Modern problems of science and education. Myocardial remodeling Concentric myocardial remodeling LV treatment

The term "heart remodeling" was proposed by N. Sharp in the late 70s of the last century to refer to structural and geometric changes after acute myocardial infarction (AMI). Then it received a broader interpretation. Ischemic remodeling is a dynamic, reversible process of changing the thickness of the myocardium, the size and shape of the chambers of the heart, dysfunction of the left ventricle (LV).

Left ventricular hypertrophy - the initial stage of remodeling in arterial hypertension (AH), depends not so much on the level of blood pressure - hemodynamic overload, but on the activity of the RAAS. The risk of developing chronic heart failure (CHF) increases 15 times. LVH develops according to the concentric type (adding sarcomeres inside the cardiomyocyte). A11 stimulates the growth of muscle fibers, aldosterone changes the intracellular matrix with the formation of diastolic dysfunction - DD. DD is an early stage of LV remodeling, a marker of myocardial fibrosis.

Relaxation is the most energy-dependent process; LVH suffers first of all. The LA experiences the greatest hemodynamic overload in DD. Dilatation of the LA causes mitral regurgitation. An important stage is the transition from concentric LVH to eccentric. To the systolic pressure overload is added the diastolic volume overload. LV dilatation is accompanied by systolic dysfunction. And this increases mortality by 50%. CHF is moving to the finishing stage. ACE inhibitors cause regression of concentric hypertrophy, reducing the thickness of the walls of the left ventricle; normalize diastole. The volume of muscle fibers and myocardial fibrosis decrease.

After damage and death of part of the cardiomyocytes, both in the normal and damaged zone, the process of sclerosis takes place. Myocytes hypertrophy, their mutual arrangement changes; the ratio: "base / top" is violated. The processes of maintaining cardiac output and normalizing the tension of the LV wall are activated. The radius of curvature of the LV walls changes, on which the different stiffness of the LV walls and the distribution of intraventricular volume depend.

The mechanism for maintaining cardiac output and normalizing LV wall tension is realized through the RAAS and hypertrophy of undamaged myocardial segments. Expansion of the infarct In 1978, G. Hutchius and B. Bulkley described the process of acute enlargement and thinning of the infarct zone without additional myocardial necrosis. In the first hours after the death of myocytes, edema and inflammation localize the infarction zone. Further, the proliferation of fibroblasts and the replacement of this area with collagen are observed. The infarction zone can become thinner and expand. The length of the sariomeres does not change. Thus, an increase in LV volume occurs due to the rearrangement of myofibrils without their stretching.

The wall becomes thinner due to the sliding of muscle fibers relative to each other as a result of the weakening of connections between myocytes in the infarction zone. With ECHO KG, an increase in the zone of akinesia without enzymatic shift is determined. Expansion is most likely in transmural MI and ends with CHF, aneurysm, and myocardial rupture. The anterior-apical region is more vulnerable, as it is the most curved. Possible dilatation of the unaffected zone with a total expansion of the left ventricle.

Post-infarction LV remodeling (PRLV)

A sharp stretching of the viable myocardium according to the Frank-Starling law, an increase in chrono-inotropic effects during stimulation of adrenoreceptors maintains the pumping function in conditions of a decrease in the contracting part of the myocardium. If more than 20% of the LV mass is affected, compensation will be inadequate. Enlargement of the LV cavity helps to restore SO against the background of a decrease in EF. Dilatation increases myocardial stress, a vicious circle is completed. As a compensation, myocyte hypertrophy occurs: up to 78% of the initial volume. Hypertrophy can be concentric without cavity enlargement and eccentric with dilation Hypertrophy can restore LV wall tension In extensive MI, dilatation is not proportional to myocardial mass gain

The role of cytokines

Cytokines are markers of CHF. The development of CHF is accompanied by an increase in pro-inflammatory cytokines - interleukin - - 1.6; in blood plasma and in the myocardium. No increase in anti-inflammatory cytokines, resulting in increased inflammation. Expression of cytokines and their receptors on cardiomyocyte membranes confirms central role cytokines in the pathogenesis of CHF. The level of tumor necrosis factor (TNF) directly depends on the FC of CHF. Immunomodulators increase the level of anti-inflammatory mediators.

Intravenous administration of pentoxifylline, immunoglobulin increases EF and reduces TNF - alpha Sodium - uretic peptide - (NP) Normally produced by atrial cardiomyocytes and regulates water-salt balance and reduces blood pressure. With a decrease in cardiac output in patients with asymptomatic LV dysfunction and FC I CHF, the synthesis of NP in the ventricles of the heart increases. This blocks the activity of the circulating link of the RAAS and compensates for the condition of patients. The progression of CHF activates the RAAS. The sodium-uretic response to the growth of NP activity decreases. This leads to sodium and water retention, systemic and renal vasoconstriction.

Postinfarction LV aneurysm

The classic variant of post-infarction LV remodeling is post-infarction LV aneurysm (LA), which develops in 8-34% of cases of transmural myocardial infarction: it is characterized by akinesia or dyskinesia of the LV wall. The geometry, volume and mass of the left ventricle change. Clinically manifested in the form of CHF in 50% of patients or more, ventricular arrhythmias, thromboembolic syndrome. Surgical method treatment is myocardial revascularization and left ventricular plasty. Early aneurysms in anterior MI are unfavorable prognostically. Risk factors: - more than 2 MI in history; - attacks of cardiac asthma - III, IY FC according to NYHA; - FV<25%; - КДД >24 mm. rt. Art.; - stenosis of the LCA trunk; - defeat of the three main basins coronary arteries.

PROGNOSIS LV remoderation Radiologically visible enlargement of the LV is unfavorable and increases mortality by 3 times, predicts the development of CHF. Rise from. ST with a decrease or absence of h. R on the ECG helps not only to diagnose MI, to determine its size, but also to suggest LV remodeling. Compensatory processes depend on the state of the coronary blood flow of the surviving myocardium; with inadequate blood supply, dilatation is greater, and mortality is higher. Arterial stenosis limits compensatory myocardial hypertrophy and increased workload. Cavity dilatation is directly correlated with the risk of fatal arrhythmias.

HDI correlation

Primary prevention is beyond doubt: it is the earliest and most adequate restoration of perfusion in patients with ACS. Prevention of CHF begins in the first hours of AMI. It is necessary to limit the area of necrosis: thrombolytics, nitrates. BAB, antiplatelet agents.

Surgical myocardial revascularization

1. The effect of ACE inhibitors has been proven: prolonged preparations and those acting on tissue ACE are preferred. Mortality from CHF is significantly reduced, EF - increases. ACE inhibitors are more effective in anterior MI. ACE inhibitor therapy is prescribed on the first day of MI.

2. BABs not only have an antiarrhythmic effect, but also inhibit LV remodeling. K. Shiono did not note the effect of atenolol. Metoprolol causes volume reduction and regression of LV mass; improves LV geometry.

3. Calcium antagonists are effective: ampodipine, diltiazem and isoptin, but treatment should be long.

4. Nitrates limit early postinfarction LV remodeling. 5 Digoxin, as a result of inotropic stimulation in anterior MI, can increase LV infarction without reducing collagen content. 6 L-carnitine in the acute and late period of MI reduced LV dilatation (S. Iliceto).

Concept and reasons

A sufficiently 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 during sports or during heavy physical labor leads to the formation of the so-called working hypertrophy. What else can cause the formation of this complication? We list the main factors:

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

The risk factors for developing LVH are:

elevated arterial pressure(HELL),
male gender,
patients over fifty years of age
burdened heredity for cardiovascular diseases (CVD) (diseases of the circulatory system in blood relatives),
overweight,
violation of cholesterol metabolism.

2 The 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 partial remodeling. The second concept is broader. Remodeling means the process of changing an existing structure, rearranging it or adding something to it. Myocardial remodeling is a change in its geometric structure under the influence of some specific factor. Moreover, not only the structure is being rebuilt, but functional restructuring is also taking place.

The purpose of remodeling is the adaptation of the left ventricle to the established hemodynamic conditions, which often acquire a pathological character. With constant influence high blood 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 with 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 chamber of the heart is reduced.

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

Myocardial cells are cardiomyocytes. Cardiomyoites are highly differentiated structures. This means that these cells have lost the ability to divide. Therefore, in response to increasing physical activity (FN), the concentration of biologically active substances in the body increases: norepinephrine, angiotensin, endothelin, etc. In response to this, the number of sarcoplasmic contractile units in cardiomyocytes increases. Energy exchange processes begin to flow 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, and the vascular network remains at the same level. The LV myocardium enters a state of ischemia - oxygen starvation. In response to this, the components of the connective tissue - fibroblasts - are activated. "Growing" with connective tissue, the myocardium loses its elasticity and becomes rigid. This circumstance entails a decrease in the diastolic function of the left ventricle. In simple terms, appears (LV).
Collagen. At various diseases, in particular with myocardial infarction, the collagen that provides 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 level off, and in place of weakened cardiomyocytes that have undergone necrosis during a heart attack, a scar is formed from the connective tissue.

3 Types of hypertrophy

Concentric. Concentric hypertrophy of the myocardium of the left ventricle (concentric hypertrophy of the LV myocardium) is characterized by a uniform thickening of its walls. This uniform wall thickening can lead to a reduction in the chamber lumen. 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, 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. Hence, concentric LV hypertrophy develops.

Eccentric. Unlike the previous type, eccentric hypertrophy of the left ventricle is formed if the LV is overloaded with volume. Mitral or aortic valve insufficiency, as well as some other reasons, can lead to the fact that blood from the left ventricle is not completely expelled into the aorta. There remains some of it. The walls of the left ventricle begin to stretch, and its shape resembles a swollen ball. The second name for this type of remodeling is asymmetric. With eccentric LV hypertrophy, 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 is most often found in sports. Individuals involved in rowing, skating, or cycling may have this type of LV hypertrophy.

Separately, the authors single out 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 complaints of a patient with LVH may be shortness of breath, which he experiences during intense physical exertion. With the progression of the process, this symptom can also manifest itself at the time of performing loads of lesser intensity, and after that at rest. The last point indicates the development of heart failure (HF) in the patient.

In addition to shortness of breath, patients complain about the underlying disease. Pain or discomfort in the region of the heart or behind the sternum, which are associated with stress or stress, may be disturbing. Palpitations, dizziness, headaches, fainting may also be present. The list of symptoms can be supplemented by sensations of interruptions in the work of the heart, increased fatigue, weakness, and other signs of the underlying disease.

The leading instrumental method of left ventricular myocardial hypertrophy is echocardiography (EchoCG or ultrasound of the heart). Despite the fact that such a simple and affordable method of instrumental diagnostics as electrocardiography (ECG) also has its own diagnostic criteria with respect to LVH, however, ultrasound of the heart in its diagnostic sensitivity exceeds ECG by more than 5 times. The main echocardiographic indicator that is taken into account when making a diagnosis of LVH is the mass of the left ventricular myocardium (LVML), or rather its index.

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

The normal geometric structure of the left ventricle is set on the condition that the OTC is less than 0.45; and LVMI is within the normal range.
Concentric remodeling has the following echocardiographic criteria: OTC equal to or less than 0.45; LVMI remains normal.
Eccentric remodeling is characterized by an OTC less than 0.45 with LVMI greater than normal.

Concentric LV hypertrophy is considered to be more unfavorable prognostically, since it is this type of myocardial remodeling that leads to diastolic dysfunction and electrical instability of the myocardium, thereby increasing the risk of sudden cardiac death among these patients. The severity of diastolic dysfunction, regardless of the type of hypertrophy, is affected by the relative wall thickness. The greater the degree of its increase, the worse the prognosis. But the increase in end-diastolic razer 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, due to which such a complication has developed. It includes non-pharmacological measures - the elimination of risk factors, as well as taking medicines that support heart function and prevent the progression of this complication. Treatment of left ventricular hypertrophy (LVH) is mandatory, even if the patient feels well.

With inefficiency drug therapy patients with impaired LV function surgery. Depending on what structural component suffered, the following surgical interventions are offered:

Stenting of coronary arteries, angioplasty. Such a procedure is prescribed in case of development.
Prosthetic heart valves. Such an operation may be indicated if valvular defects are the cause of LVH.
Dissection of adhesions on the valves (commissurotomy). One of the indications for such a surgical intervention is aortic stenosis. The dissection of the commissures makes it possible to reduce the resistance that the ventricular myocardium encounters when blood is expelled into the aorta.

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According to the definition of Yu. N. Belenkov (2002), the process of continuous development cardiovascular disease- from risk factors to death of the patient there is a single cardiovascular continuum (Fig. 1.). As can be seen from the presented figure, this process from the appearance of the main risk factors (FR) - arterial hypertension (AH), diabetes(DM) and dyslipidemia, which can lead to coronary disease heart disease (CHD), which can be complicated by the development of acute myocardial infarction (AMI), to remodeling of the left ventricle (LV) due to the death of cardiomyocytes (CMC) and loss of myocardial contractility can take quite a long time. The intensity of the development of CHF, leading to the death of the patient, is largely determined by both the number of dead cardiomyocytes and the quality of the patient's treatment. At the same time, the death of the patient, especially in persons with initial manifestations of CHF, may be due to the appearance of life-threatening arrhythmias. The development of CHF can also go in another way: arterial hypertension → left ventricular hypertrophy → left ventricular dysfunction → CHF or IHD → myocardial hibernation → left ventricular dysfunction → CHF.

A necessary stage in the development of the cardiovascular continuum is the remodeling of the heart muscle. According to M. Pfeffer (1985), "remodeling is structural and geometric changes in the left ventricle, including the processes of myocardial hypertrophy and dilatation of the heart, leading to a change in its geometry and a violation of systolic and diastolic function." As can be seen from the above figure, one of the most important ways to interrupt the vicious circle of cardiac muscle remodeling is to influence its main link in pathogenesis - hyperactivation of neurohormonal systems, the role of which in the cardiovascular continuum can be schematically represented as follows (Fig. 2).

As a result of overloading the heart with pressure, as, for example, with arterial hypertension, a concentric type of hypertrophy of the walls of the left ventricle develops (Fig. 3). Due to the thickening of the walls of the left ventricle (there is no increase in its cavity), the stiffness of the myocardium increases, i.e. the so-called diastolic dysfunction of the left ventricle (DDLV) develops. With such a change in the structure of the left ventricle, its function also changes, in this case, insufficient diastolic relaxation of the left ventricle is observed. The second type of remodeling develops according to a different mechanism, when the result of structural restructuring of the heart muscle is eccentric hypertrophy of the left ventricle.

The essence of the process of restructuring the geometry of the left ventricle is as follows. With volume overload, which occurs, for example, with hemodynamically significant mitral valve insufficiency, the situation is not uncommon in patients who have previously undergone acute infarction myocardial infarction (AMI), due to mitral regurgitation, eccentric hypertrophy of the left ventricle and expansion of its cavity develops. This situation, aggravated by myocardial ischemia leading to the death of cardiomyocytes, is accompanied by a significant decrease in the strength heart contraction, i.e. there is a typical picture of left ventricular systolic dysfunction (LVSD), prognostically more unfavorable than diastolic left ventricular dysfunction.

Summarizing the presented data, without dwelling on other important mechanisms for the formation of myocardial insufficiency, we highlight the main thing. On the long way from the imbalance of neurohormones that determine the degree and intensity of cellular damage to the appearance of a structural change in the heart muscle itself, up to eccentric remodeling, most patients take years. The staging of the cardiovascular continuum makes it possible to usefully influence the key links in the pathophysiological process of the development and progression of CHF. The effectiveness of the use of neuromodulators, which include, first of all, angiotensin-converting enzyme inhibitors (ACE inhibitors) and beta-blockers, has been proven by a huge number of large-scale multicenter cooperative studies.

Nevertheless, even despite a fairly clear understanding of the pathophysiology of the main causes leading to CHF (arterial hypertension, diabetes mellitus (DM) and dyslipidemia), as well as standards for their drug correction, the prognosis of the course of CHF remains pessimistic.

As one of the reasons for the development of CHF, one can note the situation in patients with arterial hypertension- the main category of patients who develop myocardial dysfunction. In Russia, according to I. E. Glazova (2002), based on research by employees of the Center for Preventive Medicine of the Russian Federation, 41.1% of women over 18 years of age and 39.2% of men suffer from arterial hypertension. However, despite such a high prevalence of arterial hypertension (according to a survey of 80,000 people aged 40-45 years in 23 cities of Russia, the average arterial hypertension in the population was 23%), only 57% of patients knew about the presence of the disease, and effective treatment was recognized only in 8% of cases. Only 27% of patients with arterial hypertension are effectively treated in the USA, Italy - 9%, Egypt - 8%, England - 6%, China - 3%, Poland - 2%.

Based on this important and only one example, a question arises before a practitioner: what should be done so that there are as few people with myocardial dysfunction as possible and in what ways can this be done? What if the use of such popular antihypertensive drugs as reserpine, adelfan, etc., tested by time and experience of clinicians, for example, the even more popular clonidine (clophelin), is evidence of the incompetence of the therapist in the field of modern cardiology and ultimately leads to an increase in deaths from stroke in patients with arterial hypertension, especially in combination with CHF?

Rapovets V.A.
Cardiologist

Ischemic remodeling is a dynamic, reversible process of changing the thickness of the myocardium,
the size and shape of the chambers of the heart, dysfunction of the left ventricle (LV).

Left ventricular hypertrophy is the initial stage of remodeling in arterial hypertension (AH),
depends not so much on the level of blood pressure - hemodynamic overload, but on the activity of the RAAS.

The risk of developing chronic heart failure (CHF) increases 15 times. LVH develops according to the concentric type (adding sarcomeres inside the cardiomyocyte). A11 stimulates the growth of muscle fibers, aldosterone changes the intracellular matrix with the formation of diastolic dysfunction - DD.

DD is an early stage of LV remodeling, a marker of myocardial fibrosis.

Relaxation is the most energy-dependent process; LVH suffers first of all. The LA experiences the greatest hemodynamic overload in DD. Dilatation of the LA causes mitral regurgitation.

An important stage is the transition from concentric LVH to eccentric. To the systolic pressure overload is added the diastolic volume overload. LV dilatation is accompanied by systolic dysfunction. And this increases mortality by 50%. CHF is moving to the finishing stage.

ACE inhibitors cause regression of concentric hypertrophy, reducing the thickness of the walls of the left ventricle; normalize diastole. The volume of muscle fibers and myocardial fibrosis decrease.

At the stage of eccentric hypertrophy, ACE inhibitors prevent myocardial thinning, reduce myocardial stress. ACE inhibitors increase EF, reduce LV volume, improve local contractility - reduce asynergy index. Acute MI In the first 72 hours of AMI, early remodeling occurs - stretching and thinning of the myocardium, dilatation and spherification of the left ventricle. With extensive transmural MI, serious
architectural restructuring that determines the prognosis of the disease. After damage and death of part of the cardiomyocytes, both in the normal and damaged zone, the process of sclerosis takes place. Myocytes hypertrophy, their mutual arrangement changes; the ratio: "base / top" is violated. The processes of maintaining cardiac output and normalizing the tension of the LV wall are activated. The radius of curvature of the LV walls changes, on which the different stiffness of the LV walls and the distribution of intraventricular volume depend.

The mechanism for maintaining cardiac output and normalizing LV wall tension is realized through the RAAS and hypertrophy of undamaged myocardial segments.

Expansion of a heart attack

In 1978, G. Hutchius and B. Bulkley described the process of acute enlargement and thinning of the infarct zone without additional myocardial necrosis. In the first hours after the death of myocytes, edema and inflammation localize the infarction zone. Further, the proliferation of fibroblasts and the replacement of this area with collagen are observed. The infarction zone can become thinner and expand. The length of the sariomeres does not change. Thus, an increase in LV volume occurs due to the rearrangement of myofibrils without their stretching. The wall becomes thinner due to the sliding of muscle fibers relative to each other as a result of the weakening of connections between myocytes in the infarction zone. With ECHO KG, an increase in the zone of akinesia without enzymatic shift is determined.

Expansion is most likely with transmural MI and ends with CHF, aneurysm and myocardial rupture. The anterior-apical region is more vulnerable, as it is the most curved. Possible dilatation of the unaffected zone with a total expansion of the left ventricle.

Post-infarction LV remodeling (PRLV)

Sharp stretching of the viable myocardium according to the Frank-Starling law, an increase
chrono-inotropic effects during stimulation of adrenergic receptors supports pumping
function in conditions of a decrease in the contracting part of the myocardium. When more than
20% LV mass compensation will be inadequate.

Enlargement of the LV cavity helps to restore SO against the background of a decrease in EF.

Dilatation increases myocardial stress, a vicious circle is completed. As a compensation, myocyte hypertrophy occurs: up to 78% of the initial volume.

Hypertrophy can be concentric without cavity enlargement and eccentric with dilation Hypertrophy can restore LV wall tension In extensive MI, dilatation is not proportional to myocardial mass gain

The role of cytokines. Cytokines - markers of CHF

The development of CHF is accompanied by an increase in pro-inflammatory cytokines - interleukin - - 1.6; in blood plasma and in the myocardium. No increase in anti-inflammatory cytokines, resulting in increased inflammation. The expression of cytokines and their receptors on the membranes of cardiomyocytes confirms the central role of cytokines in the pathogenesis of CHF.

The level of tumor necrosis factor (TNF) directly depends on the FC of CHF. Immunomodulators increase the level of anti-inflammatory mediators.

Intravenous administration of pentoxifylline, immunoglobulin increases EF and reduces TNF-alpha

Sodium - uretic.peptide - (NP)

Normally, it is produced by atrial cardiomyocytes and regulates the water-salt balance and lowers blood pressure. With a decrease in cardiac output in patients with asymptomatic LV dysfunction and FC I CHF, the synthesis of NP in the ventricles of the heart increases. This blocks the activity of the circulating link of the RAAS and compensates for the condition of patients. The progression of CHF activates the RAAS. The natriuretic response to an increase in NP activity decreases. This leads to sodium and water retention, systemic and renal vasoconstriction.

Postinfarction LV aneurysm

Surgical treatment is myocardial revascularization and plasty
LV. Early aneurysms in anterior MI are unfavorable prognostically.

Risk factors:
- more than 2 MI in history;
- attacks of cardiac asthma - III, IY FC according to NYHA;
- FV 24 mm. rt. Art.;
- stenosis of the LCA trunk;
- the defeat of the three main basins of the coronary arteries.

LV remodeling prognosis

Radiologically visible enlargement of the left ventricle is unfavorable and increases mortality by 3 times, predicts the development of CHF. Rise from. ST with a decrease or absence of h. R on the ECG helps not only to diagnose MI, to determine its size, but also to suggest LV remodeling. Compensatory processes depend on the state of the coronary blood flow of the surviving myocardium; with inadequate blood supply, dilatation is greater, and mortality is higher. Arterial stenosis limits compensatory myocardial hypertrophy and increased workload. Cavity dilatation is directly correlated with the risk of fatal arrhythmias.

LV correlation

Myocardial revascularization

1 The effect of ACE inhibitors has been proven: prolonged preparations and those acting on tissue ACE are preferred. Mortality from CHF is significantly reduced, EF - increases.
ACE inhibitors are more effective in anterior MI. ACE inhibitor therapy is prescribed on the first day
THEM.

2 BABs not only have an antiarrhythmic effect, but also inhibit LV remodeling. K. Shiono did not note the effect of atenolol. Metoprolol causes volume reduction and regression of LV mass; improves LV geometry.

3 Calcium antagonists are effective: ampodipine, diltiazem and isoptin, but treatment
should be long.

4 Nitrates limit early postinfarction LV remodeling.

5 Digoxin, as a result of inotropic stimulation in anterior MI, can increase LV infarction without reducing collagen content.

6 L-carnitine in the acute and late period of MI reduced LV dilatation (S. Iliceto).

Literature:

1 Cardiology, 2003, 8, pp. 83-94.
2 Cardiology, 2003, 8, pp. 68-72.
3 Buziashvili YI et al Cardiology, 2002, 10, pp. 88-94.

The predictive value of the shape and geometry of the left ventricle in patients with arterial hypertension (AH) continues to be debated. In earlier studies, LV remodeling was seen as an adaptive response to pressure and volume overload and was associated with a better prognosis. In fact, the process of LV adaptation to hypertension is more complex than expected. The heart is able to adapt to prolonged hypertension by developing concentric LV hypertrophy. In accordance with the compensatory response pattern, LV wall thickness increases in proportion to A/D levels to maintain normal myocardial stress. Obviously, the range of adaptation of the heart to hypertension should be associated with the difference in hemodynamic load and with the state of myocardial contractility. LV dilatation is a late transition from LV hypertrophy to myocardial insufficiency.

The widespread use of the ECHO-KG method made it possible to classify the LV architectonics in patients with AH 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 model in 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 LV wall thickness);

2) eccentric hypertrophy (weight gain with normal

small relative thickness);

3) concentric remodeling (normal weight and increase

personal relative wall thickness);

4) normal LV geometry;

A. Hanau et al. determined the hemodynamic features and the 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 only in 8% of the subjects; 27% had eccentric hypertrophy; 13% - concentric LV remodeling; 52% of the subjects were characterized by normal LV geometry. The shape of the left ventricle was the most ellipsoid in the group of patients with concentric hypertrophy and the most spherical in the group with eccentric hypertrophy.

Differences in the structural-geometric model of the left ventricle in patients with hypertension are closely related to the pathophysiology of the heart and circulation. Patients with concentric hypertrophy are characterized by almost normal end-systolic myocardial stress, normal sizes and LV shape, increased total peripheral vascular resistance (PVR) and a slight increase in cardiac index.

Patients with concentric remodeling are also characterized by normal levels of end-systolic myocardial stress and increased total peripheral resistance. However, they are characterized by reduced shock and cardiac indices. The incentive to increase relative LV wall thickness in this group is not fully understood. In part, it can be explained by a decrease in arterial compliance, as indicated by a subnormal stroke volume with a slight increase in the level of pulse A/D. Patients with eccentric left ventricular hypertrophy x- high cardiac index, normal PVR, LV cavity enlargement, end-systolic myocardial stress, indicating inadequacy of left ventricular 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 AH have normal LV geometry and are characterized by a slight increase in total PVR, systolic and diastolic blood pressure.

Even a small change in LV mass within normal limits can serve as a prognostic sign of an increased risk of cardiovascular complications. Numerous studies show that an increase in LV mass is a stronger predictor of cardiovascular events and mortality than blood pressure levels and other risk factors, with the exception of age. These data are consistent with those of other studies and support the concept that LV mass gain is a common final pathway for many adverse cardiovascular outcomes.

The configuration of the left ventricle, regardless of the mass of the myocardium, affects the prognosis of patients with hypertension. One study examined the difference in cardiovascular risk in 694 hypertensive patients with normal LV myocardial mass, in whom, during the initial ECHO-CG, either normal configuration LV, or its concentric remodeling. Duration of follow-up was 8 years (average 3 years). Cases of cardiovascular complications, including fatal ones, were 2.39 and 1.12 per 100 patients per year in groups with and without concentric remodeling, respectively (by 2.13 times).

The 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 left ventricle. Thus, the worst prognosis for cardiovascular complications (31%) and mortality (21%) was observed in the group of patients with concentric LV hypertrophy. The most favorable prognosis (no deaths and 11% of cardiovascular complications) score characteristic of a 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 left ventricle in patients with AH allows us to conclude that concentric remodeling is accompanied by "volume underload", possibly due to "pressure natriuresis". There is no obvious LV hypertrophy in response to volume underloading. The study of the mechanisms of LV underloading may provide new strategies for preventing the progression of hypertensive heart disease and optimizing antihypertensive treatment.