The main indicators of left ventricular remodeling are: Left ventricular remodeling: pathogenesis and assessment methods. Surgical myocardial revascularization

Arterial hypertension (HTN) is a major risk factor for cardiovascular morbidity and mortality. The presence of hypertension increases the risk of developing coronary heart disease (including acute myocardial infarction and sudden coronary death) by more than 2 times, and the risk of heart failure and stroke by more than 3 times.

In recent years, the attention of specialists studying essential hypertension has been drawn to the remodeling of the cardiovascular system in this disease. Cardiac remodeling is a process of complex disruption of its structure and function and includes an increase in myocardial mass, dilatation of cavities and changes in the geometric characteristics of the ventricles.

Recent studies have shown that left ventricular hypertrophy (LVH) is far from the only option for the development of a hypertensive heart. With the improvement of echocardiographic diagnosis of LVH and a more in-depth study of this problem, it has become obvious that anatomical changes in the left ventricle in hypertension are not always accompanied by an increase in myocardial mass. It turned out that in many cases a change in the geometry of the left ventricle, in particular a decrease in the size of its cavity, occurs with normal myocardial mass.

The nature of remodeling in essential hypertension is heterogeneous; on the one hand, it is a response to a damaging overload, on the other hand, it has been proven that remodeling is a process associated with a primary and neurohumorally mediated disruption of cellular ion transport. Among the humoral disorders involved in remodeling processes, the main role is played by pathological activation of the reninangiotensin system (RAS), the sympathoadrenal system and hyperinsulinemia.

Morphological changes in hypertension are characterized by a gradual change in the geometry and mass of the myocardium. The process of cardiac remodeling involves all types of cells present in the myocardium: myocytes, interstitial cells, vascular endothelium and immune cells. In the early stages of pathological LVH, the diameter of cardiomyocytes, the number of myofibrils and mitochondria, and the size of nuclei increase. In later stages of hypertrophy, some changes in the cellular organization and shape of cardiomyocytes are also noted. The last phase of hypertrophy is characterized by the loss of contractile elements and the parallel arrangement of sarcomeres in cardiomyocytes. Another important morphological sign of a hypertensive heart is an increase in the content of collagen and fibrous tissue in the myocardium. Factors such as angiotensin II, endothelin-1 and aldosterone have the effect of fibroblast proliferation. Remodeling of the coronary resistance vessels also occurs with the subsequent development of perivascular fibrosis in the intramural coronary arteries and arterioles, along with thickening of their medial layer. In addition to contractile disorders in cardiomyocytes, interstitial and perivascular fibrosis, the death of cardiomyocytes (apoptosis) is now considered as one of the possible determining factors contributing to the transition from the compensated stage of LVH to the decompensated one.

Disproportional growth of myocardial and connective tissue structures contributes to the disruption of first diastolic and then systolic function of the left ventricle and the development of congestive heart failure. Myocardial fibrosis leads to a decrease in coronary reserve, which in patients with hypertension can also be observed with intact coronary arteries. Impaired myocardial perfusion occurs due to an increase in coronary vascular resistance, a decrease in the number of capillaries per gram of muscle tissue, structural changes in the coronary arteries, and endothelial dysfunction. Decreased coronary reserve in LVH increases the heart's sensitivity to ischemia when myocardial oxygen demand increases or perfusion pressure decreases. The presence of myocardial ischemia in a hypertensive heart can explain the increased incidence of ventricular arrhythmias, atrial fibrillation, myocardial infarction and sudden coronary death in patients with hypertension.

The most common classification of types of left ventricular remodeling in hypertension is the classification of A. Ganau (1992), which is based on determining the left ventricular myocardial mass index (LVMI) and the relative wall thickness (RWT) of this ventricle. Depending on the level of LVMI and TVR, four different types of geometric adaptation of the left ventricle to hypertension are distinguished:
1) concentric left ventricular hypertrophy (increased LVMI and TVR);
2) eccentric hypertrophy (increased LVMI with normal TVR);
3) concentric remodeling (increased TPV with normal LVMI);
4) normal geometry of the left ventricle.

According to the observations of A. Ganau and R. Devereux, during an examination of 165 untreated patients comparable in severity and duration of hypertension, a normal type of LV geometry was detected in 52%, concentric remodeling in 13%, eccentric LVH in 27% and only 8% - concentric LVH. The frequency of detection of different types of left ventricular remodeling in hypertension of varying severity has not been sufficiently studied. According to E. Shlyakhto (1999), concentric remodeling options are more common in moderate hypertension than in mild hypertension, while the normal type of geometry and eccentric LVH are more common in stage I arterial hypertension (according to WHO classification, 1993).

The risk of developing cardiovascular complications depends on the type of left ventricular remodeling in hypertension. The least favorable prognosis is concentric LVH - the probability of developing cardiovascular diseases within 10 years is 30%; followed by eccentric LVH - 25%; concentric remodeling - 25%; normal geometry type - 9%. Some authors attribute this to the fact that the greatest mass of the left ventricle is observed with concentric LVH, therefore, the unfavorable prognosis is due to an increase in the mass of the left ventricular myocardium (LVMM).

It is known that the presence of LVH, regardless of blood pressure level, is an unfavorable prognostic sign. The Framingham Study found that individuals 35 to 64 years of age with electrocardiographic evidence of LVH had a 3- to 6-fold higher risk of developing cardiovascular disease than those without LVH. It has been established that an increase in LVMI by 50 g/m2 is accompanied by an increase in the risk of coronary heart disease by 50%. The relative risk of death increases by 2.1 times with an increase in LVMM by 100 g, and by approximately 7 times with an increase in the thickness of the posterior wall of the left ventricle by 0.1 cm.

According to echocardiography (EchoCG), the presence of left ventricular wall hypertrophy is recorded if the thickness of the interventricular septum and/or posterior wall of the left ventricle at the end of diastole exceeds 1.1 cm. A more accurate sign of LVH is an increased LVMM, which is calculated using the formula of R. Devereux and N . Reichek (1977):
LVMM = 1.04 ([EDR + LVAD + TMZH]3 − [EDR]3) − 13.6,
where EDR is the end-diastolic size, LVSD is the thickness of the posterior wall of the left ventricle, TMZ is the thickness of the interventricular septum, expressed in centimeters.

Since LVMM is highly dependent on gender, height and body weight, its value is indexed in relation to body surface area. There are currently no generally accepted normal values ​​for LVMI. According to the literature, echoCG criteria for hypertrophy proposed by R. Devereux (1984) are more often used: LVMI in men - more than 134 g/m2, in women - more than 110 g/m2. However, in recent years there has been a tendency to use lower values ​​of LVMM as a criterion for its hypertrophy.

Concentric LVH is generally associated with high blood pressure, while eccentric LVH is usually associated with obesity and increased blood volume.

With concentric LVH, the increase in blood pressure is mainly due to an increase in total peripheral resistance (TPR) with a slightly increased or normal cardiac output. Concentric LVH develops initially as an adaptive process to reduce the increased stress on the walls of the left ventricle. An increase in afterload leads to an increase in parallel rows of sarcomeres, thickening of the walls and an increase in the mass of the left ventricular myocardium.

In hypertensive patients with eccentric LVH, cardiac output is increased with minimally increased or normal TPS. An increase in preload increases the diastolic tension of the walls of the left ventricle, the sarcomeric rows of cardiomyocytes lengthen, the cavity expands and the shape (spherical) of the left ventricle changes.

Patients with the concentric type of left ventricular remodeling have relatively mild hypertension with increased TPS and reduced cardiac output. Patients with hypertension with a normal type of left ventricular geometry are characterized by low blood pressure values; OPS and/or cardiac output are slightly increased.

In addition to anatomical features, functional changes in the myocardium, in particular impaired diastolic function of the left ventricle, are also a reflection of the remodeling process. LVH is currently considered one of the most important causes of impaired left ventricular relaxation. Signs of impaired myocardial relaxation can be observed in patients with hypertension and without LVH and are often detected earlier than an increase in myocardial muscle mass. This is probably due to the accelerated development of myocardial fibrosis, which is an important factor leading to disruption of the process of myocardial relaxation. Research by M. Lin et al. (1995), in a comparative assessment of the structure and function of the left ventricle in patients with hypertension, demonstrated a significant decrease in diastolic function of the left ventricle, especially in the group of patients with hypertension with concentric and eccentric LVH. Systolic dysfunction was observed only with eccentric LVH.

=================
You are reading the topic:
Types of left ventricular myocardial remodeling in arterial hypertension and the possibility of drug correction

1. Types of left ventricular myocardial remodeling in arterial hypertension.
2. Possibilities of drug correction for left ventricular myocardial remodeling.

Pavlova O. S., Nechesova T. A. Republican Scientific and Practical Center “Cardiology”.
Published: "Medical Panorama" No. 6, September 2002.

Concentric remodeling of the left ventricular myocardium is considered the most common form of this disease. As a rule, it develops primarily in people with arterial hypertension. This type does not have the ability to change the internal space of the left ventricle; only changes occur in the walls of the heart and an increase in the septum between the cardiac sections. It is worth saying that this form can begin to develop against the background of existing left ventricular hypertrophy. By the way, hypertrophy, as a rule, develops with increased physical activity, or as a consequence of hypertension. In addition to the standard causes, there are others that do not have the best effect on human health, and these can be harmful habits such as smoking, alcohol abuse, etc.

The disease begins with hypertrophy of the left ventricle and is manifested by an increase in the thickness of its wall

It is important to know that self-diagnosis of myocardial remodeling will not lead to anything good, but you should still understand the initial signs that contribute to the onset of the disease, such as:

• headache;
• heart pain;
• deterioration of the general condition of the body;
• blood pressure surges;
• uneven heart rhythm.

At the first manifestation of such symptoms, you should contact a specialist who should prescribe a cardiogram. Only this research method will help determine the presence of this disease. It should be said that an advanced form can lead to irreversible consequences, for example, the development of chronic heart failure.

There is nothing more difficult than suffering from severe heart disease, which also leads to certain consequences. One of these is cardiac remodeling. Heart remodeling is a structural change in an organ that destroys its properties in response to external influences and other pathological processes in the human body.

Heart remodeling occurs under the influence of negative factors and diseases

Causes of occurrence

It is necessary to clarify that this disease can also develop due to other heart diseases, and this leads to special forms of development. In addition to negative factors such as disease, myocardial remodeling can also occur as a consequence of poor quality treatment. It is important to know that completely different reasons influence the development of one or another physiological feature of the heart. There is no need to talk about the importance of correctly diagnosing the causes of occurrence, because it is already clear that you should first of all pay attention to the factor that contributed to the occurrence of this anatomical change.

Due to high blood pressure, certain diseases arise that lead to these changes. In addition to these heart deformations, other abnormalities can also be observed:

• the thickness of cardiomyocytes has an accelerated growth;
• the number of sarcomeres increases;
• the heart walls increase in size.

Attention! Cardiomyocytes are the mononuclear cells that make up the myocardium. They, in turn, have a transverse arrangement, and cause increased strength of muscle mass.

Of great importance is the scale of myocardial remodeling, which has different meanings and is explained by two main causes:

If we talk about eccentric myocardial remodeling, it can be caused by significant overload of this muscle tissue. In addition, this is accompanied by elongation of mononuclear cells and a decrease in the size of the heart walls.

Interesting! But functional remodeling provokes. This problem is absolutely independent of geometric and atomic changes in muscle tissue.

Pathophysiology of the disease

Today, myocardial infarction does not sound as scary as it did a few years ago. In most cases, patients are able to continue their standard life activities, despite the stress they have endured for the heart and the entire body. It is worth saying that high-quality treatment and good rehabilitation bear fruit, but, unfortunately, in addition to this, the consequences of a heart attack still remain. Myocardial remodeling, the pathophysiology of which is only worsening, has quite unpleasant consequences. In this case, if qualified examinations are not carried out in a timely manner, you can give your body complications, such as poor circulation and chronic heart failure.

Important! Carrying out high-quality rehabilitation and following the recommendations of a specialist are mandatory conditions for this disease. If you do not adhere to this, you can get serious complications that lead to disastrous results.

Myocardial infarction, as a rule, leads to serious physiological changes in the left ventricle, which does not have a very good effect on the general condition of the patient. This change in the structure of the heart also leads to the following changes:

• the standard shape of the left ventricle is an oval shape, which can change after a heart attack and acquire spherical parameters;
• the muscle tissue itself deteriorates in its quality indicators, tends to stretch and decrease in size;
• the appearance of parts that die, and their size tends to increase, etc.

If you trace this feature, you will notice that all processes in the body are interconnected, and nothing arises just like that. Due to the fact that blood pressure constantly rises, our heart muscle tries to adapt to this phenomenon. As a result, there is a change in the size of muscle tissue. This is how this disease occurs, which is accompanied by a number of other ailments.

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, from 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 people on the list of those 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 left ventricle 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 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. ACEI 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 distinguished. 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)

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.

Bibliography:

1. Zimin Yu.V., Kozlova I.L., Rodomanchenko T.V. and others. Structural and functional changes in the myocardium, systolic and diastolic functions of the left ventricle of the heart in patients with the metabolic variant of hypertension // Kremlin Medicine. Clinical Bulletin. - 1999. - No. 2. - P. 5-8.
2. Conradi A.O., Zhukova A.V., Vinnik T.A. and others. Structural and functional parameters of the myocardium in patients with hypertension depending on body weight, type of obesity and the state of carbohydrate metabolism. // Arterial hypertension. - 2002. - T. 8. - No. 1. - P. 12-15.
3. Preobrazhensky D.V., Sidorenko B.A., Alekhin M.N. Left ventricular hypertrophy in hypertension. Part II. Prognostic value of left ventricular hypertrophy. //Cardiology. - 2003. - No. 11. - P. 98-101.
4. Khozyainova N.Yu., Tsareva V.M. Structural-geometric remodeling and structural-functional restructuring of the myocardium in patients with arterial hypertension, depending on gender and age. // Russian Journal of Cardiology. - 2005. - No. 3. - P. 20-24.
5. Khromtsova O.M., Arkhipova M.V. Structural and functional features of the left ventricle of the heart and their relationship with the daily blood pressure profile in patients with arterial hypertension // Rational pharmacotherapy in cardiology. - 2009. - No. 1. - P. 46-50.
6. Kannel W. Risk stratification in hypertension: new insights from the Framingham Study // Am.J. Hyper. - 2000. - V. 13(pt. 2). - P. 3-10.
7. Krumholz H.M., Larson M., Levy D. Prognosis of left ventricular geometric patterns in the Framingham Heart Study // J. Am. Coll. Cardiol. - 1995. - Vol. 25. - P. 885-887.