IBS risk 1 what. What is coronary heart disease and how to treat it? Nutrition for IHD

Currently, cardiovascular diseases are the leading cause of death and disability worldwide. The leading role in the structure of mortality from cardiovascular diseases belongs to coronary heart disease.

Coronary heart disease (CHD) – chronic illness, which develops when there is insufficient oxygen supply to the myocardium. The main reason (in more than 90% of cases) of insufficient oxygen supply is the formation of atherosclerotic plaques in the lumen coronary arteries, arteries supplying the heart muscle (myocardium).

Prevalence

According to the World Health Organization (WHO), mortality from cardiovascular diseases is 31% and is the most common cause deaths worldwide. In the territory Russian Federation this figure is 57.1%, of which IHD accounts for more than half of all cases (28.9%), which in absolute figures is 385.6 people per 100 thousand population per year. For comparison, mortality from the same cause in the European Union is 95.9 people per 100 thousand population per year, which is 4 times less than in our country.

The incidence of ischemic heart disease increases sharply with age: in women from 0.1-1% at the age of 45-54 years to 10-15% at the age of 65-74 years, and in men from 2-5% at the age of 45-54 years to 10 -20% aged 65-74 years.

Cause of development and risk factors

The main cause of the development of coronary heart disease is atherosclerotic damage to the coronary arteries. Due to certain risk factors, cholesterol is deposited on the walls of blood vessels for a long time. A plaque then gradually forms from the cholesterol deposits. An atherosclerotic plaque, gradually increasing in size, disrupts the flow of blood to the heart. When the plaque reaches a significant size, which causes an imbalance in the delivery and consumption of blood by the myocardium, then coronary heart disease begins to manifest itself in various forms. The main form of manifestation is angina pectoris.

Risk factors for coronary artery disease can be divided into modifiable and non-modifiable.

Non-modifiable risk factors are those that we cannot influence. These include

  • Floor. Male gender is a risk factor for cardiovascular diseases. However, entering menopause, women are deprived of protective hormonal levels, and the risk of adverse cardiovascular events becomes comparable to the male sex.
  • Age. After age 65, the risk of cardiovascular disease increases sharply, but not equally for everyone. If the patient has a minimal number of additional factors, then the risk of adverse events remains minimal.
  • Heredity. A family history of cardiovascular disease should also be taken into account. The risk is influenced by the presence of cardiovascular diseases in the female line before 65 years of age, and in the male line up to 55 years of age.
  • Other non-modifiable risk factors. Other non-modifiable factors include ethnicity (for example, blacks have more high risk stroke and chronic renal failure), geographical location (for example, high frequency stroke and ischemic heart disease in Russia, Eastern Europe and the Baltic countries; low risk of CAD in China).

Modifiable risk factors are factors that can be influenced by lifestyle changes or prescription medicines. Modifiable ones can be divided into behavioral and physiological and metabolic.

Behavioral risk factors:

  • Smoking. According to the World Health Organization, 23% of deaths from coronary heart disease are caused by smoking, reducing the life expectancy of smokers aged 35-69 years by an average of 20 years. Sudden death among people who smoke a pack of cigarettes or more per day is 5 times more common than among non-smokers.
  • Eating habits and physical activity.
  • Stress.

Physiological and metabolic features:

  • Dyslipidemia. This term refers to an increase in total cholesterol, triglycerides and an imbalance between cholesterol fractions. The level of total cholesterol in patients should be no higher than 5 mmol/l. The level of low-density lipoproteins (LDL) in patients who have not had a myocardial infarction should not be higher than 3 mmol/l, and in people who have had a myocardial infarction this indicator should correspond to the value< 1,8 ммоль/л. Также негативный вклад в развитие неблагоприятных сердечно-сосудистых событий вносят липопротеиды высокой плотности (ЛПВП) и триглецириды. ЛПВП должны быть выше 1,42 ммоль/л, а верхняя рекомендуемая граница для триглицеридов – 1,7 ммоль/л.
  • Arterial hypertension. To reduce the risk of cardiovascular complications, it is important to achieve the target level blood pressure less than 140/90 mm Hg. In patients with a high and very high risk of cardiovascular complications, it is necessary to reduce blood pressure to 140/90 mmHg. or less, within 4 weeks. In the future, subject to good tolerance, it is recommended to reduce blood pressure to 130/80 mm Hg. and less.
  • Obesity and the pattern of fat distribution in the body. Obesity is a metabolic and nutritional chronic disease, which is manifested by excessive development of adipose tissue and progresses in its natural course. Excess body weight can be assessed using the formula that determines the body mass index (BMI):

BMI= body weight (kg)/height 2 (m2). If your BMI is 25 or more, this is an indication for weight loss.

  • Diabetes. Considering the high risk of developing adverse cardiovascular events in diabetes, as well as the fact that the first myocardial infarction or cerebral stroke in patients with diabetes is more often fatal, hypoglycemic therapy is an important component primary prevention adverse cardiovascular events in patients with type II diabetes.

The SCORE scale has been developed to calculate the degree of risk. This scale allows you to calculate the 10-year risk of cardiovascular disease.

Clinical manifestations of coronary artery disease

The most typical complaints for coronary heart disease are:

    Substernal pain associated with exercise or stressful situations

    Dyspnea

    Interruptions in the work of the heart, a feeling of irregular heart rhythm, weakness,

From the anamnesis data great importance have the duration and nature of pain, shortness of breath or arrhythmia, their connection with physical activity, the amount of physical activity that the patient can withstand without an attack, the effectiveness of various medicines when an attack occurs (in particular, the effectiveness of nitroglycerin).

For angina pectoris pain syndrome lasts up to 30 minutes; in case of myocardial infarction, the pain can last for several hours.

Forms of IHD

Diagnosis of IHD

Diagnosis of coronary heart disease includes assessment of the patient’s complaints: nature and location pain, their duration, conditions of occurrence, effect of taking nitroglycerin preparations.

An electrocardiographic study is required (ECG monitoring is preferred), stress tests (bicycle ergometry, treadmill test, etc.), the gold standard in diagnosis is selective coronary angiography. Additionally, myocardial scintigraphy and computed tomography are used (to exclude heart defects and cardiac aneurysms). In terms of determining prognosis and assessing the risk of cardiovascular complications - determination of cholesterol and serum lipoproteins, etc.

Treatment of coronary artery disease

The main goal in the treatment of chronic coronary heart disease is to reduce the heart's oxygen demand or increase oxygen delivery. In connection with the above, treatment of coronary artery disease can be divided into drug and surgical.

Drug treatment includes drug therapy, the main groups of drugs are beta-blockers, nitroglycerin (for relief acute attacks), long-acting nitrates, calcium channel blockers. For hypercholesterolemia, statins are prescribed, and small doses of acetylsalicylic acid are prescribed to prevent thrombosis. If there is a concomitant arterial hypertension– drugs that lower blood pressure.

If there is no effect from conservative therapy surgical treatment is performed:

Prevention of coronary artery disease

Preventing a disease is always easier than treating it!

Since the main role in the development of coronary heart disease is played by atherosclerosis, the prevention of this disease should be aimed at combating the development of atherosclerotic lesions of the coronary arteries. Risk factors need to be addressed. If we cannot influence non-modifiable factors in any way, then we direct all prevention to modifiable factors:

Stop smoking! Smoking is one of the main causes of atherosclerosis, arterial hypertension, coronary heart disease and stroke. Conversely, stopping smoking leads to a reduction in the risk of disease.

Weight control and adherence to dietary recommendations. A diet low in cholesterol and fat is prescribed: the consumption of fatty meats, fatty dairy products, and rich broths is limited; It is recommended to replace some animal fats with vegetable fats. Seafood, as well as vegetables and fruits containing a large amount of fiber, are healthy.

The fight against physical inactivity is no less important. For daily cardio training, you need to perform a course of special exercises and spend enough time in the fresh air.

Blood pressure control. It is necessary to strictly follow the recommendations for drug and non-drug treatment of arterial hypertension. It is most effective to create a blood pressure diary recording morning and evening readings. This simple method will not only help you carry out daily self-monitoring, but will also give your doctor the most complete picture of the disease.

P.S. Remember, do not self-medicate, as not knowing the complications of drugs can lead to adverse consequences.

In our center we will help not only to carry out the full scope of all necessary examinations, but also to select the most effective and safe way treatment of cardiovascular diseases.

Good day, dear readers!

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

What is coronary heart disease?

Coronary heart disease (CHD) – pathological condition, which is characterized by insufficient blood supply and, accordingly, oxygen to the heart muscle (myocardium).

Synonyms for IHD– Coronary heart disease (CHD).

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

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

The heart, as you and I know, is the “engine” of a person, one of the main functions of which is pumping blood throughout the body. However, like a car engine, without enough fuel, the heart stops functioning normally and can stop.

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

The blood supply to the myocardium (heart muscle) occurs through 2 coronary vessels that arise from the aorta. The coronary vessels, divided into a large number of small vessels, go around the entire heart muscle, feeding each section of it.

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

The onset of the disease usually manifests itself during intense physical exertion (running and others), but over time, if no action is taken, pain and other signs of IHD begin to haunt the person even during rest. Some signs of IHD are also: swelling, dizziness.

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

IHD - ICD

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

The first signs of IHD are:

  • Increased blood sugar levels;
  • Increased cholesterol levels;

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

  • Angina pectoris- characterized by pressing pain behind the sternum (which can radiate to the left side of the neck, left shoulder blade or arm), shortness of breath during physical activity (fast walking, running, climbing stairs) or emotional stress(stress), increased blood pressure, ;
  • Arrhythmic form- accompanied by shortness of breath, cardiac asthma, pulmonary edema;
  • – a person develops a seizure severe pain behind the sternum, which cannot be relieved with conventional painkillers;
  • Asymptomatic form- the person has no obvious signs, indicating the development of ischemic heart disease.
  • , malaise;
  • Edema, mainly;
  • , clouding of consciousness;
  • , sometimes with attacks;
  • Heavy sweating;
  • Feelings of fear, anxiety, panic;
  • If you take nitroglycerin during painful attacks, the pain subsides.

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

Other causes of IHD include:

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

The following people are at increased risk of developing CHD:

  • Age – the older a person is, the higher the risk of developing IHD;
  • Bad habits – smoking, drugs;
  • Poor quality food;
  • Sedentary lifestyle;
  • Exposure to frequent ;
  • Male gender;

Classification of IHD

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

Diagnosis of IHD

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

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

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

Treatment of coronary heart disease usually includes the following therapies:

1. Limitation of physical activity;
2. Drug treatment:
2.1. Anti-atherosclerotic therapy;
2.2. Maintenance therapy;
3. Diet;
4. Surgical treatment.

1. Limiting physical activity

As you and I already know, dear readers, the main point of IHD is insufficient blood supply to the heart. Due to the insufficient amount of blood, of course, the heart does not receive enough oxygen, along with various substances necessary for its normal functioning and vital activity. At the same time, you need to understand that with physical stress on the body, the load on the heart muscle also increases, which in due course wants to receive an additional portion of blood and oxygen. Naturally, because If there is already not enough blood in IHD, then under load this insufficiency becomes even more critical, which contributes to the worsening of the disease in the form of increased symptoms, up to sudden cardiac arrest.

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

2. Drug treatment (medicines for ischemic heart disease)

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

2.1. Anti-atherosclerotic therapy

IN Lately For the treatment of coronary artery disease, many doctors use the following 3 groups of drugs - antiplatelet agents, β-blockers and hypocholesterolemic (cholesterol-lowering) drugs:

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

Among the antiplatelet agents we can highlight the following drugs: acetylsalicylic acid(“Aspirin”, “Acecardol”, “Thrombol”), “Clopidogrel”.

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

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

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

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

Among the fibrates, the following drugs can be distinguished: Fenofibrate.

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

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

The level of cholesterol in the blood in case of coronary artery disease should be 2.5 mmol/l.

2.2. Maintenance therapy

Nitrates. They are used to reduce the preload on the heart by dilating the blood vessels of the venous bed and depositing blood, thereby stopping one of the main symptoms of coronary heart disease - angina pectoris, manifested in the form of shortness of breath, heaviness and pressing pain behind the sternum. Especially for the relief of severe attacks of angina, intravenous drip administration of nitroglycerin has recently been successfully used.

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

Contraindications to the use of nitrates are below 100/60 mmHg. Art. Side effects include a decrease in blood pressure.

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

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

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

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

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

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

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

Antiarrhythmic drugs. They help normalize heart rate (HR), thereby improving respiratory function and easing the course of coronary artery disease.

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

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

Among ACE inhibitors The following drugs can be distinguished: “Captopril”, “Lisinopril”, “Enalapril”.

Sedatives. They are used as a calming agent for the nervous system when the cause of an increase in heart rate is emotional experiences or stress.

Among sedatives can be distinguished: “Valerian”, “Persen”, “Tenoten”.

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

The main points of the diet for ischemic heart disease include:

  • The calorie content of food is 10-15%, and in case of obesity, 20% less than your daily diet;
  • The amount of fat is no more than 60-80 g/day;
  • The amount of protein is no more than 1.5 g per 1 kg of human body weight/day;
  • The amount of carbohydrates is no more than 350-400 g/day;
  • Quantity table salt– no more than 8 g/day.

What not to eat if you have ischemic heart disease

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

What can you eat if you have ischemic heart disease?

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

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

For the treatment of coronary heart disease M.I. Pevzner developed a therapeutic nutrition system - diet No. 10c (table No. 10c). These vitamins, especially C and P, strengthen the walls of blood vessels and prevent cholesterol deposits in them, i.e. formation of atherosclerotic plaques.

Ascorbic acid also promotes the rapid breakdown of “bad” cholesterol and its removal from the body.

Horseradish, carrots and honey. Grate the horseradish root to make 2 tbsp. spoons and pour a glass of boiled water over it. Afterwards, mix the horseradish infusion with 1 glass of freshly squeezed carrot juice and 1 glass of honey, mix everything thoroughly. You need to drink 1 tbsp. spoon, 3 times a day, 60 minutes before meals.

6134 0

The choice of management tactics for patients diagnosed with acute coronary syndrome is determined by the risk of progression to acute MI and the risk of death.

Acute coronary syndromes diagnosed in a heterogeneous group of patients with a variety of clinical manifestations, differences in degree and severity coronary atherosclerosis and a different risk of thrombosis (namely, with rapid progression to MI). For personalized selection adequate treatment it is necessary to reassess the risk of occurrence severe consequences acute coronary syndrome. Such an assessment should be carried out from the moment of diagnosis or admission of the patient to the hospital, based on available clinical information and laboratory data. The initial assessment is later supplemented with information about the dynamics of symptoms, ECG signs of ischemia, laboratory test results and functional state LV. In addition to age and previous history of coronary artery disease, clinical examination, ECG and biochemical parameters are key elements of risk assessment.

Risk factors

Elderly age and male gender are associated with more severe course IHD and increased risk unfavorable outcome. A history of coronary artery disease such as severe or prolonged angina or previous myocardial infarction is also associated with more frequent subsequent events. Other risk factors include a history of LV dysfunction or congestive heart failure, as well as diabetes mellitus and hypertension. Most well-known risk factors are also indicators of a poorer prognosis in patients with unstable CAD.

Clinical picture

Important information To evaluate the forecast, provide an estimate clinical picture, duration of the period since the last episode of ischemia, presence of angina at rest and response to drug treatment. The classification proposed by J. Braunwald is based on clinical features and allows assessment of clinical outcomes. This classification is mainly used in scientific research. But other risk indicators should also be taken into account to select the optimal treatment strategy.

ECG

ECG- the most important method not only for establishing a diagnosis, but also for prognostic assessment. Patients with ST segment depression have a higher risk of subsequent cardiac events than those with isolated T-wave inversion, who in turn have a higher risk than those with a normal ECG on admission.

The results of some studies raise doubts about the prognostic value of isolated T wave inversion. A standard resting ECG does not adequately reflect the dynamics of the development of coronary thrombosis and myocardial ischemia. Almost ⅔ episodes of ischemia during destabilization of coronary artery disease are silent and therefore are unlikely to be detected during routine ECG recording. Useful information Holter ECG monitoring can provide results, but its results are obtained only a few hours or days after recording. A promising technique is computerized 12-lead ECG monitoring in real time (on-line). In 15-30% of patients with destabilized coronary artery disease, transient episodes of ST segment fluctuations, mainly depression, are detected. These patients are at increased risk of developing subsequent cardiac events. In addition to recording the resting ECG and other common clinical parameters, ECG monitoring provides independent prognostic information. In patients with the number of ischemic episodes >0-2 per day, the incidence of death or MI after 30 days was 9.5%, in patients with the number of ischemic episodes >2-5 and >5 - 12.7 and 19.7%, respectively.

Markers of myocardial damage

In patients with unstable CAD with elevated troponin levels, early and long-term clinical outcomes are poor compared with those in patients without changes in troponin levels. The appearance in the blood of markers of myocardial necrosis, in particular cardiac troponins, against the background of a cardiac event, is associated with the risk of reinfarction and cardiac death. The risk of new events correlates with the degree of troponin elevation. According to B. Lindahl, a marked increase in troponin levels is associated with high mortality during long-term follow-up, reduced LV function, but a moderate risk of reinfarction. The increased risk associated with changes in troponin levels is independent of other risk factors, such as changes in resting or continuous ECG monitoring and markers of inflammatory activity. Immediate assessment of troponin levels is useful in determining early risk in patients with acute coronary syndrome. Identifying patients with elevated troponin levels is also useful for guiding treatment decisions in individuals with unstable CAD. Recent studies have shown that low molecular weight heparins and glycoprotein IIb/IIIa receptor inhibitors provide particular benefit when troponin levels are elevated, in contrast to cases when troponin levels do not increase.

Markers of inflammatory activity

Increased fibrinogen and CRP levels have been reported as risk factors in patients with acute coronary syndrome, but these findings are not consistent in all studies. For example, in the FRISC (FRagmin during InStability in Coronary artery disease) study, increased fibrinogen levels were associated with an increased risk of death at short and long follow-up and/or increased risk further development THEM. The prognostic value of fibrinogen levels was independent of ECG data and troponin levels. However, in the TIMI III (Thrombolysis In Myocardial Infarction) study, hyperfibrinogenemia was associated with a greater number of ischemic episodes during patients' hospital stay; however, there was no association with deaths or MI during the 42-day follow-up. The prognostic value of increased CRP levels is highest in patients with signs of myocardial damage. In some studies, elevated CRP concentrations are predominantly associated with the risk of death during long-term follow-up, in contrast to fibrinogen levels, which are associated with the risk of further MI and mortality (Fig. 2.5).

Troponin T and CRP are strongly correlated with the risk of cardiac death over the long term and are independent risk factors, but their effects are additive to each other and to other clinical markers.

Elevated levels of BNP and interleukin-6 are strong predictors of mortality during short- and long-term follow-up.

In patients with acute coronary syndromes, an early increase in the content of soluble intracellular adhesion molecules and interleukin-6 was revealed. Increased levels interleukin-6 assays also allow the identification of patients with the greatest expected benefit from an early invasive strategy and long-term antithrombotic treatment. A more detailed study of these markers may provide Additional information about the pathogenesis of acute coronary syndromes.

Rice. 2.5. Prognostic value of blood concentrations of CRP and fibrinogen: relationship with mortality in unstable ischemic heart disease

Thrombosis markers

An association between increased thrombin generation and poor outcome in patients with unstable angina has been found in some but not all studies.

The formation of venous thrombosis is associated with such changes in the anticoagulant system as deficiency of protein C (activated coagulation factor XIV), protein S (protein C cofactor), and antithrombin. But the risk of acute coronary syndrome is not associated with any of these factors. In the population and in patients with unstable angina, the risk of future coronary events was higher in patients with reduced blood fibrinolytic activity. To date, only a few large studies have been conducted on fibrinolytic activity and its relationship with acute phase proteins in patients with destabilized coronary artery disease. Currently, the study of hemostasis markers is not recommended for risk stratification or selection of individualized treatment for destabilized coronary artery disease.

Echocardiography

LV systolic function is an important parameter for assessing prognosis, which can be easily and accurately assessed by echocardiography. During ischemia, areas of transient hypokinesia or akinesia of segments of the LV wall are identified, the function of which is restored after normalization of blood flow. Background LV dysfunction, as well as other conditions such as aortic stenosis or HCM, have important in the prognostic assessment and management of such patients.

Stress test before discharge

After stabilization of the patient’s condition and before discharge useful tool A stress test is used to verify the diagnosis of coronary artery disease and assess the early and long-term risk of developing coronary events.

Exercise testing has a high negative predictive value. Parameters that reflect cardiac function provide at least as valuable prognostic information as myocardial ischemia indices, and combining these parameters provides additional information for assessing prognosis. Many patients are unable to perform an exercise test, and this in itself indicates a poor prognosis. To increase the sensitivity and specificity of prognosis assessment in these cases, especially in women, cardiac imaging methods such as myocardial perfusion scintigraphy and stress echocardiography are used. But long-term studies of the prognostic value of stress echocardiography in patients who have suffered an episode of destabilization of coronary artery disease have not been sufficient until this time.

Coronary angiography

This study provides unique information about the presence and severity of CAD. Patients with multiple vascular lesions, as well as stenosis of the left main coronary artery, are at higher risk of developing severe cardiac events. Angiographic assessment of the characteristics and location of vascular injury is performed in cases where the need for revascularization is being considered. Risk indicators include complex, longitudinal and heavily calcified lesions and vascular angulations. But the risk is highest in the presence of filling defects, which indicate intracoronary thrombosis.

Risk assessment must be accurate, reliable and preferably simple, accessible and cost-effective. It is recommended to use the risk assessment method using the GRACE (Global Registry of Acute Coronary Events) program, which can be downloaded from the website: www.outcomes.org/grace. After answering the program questions, the resulting final figures are placed in the table. 2.1, which will help determine the short- and long-term risk of coronary artery disease in patients who have suffered acute coronary syndrome.


Table 2.1

M.I. Lutai, A.N. Parkhomenko, V.A. Shumakov, I.K. Sledzevskaya "Ischemic heart disease"

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

ICD-10

I20-I25

General information

Coronary heart disease is the most serious problem of modern cardiology and medicine in general. In Russia, about 700 thousand deaths caused by various forms of IHD are recorded annually; in the world, mortality from IHD is about 70%. Coronary heart disease mostly affects men of active age (55 to 64 years), leading to disability or sudden death. The group of IHD includes acutely developing and chronic conditions of myocardial ischemia, accompanied by subsequent changes: dystrophy, necrosis, sclerosis. These conditions are considered, among other things, as independent nosological units.

Causes

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

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

Factors contributing to the occurrence of IHD include:

  • hyperlipedemia

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

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

  • smoking

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

  • physical inactivity and obesity

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

  • impaired carbohydrate tolerance
  • angina pectoris (stress):
  1. stable (with determination of functional class I, II, III or IV);
  2. unstable: new-onset, progressive, early postoperative or post-infarction angina;
  • spontaneous angina (syn. special, variant, vasospastic, Prinzmetal's angina)
  • large-focal (transmural, Q-infarction);
  • small-focal (not Q-infarction);

6. Cardiac conduction and rhythm disorders(form).

7. Heart failure(form and stages).

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

Symptoms of IHD

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

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

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

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

Complications

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

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

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

Diagnostics

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

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

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

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

Treatment of coronary artery disease

Treatment tactics for various clinical forms Coronary heart disease has its own characteristics. However, it is possible to identify the main directions used for the treatment of coronary artery disease:

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

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

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

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

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

Prognosis and prevention

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

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

Coronary heart disease (CHD) is characterized by a decrease in coronary blood flow, inappropriate to the high myocardial demand for oxygen and other metabolic substrates, which leads to myocardial ischemia, its functional and structural disorders. IHD refers to a group of heart diseases, the development of which is based on absolute or relative coronary insufficiency.

Risk factors for CAD

Risk factors. Risk factors are divided into modifiable and non-modifiable, the combination of which significantly increases the likelihood of developing CHD.

Modifiable

(changeable)

Unmodifiable

(immutable)

    Dyslipidemia (LDL and VLDL)

    Gender: male

    Hypertension (BP>140/90 mmHg)

    Age: > 45 years – men;

    Smoking (risk increases 2-3 times)

> 55 – women

    Diabetes

    Family history: family

    Stress (frequent and/or prolonged)

early atherosclerosis, the appearance of ischemic heart disease in

    Obesity and atherogenic diet

relatives under the age of 40, early

    Physical inactivity

death of relatives from ischemic heart disease and others

    Coffee addiction, cocaine addiction, etc.

The cause of myocardial ischemia in 95-98% of patients with coronary artery disease is atherosclerosis of the coronary arteries, and in only 2-5% it is associated with spasm of the coronary vessels and other pathogenic factors. When the coronary arteries narrow, the blood supply to the myocardium decreases, its nutrition, oxygen delivery, and ATP synthesis are disrupted, and metabolites accumulate. The narrowing of the coronary arteries up to 60% is almost completely compensated by the expansion of distal resistive as well as collateral vessels and the blood supply to the myocardium is not significantly affected. Impairment of the patency of the coronary vessels by 70-80% of the initial value leads to cardiac ischemia during exercise. If the vessel diameter decreases by 90% or more, ischemia becomes permanent (at rest and during exercise).

The main danger to human life, however, is not the stenosis itself, but the accompanying thrombosis, leading to severe myocardial ischemia - acute coronary syndrome. In 75% of cases of death from coronary artery thrombosis, rupture of atherosclerotic plaques is observed, and in only 25% of patients it is caused by damage to the endothelium only.

Violation of the integrity of the capsule occurs as a result of activation of the local inflammatory process, as well as increased apoptosis of cells, structural elements of the atherosclerotic plaque. Rupture or damage to an atherosclerotic plaque leads to release into the lumen of the vessel large quantity factors activating local thrombus formation. Some thrombi (white) are tightly connected to the intima of the vessels and form along the endothelium. They consist of platelets and fibrin and grow inside the plaque, helping to increase its size. Others grow predominantly into the lumen of the vessel and quickly lead to its complete occlusion. These clots are typically composed primarily of fibrin, red blood cells, and a small amount of platelets (red). Spasm of the coronary vessels plays an important role in the pathogenesis of acute coronary syndrome. It occurs in a segment of the vessel located near the atherosclerotic plaque. Vasospasm occurs under the influence of activated platelet factors (thromboxane, serotonin, etc.), as well as due to inhibition of endothelial production of vasodilators (prostacyclin, nitric oxide, etc.) and thrombin.

A factor that increases myocardial hypoxia is the increased need of the heart muscle for oxygen. Myocardial oxygen demand is determined by left ventricular wall tension (LVWW), heart rate (HR) and myocardial contractility (MC). With an increase in filling or systolic pressure in the LV chamber (for example, with aortic and mitral regurgitation or stenosis, arterial hypertension), LV wall tension and O 2 consumption. are growing. On the contrary, with physiological or pharmacological interventions aimed at limiting filling and pressure inside the LV (for example, antihypertensive therapy), myocardial O2 consumption decreases. Tachycardia increases ATP consumption and increases the need for O2 in the heart muscle.

Thus, a pronounced decrease in the lumen of the coronary arteries and an increase in the energy demand of the myocardium lead to a discrepancy between the supply of oxygen and the needs of the heart muscle, which entails its ischemia and subsequent structural damage.

Drawing. The role of coronary sclerosis in the development of coronary artery disease.

IHD classification:

1. Sudden coronary death.

2. Angina pectoris

2.1. Angina pectoris.

2.1.1. New onset angina pectoris.

2.1.2. Stable angina pectoris (FC 1 to IV).

2.1.3. Progressive angina pectoris

2.2 Prinzmetal's angina (vasospastic).

3. Myocardial infarction

3.1. Large-focal MI (Q-MI).

3.2. Small focal MI (not Q-MI).

4. Post-infarction cardiosclerosis.

5. Heart rhythm disturbances (indicating the form).

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

Sudden coronary death- death that occurs within 1-6 hours after the onset of anginal pain . In most cases sudden death patients with IHD is associated with the occurrence of severe rhythm disturbances (ventricular fibrillation, asystole, etc.) due to myocardial ischemia.

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