Myocardial dystrophy is a non-inflammatory, non-degenerative lesion of the myocardial layer of the heart, the pathogenesis of which is based on metabolic disturbances in cardiomyocytes, accompanied by a significant decrease in not only the intensity but also the regularity of the heart.
The result of the dysmetabolic processes occurring in cardiomyocytes is the transition to the anoxic airway, which inevitably provokes a decrease in the effectiveness of myocardial heart trophism.
Myocardial dystrophy is not yet adequately studied as a separate nosology and requires the attention of scientists in determining the tactics of managing patients suffering from this pathology.
In daily practice, specialists of any profile, including cardiologists, use a single generally accepted classification of ICD-10, in which each nosological form is indicated by the serial number (myocardial dystrophy code according to ICD-10: I42). Practical use of this code allows a doctor to recognize a diagnosis verified in a specific patient anywhere in the world.
Causes of myocardial degeneration
The main provoking factor in the development of myocardial dystrophy is any pathological or physiological condition, accompanied by a mismatch between the requirements of the heart muscle in energy resources and the body's ability to produce this amount of energy. In most situations, this pathology is a consequence of other nosological forms and is called "myocardial dystrophy secondary."
Depending on the origin, myocardial dystrophy divides into two large categories: formed against a background of any pathology of the heart or developing against a background of diseases not accompanied by a violation of cardiac activity. As a cardiac pathology against which myocardial dystrophy may develop, any cardiovascular disease can occur, other than inflammatory myocardial damage.
The most common situation in which this energy imbalance in the myocardium develops is the prolonged deficiency of vitamins and essential nutrients in the human body, which occurs with prolonged unbalanced nutrition and hunger. In addition, with excessive physical activity in professional athletes, as well as during pregnancy, myocardial dystrophy does not develop due to inadequate intake of nutrients in the body, but as a result of excessive consumption of them.
According to the etiopathogenetic classification of this pathology, a number of specific forms are distinguished: tonsillogenic myocardial dystrophy (damage to cardiomyocytes as a result of intoxication in inflammation of the tonsils), intoxication myocardial dystrophy (alcoholic), caused by toxic effects on cardiomyocytes. For the development of alcoholic myocardial dystrophy, a long-term course of alcoholism is a prerequisite. In addition, myocardial dystrophy toxic can be provoked by prolonged exposure to the human body of toxins of various kinds (benzols, nicotine, aniline), as well as drugs during their overdose.
Neuroendocrine myocardial dystrophy is formed on the background of various violations of the hormonal status of the patient, as well as in the violation of neurohumoral regulation. Dystrophic damage to the myocardium develops because the structures of the nervous system are in a constant excited state, accompanied by excessive production and release of adrenaline into the total blood flow. The above changes inevitably provoke an increase in the load on the myocardium, which ends with the formation of irreversible dystrophic changes.
Despite the polyethiologic nature of this pathology, all etiopathogenetic variants of myocardial dystrophy are characterized by a single pathogenetic mechanism of development, based on the violation of energy intracellular metabolism. The development of myocardial dystrophy in severe anemia is explained by the formation of hemic hypoxic damage, which inevitably provokes the development of energy deficiency in the myocardium. Thus, any form of anemic syndrome, both acute and chronic, is accompanied by the development of dystrophic changes in the myocardium.
For a long time myocardial dystrophy of the heart is accompanied by the formation of only reversible changes in the myocardial layer, and only in the final stage of the disease does the patient notice the development of degenerative changes of an irreversible nature.
With regard to the development of myocardial dystrophy in childhood, the most common etiologic factor is the rickets suffered at an early age, but the debut of clinical manifestations is at school age, when the physical and psychoemotional load significantly increases. In a situation where signs of myocardial dystrophy are observed in a newborn child, one should examine such a patient for the presence of foci of intrauterine infection, as well as signs of perinatal encephalopathy, as these pathological conditions become a favorable background for the development of dystrophic changes in the myocardium immediately after birth.
Symptoms of myocardial dystrophy
All clinical manifestations of myocardial dystrophy are based on violations of cardiohemodynamics caused by a moderate or severe decrease in the contractile function of the heart. The most characteristic complaints of a patient suffering from myocardial dystrophy are a feeling of aching pain in the projection of the location of the heart, a feeling of discomfort and irregular heart rhythmicity, which are short-lived and do not involve a significant disability of a person. Nonspecific complaints due to violation of the blood filling of the brain structures are headaches, inability to perform the usual physical activity, periodic episodes of dizziness and drowsiness.
In a situation where myocardial dystrophy is accompanied by the development of degenerative changes in the myocardium and the appearance of signs of congestive heart failure, the patient develops pathognomonic symptoms in the form of pronounced edematic syndrome of both peripheral and central type, progressive respiratory disorders and cardiac arrhythmias in the form of extrasystole , tachycardia and paroxysmal atrial fibrillation . This clinical symptom complex is observed in all types of myocardial dystrophy, but each etiopathogenetic variant of this cardiac pathology is characterized by the development of specific manifestations.
Myocardial dystrophy in children has certain features of the course, manifested by a prolonged latent period, during which the child does not experience any clinical manifestations at all. This period is dangerous because without routine methods of diagnosis, early verification of the diagnosis is much more difficult and there is a high risk of developing cardiovascular complications against the background of complete well-being.
Tonsilgenic myocardial dystrophy is characterized by the fact that the development of clinical signs occurs a few days after the transference of angina and manifests itself in the form of an intense pain syndrome in the heart, progressive weakness, heart failure, subfebrile fever and arthralgia.
With regard to diagnostic measures that allow reliable verification of the diagnosis, electrocardiography, echocardioscopy and phonocardiography are used. The main electrocardiographic criteria for myocardial dystrophy is the appearance of an incorrect orientation and deformation of the T wave in several leads, a distorted U wave, and a ST segment decrease by at least 1 mm. These changes are not specific, and for their detection, an obligatory condition is the implementation of a 24-hour Holter electrocardiographic monitoring.
More specific changes are characterized by myocardial dystrophy in the performance of echocardioscopy, since in this situation, the patient shows signs of hemodynamic disorders with complete absence of organic damage to the myocardium. Changes in phonocardiography in myocardial dystrophy develop only at the stage of cardiac decompensation and are manifested in the form of recording the rhythm of gallop and systolic murmur in the projection of the apex of the heart.
Laboratory changes in myocardial dystrophy are detected only in the terminal stage and manifest as a decrease in the activity of mitochondria of cardiomyocytes. The identification of these changes reflects an extremely unfavorable course of myocardial dystrophy and is a negative prognostic sign.
In difficult diagnostic situations in which the patient has severe clinical manifestations and hemodynamic disorders that do not correspond to the detected changes in the myocardium, it is recommended that a puncture biopsy of the heart muscle is performed. For this purpose, the endomyocardial material is sampled under local anesthesia. This technique is difficult to perform, so its practical application is minimal.
In cardiological practice, specialists use the clinical classification of myocardial dystrophy, according to which it is common to divide the three stages of development of this pathology. In the initial stage there is a compensatory increase in the function of the heart muscle in response to the dysmetabolic disorders occurring in the myocardium. Clinically, this condition is manifested by nonspecific prolonged cardialgia and a certain decrease in the tolerance of physical activity. Instrumental imaging methods are not accompanied by the detection of pathological changes in the structures of the cardiovascular system. The stage of clinical compensation is characterized by the development of cardiohemodynamic and respiratory disorders. In this situation, with routine electrocardiographic studies, characteristic signs of hypertrophy of the left heart are revealed. The decompensated stage of myocardial dystrophy provokes the development of severe health disorders, and the patient's treatment must be pathogenetically grounded.
Dyshormonal myocardial dystrophy
The main etiological factor in the emergence of a disgormonal variant of myocardial dystrophy is an imbalance of normal ratios of thyroid hormones, leading to a violation of its basic functions. It should be borne in mind that equally, both hyperfunction and insufficient production of thyroid hormones equally negatively affect the state of electrolyte and energy metabolism of the myocardium. When there is insufficient production of hormones by the thyroid gland, the system slows down the metabolic processes of the whole organism. The slowing down of the metabolism in the myocardium is accompanied by the development of arterial hypotension , pain sensations in the region of the aching heart. Excessive production of thyroid hormones, on the contrary, is accompanied by an acceleration of metabolic processes, manifested in the form of the appearance of cardiac stitching, a violation of the rhythm of cardiac activity and increased irritability.
In addition, the violation of testosterone production in men, as well as estrogens in women, observed as physiological involutive changes, can become a provocateur of the development of metabolic abnormalities in the myocardium. In the cardiological classification, even there is a separate nosological form of the dyshormonal variant of this pathology called "climacteric myocardial dystrophy".
The development of dystrophic changes in cardiomyocytes with estrogen deficiency during menopause is explained by the fact that sex hormones exert a regulating effect on the electrolyte balance in the cells of the whole organism, including cardiomyocytes (increase in the concentration of iron, phosphorus, copper, stimulation of the synthesis of fatty acids), therefore, when estrogen deficiency is created conditions for the development of myocardial dystrophy. Recent studies in the study of the prevalence of dysmetabolic myocardiodystrophy in postmenopausal women have proven the need for a preventive screening survey of all women during this period.
It should be borne in mind that dyshormonal myocardial dystrophy can develop in a pregnant woman and adversely affect the normal development of the fetus, but this pathology is not an absolute indication for the termination of pregnancy, it is enough only to conduct dynamic ultrasound. The preferred method of delivery in this situation is operational.
Early verification of myocardial dystrophy is of great importance in preventing the development of possible complications and improving the prognosis for the full recovery of the patient.
Myocardial dystrophy of mixed origin
The emergence of myocardial dystrophy of mixed genesis is affected by persons of early childhood suffering from severe anemia in combination with neuroendocrine and electrolyte disorders. In addition, this form of myocardial dystrophy develops in adult patients suffering from a violation of hormonal status due to thyroid disease. The fundamental factor for establishing the diagnosis of "myocardial dystrophy of mixed genesis" is polyethiologic, that is, a combination of several provoking factors, which together form the conditions for the development of dystrophic changes in the myocardium.
Priority changes in the myocardium with myocardial dystrophy of complex genesis is a violation of its contractile function, especially the left heart. However, in the absence of timely treatment, myocardial dystrophy has an extremely negative effect on the automatism, conductivity and excitability of almost all parts of the myocardium, which provokes the development of severe cardiohemodynamic disorders.
In the onset of pathomorphological and pathogenetic manifestations of the disease, the clinical symptom complex in the form of a short pain syndrome in the projection of the location of the heart, are observed only after excessive physical activity, and in a calm state, the patient does not notice any changes in his own health.
Myocardial dystrophy of mixed genesis is characterized by rapidly progressive course and resistance to the use of drug treatment, therefore the only effective method of therapy is stem cell transplantation.
Myocardial dystrophy of a complex genesis
This variant of myocardial dystrophy is characterized by extremely severe course and its occurrence is not associated with any other cardiac pathologies. The main provoking factor in the development of myocardial dystrophy of a complex genesis still remains a systemic metabolic disorder in the body, including cardiomyocytes, which can be combined with other changes unrelated to cardiac activity.
The initial clinical manifestations of cardiomyodystrophy of complex genesis are so non-specific that in most cases it is not possible to establish a reliable diagnosis at this stage. At the stage of pronounced dystrophic changes in the myocardium, clinical manifestations can simulate other cardiac pathologies (fatigue, cardialgia, respiratory distress, cardiac rhythm disturbance). In connection with this, the fundamental criterion for verification of the diagnosis is the use of a wide range of instrumental studies with proven informativeness.
In most cases myocardial dystrophy of a complex genesis proceeds in a chronic form, however, in the presence of concomitant acute conditions present in the patient, as well as with a pronounced decrease in immunity, acute development of dystrophic changes in the myocardium can be observed. As a rule, such a background condition is significant arterial hypertension , pulmonary embolism , and in this case, the risk of lethal outcome caused by contracture dystrophy of the myocardium significantly increases.
The chronic course of myocardial dystrophy is characterized by a slow progression of pathological changes in the myocardium, as well as a prolonged latent period in respect of clinical symptoms. The most common and at the same time, a serious complication of this pathology is heart failure , which is characterized by refractoriness to drug therapy.
With regard to determining the tactics of treating a patient suffering from myocardial dystrophy of complex genesis, the priority is the normalization of the patient's lifestyle and the correction of eating behavior. In addition, bringing the main background disease into the compensation stage allows in some situations to avoid the appointment of a large volume of medicines.
Dysmetabolic myocardial dystrophy
This etiopathogenetic variant of the development of myocardial dystrophy is not a common diagnosis among the general morbidity of this cardiac pathology, and the basis for pathogenesis is the inadequate intake of necessary nutritional elements into the body. Dysmetabolic variant of myocardial dystrophy most often suffer patients with diabetes mellitus in the decompensated stage or amyloidosis . At the forefront of the clinical symptom complex are the manifestations of the main background pathology, and metabolic disturbances in the myocardium manifest themselves as the appearance of a nonspecific pain syndrome in the heart, weakness and disturbance of the rhythm of the cardiac activity.
Dysmetabolic myocardial dystrophy is characterized by rapid progression of cardiohemodynamic disorders and early development of signs of congestive heart failure. The development of decompensation of heart failure caused by atrophic and dystrophic changes in the myocardium greatly complicates the course of the background disease and has a very negative effect on the patient's duration and quality of life.
Treatment of myocardial dystrophy
The primary task of the attending physician is to conduct an explanatory conversation with the patient on the topic of lifestyle and eating behavior correction, since in many situations the elimination of the etiopathogenetic provoking factor avoids the use of medication. Indications for hospitalization of the patient depend on the stage of development of myocardial dystrophy and the need for correction of medication. In the stage of initial manifestations, patients with myocardial dystrophy are subject to dynamic observation and hospitalization in a cardiac hospital at most once a year for a planned screening examination. In this situation, drug treatment, as a rule, is not required, except for the appointment of fortifying and vitaminizing complexes.
In case of subcompensated myocardial dystrophy, the use of complex conservative treatment with the use of different groups of drugs is recommended, the action of which is aimed at eliminating metabolic and trophic disturbances in the myocardium. Patients with decompensated stage of myocardial dystrophy are subject to mandatory inpatient treatment in order to level out the signs of heart failure and prevent the development of complications.
With respect to drug treatment of any form of myocardial dystrophy, the main principle of selecting the necessary regimen and volume of medicines is the etiological focus, that is, the elimination of the underlying cause of myocardial changes, as well as the pathogenetic validity of the use of the drugs of a pharmacological group (for example, the intake of anabolic steroids that stimulate the metabolic processes occurring in the myocardium).
Pathogenetic drug therapy implies the appointment of those groups of drugs that are able to normalize the disturbed metabolism in cardiomyocytes, and long oral courses should be used (Mexicor, 1 tablet three times a day for at least two months). In connection with the fact that myocardial dystrophy is accompanied by the development of not only an energy imbalance, but also electrolyte disturbances in the myocardium, it is advisable to administer preparations containing potassium (Panangin orally 1 tablet three times a day). To eliminate the signs of increased excitability in the neuroendocrine variant of myocardial dystrophy, the appointment of daily tranquilizers (Adaptol 1 tablet once a day) is necessary, the advantages of which are the absence of negative influence on coordination of movements and sleep.
Surgical methods of treatment are used for preventive purposes in chronic tonsillitis (tonsillectomy), removal of the adrenals with their hyperplasia. The diagnosis of "dyshormonal myocardial dystrophy" should be accompanied by the appointment of drugs that normalize the hormonal status of the patient (triiodothyronine for correction of hypothyroidism in a daily dose of 25 mg). In a situation where the patient has alimentary protein or vitamin deficiency of a serious degree, one should resort to the parenteral route of introducing the missing amino acids and vitamin complexes. Myocardial dystrophy, developed against the background of an anemic syndrome, needs to be corrected for this condition, consisting of transfusion of the erythrocyte mass, and the administration of oral intake of iron-containing preparations.
In a situation where myocardial dystrophy is at the terminal stage of development and is accompanied by an expanded clinical symptomatology of heart failure, it is justified to administer preparations of the cardiac glycoside group (digoxin in a maintenance daily dosage of 0.125 mg). It should be borne in mind that with dystrophic changes in the myocardium, conditions are created for the rapid development of toxic effects of cardiac glycosides on the body, therefore, when the first signs of digitalization appear, the drug should be discontinued.
Subject to the patient's compliance with all recommendations for correcting nutrition, physical activity, and drug therapy, a favorable outcome of myocardial dystrophy is observed. In the case when the dystrophic changes in the myocardium are progressive, which is observed in chronic intoxication syndrome, diabetes mellitus, there is an early development of sclerotic changes in the myocardium in the form of diffuse or focal cardiosclerosis with the subsequent development of cardiac rhythm disturbances. The most favorable course and prognostic signs are characterized by a disgormonal variant of myocardial dystrophy, which is of a functional nature.
? Myocardiodystrophy - which doctor will help ? If there is or suspected development of myocardial dystrophy, you should immediately seek advice from such doctors as a cardiologist and endocrinologist.