Pathological physiology. Myocardial infarction pathophysiology Complications of myocardial infarction pathophysiology

Cardiovascular diseases are pathological changes in the structure and functioning of the heart and blood vessels, leading to serious consequences. There are a significant number of such diseases, and they can all manifest themselves in different ways.

Reasons for appearance

The origin of heart and vascular diseases can be very different; the main underlying factors are considered to be:

1. Inflammation.
2. Congenital pathology associated with a hereditary factor.
3. Intoxication of the body.
4. Metabolic and metabolic disorders.

Who is at risk?

Risk factors for cardiovascular diseases:

1. High blood pressure. Constant load on the heart and irreversible changes in the vascular wall during hypertension lead to the development of heart failure.
2. Diseases of the endocrine system. Disruption of the structure of blood vessels in diabetes mellitus and increased workload on the heart due to hyperfunction of the thyroid gland, as well as changes in metabolic processes in most endocrine diseases are often complicated by the development of heart and vascular diseases.
3. Increased cholesterol levels. The deposition of plaques on the walls of blood vessels leads to chronic myocardial ischemia and cerebral hypoxia.
4. Bad habits. Smoking and alcohol, as well as taking psychotropic drugs, trigger many mechanisms that ultimately lead to death, with vascular and heart pathology taking the leading place.
5. Elderly age. It is estimated that about 90% of people die as a result of coronary artery disease after 60 years of age, and the risk of developing a stroke doubles after the age of 55− years.
6. Gender. Men get sick more often than women before menopause. After this, the risk of developing diseases becomes the same.
7. Physical inactivity and obesity. Physical inactivity leads to a general weakening of the body, decreased vascular tone, blood stagnation, and susceptibility to infectious diseases. Often such people suffer from obesity, and this greatly contributes to the development of atherosclerosis, hypertension, and thrombophlebitis.
8. Living in a contaminated area. Residents of large industrial cities are many times more likely to get sick and die from a heart attack or stroke.
9. Heredity. There is a high probability of having a child with cardiac pathology in those families where relatives also have birth defects.

How to determine if a patient has heart and vascular disease?

In cardiology, the main method for studying the electrical activity of the myocardium is the ECG. A cardiogram allows you to determine the pacemaker, the frequency of contractions and their regularity, and the presence of ectopic foci of excitation. The recording sometimes reveals scars after a heart attack, indirect signs of metabolic disorders, as well as acute conditions - angina pectoris and heart attack.

If necessary, Holter monitoring is performed, that is, recording the work of the heart over a certain time. This makes it possible to record changes occurring in the patient at different times of the day and under different loads, short-term episodes of rhythm or conduction disturbances, as well as transient episodes of myocardial ischemia.

Sometimes diagnosis is made using echocardiography. Such a study helps in identifying violations of tissue structure, the size of cavities, and wall thickness. Echocardiography is prescribed for the diagnosis of heart attacks, cardiac tumors, changes associated with the valve apparatus, neurocirculatory dystonia, and cardiomyopathy.

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A more accurate picture of the structure of the heart muscle and valves can be obtained using MRI of the heart. Magnetic resonance imaging measures parameters such as the speed of movement in blood vessels and the pumping function of the heart, and evaluates the condition of the coronary arteries.

How does cardiovascular pathology manifest itself?

Symptoms of this type of disease can be different, but most often patients complain about:

1. Pain or discomfort in the left chest. With angina, pain occurs after overexertion or at rest, and passes after a certain period of time after taking nitroglycerin. Severe burning pain radiating to the left arm, under the shoulder blade, neck and back may indicate the development of myocardial infarction. If it radiates to the back of the head or groin area, aortic dissection can be assumed. Dull or aching pain in the presence of fever indicates inflammation - myocarditis or pericarditis.
2. Feeling of irregular heartbeat. It can occur against the background of excitement, with increased pressure, as a result of inflammatory phenomena during myocarditis. It is characteristic that in case of serious illnesses, the feeling of interruptions, as a rule, is absent.
3. Dyspnea. It is a sign of the development of heart failure. First it occurs during physical activity, and then at rest. It may also be a sign of congestion in the pulmonary circulation or ischemic disorders of the brain. Intensifies with excess weight, accompanied by swelling of the lower half of the body.
4. Edema. Cardiac edema is characterized by its symmetry and localization in the lower extremities, and the symptoms intensify at the end of the day. If the patient lies in bed, then swelling occurs on the back and in the sacral area. Minor swelling can be determined by pressing on it with your fingers - a dimple appears in this place, which then very slowly straightens out.
5. Change in skin color. In the presence of cardiac pathology, patients may be pale (aortic valve insufficiency, vascular spasms, rheumatic heart disease), or cyanotic in the area of ​​the nasolabial triangle and in the distal parts of the limbs (with heart failure).
6. Headache. Often occurs with pathology of cerebral vessels, high or very low pressure, and can accompany febrile conditions with myocarditis or rheumatic carditis.

Therapy methods

Treatment of cardiovascular diseases is carried out only by a cardiologist. Its main directions are to eliminate the cause that caused the disease.

Great importance is given to prevention and drug therapy, in which antihypertensive drugs are prescribed for high blood pressure, diuretics to relieve the heart and relieve swelling, drugs that reduce the need for oxygen in the myocardium and brain, improve the rheological properties of the blood, and lower cholesterol. For arrhythmia, blockers and antiarrhythmics are used. Substances that can improve blood circulation and nutrition in the heart muscle and brain are used.

Hypertension and hypotension - what is it?

The cardiovascular system plays a key role in ensuring the normal functioning of the human body and life in general. Pathologies of this vital system are in first place among the causes of mortality on the entire planet.

Tens of thousands of specialists are working on the problem of the most effective treatment of pathologies of the heart and blood vessels. One of the most common problems is considered to be a violation of blood pressure (BP) - its increase or decrease. It is about hypertension and hypotension, symptoms, methods of diagnosis and treatment that will be discussed in this article.

Who are hypertensives and hypotensives?

You should understand the issue and understand who hyper- and hypotensive people are. The etiology of these words is directly related to the underlying disease - the presence of high or low blood pressure. Statistics show that three out of four adults today can be found to have pathological blood pressure levels.

A hypertensive person has a persistent increase in the numbers obtained during tonometry, and a hypotensive person, on the contrary, has a persistent decrease. The clinical picture in these cases is different, since the hypertensive patient experiences headache, sudden loss of ability to work, and blurred vision. With hypotension, the patient will complain of weakness, “floaters” flashing before the eyes, inability to stand up, and a squeezing headache.

You can guess what type of blood pressure disorder a person most likely has by looking at the characteristic appearance of such patients. For example, people who overeat, prefer fatty foods, or abuse alcohol and tobacco products more often suffer from hypertension. These patients are usually exposed to chronic stress at work, resulting in headaches, weakness, and tinnitus.

Hypotonics can be seen from a great distance; usually these are very thin people with an asthenic build. Such patients have cold extremities, long fingers and are prone to loss of consciousness. Often there is a condition in which the eyes begin to darken, the mouth becomes dry, and nausea appears. During sports, hypotensive patients may complain of weakness and a bursting headache. They also have poor appetite, which is why all types of metabolism are disrupted, and for drug therapy the dose should be selected individually.

Can a hypertensive person become hypotensive?

According to pathophysiology, hypertension and hypotension are completely different, so it is extremely rare to find cases when one disease gradually flows into another. Usually such changes are associated with serious changes in the body.

Typically, after the transition of hypertension to hypotension, a person develops the following pathologies:

• ulcerative defects of the mucous membrane of the stomach or duodenum;
• bleeding uterine tumors;
• gynecological pathologies leading to constant blood loss;
• disturbances in the functioning of the endocrine glands;
• traumatic brain injury;
• menopausal syndrome;
• overdose of medications during treatment of hypertension.

A more common occurrence is the patient's transition from hypotension to elevated blood pressure. This is due to atherosclerotic processes in blood vessels, which reduces their elasticity. Women more often, after prolonged hypotension, become hypertensive due to certain hormonal changes at the age of about fifty to sixty years.

Such changes in the functioning of the cardiovascular system have a very negative impact on the work of the heart muscle, kidneys, and even the condition of the blood vessels of the brain. This is due to the fact that throughout life the receptors and muscle fibers have become accustomed to working in a certain mode, and after an increase in blood pressure, the loads have become unbearable - chronic heart or kidney failure often develops, and hemorrhagic strokes occur.

What are the causes of hypertension and hypotension?

More often in a doctor's practice there are hypertensive patients than hypotensive patients. There are actually a lot of reasons for this; the following factors will lead to a chronic increase in blood pressure:

• influence of stress;
• presence of hormonal imbalance;
• pathologies associated with neurohumoral regulation;
• development of atherosclerotic lesions of arteries and arterioles;
• chronic intoxication with salts of heavy metals;
• excess body weight;
• abuse of alcohol and tobacco products;
• compression of vascular structures by the uterus in a pregnant woman;
• damage to kidney tissue.

The mechanism of hypotension is quite complex; it can arise as a result of conditions leading to a decrease in the activity of the heart muscle, or as a result of an effect on reducing the resistance of the wall of peripheral blood vessels.

The following conditions can lead to such changes:

• the presence of vegetative-vascular dystonia;
• diseases of the digestive tract;
• moving to other climatic zones;
• professional sports;
• allergic conditions;
• avitaminosis.

What are the dangers of hypertension and hypotension?

Any deviations from the norm should not necessarily be regarded as negative for the body. Some people feel comfortable with certain levels of high or low blood pressure, and vice versa, after “normalizing” this indicator they complain.

Only if a person previously had a blood pressure of 120/80, and then it gradually changed, and pathological manifestations appeared, should diagnosis and immediate treatment be undertaken. Otherwise, certain complications may develop.

Hypertension in this regard is more dangerous, as it can cause the following consequences:

• pulmonary edema or acute left ventricular failure;
• development of ischemic or hemorrhagic stroke;
• myocardial infarction;
• damage to retinal vessels with subsequent hemorrhage;
• deterioration of general health and development of disability;
• development of renal failure due to the development of a “hypertensive kidney”.

Chronic hypotension significantly reduces quality of life and interferes with daily tasks due to the following manifestations:

• dizziness;
• nausea;
• “flies” before the eyes;
• periodic loss of consciousness;
• thrombotic lesions.

Conclusion

Both pathologies are harmful to health and occur not only in older people. Hypertension is more often observed in middle-aged and older men, hypotension is more typical in girls. After detecting deviations from normal blood pressure readings, you should contact a specialist to carry out diagnostic measures and select the most adequate therapy.

What are the dangers of myocardial hypoxia?

If the heart does not receive enough oxygen, myocardial hypoxia develops, which leads to tissue death. When a large number of cells die, this can cause dangerous complications and even death. With a critical lack of oxygen, the heart muscle stops working.

Definition

To understand what hypoxia of the left ventricular myocardium is, you need to understand its origin. As a rule, it occurs due to oxygen starvation of the heart. Without oxygen, the body of an adult and a child cannot fully exist, because this element takes part in energy production.

There are two forms of this disease:

• Spicy. Appears unexpectedly, and entails the rapid death of the patient.
• Chronic. This form can exist for a long time without any manifestations. It can be detected only with a pathological change in the heart muscle.

At the initial stage of the disease, muscle tissue becomes softer, which leads to cell death and necrosis.

Full heart function cannot be restored in an advanced hypoxic form.

Why does it occur?

The following reasons contribute to the development of hypoxia:

• Long stay in a stuffy room or at altitude in the mountains. In this case, a person breathes air that has a low oxygen content.
• Hemolysis of red blood cells or anemia. Blood oxygen saturation worsens due to a decrease in the ability of hemoglobin to attach oxygen molecules.
• Poisoning with toxic substances, heavy metals, carbon monoxide. In this case, body tissues lose their ability to absorb oxygen.
• Inactive lifestyle.

• Myocardial infarction, diabetes mellitus, vasculitis, cardiac pathophysiology. These diseases aggravate blood circulation or completely block it, which occurs due to damage to blood vessels.
• High physical activity.
• Bad habits.

It is possible that a combination of several factors can cause the disease.

Symptoms of cardiac oxygen deficiency

In case of poisoning and suffocation, signs of myocardial hypoxia manifest themselves in the form of drowsiness, dizziness and loss of consciousness. If assistance is provided incorrectly or is absent, death occurs.

The symptoms of myocardial hypoxia caused by blockage of the coronary artery look somewhat different. This condition occurs due to the formation of a plaque and a blood clot on it. Even with a slight blockage of the lumen, a person will experience acute pain at the time of artery spasm.

Discomfort may occur due to smoking, elevated blood pressure, or an adrenaline rush caused by stress or high physical activity.

The development of a heart attack is indicated by burning pain on the left side of the chest, which sometimes radiates under the shoulder blade or arm. Moreover, it is not possible to cope with the pain syndrome even after taking the drug Nitroglycerin. This condition requires an immediate call to an ambulance.

Diagnosis of the disease

In order for the doctor to make an accurate diagnosis, the patient must undergo a number of studies:

• pulsometry;
• blood pressure measurement;
• biochemical blood test;
• Ultrasound of the heart;
• EchoCG.

How does hypoxia manifest itself on an ECG?

Electrocardiography allows you to detect diffuse changes in the myocardium and disruption of processes in the septal-apical region of the left ventricle.

On the cardiogram, acute hypoxia manifests itself when ischemic changes in the left ventricle are detected. This is evidenced by a disturbed heart rhythm, elevation (exceeding the norm in relation to the isoline), a decrease in the ST segment, the formation of biphasic and negative T waves. The presence of a pathological Q wave is of particular danger. This means that hypoxia has caused an extensive heart attack.

Drug treatment

Treatment of myocardial hypoxia is aimed at eliminating the root cause of the disease. Drug therapy involves taking antihypoxants, which are used to restore energy mechanisms in tissues. They have antiangial, antiarrhythmic and cardioprotective properties. Most often, patients are prescribed Inosine or Amtizol.

Sometimes treatment is carried out with antioxidants, which include the drugs Emoxipin and Mexidol. With their help, more economical consumption of oxygen by tissues is ensured.

Treatment tactics may also include taking oxygen supplements, plasmapheresis, or blood transfusions.

Traditional medicine

Moderate myocardial hypoxia can be treated with traditional medicine:

• Infusion of birch buds. This recipe involves steaming 2 tablespoons of birch buds in a glass of boiling water. The broth should brew, after which it is cooled and filtered. Drink the product before meals, a quarter glass three times a day.
• Woodlice infusion. For cooking, take 1 table. l. raw materials and pour a glass of boiling water over it. The medicine is left for half an hour, after which take 1 large spoon three times a day.

Nutrition

Any heart disease requires a special diet. Patients should include pomegranate, green apples, all kinds of cereals and pork liver in their diet. The listed products improve blood properties and increase hemoglobin.

The consequence of hypoxia can be heart failure and cessation of heart function. Lack of proper assistance leads to disastrous consequences.

Among the common complications of this disease are myocardial infarction and a prolonged attack of angina. In addition, there is a risk of developing cardiosclerosis, in which connective tissue is formed in place of muscle tissue.

To prevent the development of the disease and prevent the start of irreversible processes, increased attention should be paid to prevention. It involves adjusting your lifestyle and nutrition. It is also very important to give up bad habits and spend more time in the fresh air.

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Perioperative MI is one of the most important predictors of short- and long-term morbidity and mortality associated with noncardiac surgery. Typically, perioperative MI occurs within the first three days (±5%) after surgery.

The prevalence of ACS (with clinical signs or asymptomatic), assessed by serum troponin I or T concentrations, reaches 15-25% in patients with vascular surgery. Thus, the prevention of perioperative MI can be considered a point of application for increasing the overall number of favorable outcomes of surgical interventions. To achieve this goal, knowledge about the pathophysiological mechanisms of the development of perioperative MI is necessary.

Unfortunately, the full mechanism of perioperative MI is not yet understood, but its development is presumably similar to that of other categories of infarction. Rupture of an atherosclerotic plaque in the coronary artery, leading to the formation of a thrombus and subsequent occlusion of the vessel, is the main cause of perioperative ACS (as well as in MI not associated with surgical interventions). The operation itself serves as a significant stressor leading to an increased risk of plaque rupture. The perioperative stress reaction includes the release of catecholamines into the blood with the subsequent development of hemodynamic stress, vascular spasm, decreased fibrinolytic activity, platelet activation and hypercoagulation.

Two retrospective studies focused on pathological changes in the coronary vessels in fatal perioperative myocardial infarction. A study by Dawood et al. with autopsy control showed that in 55% of cases of perioperative MI there is a tear or complete rupture of the plaque, as well as hemorrhage into the resulting defect. Similar autopsy results were obtained by Cohen and Aretz in 46% of patients with postoperative MI. The survival period in patients with plaque rupture was significantly shorter than in patients without such damage.

In patients with clinically significant coronary artery disease, perioperative MI may be caused by a discrepancy between the metabolic needs of the myocardium and their actual supply, associated with tachycardia or an increase in the force of heart contractions. Episodes of perioperative ST segment depression, reflecting subendocardial myocardial ischemia and occurring mainly during the first two days after surgery, have been described in 41% of patients with vascular surgery. The association of perioperative MI with myocardial ischemia and nonpenetrating or circular subendocardial infarction supports this mechanism.

Landesberg et al. demonstrated that 85% of postoperative cardiac complications were associated with prolonged ST segment depression. In a study by Fleisher et al. 78% of patients with cardiac complications experienced at least one episode of prolonged (more than 30 minutes) myocardial ischemia either before or during a cardiovascular event. In most cases, it was not accompanied by a Q wave. The hypothesis that ST segment depression may lead to perioperative MI is supported by the increase in serum troponin T concentrations during or immediately after prolonged ischemia with ST segment depression.

Ischemia with ST-segment elevation is considered less common, as demonstrated by a study by London et al., which reported an incidence of 12% of ST-segment elevation during surgery. There is currently little data on this topic. Using various diagnostic methods, it is possible to assess the risk of ischemic complications in a patient, but it is difficult to predict the localization of perioperative MI. This is due to the impossibility of predicting the rate of destabilization of the atherosclerotic plaque of the coronary artery under conditions of surgical stress in a patient with asymptomatic coronary artery disease.

Sanne Hoeks and Don Poldermans

Non-cardiac surgical interventions in cardiac patients

A heart attack is a focus of necrosis that develops as a result of circulatory disorders. Infarction is also called circulatory or angiogenic necrosis. The term “infarction” (from the Latin to stuff) was proposed by Virchow for a form of necrosis in which a dead area of ​​tissue becomes saturated with blood.

Acute myocardial infarction is determined using clinical, electrocardiographic, biochemical and pathomorphological characteristics. It is recognized that the term “acute myocardial infarction” reflects the death of cardiomyocytes caused by prolonged ischemia.

Thrombosis of vessels of various locations occupies one of the leading places among the causes of disability, mortality and reduction in the average life expectancy of the population, which determine the need for widespread use of drugs with anticoagulant properties in medical practice.

The accumulated experimental and clinical experience in the treatment of myocardial infarction, the lack of the expected positive effect from thrombolytic therapy indicates that restoration of coronary blood flow is a “double-edged sword”, often leading to the development of “reperfusion syndrome”.

Blood lipid disorders occupy a leading place in the list of risk factors for major diseases.

How is myocardial infarction diagnosed?

What is the pathophysiology of acute myocardial infarction (MI)?

The modern view of the pathophysiology of myocardial infarction is based on Herrick's observation made in 1912 and confirmed by Dewood in 1980. They described the occlusion of stenotic coronary arteries by thrombus in the area of ​​acute MI. A thrombus most often forms at the site of a ruptured atherosclerotic plaque. The degree of obstruction and thrombosis varies. It is caused by many factors, including disruption of the coronary vascular endothelium, extent of obstruction, platelet aggregation, and changes in vascular tone. These mechanisms are thought to underlie 85% of MI cases.

Other causes of MI include coronary vasculitis, embolism, coronary spasm, congenital anomalies, and hyperviscosity. Multiple factors underlie cocaine-induced MI, as severe vasospasm and acute thrombosis occur in both stenotic and normal arteries.

In most cases, the cause of atherosclerotic plaque rupture cannot be determined. To some extent, MI has been associated with severe physical stress, emotional stress, trauma, and neurological impairment. It has been proven that MI often develops in the early morning hours, which may be due to a circadian increase in catecholamine levels and platelet aggregation. The rupture of atherosclerotic plaques and the development of MI are associated with infections of Chlamydia pneumonia, Helicobacter pylori, etc.

Classic symptoms of myocardial infarction are chest pain, shortness of breath, nausea, sweating, palpitations and fear of death. Chest pain usually lasts at least 15-30 minutes and may radiate to the arms, jaw, or back. In older adults, myocardial infarction often presents with atypical symptoms such as shortness of breath, confusion, dizziness, fainting, and abdominal pain. In approximately 25% of cases, MI is asymptomatic or undiagnosed and is therefore called “silent.”

The main signs are paleness, sweating and agitation. Abnormal changes in blood pressure, heart rate, and respiration vary depending on the type and extent of myocardial infarction. Low-grade fever may be observed, and a fourth heart sound is almost always heard. In addition, depending on the location and extent of the MI, the jugular veins may swell and a third heart sound may be heard. Later, a pericardial friction rub and peripheral edema may appear, but these signs are not typical for the first hours of MI. When the function of the papillary muscles is impaired and avulsed, a systolic murmur is heard over the mitral valve, although it is often shorter and softer than usual with mitral valve insufficiency.

How is myocardial infarction diagnosed?

The diagnosis of myocardial infarction is made on the basis of clinical symptoms, ECG signs and increased activity of cardiac-specific enzymes in the blood serum.

Does echocardiography help in diagnosing acute MI?

Yes. Echocardiography detects abnormal movements of the myocardial wall, even if there are no signs of MI on the ECG. Echocardiography plays an essential role in the diagnosis of mechanical complications.

How to differentiate the symptoms of angina and myocardial infarction?

Pain during an acute heart attack is usually more intense and prolonged (1-8 hours), often accompanied by shortness of breath, sweating, nausea, and vomiting. In addition, on a standard 12-lead ECG, ST segment elevation is more common than ST depression. A negative T wave and an abnormal Q wave may also be observed.

What results can be obtained from a physical examination of patients with myocardial ischemia?

Physical examination findings may be normal. The gallop rhythm (fourth heart sound) may be associated with atrial contraction overcoming the rigidity of a rigid left ventricle. If the IV tone appears and disappears along with the symptoms of angina pectoris, this indicates a violation of ventricular distensibility and is an argument in favor of the assumption that the patient has myocardial ischemia. The gallop rhythm associated with the IV sound may appear before the onset of angina symptoms (and persist after the onset of myocardial ischemia symptoms) and be caused by other causes of impaired ventricular distensibility, such as its hypertrophy, hypertension, aortic stenosis, or previous myocardial infarction. You can detect signs of congestive heart failure (increased pressure in the jugular veins, wheezing in the lungs, additional third sound). Upon examination, you can see and upon palpation feel a protrusion of the chest wall associated with myocardial dyskinesia during acute ischemia or infarction. Murmurs, especially new ones, may be associated with ischemia. Ischemia of the papillary muscles can lead to mitral regurgitation. Rupture of the interventricular septum leads to the appearance of a ventricular septal defect and, consequently, an associated murmur. Aortic stenosis and obstructive cardiomyopathy are accompanied by corresponding murmurs and can cause myocardial ischemia and angina.

What other symptoms may be associated with myocardial ischemia?

Along with typical complaints of chest pain with myocardial ischemia, the following may also be observed:

• dyspnea;
• sweating;
• nausea and vomiting.

Myocardial infarction - Pathophysiology

Myocardial infarction occurs when an atherosclerotic plaque slowly forms on the inner lining of a coronary artery and then suddenly breaks off, causing catastrophic blood clot formation, leading to total occlusion of the artery and cessation of blood flow.

Acute myocardial infarction is classified into two sub-types according to acute coronary syndrome, namely non-ST-segment elevation myocardial infarction and ST-segment elevation myocardial infarction, which are most often (but not always) a manifestation of atherosclerotic heart disease. The most common cause of this disease is the rupture of an atherosclerotic plaque in the epicardial coronary artery, which leads to the formation of a cascade of blood clots, sometimes leading to complete occlusion of the artery. Atherosclerosis is the formation of fibrous plaques located on the walls of arteries (in this case, the coronary arteries), a process that usually lasts decades. Abnormalities in the blood flow column, which are observed on angiography, reflect a narrowing of the arterial cavity resulting from the long-term formation of atherosclerosis. Plaques become unstable, break off and provoke the formation of thrombi (blood clots) that clog the arteries; this process occurs within minutes. When a significant plaque rupture occurs in the vascular system, myocardial infarction occurs (necrosis of an area of ​​the myocardium).

If reduced bleeding to the heart continues long enough, the conditions are created for a process known as the ischemic cascade; heart cells in the area where coronary artery occlusion occurs die (mainly through necrosis), and new cells are not formed. A collagen scar remains in this place. Recent research suggests that another form of cell death called apoptosis also plays a role during the tissue damage process of myocardial infarction. As a result, the patient's heart undergoes long-term changes. This process of myocardial scar formation also increases the risk of developing fatal types of arrhythmia, and in addition, this phenomenon can result in the formation of a ventricular aneurysm, which can rupture, leading to catastrophic consequences.

Damaged heart tissue conducts electrical impulses more slowly than normal heart tissue. The difference in conduction velocity between damaged and undamaged tissues can cause the impulse to return repeatedly to the same area of ​​the myocardium, which leads to many types of arrhythmias, even fatal ones. The most serious of these types of arrhythmias is ventricular fibrillation (VF), an incredibly fast and chaotic heart rhythm that is one of the most common causes of sudden cardiac death. Another life-threatening type of arrhythmia is ventricular tachycardia (VT), which may or may not be a cause of sudden cardiac death. However, ventricular tachycardia often results in an increased heart rate, which reduces the efficiency of blood flow through the heart. Thus, blood output and pressure can reach dangerous levels, which can lead to subsequent coronary ischemia and progress to infarction.

A cardiac defibrillator is a special device that was created to combat fatal types of arrhythmias. This device functions by delivering an electrical shock to the patient to depolarize a critical mass of the heart muscle, thereby producing a "reboot" effect on the heart. This procedure is time dependent, and the chances of successful defibrillation decrease rapidly after the onset of cardiopulmonary shock.

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Coronarogenic necrosis (infarction) of the myocardium arise when absolute or relative insufficiency of coronary circulation.

Absolute coronary vascular insufficiency is a condition in which less blood is delivered to the myocardium through the coronary artery system than normal.

The main causes of absolute coronary insufficiency include the following.

1. Neurogenic spasm of the coronary arteries. Necrotization of the myocardium due to spasm of the coronary vessels can occur either with a very long duration of these spasms, or due to their frequent repetition. More often, coronary spasm is clinically expressed as angina pectoris (angina pectoris, angina pectoris). Its cause is usually an autonomic imbalance in the regulation of the lumen of the coronary arteries. As is known, unlike the vessels of most other organs, in the heart sympathetic influences are vasodilatory, and parasympathetic influences are vasoconstrictive. A sharp increase in the tone of the vagus nerves (both centrogenic and reflex genesis) can lead to the development of an attack of angina pectoris. If the attack is prolonged and the blood supply to the myocardium is disrupted for tens of minutes, necrosis of the heart muscle may occur.

There are two types of angina: angina pectoris And resting angina. The first occurs against the background of emotional or physical stress, and is necessarily based on coronary spasm. The second form of angina can develop without visible psycho-emotional or physical stress. It is based, first of all, on a decrease in the patency of the coronary arteries due to a progressive atherosclerotic process leading to obliteration of the coronary arteries. Against this background, even a slight increase in parasympathetic tone that has no apparent reason can result in severe spasm of the coronary vessels. This type of angina is also called unstable angina, Pritsmetal's angina.

The main symptom of angina is severe pain, which patients often define as a “dagger blow to the chest”, accompanied by a number of characteristic features discussed in detail in “Pathophysiology of Pain”. If angina does not progress to the second stage of coronary artery disease - myocardial infarction, then either its attack passes or it ends in death.

Since, apart from pain and changes in the ECG, there are no other characteristic symptoms of angina, in the pre-electrocardiographic era, clinicians said: “Angina has only two symptoms - pain and death.”

2. Thrombosis of coronary vessels. This is a fairly common cause of necrotic lesions of the heart muscle, especially in combination with atherosclerosis of the coronary arteries, which creates conditions for the formation of a blood clot. Blood clots may also occur in coronary arteries as theory suggests retrograde and ascending (“jumping”, ascending) thrombosis. The development of such thrombosis is presented in the diagram. *****72

According to this theory, under the influence of stress or other damaging factors, the capillary circulation of some areas of the myocardium is disrupted, and multiple small foci of necrosis arise, which in some cases involve the walls of the capillaries. The resulting parietal thrombi initially cause only capillary occlusion, and then, as a result of slowing blood flow and turbulent blood flow in this area of ​​the bloodstream, the thrombosis spreads higher, capturing arterioles and larger arteries. Complete occlusion of one of these vessels disrupts the blood supply to a sufficiently large area of ​​the myocardium, that is, leads to the occurrence of coronarogenic large-focal necrosis. This theory also allows for the possibility of an ascending thrombus at a sufficient distance from the initial focus of necrosis.

3. Embolism of coronary vessels. An embolus in the coronary arteries is a rather rare occurrence, since the coronary vessels depart from the aorta almost at a right angle, and the reflux of an embolus with blood from the aorta into the coronary vascular system is unlikely. More often, a large embolus closes the entire mouth of the coronary vessels, but in this case the patient does not develop a heart attack, but dies from cardiac arrest. However, in some cases, the embolic genesis of a heart attack is possible (for example, the formation of an embolus in the main coronary arteries due to thrombosis and separation of pieces of thrombus or ulceration of an atherosclerotic plaque and blockage of smaller branches of the coronary arteries by atheromatous detritus).

4. Atherosclerosis of the coronary arteries is the most common cause of myocardial infarction. According to pathomorphological studies, pronounced atherosclerosis of the coronary vessels is detected in 89-98% of cases of infarction. Atherosclerotic changes can cause myocardial infarction for the following reasons: firstly, atherosclerotic plaques themselves narrow the lumen of the coronary vessels and interfere with the normal flow of blood to the heart muscle; secondly, under conditions of atherosclerosis, blood clots form more easily; thirdly, atherosclerotic plaques can ulcerate and their particles, turning into emboli, clog the coronary vessels; fourthly, atherosclerosis sharply increases the sensitivity of the coronary vessels to spastic influences.

Clinic myocardial infarction is extremely diverse and depends both on the state of reactivity of the body and on the size, depth and localization of the necrosis focus itself. Let us dwell in more detail on the main clinical symptoms of a heart attack.

1. Pain syndrome, as mentioned above, is described in detail in the chapter “Pathophysiology of pain”. It should be added to the above that in 18-20% of cases, heart attacks can occur without pain symptoms. It should also be emphasized once again that coronary pain increases spasm of the coronary vessels, and this, in turn, leads to an increase in pain intensity. The first vicious circle closes.

2. Weakening of myocardial contractility. An ischemic or necrotic area of ​​the heart muscle loses contractility, which leads to a weakening of the contractile activity of the heart muscle, a decrease in cardiac output, and, consequently, coronary blood flow. This may increase the infarct area, further reducing cardiac output, etc. The second vicious circle closes.

3. Arrhythmias. Due to the fact that in the ischemic zone the bioelectric properties of myocardial cells are sharply disrupted, the focus of infarction, especially in the first hours after its occurrence (and subsequently - the so-called surrounding area) necrotic zone), can become a source of ectopic activity. The potential difference between fibers located in the ischemic zone and outside it causes the generation of heterotopic impulses. This factor, combined with a sharp increase in the morpho-functional heterogeneity of the heart muscle during a heart attack, can become the basis for the occurrence of ventricular fibrillation, the most common cause of so-called sudden cardiac death in the acute stage of myocardial infarction. But even non-fatal arrhythmias (extrasystole, paroxysmal tachycardia), giving additional load on the altered myocardium, can lead to deepening of infarction, which, in turn, will increase cardiac arrhythmias. The third vicious circle is closed.

4. Typical ECG changes during a heart attack. Electrocardiographic dynamics during myocardial infarction are extremely diverse and depend on the size of the infarcted area and its location. The features of the ECG, noted in its different leads, form the basis for the topical diagnosis of a heart attack, that is, determining its exact location and size. However, there are typical ECG changes during a heart attack that are always present on the ECG. Let's look at the main ones.

The appearance of a pathological QS wave. On a normal ECG, regardless of its size, the R wave is always directed upward. *****73-A During the acute stage of myocardial infarction, a negative wave appears in certain leads between the ECG points corresponding to the Q and S waves of a normal ECG, called the QS wave. *****73-B Its appearance can be explained as follows.

Normally, when taking an electrocardiogram, the total potential of the anterior and posterior walls of the heart is recorded, which is characterized on the ECG by an upward-directed R-wave. *****73-B If, for example, a section of the anterior wall of the heart is infarcted and does not generate potential, only the potential of the posterior wall is recorded on the ECG, expressed on the ECG as a QS wave. *****73-G Thus, the QS wave indicates the presence of a necrosis focus in the heart muscle.

Displacement of the ST segment relative to the isoelectric line. Normally, the ST segment of the ECG is on its isoelectric line. *****74-a With ischemic damage to the heart, its displacement is noted either up or down from this line. *****74-b Since such an ECG change is observed both during a heart attack and during angina pectoris, it is associated either with local ischemia (the infarction zone or the surrounding so-called necrotic zone, or the zone of local vasospasm), or with diffuse ischemia (with total coronary spasm).

The appearance of a “giant” T wave. It can be positive or negative. *****75 If a “giant” T appears in the acute period of coronary heart disease, it is interpreted in the same way as ST segment displacement, that is, as a manifestation of acute myocardial ischemia. If it appears in the later stages of myocardial infarction, it is associated with the occurrence of cicatricial changes in the myocardium.

Along with pathogenetic ones, during myocardial infarction a number of sanogenetic mechanisms, the most important of which are the following.

1. Strengthening collateral circulation. At first glance, this fact looks paradoxical, since it is known that the coronary arteries are characterized by an absolute insufficiency of collaterals, that is, they are functionally terminal. However, despite this, the blood supply to the infarcted area can be improved, firstly, by expanding other branches of the coronary artery, in one of the branches of which the patency is impaired; secondly, due to the expansion of other coronary arteries (in the case when the coronary arteries are distributed in the heart according to the scattered type, that is, the same area of ​​the heart is vascularized by several arterial branches); thirdly, due to a weakening of myocardial contractility and the resulting increase in the residual systolic blood volume in the ventricular cavity and an increase in intracavitary diastolic pressure. Under these conditions, blood through the system Viesenne-Tebesia vessels can go retrograde - from the cavities of the heart to the coronary vessels, *****76 which enhances the vascularization of the ischemic area.

2. Strengthening parasympathetic influences on the myocardium. During a heart attack, there is usually an increase in parasympathetic influences on the heart muscle, which is clinically manifested by severe bradycardia in the acute period of the process. Although parasympathetic influences have a coronary-constricting effect, their increase during a heart attack also plays a certain sanogenetic role, since they reduce the myocardial oxygen demand, and this decrease “overrides” the coronary-constricting effect of parasympathetic mediators.

These are the main mechanisms for the development of myocardial infarction, which occurs as a result of absolute insufficiency of the coronary vessels.

However, myocardial necrosis can also occur with relative insufficiency of coronary circulation, When The coronary arteries deliver a normal (or even increased) amount of blood to the heart, but this does not meet the needs of the myocardium, which operates under conditions of increased stress. In experiments, such necrosis can be simulated by narrowing of the aorta or pulmonary artery, when the myocardium of the corresponding ventricle is forced to work with overstrain, and the maximum throughput of the coronary vessels is not able to provide it with the necessary amount of oxygen. A similar situation can arise in poorly trained athletes if a sharp increase in heart function when lifting weights or running is not ensured by proper blood flow to it. Relative insufficiency of the coronary vessels leads, as a rule, to the occurrence of a large number of small necroses in the heart muscle.

Regardless of the specific reason that caused the absolute or relative insufficiency of the coronary vessels, they distinguish ( E. I. Chazov, F. Z. Meerson, E. Braunvald) the following four stages of development of ischemic myocardial damage.

On first stages ischemic factors cause local myocardial hypoxia and shutdown of the mitochondrial respiratory chain, and the metabolites accumulating in the area of ​​ischemia determine the occurrence of anginal pain. In turn, pain, being a trigger for the stress response, leads to an increase in the production of catecholamines.

In the event that sanogenetic mechanisms or the therapy used do not block the further development of the pathological process, it occurs second stage characterized inhibition of major metabolic pathways. As a result of the shutdown of the mitochondrial respiratory chain at this stage of the process, the tricarboxylic acid cycle is suppressed and a deficiency of high-energy phosphorus compounds (CP and ATP) develops. In turn, these changes cause activation of glycolysis and an increase in the concentration of lactic acid in cells. The resulting acidosis inhibits glycolysis, and the developing inhibition of β-oxidation of fatty acids leads to their accumulation in cardiomyocytes. During the entire second stage of development of the process, pathological changes are reversible, but they predetermine the possibility of serious damage to the membranes of both the cardiomyocytes themselves and their subcellular structures.

It is these damages, or rather their depth, that are the triggering factor for the transition of the process to third, already irreversible, stage of pathological changes.

Under the influence of excess catecholamines and fatty acids, the lipid bilayer of biological membranes is destroyed. This leads to labilization of lysosome membranes, the release of their enzymes into the cell, as well as a change in the permeability of the membranes of the sarcolemma, sarcoplasmic reticulum and mitochondria for calcium ions. Excess calcium, on the one hand, causes contracture of myofibrils, and on the other, enhances further destruction of the lipid bilayer. Proteolytic enzymes, released in abundance from lysosomes, destroy myofibrils and irreversibly damage the membrane structures of the cell.

Necrosis of cells in the ischemic area of ​​the myocardium completes fourth, the final stage of the pathological process.

Particular III coronary circulation

The blood supply to each organ is determined by many local and general factors. Regional features of blood flow regulation in one area or another largely depend on differences in the specifics of functioning. The heart, even in conditions of complete rest, is characterized by a very high level of energy metabolism.

There are 5 main features of the coronary circulation:

1. High adaptability to different levels of functional activity of the heart muscle. At rest, coronary blood flow is 200-250 ml per minute, with increased physical activity its value reaches 3.5-4.6 liters per minute.

2. The blood supply to the heart is approximately 10 times higher than the figures characterizing the nutrition of other tissues. More than 5% of all blood flows through the coronary vessels.

3. In situations associated with a sharp drop in cardiac output, the value of coronary blood flow either does not change at all or suffers slightly.

4. Blood flow in the heart muscle is influenced by the phases of the cardiac cycle: in systole, the vascular bed is compressed and the blood flow through it sharply decreases; in diastole, the volume of the vascular bed increases and the amount of blood flowing through the coronary vessels reaches a maximum.

5. Coronary arteries are functionally terminal. Sudden and complete occlusion of a sufficiently large coronary artery results in long-term disruption of blood flow distal to the damaged portion of the vessel.

Blood flow in the coronary vascular system also depends on a number of physiological factors:

1. From the level of metabolic processes.

2. From the tone of the coronary arteries,

3. From pressure in the aorta.

4. From heart rate

5. From pressure in the cavities of the heart.

If for all organs and tissues there are two ways to satisfy the increasing need for oxygen - increasing its extraction with the same blood flow and increasing blood flow due to vasodilation and rising blood pressure, then for the heart muscle there is practically one way - increasing blood flow due to the expansion of the coronary vessels . Such a reaction can only occur with a high initial vascular tone. Significant tonic contraction of smooth vessels in combination with intense energy metabolism of the myocardium is one of the paradoxes of coronary circulation. While the increase in energy metabolism in skeletal muscles during their work to the level of metabolism in the myocardium is accompanied by almost maximum vasodilation, the reserve for dilation of the coronary vessels at comparable levels of oxygen consumption remains very high. For the constantly contracting and relaxing myocardium, it is apparently not beneficial to have a large amount of blood in its thickness, an incompressible material that physically interferes with effective contraction

An increase in heart function and a simultaneous increase in oxygen consumption is accompanied by an increase in coronary blood flow, that is, dilation of blood vessels. Hypoxia also leads to dilation of the coronary vessels. Thus, both increased energy metabolism, requiring a large supply of oxygen, and hypoxia cause the same vascular reaction of an adaptive nature. The question arises whether a single mechanism underlies this reaction. Many attempts have been made to find the metabolite or group of metabolites directly responsible for vasodilation. Such metabolites included lactate, changes in pH and osmotic environment, potassium, calcium, CO 2 ions, inorganic phosphate, prostaglandins, and the kallikrein-kinin system. Bern's adenosine hypothesis has gained great popularity, according to which vasodilation during working hyperemia is explained by the effect of ATP breakdown products on vascular smooth muscles, in particular adenosine, which has even been called a mediator of working hyperemia. This hypothesis seemed very reasonable, since it linked together an increase in contractility, its energy supply due to the breakdown of high-energy compounds and an adequate change (increase) in coronary blood flow, regulated by the products of this breakdown. However, attempts to detect adenosine in the blood flowing from the myocardium did not give unambiguous results.

The effect of metabolites on vascular smooth muscle can be mediated through the nervous system and manifest itself as a cardio-coronary reflex.

V. M. Khayutin substantiated the idea that contraction of muscle fibers, including myocardial ones, changes the tension of the smooth muscle elements of the vascular wall. This causes a shift in their membrane potential and relaxation.

Recently, prostaglandins synthesized in the heart have attracted much attention as regulators of coronary blood flow. Prostaglandins of groups A and E, as well as prostacyclins, dilate coronary vessels, while simultaneously increasing heart contractions. Prostaglandin F 2 has a vasoconstrictor effect. There is evidence of an increase in prostaglandin production during myocardial ischemia. Bradykinin dilates coronary vessels and changes the permeability of microvascular walls. Kinins may also be involved in the regulation of blood flow speed. It is possible that an increase in bradykinin content during hypoxic conditions of the myocardium is responsible for the occurrence of pain.

Due to the characteristics of the blood supply to the myocardium, coronary vasomotor reactions are completely or almost completely aimed at ensuring that the blood flow matches the energy needs of the heart. Apparently, these reactions do not take part in the redistribution of blood in the body or the regulation of blood pressure. However, it remains unclear why vasodilation occurs when the vagus nerves are irritated, when the frequency and strength of heart contractions decreases and, consequently, the myocardial oxygen demand decreases. The duality of sympathetic adrenergic reactions has not yet been explained: the presence of beta reactions (vasodilation) and alpha reactions (vasoconstriction). The overall effect will be determined by such factors as the quantitative predominance of certain receptors, their reactivity, and the level of metabolic activity of the myocardium.

Etiology and pathogenesis of coronary insufficiency

The most common cause of coronary insufficiency is impaired blood flow in the vessels supplying the heart. Impaired blood flow in the coronary arteries can be caused by: atherosclerosis of the coronary arteries; spasm of the coronary arteries, and in the vast majority of cases, sclerotic arteries spasm; closure or narrowing of the lumen of the coronary arteries by a thrombus or (less often) an embolus; compression of the coronary arteries; narrowing of the mouth of the coronary artery with mesoaortitis; a sharp decrease in diastolic pressure, especially with aortic insufficiency; venous stagnation in the vessels of the heart. Significant importance in the development of coronary insufficiency is attached to the phenomena of aggregation and adhesion of blood cells in atherosclerotic vessels.

In addition to a decrease in the level of blood supply to the heart, a sharp increase in myocardial blood demand can lead to coronary insufficiency. Thus, the resulting discrepancy between the myocardial need for oxygen and nutrients and the amount of vital compounds supplied by the blood can cause the development of coronary insufficiency. A similar situation is created by excessive physical exertion, paroxysmal tachycardia, and anemia.

The pathogenesis of coronary insufficiency is complex. If under normal conditions the oxygen content in the blood of the coronary sinus is constant and does not depend on the load on the heart, then with coronary insufficiency the oxygen content in the blood of the coronary sinus decreases. In this case, there is an increase in the extraction of oxygen by the myocardium from the inflowing blood. Sometimes a local increase in oxygen consumption in the ischemic zone is masked by increased perfusion of healthy areas of the myocardium or the phenomena of so-called shunting. The reasons for the imbalance between oxygen demand and its delivery are:

1. An increase in demand simultaneously with a decrease in coronary blood flow.

2. An increase in oxygen demand and an inadequate increase in blood flow that lags behind the need.

3. Constant need for oxygen with reduced blood flow.

As already indicated, coronary insufficiency develops, as a rule, against the background of damage to the coronary vessels by atherosclerosis (in 96% of cases). Typically, the proximal portions of the coronary arteries are affected, resulting in their stenosis. The severity of the disease is proportional to the degree of stenosis. Distal to the stenosis, blood pressure decreases (the degree of decrease depends on the severity of the stenosis). However, coronary blood flow in the narrowed artery does not decrease until the pressure reaches 60 mmHg. Art. The flow turbulence that occurs during atherosclerosis sharply increases the resistance of moving blood and reduces the flow energy. Dilatation of the coronary artery distal to the site of stenosis provides the heart with the necessary volume of blood, despite the drop in perfusion pressure in the coronary vessels. However, a drop in intravascular pressure distal to the stenosis causes a chain of processes that form vicious circles:

1. Redistribution of blood, which, in turn, causes a decrease in blood supply to the subendocardial layers of the myocardium.

2. Vasodilation distal to the site of stenosis. Vessels that have dilated due to a drop in pressure lose their ability to adequately respond to regulatory influences, turning into passive conductors of blood.

Under conditions of mental or physical stress and increased blood pressure, turbulent blood flows damage the endothelium. Platelets begin to accumulate at the sites of injury. During the adhesion and destruction of platelets, thromboxane is released, which has strong vasoconstrictor properties. In addition, adenosine diphosphate (ADP) formed during the hydrolysis of ATP is also capable of increasing the degree of release of thromboxane and other biologically active substances from blood cells. Platelet adhesion is facilitated by an increase in the content of catecholamines, thrombin, collagen in the blood, hypercholesterolemia, etc. The impact of aggregation products on the platelet membrane leads to the activation of phospholipase A 2, which causes the cleavage of arachidonic acid from membrane phospholipids. This reaction is calcium-dependent. There are two ways of further modification of arachidonic acid - cyclooxygenase and lipoxygenase (Fig. 15). Some prostaglandins and thromboxane A 2 cause a sharp contraction of arterioles. According to modern concepts, there is normally an equilibrium state in the reactions of transformation of membrane phospholipids into prostacyclins and thromboxane A2. Prostacyclin, one of the main prostanoids formed in the intima of the coronary vessels, as well as in the lungs, has a coronary dilator and antiplatelet effect. Thromboxane A 2, as it has already turned out, is a proaggregator and coronary constrictor. Under pathological conditions, cyclic fluctuations in the resistance of coronary blood vessels are associated with periodic shifts in the equilibrium in the content of thromboxane A2 and prostacyclin, which, in turn, lead to the formation or dissolution of platelet aggregates. In atherosclerosis, the reaction shifts towards increasing the formation of thromboxane A2. A spasm of a section of the coronary artery that occurs due to any reason also enhances the formation of thromboxane A 2 and inhibits the production of prostacyclin. The process can acquire an avalanche-like character, increasing the degree of vasoconstriction and thrombus formation. A shift in the equilibrium in the formation of thromboxane A 2 and prostacyclin can occur under the influence of nicotine, and therefore smoking is considered a risk factor for coronary artery disease. An increase in the formation of thromboxane A 2 and a decrease in the production of prostacyclin creates conditions for the occurrence of a “secondary” spasm.

The perfusion deficiency of the poststenotic bed can be further aggravated by the fact that under these conditions the so-called “steal” phenomenon occurs. The vascular tone in the basin of the artery that is not affected by the atherosclerotic process is normal. As the work of the heart increases, blood flow in this area increases significantly. In accordance with the basic law of hemodynamics - Bernouli's theorem - the less blood flows into the narrowed artery under these conditions, the more blood flow in the unaffected area increases. The “steal” phenomenon, as a rule, contributes to the emergence of a vicious circle of regulation of coronary blood flow at the microcirculatory level. A decrease in blood flow in the affected area leads to a decrease in the contractile activity of the heart muscle and at the same time creates conditions for the occurrence of local stagnation, deterioration of the rheological properties of blood and the regional formation of areas with plasmatic capillaries. All this leads first to the occurrence of circulatory and then histotoxic hypoxia.

Types of coronary insufficiency

In recent years, much attention has been paid to active spastic reactions of blood vessels as the pathogenetic basis of some forms of coronary insufficiency and even myocardial infarction. The views of many clinicians on spasm of the coronary vessels as a result of angioneurosis began to give way to the idea that the cause of coronary insufficiency is mechanical obstructions to blood flow when the vessel wall is damaged by an atherosclerotic process followed by thrombosis. According to this point of view, myocardial ischemia and hypoxia arise due to an increase in myocardial oxygen demand with the inability of vessels affected by atherosclerosis to adequately expand. However, it should be especially emphasized that the discrepancy between oxygen delivery and the need for it can arise under the influence of a wide variety of factors, which are not always associated with changes in the structure or tone of the coronary arteries. Often, changes in the volumetric velocity of coronary blood flow occur as a complication of other forms of heart pathology (for example, defects), a decrease in systemic pressure, anemia. Myocardial hypoxia that occurs in these cases can be accompanied by clinical manifestations characteristic of true coronary insufficiency. As a rule, a symptom complex of angina or angina pectoris occurs. However, cases of angina pectoris of “non-coronary origin” do not belong to the manifestations of coronary heart disease (CHD). Thus, only those myocardial lesions that are caused by an imbalance between coronary blood flow and the true needs of the heart muscle for oxygen and nutrients should be classified as CHD.

One of the main clinical manifestations of coronary artery disease is angina pectoris. The following types of angina are distinguished:

1 Angina pectoris

2. Angina at rest

3. The so-called variant form (Prinzmetal’s angina)

Angina pectoris occurs when there is increased load on the myocardium as a result of increased physical activity. During physical activity, both stroke and minute volume increase, blood pressure rises, and heart rate increases. Emotional stress and pain are accompanied by the release of catecholamines, which cause an inotropic effect. All this, on the one hand, increases oxygen consumption by the myocardium, and on the other, causes activation of the prostaglandin-thromboxane system, the role of which in the occurrence of coronary artery spasm was discussed above

Most often, angina pectoris occurs in cases where an increase in the need for oxygen and metabolic substrates is not accompanied by dilation of the coronary arteries. As a rule, the occurrence of this form of angina is caused by changes in the intraganglionic apparatus of the heart. Activation of the sympathoadrenal system, accompanied by an increase in metabolic demands of the myocardium, aggravates the deficiency of oxygen and nutrients. In addition, catecholamines, by increasing the “unproductive” consumption of oxygen and substrates, reduce the efficiency of the functioning of myocardial structures. An increase in the content of catecholamines in the heart muscle can prevent an increase in the volumetric velocity of coronary blood flow due to a shortening of the diastolic pause, during which the blood flow in the myocardium is maximum. In other words, the occurrence of angina pectoris is based on violations of various parts of the regulation of coronary blood flow, in which an increase in the myocardial need for oxygen and nutrients is not accompanied by a corresponding increase in the volumetric velocity of coronary blood flow

Angina at rest. With severe sclerosis of the coronary arteries, an attack of angina pectoris can occur spontaneously, at rest, without any apparent reason. In some patients, angina occurs primarily in a horizontal position, since under these conditions the blood flow to the heart increases and the volume of the left ventricle increases. The tension of the myocardial walls gradually increases, as a result of which the myocardial need for oxygen increases. When the reserve of coronary blood flow decreases, this is enough to cause an attack of angina. This type of angina occurs especially often in people with dilatation of the left ventricle. Hypertension, preventing free emptying of the left ventricle, increasing the level of peripheral resistance, increases the systolic tension of the myocardium. In addition, with hypertension, oxygen access to individual muscle fibers deteriorates due to a relative decrease in the number of capillaries per unit of muscle mass. With tachycardia, oxygen consumption by the myocardium also increases, which can cause angina at rest.

Particular importance in the mechanisms of occurrence of angina at rest is given to disturbances in the intracardial regulation of coronary blood flow. As it has already turned out, an important role in the processes of adequate provision of the myocardium with oxygen and nutrients belongs to compounds of adenyl nature and the sensitivity of the receptor apparatus of the heart muscle to ADP. Adenosine disphosphate, formed during muscle contraction, can maintain the optimal volumetric velocity of coronary blood flow only with a slight change in the structure of the coronary vessels. The decrease in ATP hydrolysis that occurs at rest leads, in turn, to a decrease in the amount of ADP, a spasm of the coronary vessels occurs, which clearly does not correspond to the decrease in the load on the contractile structures of the myocardium, and an attack of angina pectoris develops.

Some authors distinguish as a separate form the so-called dysmetabolic angina, which can occur with anemia, thyrotoxicosis, hypokalemia and other metabolic disorders. If in persons with normal coronary vessels, compensation for the lack of oxygen associated with anemia is carried out by accelerating coronary blood flow, then when anemia is combined with atherosclerosis of the coronary arteries, a similar compensation mechanism is not possible.

With an excess of thyroid hormones, two parallel processes develop. First of all, tachycardia occurs, myocardial oxygen consumption increases, but its utilization does not increase. On the other hand, with thyrotoxicosis, the “coupling factor” binds and the efficiency of phosphorylation decreases, which leads to a lack of ATP, respectively, ADP and the emergence of a discrepancy between the myocardial oxygen demand and its delivery.

Variant form of angina. In 1959, Prinzmetal and his colleagues described the so-called variant form of angina, which occurs during physical rest and is usually not provoked by daytime physical activity. Oxygen deficiency in this case did not arise as a result of an increase in the need for it (as expected), but as a result of a decrease in delivery. This allowed the authors to express the opinion that a variant form of angina is caused by spasm of the coronary arteries, which is documented by electrocardiography, radioisotope and biochemical studies, and the clinical picture of an attack of angina. Nitroglycerin, calcium channel blockers, and atropine stop the spasm. Spasm is provoked by conditions that excite the sympathoadrenal system. Recognizing the reality of neurogenic narrowing of the coronary vessels, many authors note, however, that it is usually small and cannot play a significant role in the systemic regulatory reactions of blood redistribution and in most cases cannot be the cause of coronary insufficiency.

Metabolic disorders in angina pectoris

Available experimental data and clinical observation material indicate that the phenomena of coronary insufficiency cannot be reduced only to myocardial hypoxia. When the intensity of coronary blood flow decreases, the muscle fibers are affected by accumulating lactic and pyruvic acids, as well as other under-oxidized products or metabolites. For example, during myocardial ischemia, the normal relationships between aerobic and anaerobic metabolism are disrupted. One of the indicators of such a change is a violation of the ratio between the content of lactic and pyruvic acids. Under normal conditions of coronary blood flow, this indicator, as a rule, has negative values, that is, there is more pyruvic acid than lactic acid. In conditions of decreased cardiac nutrition, the concentration of lactic acid increases sharply. Some researchers define this condition as “excess of lactate” (A G. Krasnov et al, 1962). An increase in lactic acid content indicates inhibition of the reactions of the tricarboxylic acid cycle and a decrease in the efficiency of the dehydrogenation process. The main consequence of the shift towards anaerobic metabolism is a decrease in ATP production. It is known that the anaerobic disposal route is much less energetically efficient. The resulting lack of ATP in the heart muscle, in turn, cannot but affect both the contractility of the myocardium and the volumetric velocity of blood flow. The consequence of the accumulation of lactic acid is a change in the pH of the environment. A sharp decrease in the pH of the environment leads to a disruption of enzymatic activity, in particular, the activity of succinate dehydrogenase in the heart decreases. In addition, the phenomena of acidosis can contribute to a decrease in the rate of electron transport in the terminal sections of the respiratory chain and a decrease in the amount of ionized oxygen.

With myocardial ischemia, the content of adrenaline in the heart increases significantly. Usually its concentrations are 1.5-2 times higher than the values ​​​​characteristic of normal blood supply conditions. This phenomenon is due, first of all, to an increase in the uptake of adrenaline from the blood by both neuronal and extraneuronal formations, and a decrease in the level of its destruction due to inhibition of the activity of monoamine oxidase and catecholorthomethyltransferase. In parallel, the content of norepinephrine in the myocardium decreases. It should be noted that adrenaline is an activator of lipid peroxidation in the myocardium

Lipid peroxidation to a certain extent determines the composition of biological membranes and the activity of membrane-associated enzymes. Prooxidants increase the process of lipid peroxidation, while antioxidants suppress it. The role of pro-oxidants is played by vitamins A and D, low concentrations of ascorbic acid, metabolic products of leukotrienes, prostaglandins, adrenaline, etc.

The antioxidant effect is characteristic of vitamin E, thyroxine, steroid hormones, substances containing thiol groups, iron-binding agents, etc.

The stages of lipid peroxidation can be conditionally reduced to the following processes:

1. Oxygen initiation.

2. Formation of lipid free radicals.

3. Lipid peroxide production (P.F. Litvitsky, 1986).

Increased lipid peroxidation causes damage to protein and lipid components of membranes and significantly affects the activity of membrane-related enzymes

The essence of the changes is as follows: the conformation of lipoprotein complexes and proteins that provide reception and transmembrane transport of ions is disrupted; the so-called “simplest channels” are formed, through which an uncontrolled flow of cations occurs. Due to the fact that the process of lipid peroxidation disorders during myocardial ischemia is, as a rule, not local, the resulting endoperoxides cause changes in almost all the main functions of the heart muscle: automaticity, excitability, contractility and conductivity.

Some authors consider coronary insufficiency as a set of ischemic and reperfusion syndromes, which are characterized by the alternation of myocardial ischemia with periods of resumption of coronary blood flow. The phenomena of “reperfusion” during ischemia can be caused by blood flow through neighboring vessels that have not undergone spasm, retrograde blood flow through venules and the resumption of perfusion, impaired as a result of thrombosis, through arteries and arterioles.

All forms of dynamic disturbances of coronary blood flow are accompanied by characteristic changes in the electrocardiogram. During an attack of angina pectoris, after a temporary increase in heart rate, bradycardia is observed. Sometimes extrasystoles appear. Occasionally, sinoauricular or incomplete atrioventricular block occurs. A typical change is the S-T segment and the T wave, which shift towards the isoelectric line. With a prolonged attack, the T wave initially becomes biphasic and then negative.

Thus, IHD can manifest itself as functional disorders and pain syndrome (various forms of angina) or cause necrosis of a certain area of ​​the heart muscle

Chronic coronary insufficiency

Chronic coronary insufficiency is understood as a long-term or constant decrease in the volumetric velocity of blood flow in the coronary arteries. Most often, a decrease in the amount of blood flowing through the coronary vessels is associated with atherosclerotic damage to their walls. Sometimes a prolonged spasm is caused by vasoconstrictor substances accumulating in the myocardium, resulting from metabolic disorders. Excessive levels of bradykinin, histamine, serotonin, acidosis or increased potassium levels can aggravate the manifestations of ischemia. Chronic coronary insufficiency does not always manifest itself with typical chest pain. The consequence of chronic coronary insufficiency is the development of cardiosclerosis, leading to a sharp decrease in myocardial contractile activity. However, cases of myocardial infarction have been described in individuals with no subjective manifestations of coronary insufficiency. These are the so-called “silent” heart attacks, leading to sudden death in people. Typically, the diagnosis of such a heart attack is established only at autopsy.

It is still not entirely clear why people with obvious myocardial malnutrition do not have substernal pain. Observations on a group of diabetic patients, in whom “silent” ischemia most often occurs, suggest that this phenomenon is based on a block of the myocardial chemoreceptor apparatus. It should be noted that the myocardium, devoid of pain receptors, can signal about blood flow disturbances only when the chemoreceptors are overstimulated. Subjective sensation occurs after the receipt of relevant information in the higher nerve centers.

Myocardial infarction

Myocardial infarction is focal ischemia resulting in necrosis of the heart muscle, which occurs as a result of cessation of blood flow through one of the branches of the coronary arteries or as a result of its receipt in an amount insufficient to meet energy needs. The most common cause of damage to the artery wall is atherosclerosis. Other factors contributing to myocardial infarction may be physical activity, changes in the blood coagulation system, and vasospasm.

Predisposing to the occurrence of myocardial infarction, the so-called risk factors, are: hypertension, diabetes mellitus, gout, as well as a sedentary, emotionally stressful lifestyle, excess nutrition, smoking, etc.

Large (transmural) heart attacks occur when the coronary arteries are blocked, most often due to thrombosis. It is necessary to take into account that blockage of even a small branch of the coronary artery may be accompanied by spasm of neighboring vessels. This is the so-called “coronary-coronary reflex.” In this case, the infarction is a consequence of absolute arterial ischemia. With a rapidly developing cessation of blood flow in a large branch of the coronary artery, an anatomical and histological picture of a white infarction is observed, while blockage of small branches is accompanied by the development of hemorrhagic infarctions.

Infarctions without blockage of arteries most often occur in the sub-endocardial part of the myocardium. Developing small-focal changes are explained by chronic hypoxia

The tissue of the area to which the blood supply stops becomes necrotic, gradually softens, and myomalacia occurs. Granulation tissue growing along the periphery of the necrotic lesion gradually turns into connective tissue containing elastic fibers.

Due to disturbances in the structure of the myocardium, the production and utilization of energy changes. Activation of the anaerobic metabolic pathway, which, as already indicated, is less effective, leads to a deficiency of high-energy compounds. It has been proven that when the ATP content in the cell decreases by 40-60%, it completely loses its functions. Under-oxidized products accumulate in the muscle, which also reduce the contractile function of the heart, and excess catecholamines increase the energy demand of individual cardiomyocytes. When the scar is localized in the area of ​​the conduction system, a wide variety of rhythm disturbances are associated with pronounced changes in contractility. When the focus of necrosis is located near the pericardium, pericarditis occurs, which is usually serous-fibrinous in nature.

In cases where the infarction occupies a large part of the wall of the left ventricle, bulging of this area may occur and, under the influence of intraventricular pressure, a cardiac aneurysm develops. When a coronary artery becomes blocked, circulatory failure may occur. Even under these conditions, the body strives to maintain minute volume and optimal blood supply to vital organs. With circulatory failure in the periphery at the time of development of a heart attack, peripheral resistance reflexively increases. Such a mechanism for maintaining blood pressure cannot be considered adequate due to the sharply increasing load on the myocardium. Other mechanisms are also activated that help maintain the volumetric velocity of blood flow. Due to stimulation of the juxtaglomerular apparatus, the secretion of renin by the kidneys is activated, the concentration of aldosterone increases, which in turn leads to fluid retention in the body and an increase in venous flow to the heart.

In addition, under the influence of catecholamines in the blood, the concentration of non-esterified fatty acids increases (due to increased mobilization from fat depots). This can cause arrhythmia and ventricular fibrillation. In the myocardium, the content of kinins increases, the concentration of serotonin increases, and the blood coagulation system is activated.

Some patients may experience hypoglycemia, which is most often associated with a decrease in insulin secretion due to decreased blood flow in the pancreas and increased glycogenolysis and gluconeogenesis under the influence of catecholamines and steroid hormones.

Sometimes myocardial infarction is accompanied by “post-infarction syndrome.” Its typical manifestations are pleurisy and pericarditis.

Autoimmune processes that develop during myocardial necrosis are of great importance. Protein breakdown products formed during the destruction of myocardial tissue play the role of antigens. The process of autoimmunization begins on the first day. The emerging antibodies are complementary not only to the cellular structures of the damaged myocardium, but also to intact cardiomyocytes. Long-term circulation of antibodies leads to diffuse damage to the heart muscle. Despite the variety of possible manifestations of this process, the final effect of immune damage will be the development of cardiosclerosis. Instead of specialized muscle tissue, connective tissue scars develop.

The development of connective tissue in the myocardium reduces the contractility of the heart, reduces the efficiency of the functioning of its structures, and leads to a decrease in its external work. Heart failure occurs.

Electrocardiographic manifestations of myocardial infarction

Despite the fact that electrocardiographic analysis has been used to diagnose myocardial infarction for many years, this method cannot be considered absolutely informative for determining the location and severity of damage. In most cases, only comparison of series of electrocardiograms allows a correct assessment of electrophysiological processes

The most common change in a heart attack is the ventricular QRST complex. There are two points of view on the reasons causing changes in the algebraic sum of action potentials that form this complex, one of them is a simple loss of excitability of the myocardial area that has undergone an infarction; the second is a violation of the sequence of excitation of areas of the ventricular muscle and its spread to healthy areas

As a rule, three phases of electrocardiographic changes during a heart attack can be distinguished. During the first phase (12-36 hours), the ventricular complex undergoes the following changes on the ECG. The descending limb of the R wave, having reached half, immediately passes into the T wave. The S and T waves merge and a monophasic curve is formed, most often dome-shaped. This picture is recorded when using classical leads.

During the second phase (1.5 days or more), the descending limb of the R wave gradually falls below the isoelectric line. The S-T segment, having reached the isoelectric line, forms a small arc directed upward, which turns into a negative T wave.

In the third phase (usually after 7 or more days), the T wave gradually returns to the isoelectric line

The described picture is recorded in leads I, II and III; changes in ECT in the chest leads will be discussed in a special section devoted to arrhythmias

Date added: 2015-09-03 | Views: 721 | Copyright infringement

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