Diagnosis issues: concentric remodeling of the left ventricle. Types of remodeling of the left ventricle of the heart in patients with arterial hypertension: relationship with age, metabolic syndrome and psychological status Concentric remodeling of the left ventricle

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.

There is also functional remodeling, in which a violation of LV contractility appears on its own and does not depend on geometric changes. The latter are referred to as structural remodeling, indicating 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 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. At high risk are athletes, loaders, etc. 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;
headache;
disturbances in heart rhythms;
deterioration in general health,
heartache.

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 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.

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. There are many more pathological disorders 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 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.

In contact with

Myocardial remodeling implies irreversible processes that destroy or change the properties of the organ in response to external negative, stress factors. Such pathologies are usually associated with cardiovascular changes of a structural nature, for example, heart failure, hypertrophy.

For information! The concept of “myocardial remodeling” was first introduced into clinical practice in the 70s of the last century. This proposal by N. Sharp specifically meant the designation of geometric and structural changes that tended to occur after an attack of acute infarction.

From the very beginning, this term meant only the general, its geometry, shape and weight, after a while it began to be used more widely, and therefore such interpretations as left ventricular remodeling appeared. It already speaks of a rapidly occurring, irreversible process in which phenomena such as changes in wall thickness, thickening of cardiomyocytes, increase in sarcomeres, and inflammation of necrotic tissue are observed. Other concepts such as electrical modeling and electrophysiological modeling also appeared. Also, these pathologies began to be divided into forms, for example, functional and structural.

Types of myocardial remodeling

The most common classification of remodeling types in modern medical practice is considered to be that proposed in 1992 by A. Ganau, which is based on the determination of the ventricular mass index and the relative thickness of its walls, based on which four main types were obtained:

eccentric hypertrophy (wall thickness is normal, ventricular mass index is increased);
concentric hypertrophy (both indicators are increased);
concentric remodeling of the left ventricle (wall thickness is increased, ventricular mass index is normal);
normal size of the left ventricle.

The risk of developing complications after cardiovascular diseases depends on their type. For example, concentric hypertrophy has the lowest prognosis of complications, in which the risk of developing these diseases within 10 years is about 30%, and eccentric hypertrophy and concentric remodeling give no more than 25% each. As for the ventricle, which has normal dimensions, the risk of complications does not exceed 9%.

Concentric remodeling of the left ventricular myocardium, diagnosed in people with high arterial hypertension, is today recognized as the most common type. It begins with ventricular hypertrophy, which occurs mainly against the background of an increase in the thickness of its wall; sometimes the septum thickens. There are usually no pathologies in the internal space.

Interesting! The development of hypertrophy usually occurs against the background of hypertension, but can be a consequence of excessive physical stress on the body. For this reason, the first on the list of those who are at risk are athletes, followed by loaders and masons. Active smokers and those who lead a sedentary lifestyle are also at risk.

Myocardial remodeling using the example of changes after a heart attack

For a more clear idea of the pathological process, we can consider the main points of the pathophysiology of myocardial remodeling using the example of its structural changes after a heart attack. First of all, the shape of the left ventricle changed. If earlier its shape was an ellipse, now it looks more like a sphere. The thinning and stretching of the myocardium is very clearly observed, the area of necrosis of the area of the heart muscle often increases (even in cases where there were no repeated ischemic necrosis). Many other pathological disorders also appear that can lead to unpleasant consequences.

The interrelation of the processes during which a structural change develops in the heart muscle is obvious: first, the pressure increased, the heart tries to adapt in response to it, as a result, in direct proportion, the thickening of the ventricular wall occurs, and at the same time the weight of the muscle and some others increases, changes corresponding to a given state.

This example explains how myocardial remodeling occurs and why it can be dangerous and worsen the situation, increasing the risk of complications after a heart attack. That is why, after an attack, the patient undergoes a long period of rehabilitation; he is prescribed special medications (some of which are used continuously) to prevent the development of a relapse.

How is it diagnosed and can the pathology be stopped?

Diagnosis of this disease is carried out by taking an electrocardiogram of the heart. On it, if the geometry of the left ventricle of the myocardium changes, an increase in ST and a decrease in the R wave will be observed.

The development of myocardial remodeling can be prevented if hypertension is diagnosed in a timely manner (it is characterized by frequent upward pressure surges, headaches, and deterioration in general health).

Modern medicine proves that even existing pathology can be reduced with the help of medications and more. It is possible to reduce the thickness of the walls and reduce the mass of the left ventricle with the help of antihypertensive drugs.

Beta-blockers inhibit remodeling and improve the geometry of the left ventricle of the myocardium. In addition, on the first day after a heart attack, angiotensin-converting enzyme inhibitors are prescribed to prevent heart failure and prevent relapse. Nitrates, as well as calcium antagonists (they require a long course of therapy), are effective in limiting early post-infarction remodeling.

It is also important to reduce your intake of salt and pickles, follow a specially designed diet and take control of your own weight (prevent the formation of excess kilograms).

The term “cardiac 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 changes in myocardial thickness, the size and shape of the heart chambers, and left ventricular (LV) dysfunction.

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 in a concentric manner (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; with LVH, it suffers first. During DD, the LA experiences the greatest hemodynamic overload. LA dilatation causes mitral regurgitation. An important stage is the transition of concentric LVH to eccentric. In addition to systolic pressure overload, diastolic volume overload is added. LV dilatation is accompanied by systolic dysfunction. And this increases mortality by 50%. CHF is moving towards the final stage. ACE inhibitors cause regression of concentric hypertrophy, reducing the thickness of the LV walls; normalize diastole. The volume of muscle fibers and myocardial fibrosis decreases.

At the stage of eccentric hypertrophy, ACEI prevents myocardial thinning and reduces myocardial stress. ACE inhibitors increase EF, reduce LV volume, improve local contractility - reduce the asynergia index. Acute MI In the first 72 hours of AMI, early remodeling occurs - stretching and thinning of the myocardium, dilatation and spherification of the LV. With extensive transmural MI, a serious architectural restructuring occurs, which determines the prognosis of the disease.

After damage and death of some cardiomyocytes in both normal and damaged zones, the process of sclerosis occurs. Myocytes hypertrophy, their relative position changes; the “base/top” ratio is disrupted. The processes of maintaining cardiac output and normalizing LV wall tension are activated. The radius of curvature of the LV walls changes, which determines the different stiffness of the LV walls and the distribution of intraventricular volume.

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

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

Post-infarction LV remodeling (PLR)

A sharp stretch of the viable myocardium according to the Frank-Starling law, an increase in chrono-inotropic effects upon stimulation of adrenergic receptors, supports 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 restore SV against the background of decreased EF. Dilatation increases myocardial stress, a vicious circle is completed. As compensation, myocyte hypertrophy occurs: up to 78% of the original volume. Hypertrophy can be concentric without increasing the cavity and eccentric with dilatation Hypertrophy can restore the tension of the LV wall In case of extensive MI, dilatation is not proportional to the increase in myocardial mass

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 myocardium. Without increasing anti-inflammatory cytokines, which leads to 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, an 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 RAAS and compensates for the condition of patients. The progression of CHF activates the RAAS. The sodium uretic response to increased NP activity decreases. This leads to sodium and water retention, systemic and renal vasoconstriction.

Post-infarction 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: characterized by akinesia or dyskinesia of the LV wall. The geometry, volume and mass of the LV changes. Clinically manifests itself in the form of CHF in 50% of patients or more, ventricular arrhythmias, thromboembolic syndrome. The surgical treatment method is myocardial revascularization and LV plastic surgery. Early aneurysms in anterior MI are prognostically unfavorable. Risk factors: - more than 2 MI in history; - attacks of cardiac asthma - III, IY FC according to NYHA; - FV<25%; - КДД >24 mm. Hg Art.; - stenosis of the left coronary artery trunk; - damage to the three main basins of the coronary arteries.

PROGNOSIS of LV remodeling Radiologically visible enlargement of the LV is unfavorable and increases mortality by 3 times, predicts the development of CHF. Rise from. ST with decreased or absent z. R on the ECG helps not only to diagnose MI, determine its size, but also to suggest LV remodeling. Compensatory processes depend on the state of 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 load. Cavity dilatation directly correlates with the risk of fatal arrhythmias.

Correlation of LVRI

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: long-acting drugs that act on tissue ACE are preferable. Mortality from CHF significantly decreases, EF increases. ACE inhibitors are more effective in anterior MI. ACE inhibitor therapy is prescribed on the first day of MI.

2. Beta blockers not only have an antiarrhythmic effect, but also inhibit LV remodeling. K. Shiono noted no effect from atenolol. Metoprolol causes volume reduction and regression of LV mass; improves LV geometry.

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

4. Nitrates limit early post-infarction LV remodeling. 5 Digoxin, as a result of inotropic stimulation during anterior MI, may increase LV infarct bulge without reducing collagen content. 6 L-carnitine in the acute and long-term period of MI reduced LV dilatation (S. Iliceto).

Collection output:

TYPES OF REMODELING OF THE LEFT VENTRICLE OF THE HEART IN PATIENTS WITH ARTERIAL HYPERTENSION: RELATIONSHIP WITH AGE, METABOLIC SYNDROME AND PSYCHOLOGICAL STATUS

Bobylev Yuri Mikhailovich

Ph.D. honey. Sciences, Associate Professor, Perm State Medical Academy named after. ak. E.A. Wagner, Russian Federation, Perm

TYPES OF THE LEFT VENTRICULAR REMODELING OF THE HEART IN PATIENTS WITH HYPERTENSION: RELATING TO AGE, MATABOLIC SYNDROME AND PSYCHOLOGICAL STATUS

Yuri Bobylev

candidate of Medical Science, Associate Professor, Perm State Medical Academy named after academician E.A. Vagner, Russia, Perm

ANNOTATION

The features of left ventricular remodeling in women with arterial hypertension (AH) were studied depending on age, the presence of metabolic syndrome (MS) and psychological status. The results obtained showed that concentric left ventricular hypertrophy (LVCH) predominates in elderly and senile patients. It has been shown that left ventricular hypertrophy (LVH) occurs with equal frequency in patients with and without MS, but LVCH is more common in patients with MS. The highest level of reactive and personal anxiety is observed in patients with LVCH.

ABSTRACT

Peculiarities of left ventricular remodeling in women who have hypertension depending on age, metabolic syndrome and psychological status are under study. Obtained results show that concentric hypertrophy of left ventricle prevails in patients of elderly and old age. It is presented that left ventricular hypertrophy occurs with the same frequency in patience with absence and presence of metabolic syndrome; however, concentric hypertrophy of left ventricular often occurs in patience with metabolic syndrome. Higher level of reactive and trait anxiety is observed in patients with concentric hypertrophy of left ventricular.

Keywords: arterial hypertension; heart; remodeling; age; metabolic syndrome; anxiety; depression.

Keywords: hypertension; heart; remodeling; age; metabolic syndrome; anxiety; depression.

Introduction. Arterial hypertension (AH) remains one of the most pressing health problems. This is due to the high prevalence of the disease and the high risk of its complications - coronary heart disease (CHD), cerebral strokes, heart and kidney failure. It is known that hypertension leads to the development of cardiac remodeling. Cardiac remodeling in patients with hypertension is identified primarily with left ventricular myocardial hypertrophy, which is an independent risk factor for cardiovascular diseases (CVD) and sudden death. The classification of left ventricular remodeling in patients with hypertension includes 4 types of geometric models depending on the relative thickness of the left ventricular (LV) wall and LV myocardial mass index. According to the literature, the main manifestation of structural and functional changes in the LV in patients with hypertension is concentric remodeling and concentric hypertrophy of the LV, while the highest rates of CVD risk and mortality are observed in patients with LVCH.

The purpose of this study was to study the features of structural and functional parameters of the heart in women with hypertension.

Materials and methods. We examined 74 women aged from 31 to 80 years, average age 61.64±1.83 years, with stage I-II hypertension according to the WHO classification, with varying duration of the disease.

During the study, anamnesis was studied, anthropometric data were analyzed - height, weight, body mass index (BMI), waist circumference (WC), and blood pressure (BP) levels were measured. According to the WHO classification (1997), a BMI of 25-29.9 was assessed as overweight, 29.9-34.9 as class I obesity, 35.0-39.9 as class II, and more than 40 as class 3 obesity.

In blood serum taken in the morning on an empty stomach, total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), very low-density lipoprotein cholesterol (VLDL-C), and triglycerides (TG) were determined.

Glucose levels were determined and a standard glucose tolerance test (GTT) was performed according to indications. Blood plasma glucose level at 120 min. GTT from 7.8 to 11.0 mmol/L was considered as impaired glucose tolerance (IGT).

The diagnosis of MS was made according to the criteria of the US National Cholesterol Education Program in the presence of any three or more criteria (ATP III): WC > 88 cm, BAP ≥130 mm Hg. art., blood pressure ≥ 85 mm Hg. Art., HDL cholesterol< 1,3 ммоль/л, ТГ ≥ 1,7 ммоль/л, глюкоза ≥ 6,1 ммоль/л.

All patients underwent echocardiographic examination (EchoCG) using a standard technique using the Vivid 3 Pro apparatus. The following structural, geometric and functional indicators of the LV were calculated: end-diastolic (EDD, cm) and end-systolic (ESR, cm) dimensions, thickness of the posterior wall of the LV (PLWW, cm) and thickness of the interventricular septum (IVS, cm) in diastole, LV ejection fraction (EF%). Left ventricular myocardial mass (LVMM) was calculated using the formula of R. Devereux and N. Reicheck. The LVMM index (LVMI) was determined using the Dobios formula. The criteria for diagnosing LVH were the Framingham criteria - LVMI for women more than 110 g/m2. Relative left ventricular wall thickness (LVW) was calculated as (LVLT+LVAD)/LVRD. Based on the values of LVMI and TVR, 4 types of remodeling were identified. Patients with normal LV geometry (LVNG): (LVMI<110 и ОТС<45), больные с признаками КГЛЖ: (ИММЛЖ>110 and OTC>0.45); patients with signs of LV concentric remodeling (LVCR): (LVMI<110 и ОТС>0.45); patients with signs of eccentric LV hypertrophy (LVEH): (LVMI>110 and TVR<0,45).

Statistical data processing was carried out using the STATISTICA 6.0 software package. Differences at p<0,05.

Results and discussion

According to echocardiography, LVH was detected in 56 (75.7%) patients, and depending on LVMI and TVR, patients were divided into the following groups. With normal LV geometry - 18 (24.3%) patients, patients with LVCR - 23 (31.1%) patients, patients with LVEF - 12 (16.2%) patients and patients with LVCH - 21 (28.4%) ) patient (Table 1).

Table 1.

Echocardiographic criteria for left ventricular remodeling in the studied patients (M±m)

Indicators	Normal geometry	KRLZH	LVEF	LVCH
Age, years


TZSLZh, cm



LVMI, g/m2

Note: *p<0,05 по сравнению с нормальной геометрией ЛЖ и КГЛЖ, # р<0,05 по сравнению с КРЛЖ и ЭГЛЖ

Age had a significant effect on the incidence of LVH in the examined patients. If in young and middle-aged patients the frequency of LVH was 71.9%, then in elderly patients it was 80.0%, which corresponds to the data of the authors who studied remodeling processes in hypertension. At the same time, age had a significant effect on myocardial mass; we identified a close relationship between age and LVMM (r = 0.41, p<0,05), а так же связь возраста и ТЗСЛЖ (r=0,41, р<0,05), связь возраста и ТМЖП (r=0,34, р<0,05).

The following types of LV remodeling were observed in the examined patients depending on age (Table 2).

Table 2.

Types of left ventricular remodeling depending on age

As can be seen from Table 2, in young and middle-aged people, LV CO predominated, in contrast to the data of other authors, which showed the predominance of LV EH at this age. The frequency of LVCH, which is the most unfavorable type of remodeling, begins to predominate in elderly and senile patients, which indicates the highest level of cardiovascular risk.

According to our data, patients with LVCH had the greatest myocardial mass (Table 1), which corresponds to the observation of other authors. Ejection fraction allows you to assess the state of LV systolic function. According to our data and the data of other researchers, the decrease in EF was most significant in patients with LVEF compared with patients with normal LV geometry and LVEF (p<0,05). Это говорит о том, что на величину ФВ левого желудочка выраженность гипертрофии его существенно не влияет.

Subsequently, we divided the patients into two groups: group 1 29 patients, average age 61.14±2.17 years with no MS, group 2 45 patients, average age 61.60±1.79 years with the presence of MS (Table 3).

Table 3.

Indicators of left ventricular remodeling in patients with and without metabolic syndrome (M± m)

Systolic function indicators, namely EF, did not differ significantly between patients with and without MS (57.38±1.22 and 58.30±0.52%, respectively). The mass of the LV myocardium was slightly larger in patients with MS compared to patients without MS, but no significant difference was found.

In group 1, LVH was detected in 75.9% of patients, in group 2 - in 75.5% of patients, i.e. LVH occurred with the same frequency both in patients without MS and in patients with MS . In the group of patients without MS (Table 4), LVDC was most common; in the group of patients with MS, in contrast to the data of other authors, LVDC and LVCH were found with equal frequency, and the percentage of LVEF decreased from 27.3% in group 1 to 17.6% in patients with MS.

Table 4.

Type of left ventricular remodeling depending on the absence and presence of metabolic syndrome

Prevalence of anxiety and depressive symptoms in the studied patients according to the HADS scale. The average score on the anxiety scale in patients with hypertension without LV hypertrophy was 8.33±1.21, on the depression scale - 5.13±0.79, in patients with LVH - 7.91±0.61 on the anxiety scale and 6. 02±0.52 on the depression scale. When assessing the severity of anxiety and depressive symptoms, it was found that in the group of patients with normal LV geometry, the subclinical and clinical level of anxiety was 11.44±0.91, the level of depression was 8.75±0.48. In the group of patients with LVH, the subclinical and clinical levels of anxiety and depression were 10.56±0.58 and 9.65±0.51, respectively. There were no significant differences in the severity of anxiety and depressive symptoms between the two groups of patients.

An analysis was carried out on the severity of anxiety and depressive symptoms on the HADS scale depending on the type of LV remodeling (Table 5).

Table 5.

Scale indicatorsHADSdepending on the type of LV remodeling (M± m)

At the same time, subclinically expressed anxiety was observed in patients with LVCR, and clinically pronounced anxiety was observed in patients with LVEF and LVCH. Depression in all three types of remodeling corresponded to a subclinical level. Thus, anxiety acts as a prodromal symptom of depression.

The indicators of the Spielberger-Khanin self-assessment scale of anxiety are shown in Table 6.

Table 6.

Indicators of the Spielberger-Khanin questionnaire depending on the type of LV remodeling (M± m)

Note: *<0,05 по сравнению с КРЛЖ

The results of a study of the level of anxiety on the Spielberger-Khanin scale showed. A high level of reactive anxiety (RA), as a reaction to the disease, was observed in patients with LVCH; in other types of remodeling, the level of RA corresponded to a moderate one. The level of personal anxiety (PT) was also highest in patients with LVCH.

Conclusions:

In elderly and senile patients with hypertension, LVCH predominates, which indicates a high level of cardiovascular risk. There was a significant relationship between age and LVMM, LVAD and LVAD.

The decrease in EF was most pronounced in patients with LVEF, but LVMM was greater in patients with LVCH, which suggests that the EF value is not affected by the severity of LVH.

In the group of patients with and without MS, LVH occurs with the same frequency, however, in patients with MS, the frequency of LVH, the most unfavorable type of remodeling, increases.

It should be noted that there is a close comorbidity of anxiety and depressive states in patients with hypertension, both with the absence and presence of LVH, which is most pronounced in patients with LVH. The highest level of reactive and personal anxiety is observed in patients with LVCH.

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Myocardial remodeling is the restructuring of the existing structure and progressive dysfunction of the myocardium in response to prolonged damaging overload or loss of part of the functioning myocardium (E.

Braunwald).

Options for restructuring the myocardial structure (remodeling):

Myocardial hypertrophy;

Changes in the geometry of the ventricles (violation of the ellipsoidal shape and increase in sphericity);

Dilatation of the heart cavities;

Myocardial fibrosis.

Table 3

Hemodynamic options for myocardial remodeling

Long-term intracardiac mechanisms. With prolonged stress on the heart (for example, with valve defects, primary arterial hypertension), compensatory hyperfunction of the heart develops

(CGS) (according to F.Z. Meerson) is myocardial remodeling, which is based on hypertrophy of certain parts of the heart muscle, which occurs to compensate for the long-term load on cardiomyocytes. CGS has the following stages of development:

1) emergency;

2) completed hypertrophy and relatively stable hyperfunction;

3) gradual exhaustion and progressive cardiosclerosis.

The emergency stage develops immediately after an increase

load and is characterized by a combination of pathological and compensatory-adaptive changes in the myocardium (disappearance of glycogen, decrease in creatine phosphate level, decrease in intracellular potassium content and increase in sodium content, activation of glycolysis and accumulation of lactate) with the mobilization of reserves of the myocardium and the body as a whole. Characterized by an increase in the intensity of functioning of the structures (IFS) (this is the load per unit of muscle mass of the heart), the accumulation of under-oxidized metabolic products, which leads to activation of the genetic apparatus of cells, increased synthesis of nucleic acids and proteins, an increase first in the mass of energy-producing structures (mitochondria), then in functioning structures (myofibrils) and the development of myocardial hypertrophy within several weeks.

The stage of completed hypertrophy and relatively stable hyperfunction. At this stage, the hypertrophy process is complete, the myocardial mass is increased and no longer grows. IFS is close to normal. Oxygen consumption, energy production, and macroerg content do not differ from normal values. Normal level of activity of the genetic apparatus. Hemodynamic parameters normalized. The hypertrophied heart has adapted to the new loading conditions and can compensate for them for a long time.

The following features of hypertrophied myocardium should be noted:

1) dysregulation of a hypertrophied heart due to a lag in the growth of nerve endings and an increase in the mass of cardiomyocytes;

2) a decrease in the vascular supply of the myocardium as a result of a lag in the growth of arterioles and capillaries from an increase in the size and mass of muscle cells, i.e., the development of relative coronary insufficiency;

3) increase in mass per unit surface area of myocardial cells. Considering that enzymes for the transport of cations, metabolic substrates, and receptor proteins are localized in the sarcolemma, these changes cause the development of ionic imbalance, disturbances in the metabolism of cardiomyocytes and the regulation of their functions;

4) a decrease in the level of energy supply to myocardial cells due to a lag in the increase in the mass of mitochondria compared to the mass of myofibrils;

5) disruption of plastic processes in cardiomyocytes as a result of a relative decrease in the number of mitochondria, a decrease in the cell surface area, the volume of the microvasculature and a deficiency of energy and substrates necessary for the biosynthesis of structures;

6) decreased contractile function of the heart.

The stage of gradual exhaustion and progressive cardiosclerosis is characterized by profound disturbances in the metabolism and structure of the myocardium, the development of a “wear complex of a hypertrophied heart” - the development of a large amount of connective tissue in the myocardium, loss of elasticity by myofibrils, deterioration of the conditions of cardiac regulation, leading to disruption of the contractile properties of the heart muscle. The main reason for the development of the “wear complex” is the lag in the growth of mitochondria from the growth of myofibrils during the development of hypertrophy, part of the myocardium becomes energy unsupplied, as a result of which the contractile elements die and are replaced by connective tissue, and the functioning muscle fibers change a number of their physicochemical properties and cannot carry out the processes of transformation of ATP energy into actomyosin energy. Progressive depletion of the compensatory reserves of the heart leads to heart failure, and subsequently to circulatory failure.