Myocardium and its diseases

Table of contents:
  • How the heart muscle system is arranged
  • What does the mass of the myocardium indicate?
  • Heart reduction mechanism
  • What affects the contractility process?
  • Properties of the heart muscle
  • Types of myocardial lesions
  • Features of myocarditis
  • Disorders of myocardial metabolism
  • When does myocardial hypertrophy occur?
  • Myocardial infarction in ischemia
  • How does the myocardium change with thrombosis of the coronary arteries?
  • Is it possible to confirm necrosis by laboratory methods?

If you forget about lyrical digressions, then the heart is a hollow organ, "suspended" and fixed in a special bag of powerful ligaments. The size of a normal heart can be judged by comparison with the volume of a person's fist.

For the organism the pumping function is irreplaceable - pumping the blood, which allows transportation of oxygen and nutrients to any tissues, delivery of waste for processing.

Any changes in the myocardium( muscle layer) affect the usefulness of the heart, contribute to physiological and pathological abnormalities, cause acute and chronic diseases.

How the heart muscle system is arranged

The myocardium is the thickest layer of the heart, located midway between the endocardium( inner layer) and the epicardium from the outside. A feature of the heart is the ability of the atria and ventricles to contract independently, independently of each other, even to "work" in an autonomous mode.

The contractility is provided by special fibers( myofibrils).They combine the signs of skeletal and smooth muscle tissue. Therefore:

  • distributes the load evenly across all departments;
  • have striated striation;
  • provides non-stop work of the heart for a lifetime;
  • shrink regardless of the influence of consciousness.
The basis of the muscle tissue is the cells of the myocytes

In each cell there is an elongated nucleus with a large number of chromosomes. Due to this, myocytes are more "tenacious" than cells of other tissues and capable of withstanding significant loads.

Atrial and ventricles have different myocardial densities:

  1. In the atria, it consists of two layers( surface and deep) that differ in the direction of the fibers, outwardly there are transverse or circular myofibrils, and inside are longitudinal ones.
  2. The ventricles are provided with an additional third layer lying between the first two, with the horizontal direction of the fibers. Such a mechanism strengthens and supports the force of contraction.

As indicated by the mass of the myocardium

The total mass of the heart in an adult is about 300 g. The development of methods of ultrasound diagnostics made it possible to calculate from this weight the part related to the myocardium. The average mass index of myocardium for men is 135 g, for women - 141 g. The exact mass is determined by the formula. It depends on:

  • the size of the left ventricle in the diastole phase;
  • thickness of the interventricular septum and posterior wall.

Even more specific for diagnosis is the index, such as the index of the mass of the myocardium. For the left ventricle, the norm for men is 71 g / m2, for women - 62. This value is calculated automatically by the computer when entering data on the growth of a person, body surface area.

Studies of the nature of myocardial hypertrophy are important in the differential diagnosis of cardiomyopathies, the effects of hypertension, the appointment of therapy to reduce the burden on the heart.

Heart reduction mechanism

Thanks to the development of electron microscopy, the internal structure of the myocardium, the structure of the myocyte, providing the property of contractility, is established. Thin and thick protein chains, called "actin" and "myosin", were detected. When the actin fibers glide over myosin, the muscle contraction( systole phase) occurs.

The biochemical reduction mechanism consists in the formation of the common substance "actomyosin".An important role is played by potassium. Leaving the cell, it promotes the combination of actin and myosin and the absorption of energy.

The energy balance in myocytes is maintained due to replenishment in the phase of relaxation( diastole).In this process, biochemical components:

  • oxygen,
  • hormones,
  • enzymes and coenzymes( B vitamins are especially important in their role),
  • glucose,
  • lactic and pyruvic acids,
  • ketone bodies.
  • amino acids.

What affects the contractility process?

Recommended reading: Myocardial infarction Moderate hypoxia of the myocardium

Any diastolic dysfunction disrupts the production of energy, the heart loses its "makeup", does not rest. The metabolism of myocytes is affected by:

  • nerve impulses coming from the brain and spinal cord;
  • deficiency or excess of "components" for a biochemical reaction;
  • infringement of receipt of necessary substances on coronary vessels.

Blood supply to the myocardium is carried out by coronary arteries that extend from the base of the aorta. They are sent to different parts of the ventricles and atria, break down into small branches feeding deep layers. An important adaptive mechanism is the system of collateral( auxiliary) vessels. These are reserved arteries, normally in a collapsed state. For their inclusion in the channel of blood circulation, the main vessels( spasm, thrombosis, atherosclerotic damage) should fail. It is this reserve that can limit the infarction zone, provides nutrition compensation in case of myocardial thickening during hypertrophy.

Support for satisfactory contractility is needed to prevent heart failure.

Properties of the heart muscle

In addition to contractility, the myocardium has other exceptional properties that are inherent only in muscle tissue of the heart:

  1. Conductivity - equates myocytes to nerve fibers, because they are also capable of impulses, transferring them from one area to another.
  2. Excitability - for 0,4 seconds.the whole muscle structure of the heart comes into excitement and provides a complete discharge of blood. The correct rhythm of the heart depends on the occurrence of excitation in the sinus node located in the depth of the right atrium and further passage of the pulse along the fibers to the ventricles.
  3. Automatism - the ability to independently form a focus of excitation around the established direction. This mechanism causes a violation of the correct rhythm, as other sites take on the role of driver.
The focus is called "ectopic", it appears on the ECG

. Different myocardial diseases are accompanied by minor or severe disorders of the listed functions. They determine the clinical features of the course and require a special approach to treatment.

Consider the pathological changes in the myocardium and their role in the occurrence of certain diseases of the heart muscle.

Types of myocardial lesions

All myocardial lesions are divided into:

  1. Non-coronary myocardial diseases - characterized by a lack of connection of causes with coronary artery disease. These include inflammatory diseases or myocarditis, dystrophic and nonspecific changes in the myocardium.
  2. Coronarogenic - consequences of impaired permeability of coronary vessels( foci of ischemia, necrosis, focal or diffuse cardiosclerosis, cicatricial changes).

Features of myocarditis

Myocarditis is often found in men, women and in childhood. Most often they are associated with inflammation of certain areas( focal) or the entire muscle layer of the heart( diffuse).The causes are infectious diseases( influenza, rickettsiosis, diphtheria, scarlet fever, measles, typhus, sepsis, poliomyelitis, tuberculosis).

Carrying out of preventive work on formation of sufficient protective reaction with the help of vaccinations allowed to limit the disease. However, serious heart problems remain after nasopharyngeal diseases, because of the development of a chronic rheumatic process. Non-rheumatic myocarditis is associated with a severe stage of uremic coma, acute nephritis. An autoimmune character of the inflammatory reaction is possible, proceeding as an allergy.

In a histological study, among the muscle cells,

  • granulomas of a typical structure are found in rheumatism;
  • edema with congestion of basophils and eosinophils;
  • death of muscle cells with proliferation of connective tissue;
  • accumulation of fluid between cells( serous, fibrinous);
  • sites of dystrophy.

The result in all cases is impaired myocardial contractility.

The clinical picture is diverse. It consists of the symptoms of cardiac and vascular insufficiency, rhythm disturbances. Sometimes the endocardium and pericardium are affected simultaneously.

Usually, right ventricular failure is more common, since the right ventricular myocardium is weaker and first fails.

Pain in the heart - the main sign of myocarditis

Patients complain of shortness of breath, palpitation, a sense of disruption on the background of an acute disease or after an infection.

Rheumatic inflammation is always accompanied by endocarditis, necessarily the process extends to the valve apparatus. When delaying treatment, a vice is formed. For a good response to therapy, temporary disturbances of rhythm and conductivity are typical without consequences.

Disorders of myocardial metabolism

Exchange disorders often accompany myocarditis and coronary heart disease. To find out what is primary is not possible, so this pathology is connected. Because of the lack of substances for energy production in cells, lack of oxygen in the blood in thyrotoxicosis, anemia, beriberi, myofibrils are replaced by scar tissue.

The heart muscle begins to atrophy, to weaken. This process is typical for senile age. A special form is accompanied by the deposition of lipofuscin in the cells, which, in histology, the heart muscle changes color to brownish-red, and the process is called "brown atrophy of the myocardium."At the same time, dystrophic changes are found in other organs.

Muscle of the heart loses tone, elasticity is reduced, conduction and automatism are violated. Patients with myocardial dystrophy can manifest atrial fibrillation and different degrees of blockade.

When does myocardial hypertrophy occur?

The most common cause of hypertrophic changes in the heart muscle is hypertensive disease. Increased resistance to blood vessels causes the heart to work against a high load.

For the development of concentric hypertrophy is typical: the volume of the cavity of the left ventricle is preserved unchanged with a general increase in size.

Symptomatic hypertension in diseases of the kidneys, endocrine pathology are less common. The moderate thickening of the ventricular wall makes it difficult to grow the vessels deep into the mass, so it is accompanied by ischemia and the state of oxygen deficiency.

Cardiomyopathies - diseases with unexplained causes, combine all possible mechanisms of myocardial damage from increasing dystrophy, leading to an increase in ventricular cavity( dilated form), to severe hypertrophy( restrictive, hypertrophic).

Hypertrophy of the myocardium
Muscle of the left ventricle reaches a thickness of 3 cm

A special variant of cardiomyopathy - spongy or noncompact myocardium of the left ventricle is congenital in nature, often associated with other heart and vascular malformations. Normally, the noncompact myocardium forms a certain proportion in the mass of the heart. It increases with hypertension, hypertrophic cardiomyopathy.

Pathology is detected only in the adult state due to symptoms of heart failure, arrhythmia, embolic complications. In color Doppler study, an image is obtained in several projections, and the thickness of noncompact sites is measured during systole, and not diastole.

Myocardial infarction in ischemia

In 90% of cases in coronary vessels with ischemic disease, atherosclerotic plaques overlapping the diameter of the feeding artery are found. A certain role is played by metabolic changes under the influence of impaired nervous regulation - the accumulation of catecholamines.

With angina pectoris, the condition of the myocardium can be characterized as forced "hibernation"( hibernation).Hibernating myocardium is an adaptive response to oxygen deficiency, adenosine triphosphate molecules, potassium ions, major calorie suppliers. Occurs in local areas with prolonged circulatory disturbance.

A balance is maintained between a decrease in contractility in accordance with impaired blood supply. In this case, the cells-myocytes are quite viable and can be fully restored with improved nutrition.

"Stunned myocardium" is a modern term that characterizes the condition of the heart muscle after the restoration of the coronary circulation in the heart site. The cells accumulate energy for several days, the contractility in this period is disturbed. It should be distinguished from the phrase "myocardial remodeling", which means actual changes in myocytes under the influence of pathological causes.

Most often, these changes are accompanied by unstable angina. But, if there is a more persistent reduction in the delivery of nutrients or a sharp increase in demand( physical activity), then the process of ischemia proceeds according to a more severe type to necrosis of the muscle layer.

How does the myocardium change with thrombosis of the coronary arteries?

Prolonged spasm or blockage of the coronary arteries causes necrosis of that part of the muscle that they supply with blood. If this process is slow, collateral vessels will take on "work" and prevent necrosis.

Myocardial infarction
The left ventricle is most often affected in the basin of the anterior descending artery

. The hearth is located in the region of the apex, anterior, posterior and lateral walls of the left ventricle. It rarely seizes the septum and right ventricle. Necrosis in the lower wall occurs when the right coronary artery is blocked.

If the clinical manifestations and the ECG picture converge in the confirmation of the form of the disease, then the diagnosis can be confident and use a combination treatment. But there are cases that require confirmation of the opinion of the doctor, primarily with the help of accurate, undeniable markers of myocardial necrosis. As a rule, the diagnosis is based on the quantitative determination of more or less specific for necrotic tissues decay products, enzymes.

Is it possible to confirm necrosis by laboratory methods?

The development of modern biochemical diagnosis of the infarction allowed us to identify standard markers of myocardial necrosis for early and late manifestations of myocardial infarction.

Markers of myocardial necrosis
The most significant is the increase in the content of substances in the dynamics 6-9 hours, 9-12 hours after the onset of the pain syndrome

The early markers are:

  • Myoglobin - increases in the first 2 hours, the optimal use of the indicator to monitor the effectiveness of fibrinolytic therapy.
  • Creatine phosphokinase( CKF) - a fraction of cardiac muscle is only 3% of the total mass, so if it is not possible to determine only this part of the enzyme, the test does not have a diagnostic value. With necrosis, the myocardium rises by a second or third day. It is possible to increase the index in case of renal failure, hypothyroidism, oncological diseases.
  • Cardiac type of protein that binds fatty acids - in addition to the myocardium there is a wall of the aorta, the diaphragm. It is regarded as the most specific indicator.

The late markers are:

  • Lactate dehydrogenase, the first isoenzyme - reaches the highest level by the sixth-seventh day, then decreases. The test is considered to be low specific.
  • Aspartate aminotransferase - reaches a maximum by the 36th hour. Due to its low specificity it is used only in combination with other tests.
  • Cardiac troponins - stored in the blood for up to two weeks. They are considered the most specific indicator of necrosis and are recommended by international standards for diagnosis.

The data on myocardial changes are confirmed by anatomical, histological and functional studies of the heart. Their clinical significance allows us to timely identify and assess the degree of destruction of myocytes, the possibility of their recovery, and control the effectiveness of treatment.