Diabetic cardiomyopathy. Diabetic cardiomyopathy: development and treatment of the disease Diabetes mellitus and secondary cardiopathy

Diabetic cardiomyopathy is a serious complication of the “sweet disease”, which develops as a result of metabolic disorders in the heart muscle due to increased amounts of sugar in the blood.

The main difference from classical cardiopathy is the absence of a connection between this problem and arterial hypertension, the patient’s age, the presence of heart defects and other factors.

Mechanism of development of diabetic cardiomyopathy

There are 2 types of this pathology:

Primary. It is characterized by disorders in the metabolic processes of the myocardium. It accumulates under-oxidized cell breakdown products, glucuronates, glycated protein and abnormal collagen. All this gradually worsens the ability of the heart to contract and leads to the development of failure with systolic or diastolic dysfunction.
Secondary. Develops as a result. Microscopic examination of the heart vessels can reveal their sclerosis, proliferation or thinning of the epithelium, and the formation of microaneurysms. A state of constant oxygen starvation leads to functional disorders that directly affect the ability of the myocardium to contract.

Diabetic cardiomyopathy rarely develops through only one of the pathways described above. Basically, a combined metabolic disorder with pathology of small vessels is observed.

Why does heart damage progress?

At the moment, it has been scientifically proven that several important factors play a role in the development of the disease.

The main causes of cardiopathy:

Long lasting. The heart does not suffer immediately. It often takes many years for the pathology to manifest itself clinically. Most patients are not even aware of the presence of already formed problems with the main organ in the chest.
Disruption of redox chemical processes inside myocytes.
Oxygen transport disorders due to changes in the structure of hemoglobin.

Excess blood sugar leads to insufficient supply of nutrients to the heart. The process of alternative formation of ATP molecules using proteins and fats is launched. Toxic metabolic products are synthesized, which negatively affect the functioning of the muscle and conductive cells of the organ.

Ultimately, the heart cannot provide the necessary contraction and relaxation. Its insufficiency progresses. Disturbances in the process of myocyte depolarization and disorders in the production of NO (the main vasodilator of coronary vessels) further aggravate the course of the disease.

How does diabetic cardiomyopathy manifest itself?

It should be noted that the clinical picture of the pathology occurs only with severe damage to the myocardium, when the number of its cells decreases to the limit. Then he loses the ability to adequately contract. A complex of characteristic signs of the problem develops.

Symptoms of diabetic cardiomyopathy:

Aching, diffuse pain in the heart area. It is important to be able to differentiate it from acute coronary syndrome. It does not spread to the left side of the human body and often goes away on its own without the use of nitroglycerin.
Dyspnea.
Swelling in the legs.
A wet cough appears.

In parallel, other late ones develop: retino-, neuro-, microangio-,.

When performing an ECG, the following characteristic electrophysiological changes in heart function can be noted:

Deformation of the P and R waves. This is often a sign of morphological disorders in the organ cavities. They can hypertrophy.
Lengthening or shortening of the P-Q and Q-T intervals are observed.
Deformations of the T wave are possible, which often indicates the addition of myocardial ischemia.
Heart disorders often progress in the form of arrhythmias (tachycardia, bradycardia, pacemaker migration, extrasystole, episodes of atrial flutter, various impulse conduction blockades).

It is extremely difficult to identify any special and specific changes in the functioning of the heart that would be inherent in purely diabetic pathology. Almost any cardiomyopathy will mimic a similar clinical picture, so it is important to know the medical history and take into account the patient’s problems with carbohydrate metabolism.

Diagnosis and therapy of diabetic heart disease

To verify the diagnosis, they mainly use:

Echo-KG;
Scintigraphy with Thalium-201.

These methods can demonstrate the functionality of the myocardium and indicate pathological foci.

Treatment of diabetic cardiomyopathy is based on the following principles:

Normalization of hyperglycemia.
Use of thiazolidinediones (Pioglitazone, Rosiglitazone). They prevent proliferation of the muscular component of blood vessels and reduce their spasm.
Statins to slow the progression of atherosclerosis. The most commonly used are Atorvastatin and Rosuvastatin.
Symptomatic treatment of heart failure and other concomitant diseases.

The process of treating this pathology remains very complex, since it is necessary to comprehensively influence metabolic reactions throughout the human body. However, with timely diagnosis of the problem, good therapeutic results can be achieved and the patient’s quality of life can be improved.

Cardiomegaly (CMG) is understood as a significant increase in the size of the heart due to its hypertrophy and dilatation (less commonly, infiltrative processes), or the accumulation of products of impaired metabolism, or the development of neoplastic processes.

Specific signs are determined by the disease that led to CMG (cardiomyopathies, heart defects: acquired and congenital, pericarditis, myocarditis, arterial hypertension, coronary heart disease and others).

Rice. 1. Dependence of end-diastolic pressure (EDP) and stroke work (SW) on the type of myocardial remodeling.

(according to Zeldin P.I., 2000)

Myocardial hypertrophy (with the exception of CGM) is a compensatory reaction that allows the heart to maintain normal blood circulation in the presence of a particular pathological condition. Hypertrophy never leads to a significant increase in the size of the heart and is accompanied by only a moderate expansion of its boundaries. CMH occurs, as a rule, with the development of myogenic dilatation of the heart and is characterized by various symptoms of heart failure and rhythm disturbances. Depending on the reasons causing an increase in the size of the heart, the development of partial CMG (a significant increase in a separate cardiac chamber) is initially possible. Subsequently, total KMG develops. Diffuse myocardial lesions immediately lead to total CMG. Most often, the degree of CMH depends on the duration of the pathological process causing an increase in the size of the heart and its severity (Fig. 1).

Myocardial diseases

Myocardial lesions, varied in cause and nature, are quite common. Allocate myocarditis, myocardial dystrophy and cardiomyopathy.

The term “myocardial dystrophy” combines non-inflammatory lesions of the myocardium, which are based on metabolic and trophic disorders.

Myocarditis is an inflammatory lesion of the myocardium.

The most common cause of myocarditis is a viral infection, with Coxsackie viruses accounting for 30 to 50% of all myocarditis. A distinctive feature of viral myocarditis is severe disturbances in the microvasculature. Destruction of the capillary endothelium under the influence of the virus is accompanied by increased permeability, stasis, and thrombosis in the vessels, which facilitates the penetration of the virus into the parenchyma. Viruses replicate from cell materials in myocytes. Replication is most pronounced on the 3-5th day of invasion. Activation of humoral immunity is manifested by a high level of AT type IgM, an increase in the titer of immune complexes in the blood. In most cases, viruses are not detected in the myocardium 10-14 days after the onset of the disease; foci of necrosis are eventually replaced by fibrous tissue. However, cells and products of disrupted protein metabolism exposed to viruses can acquire antigenic properties, causing the formation of antibodies that cross-react with unaffected myocardial cells, triggering an autoimmune reaction.

In the first place in the clinical picture are signs of heart failure (shortness of breath, edema, tachycardia, congestion in the pulmonary circulation). For all forms of myocarditis, the following syndromes are distinguished: cardiomegaly, rhythm disturbances (tachyarrhythmias, atrial fibrillation, ventricular paroxysmal tachycardia, and, to a greater extent, conduction disturbances - blockades), as well as cardialgia.

Auscultatory symptoms: weakening of the 1st sound, development of relative mitral valve insufficiency, systolic murmur at the apex, emphasis of the 2nd tone on the pulmonary artery, appearance of the 3rd and 4th sounds (III tone - diastolic gallop rhythm due to myocardial weakness, non-simultaneous contraction of the ventricles, IV - non-simultaneous contraction of the atria ). This picture is similar to the symptoms of combined mitral valve disease (pseudovalvular variant).

Thromboembolic syndrome (inflammation of the endocardial walls leads to a change in the electrical charge to (+), as a result, platelet adhesion, disruption of intracardiac hemodynamics, and parietal thrombus formation).

ECG changes in myocarditis are varied and transient: rhythm and conduction disturbances. Changes in the P wave (reduction, splitting) and the QRS complex (decrease in the voltage of the teeth and their splitting), decreased S-T interval, reduction, biphasicity and inversion of the T wave.

With myocarditis, the number of CD 4 increases and the ratio of CD 4 \CD 8 changes, the number of CD 22, Jg M, G, A, CEC increases.

Diagnostic criteria

Clinical diagnostic scheme for myocarditis proposed by NYHA (1973).

1. Relationship with previous infection, proven clinically and laboratory data: isolation of the pathogen, results of the neutralization reaction, complement fixation reaction, hemagglutination reaction, acceleration of ESR, appearance of C-reactive protein

2. Signs of myocardial damage

Big signs:

Pathological changes on the ECG (repolarization disturbances, rhythm and conduction disturbances);

Increased blood concentrations of cardioselective enzymes and proteins (creatine phosphokinase (CPK), CPK-MB, lactate dehydrogenase (LDH), aspartate aminotransferase (AST), troponin T);

Increased heart size according to radiography or echocardiography;

Congestive circulatory failure;

Cardiogenic shock

Minor signs:

Tachycardia (sometimes bradycardia);

Weakening of the first tone;

Gallop rhythm

The diagnosis of myocarditis is valid when a previous infection is combined with one major and two minor signs.

The NYHA criteria are the initial stage for diagnosing non-coronary myocardial diseases. To establish a final diagnosis, additional examination with visual (MRI) or histological confirmation of the clinical (preliminary) diagnosis is necessary.

Morphological criteria for diagnosing myocarditis: the presence of inflammatory infiltration (neutrophils, lymphocytes, histiocytes) of the myocardium and necrosis and/or damage to adjacent cardiomyocytes.

Inflammatory infiltration in the myocardium and cardiosclerosis can be detected by MRI with paramagnetic contrast agents. The contrast selectively accumulates in areas of accumulation of extracellular fluid (water), which makes it possible to judge the localization and extent of inflammation in the myocardium.

3. Laboratory methods confirming inflammatory damage to the heart: basophil degranulation test, the presence of cardiac antigen and antibodies to the myocardium, as well as a positive test for inhibition of lymphocyte migration with cardiac antigen, polymerase chain reaction to detect antibodies to pathogens.

4. Myocardial cardiosclerosis is characterized by:

The presence of “mesh” fibrosis in myocardial morphobiopsy specimens;

Impaired myocardial perfusion during cardiac MRI with contrast.

Cardiomyopathies

The term “cardiomyopathy” (CM) refers to heart pathology of unknown etiology and non-coronarogenic origin. According to the WHO classification (1995), there are:

1) dilatation, or stagnation;

2) hypertrophic;

3) restrictive;

4) specific (metabolic: diabetic, alcoholic, ischemic; valvular, inflammatory, etc.);

5) arrhythmogenic right ventricular cardiomyopathy – when there is a constant tachyarrhythmia leading to an increase in the right ventricle;

6) unclassified (fibroelastosis, “spongy myocardium”, systolic dysfunction with minimal dilatation, etc.)

Exclude: IHD, arterial hypertension, defects, myocarditis, pericarditis, pulmonary hypertension.

Dilated cardiomyopathy (DCM)

The leading role in the development of the disease is given to chronic viral infection (enteroviruses, Coxsackie), autoimmune influence (presence of cardiac organ-specific autoantibodies), and genetic predisposition.

In the clinical picture, the leading syndromes are: cardiomegaly, progressive heart failure, resistant to therapy; rhythm disturbances (atrial fibrillation, extrasystole, other forms of tachyarrhythmias; conduction blockades), thromboembolic syndrome. Auscultatory symptoms are similar to myocarditis: the first tone is weakened, regurgitation (systolic murmur at the apex), the accent of the second tone on the pulmonary artery, gallop rhythm.

During DCM, the following are distinguished:

I period – asymptomatic course (from the moment of detection of dilatation of the left ventricle),

II period – heart failure FC I-II,

III period – heart failure FC III, dilatation of both ventricles.

IV period – stabilization of the condition against the background of maintenance therapy, often with “small output” syndrome,

V period – terminal stage, heart failure, class IV and ischemic damage to internal organs.

Currently, the diagnosis of DCM most often begins after identifying LV dilatation of the heart with low systolic function in a patient who presents with complaints of shortness of breath, edema and weakness.

Laboratory data: no signs of inflammation, no morphological tests.

The main morphological manifestation of DCM is dilatation of both ventricles. Microscopically, hypertrophy and degeneration of cardiomyocytes, interstitial fibrosis of varying severity, and small accumulations of lymphocytes (usually less than 5 per field of view) are detected.

X-ray of the chest organs: enlargement of all chambers of the heart, smoothness of the “waist”, convexity of the left ventricular arch, absence of atherosclerosis of the aorta, moderate changes in the pulmonary circulation, mainly due to venous stagnation.

The ECG shows nonspecific repolarization disorders, conduction disturbances, and atrial fibrillation.

An echocardiogram can reveal dilation of the cavities, primarily dilatation of the left ventricle. Typically, with DCM, there is a decrease in cardiac output, a global impairment of contractility, and segmental LV dysfunction is detected in almost 60% of patients.

Atrial dilatation is also common, but is less significant than ventricular dilatation. Intracavitary thrombi are most often detected in the apex of the left ventricle.

Doppler studies can identify moderate mitral or tricuspid regurgitation.

Myocardial scintigraphy with 99 mTc allows quantitative assessment of systolic and diastolic function of the LV and is used in situations where echocardiography is not possible. Right side catheterization is used to guide therapy in patients with severe disease, but initial hemodynamic assessment before treatment is rarely indicated.

An endomyocardial biopsy is necessary in the presence of myocardial dysfunction and a systemic disease affecting the myocardium and amenable to specific treatment (sarcoidosis, eosinophilia). Most often, difficulties arise when excluding ischemic heart disease and current myocarditis as causes of LV dilatation. In doubtful cases, coronary angiography is indicated for patients with heart failure and left ventricular dilatation, since revascularization in the presence of coronary artery stenosis can lead to restoration of systolic function.

A more rare cause of LV dilation and decreased systolic function is a long-standing arrhythmia with a rapid ventricular rate (tachycardia-induced cardiomyopathy). The differential diagnostic criterion is the restoration of LV systolic function and the complete reversibility of its dilatation after restoration of sinus rhythm or heart rate control.

Hypertrophic cardiomyopathy (HCM) - a rare disease of the heart muscle, characterized by severe hypertrophy of the left ventricular myocardium in the absence of etiological factors for increasing heart mass (primarily arterial hypertension and aortic stenosis).

HCM is characterized by massive (more than 1.5 cm) hypertrophy of the myocardium of the left ventricle (Fig. 2) and/or in rare cases of the right ventricle, often asymmetric in nature due to thickening of the interventricular septum with the frequent development of obstruction (systolic pressure gradient) of the LV outflow tract in the absence of known causes (arterial hypertension, defects and specific heart diseases).

Rice. 2. Scheme of obstruction in hypertrophic cardiomyopathy.

(according to Zeldin P.I., 2000)

The most common clinical manifestations are shortness of breath, various pain sensations in the chest of a cardiac or angina nature, cardiac arrhythmias (interruptions, rapid heartbeat), dizziness, pre- and syncope.

There are five main variants of the course and outcomes:

Stable, benign course,

Sudden death (SD),

Progressive course: increased shortness of breath, weakness, fatigue, pain (atypical pain, angina), the appearance of presyncope and syncope, impaired LV systolic function,

- “end stage”: further progression of congestive heart failure (HF) associated with LV remodeling and systolic dysfunction,

The development of atrial fibrillation and associated complications, in particular thromboembolic ones.

The main diagnostic method is echocardiography. A hypercontractile state of the myocardium is characteristic with a normal or reduced LV cavity, up to its obliteration in systole. Typical for HCM are morphological changes: anomaly in the architectonics of the contractile elements of the myocardium (hypertrophy and disorientation of muscle fibers), the development of fibrotic changes in the heart muscle.

Diagnostic criteria for hypertrophic cardiomyopathy are presented in Table 1.

Table 1

Diagnostic criteria for hypertrophic cardiomyopathy(McKenna W.J., Spirito P., Desnos M. et al, 1997)

Research methods	Manifestations
Large criteria
Echocardiography	Left ventricular wall thickness 13 mm in the anteroseptal region or on the posterior wall or 15 mm in the posteroseptal region or on the free wall of the left ventricle; Systolic displacement of the mitral valve leaflets (contact of the mitral leaflet with the interventricular septum)
Electrocardio	Signs of left ventricular hypertrophy with repolarization disorders; Inversion of the T wave in leads I and aVL (>3 mm), leads V 3 -V 6 (>3 mm) or leads II, III and aVF (>5 mm); Abnormal Q waves (>25 ms or >25% of the R wave) in at least two leads II,III,aVF and V 1 -V 4 or I,aVL,V s -V 6
M scarlet criteria
Echocardiography	Left ventricular wall thickness 12 mm in the anteroseptal region or on the posterior wall or 14 mm in the posteroseptal region or on the free wall of the left ventricle; Moderate systolic displacement of the mitral valve leaflets (there is no contact of the mitral leaflet with the interventricular septum); Enlarged mitral valve leaflets
Electrocardio	Blockade of one of the His bundle branches or moderate conduction disturbances (in the left ventricular leads); Moderate repolarization disturbances in the left ventricular leads; Deep wave S in lead V 2 (>25 mm)
Clinical signs	Fainting, chest pain, and shortness of breath that are otherwise unexplained.

Restrictive cardiomyopathy (RCMP) includes : endomyocardial fibrosis (EMF) and eosinophilic Loeffler's endocarditis. It is proposed to call both forms the single term “endocardial disease”

With restrictive cardiomyopathy, the diastolic function of the myocardium is impaired and heart failure develops without pronounced myocardial hypertrophy and dilatation of the cavities. It is assumed that when exposed to a nonspecific agent (infectious, for example, a type of filariasis, or toxic) in the presence of impaired immunity, eosinophilia occurs (36-75% of eosinophils in the blood), and degranulation of eosinophils occurs. Pathologically altered eosinophils produce a protein that penetrates into cardiomyocytes, causing their death, and has a procoagulant effect.

Clinical picture depends on which part of the heart is affected, as well as on the severity of fibrosis. In general, these are signs of heart failure associated with a sharp decrease in diastolic compliance of the myocardium due to severe endomyocardial fibrosis and valvular insufficiency. With damage to the right ventricle, there is a significant increase in central venous pressure, swelling and pulsation of the jugular veins, exophthalmos, “moon-shaped” puffiness of the face with cyanosis, an increase in abdominal volume due to hepatomegaly and ascites.

Damage to the left ventricle, especially when accompanied by mitral regurgitation, is characterized by symptoms of pulmonary hypertension, which is clinically manifested in shortness of breath and cough. Pericarditis is quite common. Atrial rhythm disturbances are characteristic. There are several types of EMF: arrhythmic, pericardial, pseudocirrhotic, calcific.

The arrhythmic type is manifested by rhythm disturbances of atrial origin.

The pericardial type is characterized by chronic or recurrent effusion.

With the pseudocirrhotic type, pronounced ascites and a dense liver are noted.

The calcific type is characterized by linear calcification of the apex or region of the outflow tract from the right ventricle. The liver, spleen and kidneys are involved in the process, and hypereosinophilia is often detected.

There are also right-, left- and biventricular EMFs.

In right ventricular EMF, bilateral proptosis and sometimes cyanosis and enlargement of the parotid gland are often observed. Ascites, an enlarged liver, and swelling in the ankle joints are often detected. We can palpate a push in the II-III intercostal space, which is caused by the expansion of the right ventricle. A sharp, loud early diastolic III sound is almost always heard.

Symptoms and signs of left ventricular EMF are less typical. Left ventricular failure with pulmonary hypertension is usually observed. The murmur of mitral insufficiency is heard in combination with the diagnostic III sound.

With biventricular EMF, symptoms of right and left ventricular failure are combined.

ECG reveals signs of ventricular hypertrophy and overload, supraventricular arrhythmias, the presence of pathological Q, mainly in leads V1-2.

During X-ray examination detect pronounced hypertrophy of the right or left atria. Calcium deposits may be seen near the apex and in the inflow tract area.

EchoCG- the most informative method for diagnosing EMF. Thickening of the endocardium, a decrease in the cavity of one or another ventricle, paradoxical movement of the interventricular septum, and pericardial effusion in 50-70% are detected.

Differential diagnosis in the right ventricular form, EMF is performed with constrictive pericarditis and all diseases that occur with enlargement of the right atrium (atrial myxoma, Ebstein's anomaly, etc.). All cases of RCM accompanied by hydropericardium require differentiation from pericarditis of any etiology.

Alcoholic cardiomyopathy. Develops in some people who abuse alcohol for many years (usually at least 10 years). There is no direct correlation with the dose of alcohol and the type of drinks predominantly consumed. Among damage to internal organs in alcoholics, cardiac pathology ranks third in frequency after alcoholic diseases of the liver and pancreas and is often combined with them. Patients with alcoholic myocardial dystrophy without clinically significant dysfunction of other organs are described. In addition to the classic form of heart damage in alcoholics - alcoholic myocardial dystrophy with cardiomegaly - sometimes there is a pseudo-ischemic form of damage, simulating angina, and an arrhythmic form, manifested by various rhythm disturbances (atrial fibrillation, various conduction disturbances). With these forms there is no significant increase in heart size.

Clinically, alcoholic heart damage resembles the course of primary DCM; in addition, there are “alcoholic stigmas”: a puffy face with reddened skin and a “drunkard’s nose”, swollen veins, small telangiectasias, tremors of the hands, lips, tongue, Dupuytren’s contracture - shortening and wrinkling of the aponeurosis of the palms with ulnar contracture of the fingers. Polyneuritis, damage to the central nervous system with mental changes, and chronic parotitis often develop. Gastric ulcers complicated by perforation are significantly more often diagnosed in alcoholics. Typical manifestations are chronic pancreatitis, usually of the pancreas, as well as liver damage (fatty hepatosis, alcoholic hepatitis, alcoholic cirrhosis).

A feature of the course of alcoholic heart damage is a slowdown in progression or even stabilization of the process with complete abstinence from drinking alcohol at the initial stage of the disease. In some alcoholics, cardiac damage with cardiomegaly can develop rapidly in combination with damage to the peripheral and central nervous system, resembling the acute form of beriberi (the so-called “Western type” of beriberi). Vitamin B1 deficiency may play a role. In the blood, the activity of GGTP, acetaldehyde, AST, ferritin, ethanol is often increased without obvious signs of intoxication (indicators of constant alcohol abuse). Even at the early stage of alcoholic heart damage, prolongation of electrical systole (QT interval more than 0.42 s) is common, which is rarely found in non-alcoholics. Prolongation of the QT interval can lead to acute arrhythmias and sudden death in alcohol abusers. An early nonspecific change in the ECG of the final part of the ventricular complex is also possible, with negative dynamics of these changes with the “ethanol” test and the absence of positive dynamics when using a test with nitroglycerin and obsidan.

Endocrinopathies. In endocrine diseases that occur with arterial hypertension, changes in the heart depend mainly on the level of blood pressure and concomitant ischemic heart disease. In some cases, it is possible to develop non-coronogenic changes in the myocardium up to focal necrosis (Itsenko-Cushing syndrome) and hypercortisonism of another nature, pheochromocytoma (Conn syndrome).

Diabetic cardiomyopathy. Damage to large arterial vessels is characteristic: atherosclerosis is the most clinically important, Menkenberg's calcific sclerosis and non-atheromatous diffuse intimal fibrosis are also found. Damage to the coronary arteries by atherosclerosis (diabetic macroangiopathy) leads to a typical picture of coronary artery disease, which develops at a younger age than classic coronary artery disease, especially in severe diabetes.

In insulin-dependent diabetes mellitus, diabetic microangiopathy also occurs, most often clinically manifested by damage to the small vessels of the kidneys and retina, nervous system and other organs, including the heart. In this case, severe myocardial damage is possible, regardless of the severity of the atherosclerotic process in the coronary arteries. Clinically, this condition, which some authors call diabetic cardiomyopathy, is manifested by progressive heart failure and various rhythm disturbances; in the advanced stage it resembles primary congestive cardiomyopathy. Damage to the cardiovascular system in diabetes mellitus is one of the most common causes of death in this disease.

Cardiomyopathywith thyrotoxicosis. In its development, a significant role is played by the indirect toxic effect of thyroid hormones on the myocardium, the development of atrial fibrillation and the severity of dystrophic changes in the myocardium. The development of heart failure is accompanied by dilatation of the heart chambers, which can sometimes precede the clinical picture of cardiac decompensation. Changes in the heart often come to the fore in patients with toxic adenoma, when the ocular symptoms and agitation typical of diffuse toxic goiter are absent.

Cardiomyopathywith hypothyroidism. Myxedema is characterized by an enlarged heart, a low pulse, and low blood pressure; Heart failure gradually develops with congestion in the systemic and pulmonary circulation. Patients complain of shortness of breath and heart pain. Often there is an effusion in the pericardial cavity. In rare cases, asymmetric myocardial hypertrophy similar to hypertrophic subaortic stenosis has been described. In severe cases, the heart X-ray resembles a bag spread out on the diaphragm with smoothed contours; the ECG typically shows a decrease in the voltage of all waves; there may be a slowdown in AV conduction, a decrease in the ST segment, smoothness or inversion of the T wave.

Cardiomyopathywith acromegaly. Acromegaly is a consequence of pituitary adenoma and excessive secretion of growth hormone. More often develops after 30 years. Headaches are typical, there may be visual impairment (bitemporal hemianopsia, complete blindness) due to damage to the chiasm, the patient’s body size increases, which is sometimes the first sign of the disease. The hands and feet become wide, the fingers take on the shape of sausages, and exostoses are possible. First, there is hyperfunction of some endocrine glands (thyroid, genital, adrenal cortex), later - their hypofunction. Diabetes mellitus is characteristic. There is an increase in internal organs. Due to the enlargement of the larynx, the voice becomes low. Cardiomegaly develops, in the progression of which arterial hypertension, typical of acromegaly, also plays a certain role, in particular due to secondary hyperaldosteronism.

At the very beginning, an increase in heart size does not lead to the development of heart failure. It occurs later in connection with the development of myocardial dystrophy and cardiosclerosis, since growth hormone stimulates excessive formation of connective tissue. In addition to the development of symptoms of heart failure, rhythm and conduction disturbances occur. Some patients develop severe damage to the heart muscle, which can be fatal.

A pituitary tumor is detected by X-ray (images of the skull and sella turcica, tomography, computed tomography). It is necessary to examine the fundus and visual fields (signs of increased intracranial pressure, tumor pressure on the chiasm), a neurological examination (signs of increased intracranial pressure, disturbances in the intracranial innervation of 3, 4, 6, 7, 12 pairs of nerves). High diagnostic value of determining increased activity of growth hormone in blood serum. The ECG reveals left ventricular hypertrophy, signs of myocardial ischemia, there may be cicatricial changes, diffuse muscle changes.

Obesity. Most authors highlight metabolic-nutritional (alimentary-constitutional) obesity, which is the most common, primary cerebral obesity and endocrine obesity in hypothyroidism, Cushing's syndrome and disease, decreased ovarian function and a number of other syndromes.

Changes in the cardiovascular system play a leading role in the clinical picture of obesity. As obesity progresses, the heart is surrounded by a fatty shell, fat is deposited in the connective tissue layers of the myocardium, complicating its contractile function. In addition, the risk of developing atherosclerosis increases and blood pressure rises, including in young patients. All these factors lead to an increase in the size of the heart due to hypertrophy and dilatation of both ventricles, especially the left. The clinical picture of heart damage is practically no different from that of ischemic heart disease and arterial hypertension. The obesity-hypoventilation syndrome (Pickwick syndrome) requires special attention. Typically, a combination of leading primary symptoms (obesity, hypoventilation, increased drowsiness) with secondary symptoms: diffuse cyanosis, mental disorders. Emphysema and the formation of cor pulmonale are characteristic. Some authors consider this symptom complex to be hereditary. Women get sick more often.

Cardiac ischemia. CMG is possible in some forms of IHD (even without hypertension). The development of myocardial hypertrophy in these cases is also a compensatory process. An increase in heart size is typical for any extensive myocardial infarction complicated by heart failure, post-infarction cardiosclerosis, or left ventricular aneurysm.

For diagnosis, ECG and echocardiography are widely used, which reveal segmental impairment of contractility - various types of asynergia: hypokinesia, dyskinesia, akinesia. Coronary angiography reveals varying degrees of stenosis of the coronary arteries and confirms the atherosclelic nature of ischemic cardiomyopathy.

CHF– a complex of characteristic symptoms (shortness of breath, fatigue and decreased physical activity, edema, etc.) that are associated with inadequate perfusion of organs and tissues at rest or during exercise and often with fluid retention in the body.

The most common causes of the development of CHF in Europe and Russia are ischemic heart disease and myocardial infarction, which are associated primarily with impaired systolic function of the left ventricle. Among other reasons for the development of CHF, dilated cardiomyopathy, rheumatic heart defects, arterial hypertension and hypertensive heart, myocardial lesions of any etiology, pericarditis, etc. should be noted.

In response to constant overload of the ventricles in CHF, their hypertrophy develops. With volume overload (for example, caused by valvular insufficiency), eccentric hypertrophy develops - dilation of the cavity with a proportional increase in myocardial mass, so that the ratio between wall thickness and ventricular volume remains almost unchanged.

With pressure overload (aortic stenosis, untreated arterial hypertension), on the contrary, concentric hypertrophy develops, which is characterized by an increase in the ratio between wall thickness and ventricular volume. In both cases, the compensatory capabilities of the myocardium are so great that overt heart failure often occurs many years later.

Criteria used to determine the diagnosis of CHF:

symptoms (complaints) – shortness of breath (from slight to suffocation), fatigue, palpitations, cough, orthopnea;

clinical signs – pulmonary congestion (wheezing, x-ray), peripheral edema, tachycardia (90 – 100 beats/min);

objective signs of cardiac dysfunction - ECG, chest x-ray; systolic dysfunction (decreased contractility, normal level of LV ejection fraction more than 45%), diastolic dysfunction (Doppler echocardiography, increased pressure in the pulmonary artery, hyperactivity of brain natriuretic hormone).

Cardiac aneurysm. Develops in 12-15% of patients who have had transmural myocardial infarction. One of the early symptoms of an aneurysm of the anterior wall of the left ventricle is precordial pulsation in the 3-4 intercostal spaces to the left of the sternum, which is determined by palpation and by eye (the “rocker arm” symptom). Aneurysms located at the apex of the heart often reveal the phenomenon of a double apex beat: its first wave occurs at the end of diastole, and the second is the apex beat itself. Rarer aneurysms of the posterior wall of the left ventricle are more difficult to diagnose due to the absence of pathological pulsation of the anterior chest wall. The apical impulse in patients is usually increased. There is a discrepancy between the increased pulsation at the apex of the heart and the small pulse at the radial artery. Pulse blood pressure is reduced. ECG: absence of dynamics of acute myocardial infarction (frozen nature of the curve: upward displacement of the S-T segment, appearance of the QS complex in the corresponding leads) is an important diagnostic sign of cardiac aneurysm. Electrokymography reveals paradoxical pulsation of the cardiac circuit. X-ray and tomography of the heart are also used. Echocardiography reveals an area of dyskinesia and akinesia. Radionuclide ventriculography and coronary angiography are also used.

Arterial hypertension are one of the common causes of heart enlargement. As a rule, the severity of arterial hypertension and the duration of its existence correspond to the severity of CMH, but there are exceptions.

An increase in heart size in hypertension is a mandatory symptom and goes through several stages. Initially, concentric hypertrophy develops, involving the “outflow tract” from the left ventricle from its apex to the aortic valves. During this period, the enlargement of the left ventricle may not be physically detected, although an increased apical impulse is often palpated, especially in the position on the left side. In the case of moderate hypertension, this condition can last for years.

Subsequently, hypertrophy and dilatation develop along the “inflow path” from the left ventricle to the apex; hypertrophy takes on an eccentric character, the left border of the heart shifts to the left and down, the apical impulse becomes high and lifting. At this stage, it is also possible that the left atrium is enlarged and some smoothing of the heart’s waist is detected during percussion of the boundaries of relative cardiac dullness.

The next stage is an enlargement of all parts of the heart, the development of total CMG. In the case of pronounced progression of hypertension and malignant hypertension, this condition can develop relatively quickly. Slowly progressing hypertension rarely leads to the formation of significant CMH, and symptoms of heart failure do not appear for a long time. To diagnose hypertension, blood pressure is monitored, an ECG (signs of LVH), the fundus of the eye is studied (hypertensive angiopathy), an X-ray examination of the size of the heart, and echocardiography. Other causes of CMG are excluded.

Acquired heart defects- acquired morphological changes in the valve apparatus, leading to disruption of its function and hemodynamics. Most often they arise as a result of acute rheumatic fever, infective endocarditis, systemic connective tissue diseases, trauma, and mitral valve prolapse (MVP). The main signs of acquired heart defects are shown in Table 2.

The term “diabetic cardiomyopathy” is accepted both in domestic and foreign literature. According to the classification approved by the National Congress of Cardiologists of Ukraine (2000), a group of metabolic cardiomyopathies has been identified, which includes diabetic cardiomyopathy.

In accordance with the classification of the International Federation of Cardiologists, non-coronary heart disease in diabetes mellitus is called the collective term “ diabetic cardiomyopathy».

Pathogenesis of diabetic cardiomyopathy

Currently, there are three main pathogenetic mechanisms for the formation of cardiomyopathy in type 1 diabetes mellitus:

metabolic
microangiopathic
neurovegetative-dystrophic.

Metabolic mechanism

The leading role in the development of cardiomyopathy in diabetes mellitus in children is played by metabolic disorders both in the body in general and in the myocardium itself, resulting from insulin deficiency.

It is known that insulin has direct and indirect effects on the heart. The direct effect is to increase the flow of glucose and lactate into the myocardium and stimulate their oxidation. Insulin increases and stimulates the activity of glucose transport protein 4 and its transfer of glucose into the myocardium, activates hexokinase and glycogen synthetase, and increases the formation of glycogen in the myocardium. Its indirect effect is the regulating influence of the level of fatty acids (FA) and ketone bodies in the blood plasma, inhibition of lipolysis and ketogenesis in the liver (after meals).

Insulin reduces the concentration of fatty acids and ketone bodies in plasma and inhibits their entry into the heart. In conditions of insulin deficiency and insulin resistance (IR), these mechanisms of insulin action are disrupted. The metabolism of glucose and FA changes, the amount and activity of glucose transport protein 4 and its transfer of glucose into cells decreases. In the blood plasma, the concentration of FA increases and the flow of glucose and lactate into the heart decreases.

Under physiological conditions, the body has a constant balance between the level of free radicals (oxidants) and the activity of the antioxidant defense system. Under normal conditions, free radicals are quickly neutralized by natural fat- and water-soluble antioxidants. However, in patients with diabetes, the level of natural antioxidants is significantly reduced, which leads to a pathological increase in the number of reactive radicals, that is, to oxidative or so-called oxidative stress.

Thus, low concentrations of insulin are unable to adequately suppress lipolysis in adipocytes, which leads to a sharp increase in the level of free fatty acids (FFA) in the blood. This reduces the absorption of glucose by the myocardium and its oxidation. Competition is formed at the mitochondrial level during the formation of acetyl-CoA. As a result of excess acetyl-CoA, pyruvate dehydrogenase activity is blocked. An excess of the resulting citrate inhibits the glycolytic activity of phosphofructokinase, leading to the accumulation of glucose-6-phosphate, which in turn inhibits hexokinase and thereby reduces the rate of glycolysis.

The glycolytic fraction of ATP is used to ensure membrane transport of calcium, namely Ca2+-ATPase of the ion pump of the sarcoplasmic reticulum, in reactions coupling electrophysiological and contractile processes in the myocardium.

Suppression of glycolysis leads to a constant pronounced excess of calcium inside the cell, causing the following consequences:

Myocardial contracture is provoked with impaired myocardial relaxation and the occurrence of rigidity of the heart muscle. It leads to ischemia and necrosis.
The cell's compensatory response to excess calcium in the cytoplasm is to increase its uptake by mitochondria. However, this process is energy-dependent, which means that the ATP pool is stolen, which can be used for cardiac contraction.
Activation of phospholipases that destroy cell membranes.

Impaired acetyl-CoA carboxylase activity leads to intensification of β-oxidation of fatty acids, thereby displacing long-chain FAs from this process with the subsequent accumulation of their under-oxidized metabolites in the cytoplasm and mitochondria. The result of the accumulation of fatty acid oxidation products is a decrease in the general and regional contractile function of the myocardium, a shortening of the membrane action potential, which is the leading cause of the formation of malignant rhythm disturbances, including sudden death.

Microangiopathic mechanism

Chronic hyperglycemia, leading to protein glycation and stimulation of peroxidation in the foam cells of the vascular endothelium, leads to the formation of microangiopathy of various localizations.

Excessive amounts of lipid peroxidation (LPO) products have a cytotoxic effect, which is manifested by damage to the membranes of erythrocytes and lysosomes. In this case, the structure of cell membranes changes until they rupture, and the activity of cytochrome oxidase is inhibited. The process also affects the vessels that supply the heart, which underlies ischemic damage to the heart muscle.

Neurovegetative-dystrophic mechanism

Metabolic disorders and microangiopathies lead to deterioration of trophic processes in the autonomic centers, nerve trunks, the formation of axonal degeneration and demyelination of nerve fibers - the development of autonomic cardiac neuropathy. It is manifested by the gradual development of vagal denervation of the heart, which is the main cause of disturbances in normal heart rate variability, which leads to energy deficiency in the myocardium, contributing to the progression of cardiomyopathy.

Morphological changes in diabetic cardiomyopathy

The morphological result of these processes is a violation of the ultrastructure of myocardiocytes - enlargement of the nucleus, swelling of mitochondria with a pathological configuration of crypts, a decrease in the number of ribosomes, expansion of the tubules of the sarcoplasmic reticulum, intracellular edema, the appearance of fat droplets, and the disappearance of glycogen grains. According to some data, apoptosis in cardiomyocytes in patients with diabetes mellitus occurs quite intensively.

Characteristic features of ultrastructural changes in myocardial cells in cardiomyopathy of any etiology, including diabetic, are nonspecific and reversible. After eliminating the cause, the structure of cardiomyocytes is restored due to intracellular regenerative processes. However, recent research in this area demonstrates that long-term inadequate glycemic control is associated with increased collagen fiber content and gelatinase activity in the myocardium and the formation of significant alteration and fibrosis.

Clinic

Cardiomyopathy in type 1 diabetes mellitus in the early stages of its development has minimal clinical manifestations, which are nonspecific and intensify with ketoacidosis and hypoglycemia (general weakness, moderate shortness of breath during exercise, palpitations, prolonged, often vague pain in the heart, not typical for angina localization).

An objective examination reveals a weakening of heart sounds, a systolic murmur above its apex and at the Botkin-Erb point, and an expansion of the boundaries of relative cardiac dullness.

A significant clinical result of the complex of metabolic, angiopathic, neuropathic influences are rhythm and conduction disturbances in the form of sinus arrhythmia, tachycardia, bradycardia, intraventricular conduction disorders, supraventricular extrasystole and transient atrioventricular block of the I-II degree.

One of the early manifestations of cardiac dysfunction in patients with type 1 diabetes mellitus (DM1) is the deterioration of diastolic relaxation of the myocardium, that is, the development of a “diastole defect”. Left ventricular systolic function is usually normal at rest, but may change with exercise. It has been established that disturbances in the diastolic function of the left ventricle are most pronounced in patients with type 10 diabetes mellitus with the presence of late complications.

An imbalance in the autonomic regulation of cardiac activity as a component of autonomic cardiac neuropathy is characterized by a decrease in parasympathetic influence and an increase in sympathetic influence on the regulation of sinus rhythm, which is manifested by tachycardia at rest, orthostatic hypotension with dizziness, and a decrease in blood pressure when getting out of bed by more than 30 mm Hg. Art., arrhythmia; persistent tachycardia (including resting tachycardia), fixed heart rate and decreased heart rate variability during deep breathing. In this case, a negative Valsalva maneuver or bradycardia is determined, a decrease in the Valsalva ratio ≤ 0.21 (ECG norm: max R-R on exhalation / max R-R on inhalation > 0.21). Cardiac arrhythmias are predictors of sudden death.

Diagnosis of diabetic cardiomyopathy

The list of diagnostic measures when establishing a diagnosis of diabetic cardiomyopathy includes the following:

complaints, anamnesis, clinic;
glycemic and glucosuric profile;
electrocardiography;
echocardiography using functional tests;
doppler echocardiography (according to indications);
study of the lipid spectrum of blood;
daily monitoring of blood pressure and ECG.

Treatment of diabetic cardiomyopathy

The main treatment strategy for diabetic cardiomyopathy consists of the following areas:

Rationalization of diet therapy, insulin therapy, and physical exercise regimens in order to achieve optimization of glycemic control.
Use of potassium, L-carnitine, ATP, etc. preparations for metabolic and cardiotrophic purposes.
Prescription of B vitamins for the purpose of neurotropic effects; drugs that improve neuromuscular conduction.
If arrhythmia is present, use antiarrhythmic drugs.
If there are signs of heart failure - diuretics, ACE inhibitors, cardiac glycosides.

From the monograph “Diabetes mellitus: from child to adult”

Senatorova A.S., Karachentsev Yu.I., Kravchun N.A., Kazakov A.V., Riga E.A., Makeeva N.I., Chaichenko T.V.
State Institution “Institute of Endocrine Pathology Problems named after. V.Ya. Danilevsky AMS of Ukraine"
Kharkov National Medical University
Kharkov Medical Academy of Postgraduate Education of the Ministry of Health of Ukraine

Definition
Diabetic cardiomyopathy is a heart pathology that develops in children with diabetes or in children born to mothers with diabetes. In the latter case, it is one of the manifestations diabetic embryofetopathy. In a pregnant woman with diabetes, the risk of congenital malformations is 4-6 times higher than the general population risk. The most common malformations are malformations of the brain and nervous system (anencephaly, spinal hernia), as well as malformations of the urinary system, skeleton, and heart. About 30% of children born to mothers with diabetes have diabetic cardiomyopathy.

Etiology and pathogenesis
Insufficient compensation of diabetes mellitus in the mother and persistent hyperglycemia are risk factors for the development of diabetic cardiomyopathy in the fetus and newborn.

Since glucose easily crosses the placenta, its concentration in fetal blood is 70-80% of that of the mother. Fetal hyperglycemia leads to Langerhans cell hyperplasia in the fetus, followed by hyperinsulinemia, stimulation of glucose and amino acid uptake by tissues, increased gluconeogenesis and lipogenesis. Myocardial hypertrophy is one of the symptoms of diabetic embryofetopathy (DF), a special case of generalized organomegaly.

The genesis of diabetic myocardial hypertrophy lies in the anabolic effect of insulin, which causes hypertrophy and hyperplasia of the cardiomyocyte by acting on myocardial insulin receptors, followed by an increase in protein synthesis. If the number of insulin receptors does not decrease in the postnatal period, then myocardial hypertrophy also persists. Recently, in patients with DF, considerable attention has been paid to the insulin-like growth factor IGF-I. Normally, its concentration in the mother's blood increases during pregnancy and by the 36th week of gestation averages 302–25 ng/ml; with a lack of IGF-I, fetal growth retardation occurs, and the child is born with low body weight.

In mothers with diabetes mellitus, the level of IGF-I by the 36th week of gestation is significantly increased compared to healthy mothers (mean 389–25 ng/ml). A similar increase in IGF-I (up to 400–25 ng/mL) is noted in the presence of ventricular septal hypertrophy in newborns, which may also indicate the role of this factor in the development of secondary cardiomyopathy.

It can manifest as symmetrical or asymmetric (45%) myocardial hypertrophy; in rare cases, obstruction of the left ventricular outflow tract is possible. The thickness of the interventricular septum can reach 14 mm (with a normal value of M + 2SD up to 8 mm in a newborn child). This is accompanied by a violation of both systolic and diastolic myocardial function. The same patient may have a combination of congenital heart disease and myocardial hypertrophy.

Clinical picture
A newborn with diabetic fetopathy of large size, often of a “Cushingoid” appearance: facial hyperemia or cyanosis, lethargy, and swelling are noted. Possible respiratory failure due to RDS syndrome, hemorrhagic syndrome. Body weight often exceeds 4 kg. The clinical picture of cardiomyopathy depends on the severity of hypertrophy. Along with asymptomatic variants, systolic murmur of varying intensity can be heard. Possible heart rhythm disturbances. Symptoms of heart failure appear when the systolic or diastolic function of the ventricles is impaired.

Diagnostics
Regardless of symptoms, all newborns born to mothers with diabetes mellitus are advised to undergo a screening echocardiographic study.

1. Electrocardiography. ECG changes are nonspecific. There may be signs of right ventricular or biventricular hypertrophy, more often noted when the left ventricular outflow tract is narrowed.

2. Chest X-ray. The changes are non-specific. In approximately 50% of cases there is moderate cardiomegaly.

3. Echocardiography. The most common finding is hypertrophy of the interventricular septum; hypertrophy of the free wall of the ventricles is also possible. In approximately 45% of cases, hypertrophy is asymmetrical (the ratio of the thickness of the IVS to the thickness of the posterior wall of the left ventricle is equal to or more than 1.3). The cavity of the left ventricle can be reduced to the point of being slit-like. Doppler sonography reveals signs of impaired diastolic function. Myocardial systolic function may be normal.

Treatment
Newborns with diabetic embryofetopathy often require resuscitation measures immediately after birth in the form of sanitation of the upper respiratory tract and various types of respiratory support, including mechanical ventilation, incubation, infusion therapy, and cardiotonic support. For obstruction of the left ventricular outflow tract, b-blockers are used. The use of inotropic drugs (including digoxin) is contraindicated. Diuretics are prescribed according to indications. Hypoglycemia, hypomagnesemia, and hypocalcemia are corrected.

Forecast
Intrauterine fetal death in mothers with diabetes mellitus is more common than the average population. However, this is associated not so much with the pathology of the fetus itself, but with problems related to the mother - hyperglycemia, vascular damage, polyhydramnios, preeclampsia.

After birth, the prognosis is usually favorable; by the sixth month of life, complete regression of myocardial hypertrophy occurs. However, hypertrophy may persist in the presence of persistent hyperinsulinemia, as is seen in nesidioblastosis. Cases of death have been described.

New articles

Effective: topical corticosteroids. Effectiveness is assumed to be: control of house dust mites. Effectiveness not proven: dietary interventions; long-term breastfeeding in children prone to atopy. go

WHO recommendations for tertiary prevention of allergies and allergic diseases: - products containing milk are excluded from the diet of children with a proven allergy to cow's milk proteins. When supplementary feeding, hypoallergenic mixtures are used (if so. go

Allergic sensitization in a child suffering from atopic dermatitis is confirmed by an allergological examination, which will identify causally significant allergens and take measures to reduce contact with them. In children. go

In infants with a family history of atopy, exposure to allergens plays a critical role in the phenotypic manifestation of atopic dermatitis, and therefore elimination of allergens at this age may lead to a reduction in the risk of developing allergens. go

The modern classification of prevention of atopic dermatitis is similar to the levels of prevention of bronchial asthma and includes: primary, secondary and tertiary prevention. Since the causes of atopic dermatitis are not up to date. go

Diabetic cardiomyopathy

… is one of the variants of dysmetabolic cardiopathy.

Diabetic cardiomyopathy is a pathology of the heart muscle in patients with diabetes mellitus, unrelated to age, arterial hypertension, valvular heart disease, obesity, hyperlipidemia and pathology of the coronary vessels, manifested by a wide range of biochemical as well as structural disorders, which subsequently lead to systolic and diastolic dysfunction, and in ending in congestive heart failure.

Diabetic cardiomyopathy is divided into primary and secondary. Primary is the result of the accumulation of glycoprotein complexes, glucuronates and abnormal collagen in the interstitial tissue of the myocardium. Secondary develops due to extensive damage to the capillary bed of the myocardium by a microangiopathic process. As a rule, these two processes develop in parallel. Histological examination reveals (1) thickening of the capillary basement membrane, as well as (2) proliferation of endothelial cells, (3) microaneurysms, (3) myocardial fibrosis, degenerative changes in muscle fibers.

Main reason diabetic cardiomyopathy is a violation of redox reactions due to insufficient supply of energy substrates under conditions of hyperglycemia. The mechanism of this pathology can be presented as follows: absolute or relative deficiency of insulin leads to a sharp decrease in glucose utilization in target cells. Under such conditions, the need for energy expenditure is met through the activation of lipolysis and proteolysis; the basis for replenishing the energy needs of the myocardium is the utilization of free fatty acids and amino acids. In parallel, there is an accumulation of triglycerides, fructose-6-phosphate, glycogen and other polysaccharides in the heart muscle. These biochemical changes are complicated by a parallel disruption of intracellular metabolism of NO, Ca2+ and proliferative processes in blood vessels caused by the action of insulin and/or insulin-like growth factor. Impaired liver function as a result of the development of diabetic hepatosis aggravates and accelerates the development of metabolic disorders in the myocardium. (!) Since the pathogenetic basis of diabetic cardiomyopathy is deep decompensation of diabetes mellitus, it develops, as a rule, in patients with insulin-dependent diabetes mellitus with frequent ketoacidosis.

Thus, diabetic cardiomyopathy is pathogenetically one of the variants of dismetabolic cardiopathy and implies dystrophic changes in the myocardium specific to diabetes due to long-term metabolic disorders in the form of disorders inherent in diabetes: (1) energy supply to cells, (2) protein synthesis, (3) electrolyte exchange and exchange of microelements, (4) redox processes, (5) oxygen transport function of blood, etc. Microangiopathy, as well as dishormonal disorders, play a certain role in the origin of diabetic cardiomyopathy.

Clinical manifestations diabetic cardiomyopathy is caused by impaired myocardial contractility due to a decrease in the mass of myocardial cells. At the same time, patients note aching, diffuse pain in the heart area that is not clearly related to physical activity and, as a rule, does not have the irradiation characteristic of IHD and goes away on its own, without the use of coronary lytics. Signs of heart failure gradually increase (shortness of breath, swelling, etc.). At the same time, patients almost always develop other late complications of diabetes mellitus, such as retinopathy, nephroangiopathy, etc. Further progression of diabetic cardiomyopathy depends on the duration and degree of decompensation of diabetes mellitus, as well as on the severity of arterial hypertension. (!) Remember: diabetic cardiomyopathy is asymptomatic for a long time, and in most patients there is a significant gap (interval) in time between (1) the appearance of structural and functional disorders and its (2) clinical manifestation.

Diabetic cardiomyopathy in young people has no specific symptoms and in most cases occurs without subjective symptoms. However, special studies quite often reveal functional changes in the myocardium. Thus, in 30-50% of people with diabetes under 40 years of age, the ECG reveals smoothness, deformation of the P and R waves, changes in the duration of the P-Q, Q-T intervals, a decrease in the amplitude of the QRS complex, and an increase in the Macruse index. After physical activity (and sometimes at rest), a shift in the S-T interval and various changes in the T wave occur, which are interpreted without sufficient grounds as manifestations of myocardial ischemia. Various disorders of heart rhythm and conduction are common: (1) sinus tachy and (2) bradycardia, (3) sinus arrhythmia, (4) periodically occurring lower atrial rhythm, (5) partial disruption of intraventricular conduction, etc.

Diagnostics. Since the clinical signs of diabetic cardiomyopathy are very nonspecific, instrumental methods such as (1) phonocardiography and electrocardiography are used to verify the diagnosis; (2) echocardiography; (3) myocardial scintigraphy with thallium-201. The most informative methods are echocardiography and scintigraphy, which allow reliably assessing changes in heart mass, as well as a decrease in myocardial contractility. The development of cardiac inactivity syndrome is accompanied by a decrease in stroke and minute volume.

Principles of treatment. Correction of glycemic levels is a prerequisite. As diabetes is compensated, myocardial contractile function improves. For the treatment of cardiac pathology in diabetes mellitus, the use of thiazolidinediones (Thiazolidinediones), which reduce the proliferation of vascular smooth muscle cells and the contractility of the vascular walls, is indicated. Metformin promotes glucose uptake into vascular smooth muscle cells in combination with autophosphorylation of insulin receptors and insulin-like growth factor-1 (IGF-1). These effects may lead to overcoming the vascular resistance to insulin and IGF-1 that is observed in type 2 diabetes. One of the thiazolidinediones, troglitazone, eliminates the delay in diastolic relaxation proven in a model of diabetic cardiomyoptia. However, to prove the effect of these drugs on mortality from cardiovascular pathology in diabetes, (!) it is necessary to conduct prospective controlled studies of morbidity and mortality with their use.

Given that LDL (low-density lipoprotein) is generally more atherogenic in people with diabetes, and that they have lower HDL (high-density lipoprotein) levels and elevated triglyceride concentrations, it is recommended that they receive a treatment regimen secondary prevention to reduce LDL levels to

Diabetic cardiomyopathy. Diagnosis and treatment of diabetic cardiomyopathy.

Insufficient compensation for diabetes mellitus in the mother and persistent hyperglycemia are risk factors for the development of cardiomyopathy in the fetus and newborn. Since glucose easily penetrates the placenta, its concentration in fetal blood is 70-80% of maternal blood. Fetal hyperglycemia leads to subsequent hyperinsulinemia, increased glycogenesis, lipogenesis, and protein synthesis; as a result, macrosomia and increased fat deposits in organs occur; cardiac hypertrophy is a special case of generalized organomegaly. Recently, the insulin-like growth factor IGF-I has received considerable attention in these patients. Normally, its concentration in the mother’s blood increases during pregnancy and by the 36th week averages 302 ± 25 ng/ml; with a lack of IGF-I, fetal development is delayed, and the child is born with a low birth weight. In mothers with diabetes, the level of IGF-I by week 36 was significantly increased compared to healthy mothers (average 389 ± 25 ng/ml). A similar increase in IGF-I (up to 400±25 ng/ml) is noted in the presence of hypertrophy of the interventricular septum in newborns, which may also indicate the role of this factor in the development of cardiomyopathy.

Diabetic cardiomyopathy found in approximately 30% of children born to mothers with diabetes. It can appear as symmetrical or asymmetrical (

45%) myocardial hypertrophy; in rare cases, narrowing of the left ventricular outflow tract is also possible. The thickness of the interventricular septum can reach 14 mm (with a normal value of M+2SD up to 8 mm in a newborn child). This is accompanied by impaired systolic and diastolic function of the heart. A combination of congenital heart disease and myocardial hypertrophy in the same patient is possible.

Natural history of diabetic cardiomyopathy. Intrauterine fetal death in mothers with diabetes mellitus is more common than the average population. However, this is associated not so much with the pathology of the fetus itself, but with problems related to the mother - hyperglycemia, vascular damage, polyhydramnios, preeclampsia.

After birth forecast usually favorable, by the sixth month there is a complete regression of myocardial hypertrophy. However, hypertrophy may persist with persistent hyperinsulinemia, as seen in nesidioblastosis.

Clinical symptoms of diabetic cardiomyopathy. In most cases, the disease is asymptomatic. However, respiratory disorders, hypocalcemia, hypoglycemia, hypomagnesemia and hyperbilirubinemia are possible as general somatic consequences of diabetes mellitus, as well as systolic murmur of varying intensity and rhythm disturbances. Symptoms of heart failure develop when systolic or diastolic ventricular function is impaired. Regardless of symptoms, all newborns born to mothers with diabetes mellitus should undergo screening echocardiography.

Electrocardiography. ECG changes are nonspecific. There may be signs of right ventricular or biventricular hypertrophy, more often observed with narrowing of the outflow tract of the left ventricle.

Chest X-ray. The changes are non-specific. In approximately 50% of cases there is moderate cardiomegaly.

Echocardiography. In this study, hypertrophy of the interventricular septum is most often detected; hypertrophy of the free wall of the ventricles is also possible. In approximately 45% of cases, hypertrophy is asymmetric (the ratio of the thickness of the IVS to the thickness of the posterior wall of the left ventricle is equal to or greater than 1.3). The cavity of the left ventricle is normal or slightly reduced. Systolic and diastolic functions of the ventricles are slightly impaired.

Treatment of diabetic cardiomyopathy. Treatment is symptomatic. The use of inotropic drugs (including digoxin) is contraindicated. Although children with diabetic cardiopathy often appear edematous, this is more often associated with fatty deposits than with true edema, so the use of diuretics is not always justified. Important is the correction of hypoglycemia, as well as hypocalcemia. In cases with obstruction of the outflow department of the left ventricle, adrenoblockers may be used.