is placed at the site of the narrowing.

Stenting procedure.

In this case, the cholesterol plaque is “pressed” by the balloon into the wall of the vessel. Sometimes a stent with a spring is used - a special support for the walls of an artery affected by atherosclerosis.

Bypass surgery

Surgical treatment of coronary heart disease is carried out using bypass surgery, which requires long-term rehabilitation. The essence of the operation is the flow of blood to the heart muscle due to the development of a new vascular bed, bypassing the coronaries affected by atherosclerosis. During the recovery period (six months) you must:

  • limit physical activity;
  • eliminate stress;
  • follow a diet;
  • give up alcohol and cigarettes.

The validity period of the shunts is 6 years.

Folk remedies

Cardiac ischemia requires a healthy lifestyle. Folk remedies will help with this. Herbs and plants can have a positive effect on blood vessels, myocardium, lipid metabolism, and blood viscosity. The most popular in herbal medicine for coronary artery disease:

  • Hawthorn, which strengthens the myocardium, reduces the heart rate, but the plant has a cumulative effect and affects blood pressure, so you need to take hawthorn tea with caution. Hawthorn fruits can be used all year round: dry berries (a large spoon) pour 500 ml of boiling water, leave for 15 minutes, drink in two doses with an interval of at least 6 hours.
  • You can prepare a decoction based on the berries of hawthorn, rose hips and motherwort: pour 100 g of each plant into a liter of water, bring to a boil, after 7 minutes remove from heat, cool, filter, take in the morning, half a glass on an empty stomach.
  • Horseradish leaves for ischemic heart disease - improve microcirculation. But those patients who have digestive problems should take decoctions from the plant with caution. An alternative is inhalation with horseradish root: rub the plant, take a spoonful of the mixture, pour boiling water over it and breathe in the steam for 15 minutes.
  • You can combine horseradish with honey in equal parts (100 g each). The mixture is eaten after breakfast, one and a half teaspoons, washed down with tea. Course for a month, repeat after a three-week break.
  • Garlic is a vegetable rich in phytoncides, a natural antibiotic, it relieves inflammation, that is, pain. Improves microcirculation. The recommended dose is a clove of garlic per day with lunch.

All folk recipes for the treatment of coronary artery disease must be approved by a doctor.

Prevention, prognosis

Preventing coronary disease is easier than treating it. There are a number of rules:

  • constant monitoring of blood pressure and pulse;
  • adherence to a low-cholesterol diet;
  • control of lipid spectrum, blood sugar;
  • healthy sleep;
  • walks in the open air;
  • eliminating alcohol from the diet, stopping smoking, giving up drugs, strong coffee, energy drinks, sweet soda;
  • clinical examination.

By adhering to this lifestyle, you can prevent the development of IHD, maintaining your usual quality of life for many years.

Literature

  1. Bogorad, I. V. I. V. Bogorad. Medical examination is the basis of prevention. V. M. Panchenko, V. N. Svistukhin. Cardiac ischemia. Prevention and rehabilitation / I.V. Bogorad, V.M. Panchenko, V.N. Svistukhin. - M.: Knowledge, 1987
  2. Heart disease according to Braunwald. Guide to Cardiovascular Medicine. In 4 volumes. Volume 1. - M.: Reed Elsiver, 2010
  3. Braunwald, E. Heart disease according to Braunwald. Guide to Cardiovascular Medicine. In 4 volumes. Volume 2 / E. Braunwald, ed. P. Libby, R.G. Oganova. - M.: Logosphere, 2012
  4. Chazov, E.I. Diseases of the heart and blood vessels: monograph. / E.I. Chazov. - M.: Medicine, 1992
  5. Okorokov, A. N. Diagnosis of diseases of internal organs. Volume 8. Diagnosis of heart and vascular diseases / A.N. Hams. - M.: Medical literature, 2007
  6. Malysheva, I.S. 100 questions about heart disease / I.S. Malysheva. - M.: Tsentrpoligraf, 2011
  7. Moiseev, V.S. Alcohol and heart disease / V.S. Moiseev, A.A. Shelepin. - M.: GEOTAR-Media, 2009.
  8. ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation–executive summary. 2006;
  9. Ageno W., Turpie A.G. Clinical trials of deep vein thrombosis prophylaxis in medical patients. Cornerstone. 2005;
  10. Cleland J.G., Coletta A.P., Lammiman M. et al. Clinical trials update from the European Society of Cardiology meeting 2005: CARE.HF extension study, ESSENTIAL, CIBIS.III, S.ICD, ISSUE.2, STRIDE.2, SOFA, IMAGINE, PREAMI, SIRIUS.II and ACTIVE. J. Heart Fail. 2005;
  11. Healey J.S., Baranchuk A., Crystal E. et al. Prevention of atrial fibrillation with angiotensin–converting enzyme inhibitors and angiotensin receptor blockers: a meta–analysis. Am. Coll. Cardiol. 2005;
  12. Javaheri S. Acetazolamide improves central sleep apnea in heart failure: a double.blind, prospective study. J. Respira. Crit. Care Med. 2006.
Last updated: January 27, 2020

Coronary heart disease (CHD), (synonym "coronary heart disease" comes from the term "ischemia" - to hold back, stop blood. IHD is a disease caused by deterioration of coronary circulation due to atherosclerotic lesions (narrowing) of the coronary arteries or functional impairment (spasm), changes in the rheological properties of blood and other causes leading to myocardial ischemia. The concept of coronary artery disease covers only those pathological conditions of the myocardium that are caused by atrosclerotic lesions of the coronary arteries (atrosclerotic plaque, thrombosis) or a violation of their functional state (spasm). Myocardial ischemia can also develop with lesions coronary arteries of a different origin (infectious, systemic red, etc.), as well as with heart defects (especially aortic), however, these cases do not apply to IHD. IHD is one of the main causes of mortality in industrialized countries (40-55%) Epidemiological studies have established that IHD occurs in 11-20% of the adult population. The incidence of IHD increases with increasing age.

Sudden coronary death (SCD)- death occurring immediately or within 6 hours from the onset of a heart attack.

Angina pectoris. It is characterized by paroxysmal chest pain, resulting from the fact that the myocardial need for oxygen exceeds its delivery.

Unstable angina (acute coronary syndrome)- a syndrome with coronary artery disease, located in its manifestations between stable angina and myocardial infarction.

Unstable angina includes:

  • new-onset (less than 30 days old) angina pectoris;
  • progressive exertional angina; early (in the first 14 days of myocardial infarction) post-infarction angina;
  • angina pectoris that first occurred at rest.

Myocardial infarction (MI)- acute necrosis of a section of the heart muscle resulting from absolute or relative coronary circulation. The incidence of myocardial infarction increases with age. Thus, for men aged 20-29 years, it is 0.08 per 1000 people; at 30-39 years old - 0.76; at 40-49 years old - 2.13; at 50-59 years old - 5.8; in 60-64 years - 17. In women aged 50 years, MI is 6 times less common than in men. In later age periods this difference is leveled out.

Post-infarction cardiosclerosis.

This diagnosis is made to patients who have had an MI after the scarring process is complete, i.e. 2-4 months after MI (with a protracted, recurrent course and later).

Causes

The main cause of IHD is atherosclerosis of the coronary arteries; it is detected in varying degrees of severity in more than 90% of patients with this disease. Most often, the atherosclerotic process is the basis for the deployment of numerous complex mechanisms that change coronary blood flow, metabolism and myocardial function. Factors predisposing to the development of atherosclerosis of the coronary arteries are considered risk factors for coronary artery disease. Among them, the most significant are the following: high-calorie diet; hyperlipidemia (hypercholesterolemia); AG; smoking; physical inactivity; excess body weight; diabetes; hereditary predisposition.

Developed coronary atherosclerosis can lead to spasm of the affected arteries, the formation of intravascular platelet foci with the formation of thrombosis in various vascular zones. Depending on the degree of discrepancy that has arisen between the energy needs of the myocardium and the capabilities of the blood supply, myocardial ischemia develops of varying severity. Pain is the most striking clinical manifestation of myocardial ischemia; it is also called anginal. The main pathogenetic mechanism of anginal pain is the excess of the myocardial oxygen demand over the possibilities of its delivery. Most often, delivery is limited due to narrowing of the lumen of the arteries that supply the heart muscle, atherosclerotic plaques or due to arterial spasm. Depending on the severity and duration, ischemia can lead to angina pectoris, when the process is expressed by a painful angina attack (angina pectoris), or in a more severe case, lead to the death of part of the heart muscle, that is, the development of myocardial infarction or the onset of sudden coronary death. In addition to the above-mentioned forms, IHD can manifest itself as various heart rhythm disturbances and circulatory failure, in which pain fades into the background. Anginal pain is characterized by clear clinical features that, with proper history taking, make it possible to recognize it from the patient’s story. When questioning, it is recommended to find out the following points: 1) the nature of the pain; 2) localization; 3) conditions of occurrence; 4) duration of pain; 5) irradiation; relieving effect of nitroglycerin.

Classification of coronary heart disease.

Currently, the classification of coronary artery disease proposed by WHO experts (1979) and adapted to our terminology by the All-Union Cardiology Research Center (1983) is most widespread throughout the world. According to this classification, the following forms of IHD are distinguished:

I. Sudden coronary death (primary cardiac arrest);

P. Angina pectoris:

1. Angina pectoris:

a) new-onset angina pectoris,

b) stable angina pectoris (indicating the functional class, from I to IV),

c) progressive exertional angina;

2. Spontaneous (special) angina;

3. Unstable angina;

Sh. Myocardial infarction:

1. Large focal (transmural) myocardial infarction,

2. Small focal myocardial infarction;

IV. Post-infarction cardiosclerosis;

V. Heart rhythm disturbances (indicating the form);

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

Sudden coronary death (SCD).

VCS includes cases with an unknown diagnosis and presumably associated with electrical failure of the myocardium, most often with the development of ventricular fibrillation. In 90% of those who died from ischemic heart disease, autopsy reveals significant stenosis of the main branches of the coronary arteries (more than 50-75%), in some cases underdevelopment of the coronary arteries, anomalies of their origin, prolapse of the mitral valve, and pathology of the conduction system of the heart are found.

It is believed that the main pathogenetic mechanism of VCS is acute coronary insufficiency, which develops against this background in the presence of such predisposing factors as various heart rhythm disturbances (especially ventricular fibrillation), myocardial hypertrophy, alcohol intake, previous myocardial infarction or the presence of other forms of coronary artery disease. Ventricular fibrillation always occurs suddenly. After 15-20 s from its onset, the patient loses consciousness, after 40-50 s characteristic convulsions develop - a single tonic contraction of skeletal muscles. At this time, the pupils begin to dilate. Breathing gradually slows down and stops at the 2nd minute of clinical death. In case of ventricular fibrillation, emergency care is limited to immediate defibrillation. In the absence of a defibrillator, a single punch should be given to the sternum, which sometimes interrupts ventricular fibrillation. If it is not possible to restore the heart rhythm, it is necessary to immediately begin closed cardiac massage and artificial ventilation.

Angina pectoris. When there is insufficient oxygen access to the myocardium, ischemia occurs. Ischemia can develop with spasm of unchanged coronary arteries due to the fact that under conditions of functional stress on the heart (for example, physical activity), the coronary arteries cannot expand according to needs. Angina pectoris, being the main manifestation of coronary artery disease, can also be observed as a symptom of other diseases (aortic defects, severe anemia). In this regard, the term “angina pectoris”, if the disease that caused it is not indicated, is used as a synonym for the concept of ischemic heart disease. Attacks of pain due to ischemic heart disease are also called “anginal” attacks.

Acute coronary syndrome. The main cause of unstable angina is parietal thrombosis of the coronary artery. Schematically, the process develops as follows: damage to the endothelium or rupture of an atherosclerotic plaque → platelet activation → fibrin deposition → mural thrombus in the coronary artery → unstable angina. There is an opinion about the existence of special, “vulnerable” atherosclerotic plaques that predispose to unstable course of coronary artery disease, myocardial infarction and sudden death - “lethal” plaques.

Myocardial infarction (MI). In the vast majority of cases, the immediate cause of MI is thrombotic occlusion of the coronary arteries. A thrombus in a coronary artery occurs in damaged endothelium at the site of rupture of an atherosclerotic plaque. Much less often, MI is caused by prolonged spasm of the coronary arteries or a sharp and prolonged increase in myocardial oxygen demand. There are known cases of the development of MI due to trauma; arteritis; anomalies, dissection, embolism of the coronary arteries; blood diseases; aortic heart defects; dissecting aortic aneurysm; severe hypoxia; anemia and other diseases and conditions.

Penetrating large-focal (with a pathological Q wave or QS complex on the ECG) MI develops as a result of complete or stable occlusion of the coronary artery. Small-focal (without pathological Q wave) MI occurs with non-occlusive or intermittent thrombosis, rapid lysis of an occlusive thrombus, or against the background of developed collateral blood supply.

Symptoms

Angina pectoris. The main manifestations of angina are attacks of pressing, squeezing pain in the chest. The pain is dull, painful, and if it is perceived as sharp, then this indicates its severity. Sometimes it gives the impression of a foreign body and is felt as numbness, burning, rawness, heartburn, less often as a pinching, boring, aching pain. The most typical localization of anginal pain is behind the upper or middle part of the sternum or slightly to the left of it in the depths of the chest. Most often, pain occurs during physical activity (for example, walking), and gradually its severity and prevalence increase. Usually the pain radiates to the left arm, neck, lower jaw, teeth, and is accompanied by a feeling of discomfort in the chest. The pain may be accompanied by a feeling of fear, which causes patients to freeze in a motionless position. The pain quickly disappears after taking nitroglycerin or eliminating physical effort (stopping while walking or climbing stairs) and other conditions and factors that provoked the attack (emotional stress, cold). When examining a patient during an attack of angina, no characteristic signs of either the cardiovascular system or other organs can be identified. Outside of an attack of angina, there are no characteristic changes on the ECG. However, if it is possible to register an ECG at the time of an attack, a decrease in the ST segment is detected. The same changes can be detected when performing a test with physical activity (bicycle ergometry). This test is important in recognizing angina pectoris in people whose pain is not quite typical. ECG registration is indicated in cases of prolonged attacks of angina (possibility of developing acute myocardial infarction). Angina attacks do not last long - only a few minutes (from 1 to 15). After an attack of angina, a person feels completely healthy; attacks of pain may appear several times a day, but may not occur for many months. Angina pectoris occurs at heights of physical, emotional or hemodynamic stress (with increased blood pressure, tachycardia) due to the inability to increase coronary blood flow.

New-onset angina pectoris noted when anginal attacks appear in the last 30 days. With it, anginal pain does not appear at the onset of the disease, but already with significant damage to the endothelium of the coronary artery, narrowing of its lumen by an atherosclerotic plaque, so it is impossible to immediately predict the further course of the disease. Within a month after the onset of the first anginal attacks, angina pectoris can lead to sudden death, myocardial infarction, progress or become stable.

Stable angina pectoris The occurrence of anginal attacks during the same physical activity is typical. Depending on the load that causes an anginal attack, stable angina pectoris is divided into four functional classes. Angina pectoris (functional class occurs only under extreme stress, functional class II - when quickly climbing uphill or stairs, walking quickly against the wind, in cold weather, after a heavy meal. With angina pectoris of functional class III, anginal attacks develop when walking at a normal pace, and with angina pectoris of functional class IV - at the slightest physical stress, as well as at rest in case of changes in blood pressure or the number of heartbeats.For angina pectoris III-IV functional classes, a warm-up phenomenon is characteristic, when in the morning after waking up the pain develops with minimal physical stress, and during day, load tolerance increases.In such patients, attacks occur at the slightest load, performed with raised arms.

Progressive angina pectoris characterized by an increase in the frequency of anginal attacks and their occurrence in response to a lesser load than before, an increase in the strength and duration of pain, the emergence of new zones of localization and irradiation of pain.

Spontaneous angina(special, variant, Prinzmetal's angina) occurs as a result of spasm of the coronary arteries without connection with physical stress. It usually occurs in young and middle-aged people with good exercise tolerance. It is characterized by more severe and prolonged (compared to angina pectoris) pain syndrome, often developing at the same time of day, and low effectiveness of nitroglycerin. In a small proportion of patients, at the height of pain, elevations of the st segment or other changes in repolarization on the ECG are noted. Almost 30% of patients with new-onset spontaneous angina develop myocardial infarction within 1-2 months. If this does not happen, then over time spontaneous angina can completely transform into exertional angina.

Acute coronary syndrome. According to the severity of clinical manifestations, unstable angina is divided into classes.

  • Class I. Patients with new (less than 2 months old) or progressive angina. Patients with newly emerging severe or frequent (3 times a day or more often) exertional angina. Patients with stable angina in whom attacks have definitely become more frequent, intense, prolonged, or are provoked by less exercise than before (patients with resting angina pectoris for the previous 2 months are excluded).
  • Class II. Patients with subacute angina at rest, i.e. with one or more attacks of angina at rest during the last month, but not in the previous 48 hours.
  • Class III. Patients with acute angina pectoris, i.e. with one or more attacks of angina at rest during the last 48 hours (patients with class II and III angina may also have signs of class I angina).
Myocardial infarction (MI). The symptoms of MI vary significantly depending on the period of the disease. There are five periods of MI: prodromal, acute, acute, subacute, post-infarction.

Prodromal period of MI(acute coronary syndrome or unstable angina) lasts from a few minutes to 30 days and is characterized by the appearance for the first time or an increase in frequency and intensification of habitual anginal pain, a change in their nature, localization or irradiation, as well as a change in the reaction to nitroglycerin. During this period of the disease, dynamic ECG changes may be observed, indicating ischemia or damage to the heart muscle. Pain syndrome and electrical instability of the myocardium can manifest as acute rhythm and conduction disturbances.

The most acute period lasts several minutes or hours, it lasts from the onset of pain until the appearance of signs of cardiac muscle necrosis on the ECG. Blood pressure at this time is unstable; more often, against the background of pain, there is an increase, less often - a decrease in blood pressure up to shock. In the acute period, the probability of ventricular fibrillation is highest. Based on the main clinical manifestations of the disease in this period, the following variants of the onset of MI are distinguished: painful (anginal), arrhythmic, cerebrovascular, asthmatic, abdominal, asymptomatic (painless). The anginal variant - the most common - is manifested by severe pain, the intensity of which is perceived as “dagger-like”, tearing, tearing, burning, scorching pain in the chest, lasting from 20 minutes to 12 hours or more. The arrhythmic variant includes those cases when MI begins with acute disturbances in the rhythm or conduction of the heart in the absence of pain. More often it manifests itself as ventricular fibrillation, less often - arrhythmic shock caused by a paroxysm of tachycardia (tachyarrhythmia) or acute bradycardia. The cerebrovascular variant is associated with an increase in blood pressure when MI develops against the background of a hypertensive crisis. The asthmatic variant occurs in patients with initial circulatory failure and manifests itself as a sudden, often unmotivated attack of shortness of breath or pulmonary edema. The abdominal variant occurs with localized pain in the epigastric region and is accompanied by nausea, vomiting, flatulence, stool disorder and intestinal paresis. The low-symptomatic (painless) variant of MI is manifested by weakness and a feeling of discomfort in the chest; observed in elderly and senile people.

Acute period of MI lasts (in the absence of disease relapse) from 2 to 10 days. At this time, a focus of necrosis is formed, resorption of necrotic masses occurs, aseptic inflammation in the surrounding tissues occurs, and scar formation begins. With the end of necrotization, the pain subsides and if it occurs again, it is only in cases of recurrent MI or early post-infarction angina. The likelihood of acute heart rhythm disturbances decreases every day. From the second day of MI, signs of resorption-necrotic syndrome appear (increased body temperature, sweating, leukocytosis, increased ESR). From the third day, due to myocardial necrosis, hemodynamics worsen - from a moderate decrease in blood pressure (mainly systolic) to pulmonary edema or cardiogenic shock. At the height of myomalacia in the first week of transmural MI, the risk of cardiac muscle rupture is highest.

Subacute period lasts on average 2 months. The scar is being organized. Manifestations of resorption-necrotic syndrome disappear. Symptoms depend on the degree of exclusion of the damaged myocardium from contractile function (signs of heart failure, etc.).

Post-infarction period (late)- time of complete scarring of the necrosis focus and consolidation of the scar. In typical cases of transmural MI, already during an attack of pain, characteristic ECG changes can be detected - a rise in the ST segment, a decrease in the P wave, the appearance of a deep and wide Q, and later a negative T is formed. Subsequently, over the course of several weeks or months, the signs of MI undergo a slow reverse development. Later than others, the enlarged Q wave disappears, which often remains a lifelong sign of previous transmural MI. ECG changes can be expressed in different leads, depending on the location of the MI. ECG has limited diagnostic value in case of repeated MI, with old blockade of the left bundle branch. Of great diagnostic importance is a short-term (on the 2-4th day) increase in the activity of blood enzymes - creatine phosphokinase, lactate dehydrogenase, glutamic transaminase or the appearance of cardiac-specific proteins in the blood (troponin T, etc.).

Complications.

Numerous complications aggravate the course of MI. Arrhythmias, primarily sinus tachycardia and extrasystole, are observed in most patients, especially in the first 3 days of the disease. The most dangerous are ventricular fibrillation and complete transverse blockade at the level of the intraventricular conduction system. Ventricular fibrillation is often preceded by ventricular tachycardia and extrasystole, and blockade is preceded by increasing conduction disturbances. Left ventricular heart failure (congestive wheezing, cardiac asthma, pulmonary edema) is often detected in the acute period of the disease. The most severe form of left ventricular failure is cardiogenic shock, which can occur with a particularly large infarction and usually leads to death. Its signs are a drop in systolic blood pressure (below 80 mm Hg), tachycardia and signs of deterioration of peripheral circulation: cold pale skin, cyanosis, impaired consciousness, drop in diuresis. Embolisms in the pulmonary artery system (can cause sudden death) or in the systemic circulation are possible. Mitral regurgitation often occurs if the MI involves one of the papillary muscles. An acute large left ventricular aneurysm can be recognized clinically by distorted pulsation of the atrial region, ECG stabilization characteristic of the acute phase of MI, and can be confirmed radiographically or by echocardiography. Such patients also experience circulatory failure. Sometimes patients with extensive transmural MI die from external cardiac rupture, which is accompanied by signs of acute cessation of blood circulation. Post-infarction syndrome is a late complication (a week or later after MI), manifested by signs of pericarditis (most often), pleurisy, arthralgia, eosinophilia.

Post-infarction cardiosclerosis. The symptoms of post-infarction cardiosclerosis are determined by the size and location of the post-infarction scar, as well as the state of the coronary circulation in the functioning parts of the myocardium. The most common causes of cardiac arrhythmia and conduction disturbances are heart failure. The presence of pain syndrome such as angina pectoris is not necessary. The ECG is characterized by the presence of a persistent pathological QS complex in large-focal and transmural MI or a Q wave in non-transmural MI. In some cases, the Q wave in non-transmural large-focal MI may disappear after several months (years). In small-focal MI, the pathological Q wave is not formed, so it is also absent in post-infarction cardiosclerosis. The diagnosis of “atherosclerotic cardiosclerosis” encountered in clinical practice also has a right to exist. In a number of patients, as a result of frequently repeated and long-lasting ischemia, diffuse small foci of myocardial damage develop, which differ from post-infarction scars, but ultimately sometimes lead to the same consequences as post-infarction cardiosclerosis - circulatory failure, various rhythm and conduction disturbances.

Diagnostics

Angina pectoris. It is based mainly on the identification of characteristic attacks and on data from repeated electrocardiographic studies. In unclear cases, the patient is hospitalized and additionally carried out long-term monitoring of the ECG (in this case, episodes of ischemia are detected, most of which are asymptomatic), tests with nitroglycerin and bicycle ergometry. Sometimes, to confirm the diagnosis, coronary angiography is required (performed in a cardiac surgery hospital), which makes it possible to establish the distribution and severity of coronary sclerosis, which is important when discussing the issue of surgical treatment.

Acute coronary syndrome. In all cases, with unstable angina, there is an appearance or change in habitual anginal attacks, an increase in their frequency, strength, duration or conditions of occurrence. The ECG shows changes in repolarization (ST segment and T wave). It is important to distinguish between cases of unstable angina with ST segment elevation and depression. In some patients, changes on the ECG may be absent. For differential diagnosis of non-penetrating (without pathological Q wave) myocardial infarction and unstable angina, an ECG is recorded before and immediately after taking sublingual nitroglycerin. With irreversible changes in the heart muscle, the dynamics of repolarization are not observed on the ECG, but with angina pectoris it is observed.

Myocardial infarction (MI). MI is based on a thorough analysis of the pain syndrome, the appearance of dynamic ECG changes and an increase in enzyme activity or the content of cardiac-specific proteins in the blood (troponin T). Highlight; large-focal (transmural) MI - the diagnosis is made in the presence of pathognomonic changes on the ECG: pathological Q or QS wave and enzyme activity in the blood serum, even with an atypical clinical picture; and small-focal (subendocardial, intramural) MI - the diagnosis is made when changes in the ST segment or wave develop over time T without pathological changes in the QRS complex in the presence of typical changes in enzyme activity. The diagnosis of MI indicates the date of occurrence, period of the disease, localization, features of the course and complications. It is reasonable to speak of recurrent MI when repeated foci of necrosis occur in the period from 3 to 28 days from the onset of the disease. In subsequent periods (over 28 days), a diagnosis of “recurrent myocardial infarction” is made.

Treatment

Angina pectoris. If an angina attack occurs, the patient should immediately stop exercising, sit down, and take nitroglycerin under the tongue. The cessation or significant reduction of pain occurs within 1 to 5 minutes. Nitroglycerin should be taken immediately with every attack of angina. The aerosol form of nitroglycerin has certain advantages (speed of onset and stability of the effect). In the absence of nitroglycerin at hand, the attack can often be interrupted by massage of the carotid sinus. The massage should be carried out carefully, on one side, for no more than 5 seconds. Arterial hypertension or tachycardia increases the myocardial oxygen demand and is often the cause of anginal pain. Repeated administration of sublingual nitroglycerin is often sufficient to reduce high blood pressure. A decrease in blood pressure can be achieved by administering clonidine (clonidine) sublingually (0.15 mg) or slowly intravenously (1 ml of 0.01% solution). In addition to the hypotensive effect, clonidine has a pronounced sedative and analgesic effect. For tachycardia (tachyarrhythmia), β-blockers are used to reduce the heart rate, and if their use is contraindicated, calcium antagonists (verapamil, diltiazem, 1 tablet 3 times a day) are used. The main medications for the systematic treatment of coronary insufficiency are long-acting nitrates (nitrosorbide, nitrong, sustak, isoket, isomac, nitromac, etc.) and β-blockers (propranolol, atenalol, obzidan, anaprilin). The most effective combination of drugs from these groups. Treatment begins with small doses. The initial dose of nitrosorbide is 20 mg 4 times a day, atenalol 20 mg 2 times a day. If well tolerated, the dose is gradually (every 2-3 days) increased until the full effect is achieved. The most common signs of poor tolerability are headache (for nitrates), which usually decreases with continued treatment, and bradycardia (for beta-blockers). β-blockers are contraindicated in cases of severe heart failure, bronchospasm (even in history), complete or incomplete transverse blockade, severe bradycardia and hypotension. Treatment with these medications should be continued for a long time, for months, and if successful, they should be discontinued gradually, over about 2 weeks. The treatment is usually combined with an antiplatelet agent (for example, acetylsalicylic acid 0.125 g once a day), a statin is added (for example, lovastatin 40 mg once a day, after dinner), keeping serum cholesterol at the lower limit of normal. In case of exacerbation of coronary heart disease, hospitalization in the cardiology department is indicated. The possibility of surgical treatment (coronary artery bypass grafting) can be discussed in young patients with satisfactory contractile function of the heart, for whom drug treatment does not help.

Acute coronary syndrome. All patients with unstable angina should be immediately hospitalized, if possible, in intensive observation wards of specialized cardiology departments, where they are prescribed antianginal drugs. The drugs of choice are nitrates (nitroglycerin, isosorbide dinitrate), and until the patient’s condition stabilizes, their continuous action should be ensured throughout the day. In severe cases, nitrate preparations are administered slowly intravenously. In addition to nitrates, if there are no contraindications, β-adrenergic blockers (propranolol, metoprolol or atenolol) are prescribed. If there are contraindications to treatment with β-blockers, calcium antagonists are used, of which diltiazem, 1 tablet, is the most effective. (60 mg) 3 times a day. Antiplatelet agents (acetylsalicylic acid 160-325 mg/day) and anticoagulants (heparin 24,000 units/day, etc.) are important in treatment. Thrombolytic therapy is indicated for acute coronary syndrome only in patients with ST segment elevation on the ECG. For patients with severe unstable angina, surgical methods of restoring coronary blood flow (coronary artery bypass grafting, percutaneous transluminal coronary angioplasty) are of decisive importance in treatment.

Myocardial infarction (MI). Patients with MI or suspected MI are hospitalized by ambulance, if possible, in a specialized cardiology department with an intensive care unit. Treatment begins at the prehospital stage and continues in the hospital. The most important initial goals of treatment are to relieve pain and maintain heart rhythm. To relieve pain, morphine or promedrol with atropine, fentanyl with droperidol are administered, and oxygen therapy is prescribed. In the presence of ventricular extrasystoles, 50-100 mg of lidocaine is administered intravenously with the possible repetition of this dose after 5 minutes (if there are no signs of shock). For bradycardia of sinus or other nature with a ventricular rate of less than 55 beats per minute, it is advisable to administer 0.5-1 ml of a 0.1% atropine solution intravenously. In the hospital, usually under conditions of constant cardiac monitoring, treatment is carried out aimed at pain relief (narcotic analgesics, antipsychotics), restoration of coronary blood flow (thrombolytic drugs, anticoagulants, antiplatelet agents), limiting the size of necrosis (β-blockers, nitroglycerin), and preventing early complications ( reperfusion injury of the myocardium, arrhythmias): oxygen, antioxidants, for special indications - antiarrhythmic drugs. In the future, the rate of expansion of the regime is controlled. After discharge from the hospital and treatment in a cardiological sanatorium, patients, as a rule, require systematic follow-up and treatment.

Post-infarction cardiosclerosis. Aimed at suppressing heart failure, arrhythmias, angina, and progression of atherosclerosis. Heart failure and arrhythmias in cardiosclerosis are usually poorly reversible; treatment leads only to temporary improvement.

Prevention

Myocardial infarction (MI). Differential diagnosis is carried out with a severe attack of angina pectoris (without necrosis, the QRS complex on the ECG does not change, there is no noticeable hyperenzymemia, complications are uncharacteristic), acute pericarditis (pericardial friction noise, association of pain with breathing, slow increase in ECG changes), thromboembolism of a large branch of the pulmonary artery ( in the first day, differential diagnosis can be very difficult), as well as with dissecting aortic hematoma, acute pneumonia, pneumothorax, acute cholecystitis, etc. (see relevant pathology).