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Concentric remodeling of the left ventricle. Modern problems of science and education Concentric and eccentric remodeling

However, the result was the opposite. What causes serious problems with the heart of people who regularly exercise?

What is cardiac remodeling?

Remodeling is a phenomenon whose essence is to change the structure of an object. Changes in the structure and shape of the heart, including an increase in the weight of the left ventricular muscle and an increase in the size of the organ's parts, which lead to a decrease in its functionality, are called myocardial remodeling. This process can occur rapidly, but more often it is long-term. With timely diagnosis, proper treatment, and elimination of the provoking factor, this process can be stopped and reversible.

Causes

The initial stage of cardiac muscle remodeling is an increase in the mass of the muscle layer of the left ventricle. Changes in the myocardium can occur in one of two directions:

Due to an increase in the size of cardiomyocytes, a thickening of the septum between the ventricles occurs.
Due to the increase in the width and length of cardiomyocytes, thinning of the walls of the heart and an increase in the volume of its chambers develop.

These processes are often triggered by people who incorrectly distribute physical activity. So, muscle thickening of this body occurs in those who train too intensely, especially in team sports and those that require the use of force. In this case, the cells’ need for oxygen sharply increases, so the heart is forced to accelerate oxygen-rich blood into the arteries, overcoming increased resistance, which does not allow the muscle to fully relax in the diastole stage.

Compensating for these factors, the heart muscle pumps up volume. Thus, pressure loading causes concentric remodeling of the left ventricular myocardium.

Participation in dynamic sports that develop endurance can lead to the development of eccentric remodeling of the heart muscle, which consists of an increase in the length and width of cardiomyocytes. This process is a compensatory measure of the heart muscle to return the increased volume venous blood and is caused by the need to move its sharply increased volume in the artery.

In addition to athletes and people with heavy physical labor, the risk group includes:

People who, leading a sedentary lifestyle, suddenly began to actively engage in sports.
Obese people.
Patients diagnosed with aortic stenosis.
Hypertensive patients.
Patients with heart disease.

How to stop the disease?

Heart remodeling can cause the following diseases: stroke, chronic heart failure, ischemia, necrosis of cardiac cells, and heart attack. Therefore, it is very important to correctly calculate optimal physical activity, as well as promptly check with a doctor if you suspect the appearance of an illness. If this heart pathology is detected, sudden cessation of training is contraindicated. Physical activity should be calculated by a specialist and gradually reduced. With a timely and qualified approach, the heart has a chance to return to its original shape.

Left ventricular remodeling in hypertension.

Prognostic significance of LV shape and geometry in patients with arterial hypertension(AG) continues to be debated. In earlier studies, LV remodeling was considered an adaptive response to pressure and volume overload and was associated with a more favorable prognosis. In fact, the process of LV adaptation to hypertension is more complex than expected. The heart is able to adapt to long-term hypertension by developing concentric LV hypertrophy. Consistent with the compensatory response pattern, LV wall thickness increases in proportion to A/D levels to maintain normal myocardial stress. Obviously, the spectrum of cardiac adaptation to hypertension should be associated with differences in hemodynamic load and the state of myocardial contractility. LV dilation represents a late transition from LV hypertrophy to myocardial failure.

The widespread use of ECHO-CG method has made it possible to classify the LV architectonics in patients with hypertension into four geometric models based on indicators such as myocardial mass and relative LV wall thickness. The relative LV wall thickness index is a sensitive indicator of the geometric pattern of hypertrophy and is determined by the ratio of the LV wall thickness to the transverse diameter of its cavity at the end of diastole. These geometric models are:

1) concentric hypertrophy (increase in myocardial mass and

relative thickness of the LV wall);

2) eccentric hypertrophy (increase in mass at normal

small relative thickness);

3) concentric remodeling (normal weight and increased

personal relative wall thickness);

4) normal LV geometry;

A. Hanau et al. determined the hemodynamic features and state of LV contractility in 165 patients with hypertension depending on its geometric model. The results of this analysis were unexpected and do not coincide with the views of most practicing cardiologists. Concentric LV hypertrophy was observed in only 8% of subjects; 27% had eccentric hypertrophy; 13% - concentric LV remodeling; 52% of the subjects were characterized by normal LV geometry. The shape of the LV was the most ellipsoidal in the group of patients with concentric hypertrophy and the most spherical in the group with eccentric hypertrophy.

Differences in the structural and geometric pattern of the LV in patients with hypertension are closely related to the pathophysiology of the heart and circulation. Patients with concentric hypertrophy are characterized by nearly normal end-systolic myocardial stress, normal LV size and shape, increased total peripheral vascular resistance (TPR), and a slightly increased cardiac index.

Patients with concentric remodeling are also characterized by normal level end-systolic myocardial stress and increased total peripheral resistance. At the same time, they are distinguished by reduced shock and cardiac indices. The incentive to increase relative LV wall thickness in this group is not fully understood. It may be partly explained by a decrease in arterial compliance, as indicated by subnormal stroke volume with a slight increase in pulse A/D. Patients with eccentric LV hypertrophy have a high cardiac index, normal PVR, enlarged LV cavity, and end-systolic myocardial stress, indicating inappropriate LV hypertrophy. As hemodynamic prerequisites for the formation of this geometric model, a predominant increase in venous tone or bcc is given. The vast majority with hypertension have normal LV geometry and are characterized by a slight increase in total PVR, systolic and diastolic A/D.

Even a small change in LV mass within normal values may serve as a prognostic sign of increased risk of cardiovascular complications. Numerous studies show that increased LV mass is a stronger predictor of cardiovascular events and mortality than A/D levels and other risk factors except age. These data are consistent with other studies and support the concept that increased LV mass is a common pathway for many adverse cardiovascular outcomes.

The configuration of the LV, regardless of myocardial mass, influences the prognosis of patients with hypertension. One study examined the difference in cardiovascular risk in 694 hypertensive patients with normal LV myocardial mass who had either normal LV configuration or concentric remodeling at baseline echocardiography. The duration of observation was 8 years (average 3 years). The incidence of cardiovascular complications, including fatal ones, was 2.39 and 1.12 per 100 patients per year in the groups with and without concentric remodeling, respectively (2.13 times).

Observation of 253 patients with initially uncomplicated essential hypertension for 10 years, conducted by M. Koren et al., confirmed that the incidence of cardiovascular complications and mortality are quite strictly dependent on the geometric model of the LV. Thus, the worst prognosis for cardiovascular complications (31%) and mortality (21%) was noted in the group of patients with concentric LV hypertrophy. The most favorable prognosis (no deaths and 11% cardiovascular complications) is typical for the group of patients with normal LV geometry.

Patients with eccentric hypertrophy and concentric remodeling occupied an intermediate position. The study of the pathophysiology and pathogenesis of changes in the structure and geometry of the LV in patients with hypertension allows us to conclude that during concentric remodeling there is a “volume underload”, possibly due to “pressure natriuresis”. There is no obvious LV hypertrophy in response to volume underload. Studying the mechanisms of LV underload may provide new strategies to prevent the progression of hypertensive heart disease and optimize antihypertensive treatment.

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Myocardial remodeling

The definition of “myocardial remodeling” began to be used back in the late 70s. It helped to characterize structural changes in the human heart, as well as disturbances in its geometry after a myocardial infarction. Cardiac remodeling occurs under the influence negative factors– diseases that lead the organ to the development of physiological and anatomical disorders.

If we talk about remodeling of the left ventricular myocardium, then the features of its manifestation are directly related to the factors under which it was formed. For example, when overloaded with high blood pressure, which can occur with hypertension or aortic valve stenosis, the following disorders are observed:

increase in the number of sarcomeres;
increased thickness of cardiomyocytes;
increase in wall thickness;
development of concentric remodeling of the LV myocardium.

The concept of eccentric remodeling, which is caused by volume overload of the myocardium, is also known. It is accompanied by elongation of cardiomyocytes and a decrease in wall thickness.

There is also functional remodeling, in which impaired LV contractility appears on its own and does not depend on geometric changes. The latter are referred to as structural remodeling, which refers to changes in the shape and size of the LV.

Concentric remodeling of the left ventricular myocardium

The most common type is concentric remodeling, diagnosed in people with hypertension. It begins with hypertrophy of the left ventricle, manifested by an increase in the thickness of its wall. Often accompanied by changes in the septum. The internal space remains without pathologies.

Myocardial hypertrophy - remodeling

Interesting to know! Hypertrophy is increasingly being diagnosed in young people, who suffer from it no less often than older people. arterial hypertension. Therefore, the issue of timely diagnosis and prevention of the development of consequences is very acute.

Despite the fact that most often LVH develops in people against the background of hypertension, it can also appear under the influence of constant physical activity, negatively affecting the functioning of the heart. Athletes, loaders, etc. are also at increased risk. The stress on the heart, which is typical for people with a predominantly sedentary lifestyle, as well as for smokers and alcohol drinkers, is also dangerous.

In order to be able to prevent further cardiac remodeling, it is necessary to promptly identify hypertension and LVH, which are the main factors provoking worsening changes. They are manifested by the following symptoms:

constantly elevated blood pressure, its systematic jumps upward;
headaches;
disturbances in heart rhythms;
deterioration in general health,
pain in the heart.

ECG as a method for diagnosing LV remodeling and its degree

A cardiogram will help diagnose heart disease, which must be done if the symptoms listed above are present. It is performed using special equipment - an electrocardiograph. The ST segment elevation will be seen here. A decrease or complete disappearance of the R wave may be observed. Such indicators indicate the presence of concentric remodeling of the left ventricular myocardium and may indicate a previous myocardial infarction. The latter will only aggravate the structural and geometric changes of the heart, because dead areas of the heart muscle will be replaced by connective tissue, losing their original characteristics and functions.

As a result, there is a high risk of complications, the most serious of which is chronic heart failure. It significantly increases the likelihood of death.

What factors influence the remodeling process

Remodeling can have different scales, its manifestation depends on several factors. The first is neurohormonal activation. It occurs after a heart attack. The severity of increased activation of neurohormones is directly related to the extent of damage to the heart muscle as a result of myocardial infarction. Initially, it is aimed at stabilizing the heart and blood pressure, but over time its nature becomes pathological. As a result, remodeling accelerates, it acquires a more global scale, and the development of CHF.

The second factor is the activation of the sympathetic nervous system. It entails an increase in LV tension, which results in an increase in the oxygen demand of the heart muscle.

Pathophysiology of myocardial remodeling after MI

Due to the fact that modern medicine made it possible to reduce the mortality threshold for myocardial infarction, a large number of people after an attack have the opportunity to return to almost full life after completing a rehabilitation course. But concentric remodeling of the left ventricle in this case only worsens, increasing the risk of complications: CHF, circulatory disorders. Thus, after suffering an attack, it is important to follow all the doctor’s recommendations regarding rehabilitation and prevention of its recurrence.

After MI, the structural change in the myocardium manifests itself as follows. The shape of the left ventricle changes. Previously it was ellipsoidal, but now it is becoming closer to a spherical shape. Thinning of the myocardium and its stretching are observed. The area of dead cardiac muscle may increase, even if there has been no repeated ischemic necrosis. Many more pathological disorders occur that lead to complications and increase the likelihood of their occurrence.

As we see, there is a strong and unbroken chain, during which a structural change in the heart muscle develops. It all starts with a systematically increasing blood pressure, development of hypertension. In response to constantly high blood pressure in the vessels, the heart tries to adapt to such conditions. The thickness of the ventricular wall increases. This happens in proportion to the increase in blood pressure. This increases the mass of the heart muscle, and other changes characteristic of this condition begin.

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Cardiac remodeling

The term “remodeling” entered the medical lexicon in the early 80s of the last century. Initially, it was attributed to the cardiovascular system - “cardiac remodeling”, “vascular remodeling”, and then to other structural and functional formations.

Intensive study of the process of cardiac remodeling (mainly the left ventricle) began after the SAVE studies (International multicenter randomized double-blind study), which established that inhibition of the process of post-infarction remodeling of the left ventricle is accompanied by a significant improvement in the course and prognosis of myocardial infarction

What is cardiac remodeling

According to the agreement adopted at the International Forum on Cardiac Remodeling in 2000 (USA), the concept of “cardiac remodeling” includes changes at the genetic, molecular and cellular levels that are manifested by changes in the structure, size, shape (architecture) and function of the heart that arise in response to to long-term damaging effects. The main forms of pathology that initiate cardiac remodeling include coronary heart disease, hypertension, hypertrophic cardiomyopathies and other primary heart diseases.

One of the main triggers that triggers the remodeling process is the death of cardiomyocytes - their necrosis (passive violent form of death), necroptosis (regulated necrosis), apoptosis (active programmed death), autophagy (death due to lieosome autocatalysis of organelles, proteins, lipids and other cell components ). Necrosis of cardiomyocytes is accompanied by the development of an aseptic inflammatory reaction, in which the transcription factor kappa B (NF-kB) is activated, which determines the synthesis of proinflammatory cytokines that play a key role in the pathogenesis of many processes, including cardiac remodeling.

Previously, endothelial cells and mast cells were considered the main producers of proinflammatory cytokines in damaged myocardium. It was then revealed that, in addition to these cells, fibroblasts make a significant contribution to the remodeling process. Relatively recently, it was established that these cells, in addition to participating in the proliferation of connective tissue, are capable of activating inflammasomes. Inflammasomes (from Latin inflammatio - inflammation) are cytoplasmic supramolecular formations formed in macrophages and other cells that can indirectly activate the interleukin-1 family (IL-la, IL-1J3, IL-IRa) through stimulation of caspase-1. In turn, stimulation of cardiac fibroblasts can be caused by reactive oxygen species - constant companions of ischemia, as well as pro-inflammatory cytokines. In addition, IL-la, TNF-a, oncostatin-M and other cytokines, along with angiotensin II, endothelin 1 and catecholamines, activate the production of matrix metalloproteases by fibroblasts, which are members of a family of proteolytic enzymes involved in many biological processes.

There is reason to believe that matrix metalloproteases 3 and 9 are involved in the process of cardiac remodeling. The activity of these enzymes is controlled to a large extent by tissue inhibitors of matrix metalloproteinases - TIMPs (Tissue inhibitors of matrix metalloproteinases), which form high-affinity complexes with metalloproteases, blocking their active domain, and thus preventing collagen degradation. It has now been established that the predominance of active matrix metalloproteases leads to dilatation of the left ventricle, and the active production of TIMPs can contribute to its fibrosis.

Thus, a large spectrum of cardiac biologically active molecules is involved in the mechanisms of cardiac remodeling.

The geometry of the left ventricle changes throughout the cardiac cycle from a predominantly ellipsoidal shape in systole to a more spherical shape in diastole. Such changes are natural under conditions of normal pumping function of the ventricle. Relative elongation of the left ventricle during systole is the mechanism by which the ventricle ejects a larger volume of blood with less myocardial tension. The reverse process - spherification of the left ventricle during early diastole is accompanied by an increase in ventricular volume and serves as an addition to early diastolic filling, in which only passive elongation of cardiomyocytes is involved.

Two main types of cardiac remodeling

There are two main types of cardiac remodeling: eccentric and concentric (Fig. 3.1). The criterion for their differentiation is the form of ventricular hypertrophy, which represents the initial stage of remodeling. The type of remodeling is determined by the conditions in which it is formed. For example, volume overload of the left ventricle with aortic valve insufficiency causes an increase in the length of cardiomyocytes, a decrease in wall thickness, an increase in volume and the formation of an eccentric type of left ventricular hypertrophy. In contrast to this type of remodeling, pressure overload of the left ventricle (for example, in conditions of aortic stenosis, systemic arterial hypertension) leads to an increase in the number of sarcomeres and the volume of cardiomyocytes, wall thickness and the formation of a concentric type of left ventricular hypertrophy.

In the course of studying the problem of remodeling, along with the concept of “structural remodeling” (changes in geometry, architectonics, volume, wall thickness, etc.), the concept of “functional remodeling” appeared. In relation to the pumping function of the heart, functional remodeling is associated with the concepts of “systolic and diastolic ventricular dysfunction”. Functional remodeling of the left ventricle occurs and develops independently of the process of its structural and geometric restructuring. Currently, the concept of “cardiac remodeling” applies to all forms of chronic heart failure, regardless of its origin, i.e., etiological factors.

The formation and dynamics of the process of structural remodeling of the heart are influenced by hemodynamic, neurogenic, hormonal and other factors, which are currently being actively studied.

During the formation of concentric hypertrophy, an increase in systolic pressure stimulates an increase in the synthesis of sarcomeres in their parallel orientation, which causes an increase in myocardial mass and thickening of the walls of the ventricle, but does not change the diameter of its cavity.

During the formation of eccentric hypertrophy, an increase in diastolic pressure causes the synthesis of sarcomeres located in succession. The eccentric form is characterized by an increase in the mass of the ventricle and the size of its cavity, but the average thickness of the walls remains unchanged.

Left ventricular hypertrophy naturally develops with arterial hypertension and helps maintain tension in its wall. Moreover, the development of hypertrophy depends not so much on the level of blood pressure (hemodynamic overload), but on the activity of the renin-angiotensin-aldosterone system. Initially, left ventricular hypertrophy develops in a concentric manner (adding sarcomeres inside the cardiomyocyte). Angiotensin II stimulates the growth of muscle fibers, and aldosterone changes the intracellular matrix with the formation of diastolic dysfunction. Diastolic dysfunction, which occurs already at the initial stage of left ventricular remodeling, is considered as a marker of myocardial fibrosis.

Myocardial relaxation

Relaxation of the myocardium is a very energy-demanding process, and therefore, with ventricular hypertrophy, it suffers first. The left atrium experiences the greatest hemodynamic overload during diastolic dysfunction. Dilatation of the left atrium causes mitral regurgitation, which determines the transition of concentric left ventricular hypertrophy to its eccentric form. To the systolic overload of high blood pressure, diastolic volume overload is added, i.e. the left ventricle is exposed to chronically elevated end-diastolic pressure. Left ventricular dilatation is complicated by systolic dysfunction, which increases the risk of death by approximately 50%.

Histological examination of the left ventricular wall revealed an increase in the length of individual sarcomeres and an increased number of sequentially oriented sarcomeres, which apparently lead to an increase in the length of myocytes.

During the process of hypertrophy, relative coronary insufficiency may develop due to a lag in vascular growth (angiogenesis) from the increase in myocardial mass. Due to circulatory hypoxia and relative insufficiency of mitochondria, the number of irreversibly damaged cardiomyocytes increases, which leads to a decrease in myocardial contractility. Under such conditions, the isovolumic systolic pressure curve continues to shift to the right, and the diastolic pressure curve may shift further downward (due to fibrosis), which determines a significant decrease in stroke volume and the onset of end-stage heart failure in the patient.

Cardiomyocytes

The main participants in the process of cardiac remodeling are cardiomyocytes, as well as fibroblasts and coronary vessels, and the structural and functional unit of the heart muscle tissue- contractile (typical) cardiomyocyte. These cells form functional fibers by joining with each other. The places of contact of neighboring cardiomyocytes are called intercalated discs, which indicate the cellular structure of the myocardium.

Cardiomyocytes are fully mature cells that have reached terminal differentiation and have lost the ability to divide in the early postnatal period. In this regard, an increase in myocardial mass can be achieved not by the formation of new cardiomyocytes and functional fibers, but only by the hypertrophy of pre-existing cardiomyocytes. In response to an increasing load, cardiomyocytes do not multiply, but hypertrophy - the synthesis of protein and sarcoplasmic contractile units increases in them. Inducers of hypertrophy are norepinephrine, angiotensin I, endothelium, local peptides that stimulate cell growth (insulin-like growth factor I, cardiotropin I, fibroblast growth factor, etc.), as well as physical factors that cause stretching of cardiomyocytes and increased tension in the wall of the heart cavities. By interacting with specific receptors on the membrane of cardiomyocytes, biologically active inducers trigger a cascade of intracellular signaling chains.

As a result, early response genes (so-called proto-oncogenes) are activated, responsible for the synthesis of small regulatory proteins that control the transcription of other genes. This is followed by re-expression of the fetal gene program, which, as experimental studies have shown, induces the synthesis of contractile proteins and non-contractile proteins, such as the p2 enzyme

Na+/K+-ATO-a3a, which is usually detected only in embryos, i.e. in a period characterized by total proliferation of cells in the body. Unlike other cells, cardiomyocytes arrested in the Gl phase of the cell cycle are able to respond to molecular stimuli only with hypertrophy, but not proliferation.

During the remodeling process, the proliferation of fibroblasts is activated, which leads to fibrosis - the proliferation of connective tissue with the appearance of scar changes in the heart. The increasing “stiffness” of the myocardium determines the occurrence of diastolic dysfunction, manifested by a decrease in the pumping function of the heart.

Factors regulating the remodeling process

Sympathetic nervous system

Circulatory hypoxia that develops in heart failure causes activation of the sympathetic nervous system, which is adaptive in nature and aimed at maintaining cardiac output (due to the positive chrono- and inotropic effects of catecholamines) and blood pressure. However, such prolongation is relatively imperfect, since they use only pre-prepared compensatory mechanisms that are quite limited in their capabilities; adaptation can give it a pathogenic character due to its ability to cause the progression of remodeling and, thus, aggravate the severity of heart failure.

Peripheral arterial vasoconstriction, most pronounced in the kidneys, visceral organs, skin and skeletal muscles, is aimed mainly at centralizing blood circulation, i.e., maintaining blood flow to the heart and brain.

Vasoconstriction leads to increased peripheral resistance and therefore cardiac afterload. At the same time, it is also possible to increase the preload, since when the sympathetic nervous system is activated, the tone of the venous vessels increases, which determines the increase in blood flow to the heart. In addition, the unfavorable consequences of prolonged activation of the sympathetic nervous system are due to an increase in the myocardial need for oxygen and energy substrates, as well as an increase in the processes of lipid peroxidation (the final product of the breakdown of catecholamines - xanthine is a source of reactive oxygen species) and the development of the proarrhythmogenic effect of catecholamines.

At later stages of remodeling, the activated sympathetic nervous system influences the processes of reexpression of fetal genes and hypertrophy of cardiomyocytes. A number of studies have documented that increased level circulating norepinephrine correlates with an unfavorable long-term prognosis of heart failure in patients with left ventricular dysfunction, and the use of (3-blockers reduces mortality in this form of pathology not only due to their antiarrhythmic effect, but also their ability to inhibit the process of left ventricular remodeling. For example, it was found that ( The 3-blocker metoprolol can cause volume reduction and regression of left ventricular mass, thereby improving its geometry.

Renin-angiotensin-aldosterone system

A few hours after the onset of acute heart failure, the juxtaglomerular apparatus (JGA) in the kidneys increases the synthesis of renin in response to a decrease in glomerular perfusion, more precisely to a decrease in pulse pressure in v. afferens, which is monitored by the mechanoreceptors of the JGA, and the activation of the sympathetic-adrenal system (the JGA contains |32-adrenergic receptors).

This turns on the renin-angiotensin-aldosterone system (RAAS). Modern scientific data indicate the parallel functioning of the humoral (circulating) and tissue (local) RAAS. Local RAAS function in target organs, primarily in the heart, kidneys, brain, blood vessels, and peripheral muscles. Renin catalyzes the degradation of angiotensinogen (related to α2-globulins, synthesized in the liver) into the hormone angiotensin I, which is then, under the influence of angiotensin-converting enzyme (ACE), located in the lungs, kidneys and plasma, converted into angiotensin II.

The ACE gene is mapped to chromosome 17q23. There are two forms of ACE: membrane-bound (kininase-2), which is found in macrophages, T-lymphocytes, fibroblasts; epithelial cells of the kidneys, intestines, placenta, reproductive organs, and humoral (kininase-1), which is formed in various tissues and organs, mainly in the endothelium blood vessels lungs.

It has now been established that, along with the ACE-dependent mechanism for converting angiotensin I to angiotensin II, there are alternative pathways involving chymases, cathepsin G, tonin and other serine proteases. Chymases, or chymotrypsin-like proteases, are glycoproteins with a molecular weight of approximately and have high specificity for angiotensin.

In different organs and tissues, either ACE-dependent or alternative pathways of angiotensin I formation predominate. Thus, cardiac serine protease was found in human myocardial tissue. It has been proven that the largest amount of this enzyme is contained in the myocardium of the left ventricle, where the chymase pathway of transformation to angiotensin I accounts for more than 80%. Chemase-dependent formation of angiotensin II also prevails in the myocardial interstitium, adventitia and vascular media, while ACE-dependent formation occurs in the blood plasma.

It is believed that activation of alternative pathways for the formation of angiotensin II plays an important role in the processes of cardiovascular remodeling. AT II is a powerful vasoconstrictor that increases blood pressure and stimulates the secretion of aldosterone. The biological effects of angiotensin II are carried out through a number of receptors: type I (there are subtypes A and B) and type II. Activation of type 1 receptors causes vasoconstriction and proliferation of smooth muscle cells, as well as stimulation of the process of remodeling of target organs.

At the cellular level, AT II acts as an inducer of the synthesis of transforming growth factor-β (TGF-β), which in turn stimulates the chemotaxis of macrophages and fibroblasts, inducing inflammation and activating myofibroblasts. The latter begin to synthesize components of the extracellular matrix in excess quantities, which leads to an acceleration of fibrotic restructuring of the cardiovascular system. Structural changes in the walls of coronary vessels when exposed to AT II are caused by the proliferation of smooth muscle cells and interstitial fibroblasts, as well as an increase in the synthesis of components of the extracellular connective tissue matrix.

From AT II, its metabolite ATSH is formed, which has a weak pressor property, but significantly stimulates the secretion of aldosterone by the adrenal cortex. Aldosterone is involved in the retention of sodium ions in the body, the development of secondary hyperaldosteronism, and is a factor in the stabilization of hypertension. Aldosterone has a significant profibrogenic effect, participates in the processes of remodeling of the left ventricle of the heart and the vascular wall, and promotes the development of fibrosis and functional failure in target organs.

Antidiuretic hormone

Antidiuretic hormone (ADH) is a peptide consisting of 9 amino acid residues. In most mammals, including humans, arginine is located at position 8; this form of ADH is designated arginine vasopressin (AVP). Through VlA receptors, vasopressin is able to increase vascular tone. At physiological concentrations of the hormone, its pressor vascular effect is small.

In high concentrations, ADH causes spasm of arterioles, which leads to an increase in blood pressure and, accordingly, total peripheral vascular resistance, hence the name of the hormone - vasopressin. In addition, ADH maintains the facultative reabsorption of water in the kidneys at the proper level, while reducing diuresis (antidiuretic effect). ADH is formed in the supraoptic and paraventricular nuclei of the hypothalamus, deposited in the posterior lobe of the pituitary gland, from where it is released into the blood when the osmoreceptors of the hypothalamus are excited.

When plasma osmotic pressure increases, ADH enters the blood from the neurohypophysis. By promoting the reabsorption of water in the renal tubules, ADH thereby supports venous return to the heart, i.e. its preload This effect of ADH may have a pathogenic effect on the heart in the long term, especially in the setting of heart failure.

Other factors regulating the remodeling process include natriuretic peptides, endothelin 1, pro-inflammatory cytokines, and nitric oxide.

Natriuretic peptides

There are three main representatives of the family of natriuretic peptides - atrial, medullary and C-terminal atrial. With a decrease in cardiac output in patients with left ventricular dysfunction, as well as in chronic heart failure, the synthesis of natriuretic peptides increases. Atrial natriuretic peptide is released in response to increases in atrial volume and pressure. Brain natriuretic peptide (type B) is formed in the brain when its ventricles stretch. Peripheral vasodilation and natriuresis caused by atrial and brain natriuretic peptides counteract the effects of activation of the sympathetic nervous system and the RAAS, i.e. systemic and renal vasoconstriction, sodium and water retention. In addition to their early beneficial effects on hemodynamics, fluid balance and diuresis, some have reported experimental research, the long-term effect of natriuretic peptides may be the suppression of cardiomyocyte hypertrophy and. hence, creating favorable conditions for “beneficial” remodeling.

Endothelium

The producers of this peptide hormone, represented by three isoforms, are: The endothelium is one of the strongest vasoconstrictors; it is much more active than angiotensin II. An increase in the level of endothelin in the blood can cause the occurrence and worsening of coronary heart disease. A number of studies have documented favorable results from endothelin receptor blockade in patients with heart failure. It is no coincidence that endothelium is a marker of coronary atherosclerosis and endothelial dysfunction of coronary vessels.

Experiments have established that correction of endothelial dysfunction leads to a decrease in the mass of the left ventricular myocardium, improvement of coronary hemodynamics, an increase in the force of myocardial contraction, as well as suppression of the synthesis extracellular matrix fibroblasts, which reduces the severity of perivascular fibrosis of the coronary vessels and prevents the development of interstitial remodeling of the heart.

The results of the SOLVD study (from English, Studies of Left Nfentricular Dysfunction) confirmed that in patients with progressive heart failure, the level of pro-inflammatory cytokines (TNF-a, IL-1, IL-6, etc.) increases, and abroad according to the criterion of preferential " drug therapy» XXI century called the “age of itokin therapy.” In the medical world, work on studying the remodeling process continues with the prospect of using their results to improve the effectiveness of pathogenetic therapy for patients with cardiovascular pathology.

Remodeling assessment

It has been established that remodeling occurs at all levels of the structural and functional organization of the heart and is expressed in changes in its size, shape and functionality. Pathophysiological analysis and clinical assessment remodeling of the left ventricle is carried out on the basis of measuring its linear dimensions and calculating a number of volumetric indicators: indices of relative wall thickness, sphericity, myocardial tension, and impaired ventricular contractility.

Currently, the most commonly used methods for determining the geometry and functionality of the heart are two-dimensional echocardiography, magnetic resonance imaging and radionuclide ventriculography. A necessary condition for dynamic control of the remodeling process is the use of the same method in successive observations of the condition of the left ventricle of each patient examined. The geometry (architecture) of the ventricle plays a central role in its normal function and in the process of remodeling during various diseases cardiovascular system.

When the pumping function of the ventricles of the heart deteriorates, an increase in preload is aimed at maintaining cardiac output. Prolonged overload initiates remodeling of the left ventricle: it becomes more elliptoid, expands and hypertrophies. While initially compensatory, these changes, sometimes called myocardial stress, eventually lead to increased diastolic stiffness and ventricular wall tension, which impairs the pumping function of the heart, especially during exercise.

Increased myocardial tension increases the need for macroergs and, with a certain degree of developing energy deficiency, activates apoptosis of myocardial cells. So, the loss of the normal ellipsoidal shape of the ventricle is an early morphological sign of heart damage, which can become a trigger for the development of chronic heart failure.

Cardiac remodeling precedes and accompanies the clinical manifestations of heart failure, since it can aggravate systolic and diastolic dysfunction of the ventricle. At a certain stage of development, remodeled heart syndrome (its other rare name is “structural cardiomyopathy” syndrome) overshadows the importance of the etiological factor, i.e. causes of heart damage leading to the development of heart failure.

The syndrome of “structural cardiomyopathy” comes to the fore - a pathogenetic factor of heart failure that determines the mechanisms of its development, the prognosis of this form of pathology and the quality of life of patients. Studying and understanding the adaptive and pathogenetic role of cardiac remodeling in each specific case is necessary to avoid unnecessary therapeutic interventions, i.e. to optimize the treatment of patients with cardiovascular pathology.

Concept and reasons

A fairly large number of pathological conditions and diseases lead to the formation of left ventricular (LV) myocardial hypertrophy. In addition to pathological conditions, prolonged physical activity when playing sports or performing heavy physical labor leads to the formation of so-called working hypertrophy. What else can cause the formation of this complication? We list the main factors:

arterial hypertension (AH),
ischemic disease heart (myocardial infarction, arrhythmias, conduction disturbances, etc.),
congenital malformations (CHD): aortic stenosis, underdevelopment pulmonary artery, underdevelopment of the left ventricle, truncus arteriosus, ventricular septal defect (VSD),
acquired (valvular) heart defects: mitral valve insufficiency, aortic valve stenosis,
diabetes mellitus,
hypertrophic cardiomyopathy,
hyperthyroidism (increased thyroid function),
pheochromocytoma (tumor of the adrenal medulla),
overweight, obesity,
muscular dystrophy,
smoking, alcohol abuse,
chronic emotional stress.

Risk factors for the development of LVH are the following:

high blood pressure (BP),
male gender,
patient age over fifty years,
family history of cardiovascular diseases (CVD) (diseases of the circulatory system in blood relatives),
excess body weight,
disturbance of cholesterol metabolism.

2 Formation of “perestroika”

You can find the definition of hypertrophy as remodeling. These terms are synonymous with each other, although it is correct to say that hypertrophy is a particular remodeling. The second concept is broader. Remodeling means the process of changing an existing structure, rebuilding it, or adding something to it. Myocardial remodeling is a change in its geometric structure under the influence of a specific factor. Moreover, not only the structure is being rebuilt, but functional restructuring is also taking place.

The purpose of remodeling is to adapt the left ventricle to the established hemodynamic conditions, which often become pathological. With the constant influence of increased pressure on the LV myocardium, there is a response increase in the number of sarcomeres and the thickness of the heart cell (cardiomyocytes). As a result, the LV wall thickens, which occurs during concentric remodeling of the left ventricular myocardium. In the case of eccentric remodeling, the ventricle experiences volume overload. In this case, the cardiomyocytes are stretched, and the wall of the heart chamber decreases.

The following components are involved in the development of left ventricular (LV) myocardial remodeling:

Myocardial cells are cardiomyocytes. Cardiomyoitis are highly differentiated structures. This means that these cells have lost the ability to divide. Therefore, in response to increasing physical activity (PE), the concentration of biologically active substances in the body increases. active substances: norepinephrine, angiotensin, endothelin, etc. In response to this, the number of sarcoplasmic contractile units in cardiomyocytes increases. Energy exchange processes begin to occur more intensively in the cell.
Fibroblasts are components of connective tissue. While the myocardium thickens and hypertrophies, the vessels do not have time to provide such muscle mass oxygen and nutrients. Oxygen requirements increase, but the vascular network remains at the same level. The LV myocardium enters a state of ischemia - oxygen starvation. In response to this, connective tissue components—fibroblasts—are activated. “Growing” with connective tissue, the myocardium loses its elasticity and becomes rigid. This circumstance entails a decrease in diastolic function of the left ventricle. In simple terms speaking, (LJ) appears.
Collagen. In various diseases, in particular myocardial infarction, collagen, which ensures the relationship between cardiomyocytes, begins to weaken and disintegrate. The process of collagen formation does not keep pace with its breakdown in the first weeks of a heart attack. Then these processes are leveled out, and in place of weakened cardiomyocytes that have undergone necrosis during a heart attack, a connective tissue scar is formed.

3 Types of hypertrophy

Concentric. Concentric hypertrophy of the left ventricular myocardium (concentric hypertrophy of the left ventricular myocardium) is characterized by uniform thickening of its walls. Such uniform thickening of the wall can lead to a decrease in the lumen of the chamber. Hence the second name for this type of hypertrophy is symmetrical. Most often, concentric LV hypertrophy develops due to pressure overload. Some pathological conditions and diseases, such as aortic stenosis and arterial hypertension (AH), lead to an increase in vascular resistance in the aorta. The left ventricle has to work harder to push all the blood into the aorta. This is where concentric LV hypertrophy develops.

Eccentric. Unlike the previous type, eccentric hypertrophy of the left ventricle is formed if the LV is overloaded with volume. Insufficiency of the mitral or aortic valve, as well as some other reasons, may lead to the fact that blood from the left ventricle is not completely expelled into the aorta. There remains some amount of it. The walls of the left ventricle begin to stretch, and its shape resembles an inflated balloon. The second name for this type of remodeling is asymmetric. With eccentric hypertrophy of the left ventricle, the thickness of its wall may not change, but the lumen, on the contrary, expands. Under such conditions, the pumping function of the left ventricle decreases.

The mixed type of hypertrophy most often occurs when playing sports. Individuals involved in rowing, speed skating or cycling may have this type of LV myocardial hypertrophy.

Separately, the authors highlight concentric remodeling of the LV myocardium. Its difference from concentric LVH is the unchanged mass of the LV myocardium and the normal thickness of its wall. With this type, there is a decrease in end-diastolic size (EDD) and LV volume.

4 Diagnosis and treatment

The main methods for diagnosing LVH are echocardiography (ultrasound of the heart), magnetic resonance imaging and other methods. However, at the very beginning, the entire diagnostic search is aimed at establishing the underlying disease. The first complaint of a patient with LVH may be shortness of breath, which he experiences when performing intense physical activity. As the process progresses, this symptom may appear during lower-intensity exercise, and then at rest. The last point indicates the development of heart failure (HF) in the patient.

In addition to shortness of breath, patients present complaints related to the underlying disease. May disturb painful sensations or discomfort in the heart area or behind the sternum, which are associated with stress or stress. Palpitations, dizziness, headaches, and fainting may also be present. The list of symptoms can be supplemented by sensations of interruptions in the functioning of the heart, increased fatigue, weakness and other signs of the underlying disease.

The leading instrumental method for left ventricular myocardial hypertrophy is echocardiography (EchoCG or ultrasound of the heart). Despite the fact that such a simple and accessible method of instrumental diagnostics as electrocardiography (ECG) also has its own diagnostic criteria with regard to LVH, however, cardiac ultrasound is more than 5 times superior to ECG in its diagnostic sensitivity. The main echocardiographic indicator that is taken into account when diagnosing LVH is the left ventricular myocardial mass (LVMM), or rather its index.

To distinguish between concentric and eccentric remodeling, an echocardiographic indicator such as relative wall thickness (RWT) is also used. Depending on the state of these two indicators - LVMI and TVR, the type of LV myocardial remodeling is determined:

The normal geometric structure of the left ventricle is set if the TPV is less than 0.45; and LVMI is within normal limits.
Concentric remodeling has the following echocardiographic criteria: TVR equal to or less than 0.45; LVMI remains normal.
Eccentric remodeling is characterized by TVR less than 0.45 with LVMI greater than normal.

Concentric LV hypertrophy is considered more unfavorable prognostically, since it is this type of myocardial remodeling that entails diastolic dysfunction and electrical instability of the myocardium, thereby increasing the risk of sudden cardiac death among such patients. The severity of diastolic dysfunction, regardless of the type of hypertrophy, is influenced by the relative wall thickness. The greater the degree of its increase, the more unfavorable the prognosis. But the increase in end-diastolic size correlates with the severity of LV systolic dysfunction.

Untreated LVH can be complicated by conditions such as arrhythmias, coronary heart disease (CHD), heart failure, ventricular fibrillation, and sudden cardiac death.
Treatment of LV hypertrophy includes treatment of the underlying disease that caused this complication. It includes non-drug measures - eliminating risk factors, as well as taking medicines, supporting heart function and preventing the progression of this complication. Treatment of left ventricular hypertrophy (LVH) must be carried out without fail, even if the patient feels satisfactory.

If drug therapy is ineffective in patients with impaired LV function, it is indicated surgical treatment. Depending on which structural component is damaged, the following surgical interventions are offered:

Stenting of coronary arteries, angioplasty. This procedure is prescribed in case of development.
Heart valve replacement. Such an operation may be indicated if valve defects are the cause of LVH.
Dissection of adhesions on the valves (commissurotomy). One of the indications for such surgical intervention is aortic stenosis. Dissection of the commissures reduces the resistance that the ventricular myocardium encounters when expelling blood into the aorta.

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Myocardial remodeling is a term used by doctors to refer to structural changes in the heart muscle after a person has suffered illnesses, such as a heart attack. Moreover, the features of the manifestation of violations directly depend on the cause that provoked their appearance.

For example, if we talk about remodeling that arose against the background of a systematic increase in blood pressure, it will manifest itself as follows:

increase in the number of sarcomeres;
increased thickness of cardiomyocytes;
thickening of the walls;
formation of concentric remodeling of the LV.

The term eccentric remodeling is also used in practice. It denotes the elongation of cardiomyocytes, a decrease in wall thickness. The condition is caused by volume overload of the heart muscle. As for the functional remodeling of the LV, this only implies a violation of its contractility. The geometry and dimensions of the ventricle do not change. If they are modified, we will talk about a structural variant of the pathology.

Concentric shape

Concentric remodeling of the left ventricular myocardium is a fairly common finding that applies to patients with hypertension. The process begins with LV hypertrophy, which is manifested by an increase in the thickness of its wall. Changes in the septum are also noted. The interior space has not been changed.

It should be noted that the cause of LVH can be not only a persistent increase in blood pressure, but also other factors, such as:

intense physical activity to which a person constantly subjects his body;
sedentary lifestyle, often found among office workers;
smoking, regardless of the number of cigarettes smoked;
systematic alcohol abuse.

Thus, we can conclude that in order to prevent the start of the myocardial remodeling process, it is necessary to diagnose hypertension or LVH as early as possible and treat them effective treatment. To do this, you need to study the symptoms that may indicate the presence of such diseases, these are:

systematic increase in blood pressure;
frequent headaches and dizziness;
periodic tremors in the limbs;
heart rhythm disturbances;
difficulty breathing, shortness of breath;
decreased performance;
pain in the heart area.

If such signs occur, you should contact medical care, undergo a full examination that allows you to get full information about your own health.

Important! Electrocardiography remains the main diagnostic method. It allows you to determine myocardial remodeling in the elevated segmentSTand a reduced or completely absent toothR. Similar indicators indicate the concentric type pathological condition, may indicate a heart attack, which aggravates the situation.

Remodeling after MI

The main factor contributing to the development of remodeling is neurohormonal activation. It is observed after a person has suffered a myocardial infarction. The activity of neurohormones is directly comparable to the extent of damage to the heart muscle. Initially, it helps normalize blood pressure and heart activity. But after some time, the activity of hormones becomes pathological. As a result, the remodeling process accelerates, acquiring greater proportions, and chronic heart failure develops, which poses a danger to human health and life.

The next factor is the activation of the sympathetic nervous system. It contributes to an increase in the tension of the left ventricle, as a result of which the myocardial need for oxygen increases.

Pathophysiology of the process

If we talk about the pathophysiology of myocardial remodeling, then changes after a heart attack manifest themselves as follows:

change in the shape of the left ventricle. If before the attack it was ellipsoidal, now it has become closer to spherical;
the heart muscle is thinned. Its stretching is observed;
an increase in the necrotic part of the myocardium. It can happen even in the absence of a recurrent attack.

It should be noted that thanks to the capabilities of modern medicine, the survival rate after MI has become much higher. But the remodeling process has not yet been prevented, because it is a natural consequence of an unbroken chain of natural stages. The only thing that depends on the person himself is the ability to minimize the consequences of a heart attack. To do this, it is enough to follow the recommendations of the attending physician regarding the rehabilitation period, and also do not forget about the rules for preventing a recurrent attack.

Conclusion

Let's summarize. In most cases, the remodeling process is triggered by a systematic increase in blood pressure. As a response to constantly increased pressure in the vessels - thickening of the wall of the left ventricle. Moreover, the higher the blood pressure, the greater the thickness. As a result of this process, the mass of the myocardium increases, which triggers a chain of subsequent pathological changes.

The result is a disruption of the heart as a whole, a deterioration in a person’s well-being, and the appearance of numerous symptoms that cause significant discomfort.

The same process is also characteristic of the remodeling of the heart muscle, which develops against the background of myocardial infarction, leading to complications in the form of chronic heart failure.

That is why, in order to avoid serious consequences, you need to carefully monitor your own health. As soon as signs are noticed cardiovascular diseases, it is necessary to consult a doctor as soon as possible, undergo diagnostics and a course of effective treatment.

Modern cardiology is increasingly faced with the fact that heart disease is caused not by congenital pathologies, but by an incorrect lifestyle. Moreover, many patients were confident that their actions would achieve health and longevity, because they led a healthy lifestyle and were fond of sports training. However, the result was the opposite. What causes serious heart problems in people who regularly exercise?

What is cardiac remodeling?

Causes

The initial stage of cardiac muscle remodeling is an increase in the mass of the muscle layer of the left ventricle. Changes in the myocardium can occur in one of two directions:

Due to an increase in the size of cardiomyocytes, a thickening of the septum between the ventricles occurs.
Due to the increase in the width and length of cardiomyocytes, thinning of the walls of the heart and an increase in the volume of its chambers develop.

These processes are often triggered by people who incorrectly distribute physical activity. Thus, thickening of the muscles of this organ occurs in those who train too intensely, especially in team sports and those that require the use of force. In this case, the cells’ need for oxygen sharply increases, so the heart is forced to accelerate oxygen-rich blood into the arteries, overcoming increased resistance, which does not allow the muscle to fully relax in the diastole stage.

Compensating for these factors, the heart muscle pumps up volume. Thus, pressure loading causes concentric remodeling of the left ventricular myocardium.

Participation in dynamic sports that develop endurance can lead to the development of eccentric remodeling of the heart muscle, which consists of an increase in the length and width of cardiomyocytes. This process is a compensatory measure of the heart muscle to return the increased volume of venous blood and is caused by the need to move its sharply increased volume into the arteries.

In addition to athletes and people with heavy physical labor, the risk group includes:

People who, leading a sedentary lifestyle, suddenly began to actively engage in sports.
Obese people.
Patients diagnosed with aortic stenosis.
Hypertensive patients.
Patients with heart disease.

How to stop the disease?

The definition of “myocardial remodeling” began to be used back in the late 70s. It helped to characterize structural changes in the human heart, as well as disturbances in its geometry after a myocardial infarction. Heart remodeling occurs under the influence of negative factors - diseases, which lead the organ to the development of physiological and anatomical disorders.

If we talk about remodeling of the left ventricular myocardium, then the features of its manifestation are directly related to the factors under which it was formed. For example, when overloaded with high blood pressure, which can be observed with hypertension or, the following disorders are observed:

increase in the number of sarcomeres;
increased thickness of cardiomyocytes;
increase in wall thickness;
development of concentric remodeling of the LV myocardium.

The concept of eccentric remodeling, which is caused by volume overload of the myocardium, is also known. It is accompanied by elongation of cardiomyocytes and a decrease in wall thickness.

Concentric remodeling of the left ventricular myocardium

Myocardial hypertrophy - remodeling

Interesting to know! Hypertrophy is increasingly being diagnosed in young people, who suffer from arterial hypertension no less often than older people. Therefore, the issue of timely diagnosis and prevention of the development of consequences is very acute.

Despite the fact that most often LVH develops in people against the background of hypertension, it can also appear under the influence of constant physical activity, which negatively affects the functioning of the heart. Athletes, loaders, etc. are also at increased risk. The stress on the heart, which is typical for people with a predominantly sedentary lifestyle, as well as for smokers and alcohol drinkers, is also dangerous.

constantly elevated blood pressure, its systematic jumps upward;
headaches;
disturbances in heart rhythms;
deterioration in general health,
pain in the heart.

As a result, there is a high risk of complications, the most serious of which is chronic heart failure. It significantly increases the likelihood of death.

What factors influence the remodeling process

The second factor is the activation of the sympathetic nervous system. It entails an increase in LV tension, which results in an increase in the oxygen demand of the heart muscle.

Pathophysiology of myocardial remodeling after MI

Due to the fact that modern medicine has reduced the mortality threshold for MI, a large number of people, after suffering an attack, have the opportunity to return to an almost full life by undergoing a rehabilitation course. But concentric remodeling of the left ventricle in this case only worsens, increasing the risk of complications: CHF, circulatory disorders. Thus, after suffering an attack, it is important to follow all the doctor’s recommendations regarding rehabilitation and prevention of its recurrence.

As we see, there is a strong and unbroken chain, during which a structural change in the heart muscle develops. It all starts with systematically increasing blood pressure and the development of hypertension. In response to constantly increased pressure in the blood vessels, the heart tries to adapt to such conditions. The thickness of the ventricular wall increases. This happens in proportion to the increase in blood pressure. This increases the mass of the heart muscle, and other changes characteristic of this condition begin.