Persistent cardiomyopathy

Constant cardiomyopathy (ZKMP) is still defined as dilatation, since with its development, the heart chambers expand, the myocardium begins to contract less and the pumping function decreases. This results in "stagnation" of the blood in the bloodstream, which is expressed in edema, an increase in the liver, ascites.

The incidence of cardiomyopathy according to various data is 400,000-550,000 cases per year, with a prevalence of 4-5 million people.

During the examination of the patient, in addition to physical examination, instrumental methods are used. In particular, ECG and echocardiography are performed, which allows us to evaluate the functional capacity of the heart and the degree of myocardial infarction. Depending on the indications, combined therapy is chosen, since cardiomyopathy is often a disturbance in the activity of other organs and systems of the body, except for the heart.

Video cardiomyopathy is a general characteristic

Description

Persistent (dilatatory) cardiomyopathy is a progressive pathology of the myocardium, characterized by an enlargement of the chamber of the left ventricle and a decrease in the strength of its contractions.

The term "cardiomyopathy" is used in cases where the disorder directly affects the myocardium. Other heart diseases like coronary artery disease and valve malformations can also ultimately lead to an increase in ventricles and heart failure. However, doctors do not classify heart muscle problems caused by these disorders, such as cardiomyopathy.

For stagnant cardiomyopathy, the following features are characteristic:

• It can develop at any age, but is more often defined in the period from 20 to 50 years.
• About 10% of people who develop congestive cardiomyopathy are over 65 years of age.
• Disorder occurs approximately 3 times more often in men than in women, and 3 times more often in blacks than whites.
• Every year, 5-8 out of every 100,000 people develop congestive cardiomyopathy.

A person with cardiomyopathy may have asymptomatic systolic dysfunction of the left ventricle, diastolic LV dysfunction, or both. When compensatory mechanisms can no longer compensate for the impaired function of the left ventricle, the disease is expressed by symptoms that collectively present a pathological condition such as chronic heart failure (CHF).

Pathogenesis of development

Stable cardiomyopathy is characterized by an increase in the ventricular chamber and systolic dysfunction with a change in the larger side of the size of the cavities of the left ventricle with or without a slight hypertrophy of the wall.

Hypertrophy can be estimated as the ratio of the mass of the ventricle to the size of its cavity.This ratio is reduced in individuals with dilated cardiomyopathies.

The increase in the remaining heart cells is due primarily to a violation of the work of the left ventricle.

Progressive dilatation can lead to significant mitral and tricuspid regurgitation, which in turn reduces cardiac output and increases systolic volumes and damage to the ventricular wall. This leads to further expansion and dysfunction of the myocardium.

In the period of early compensation, the impact volume and heart rate increase, which is accompanied by an increase in the peripheral vascular tone. The last compensatory mechanism helps maintain blood pressure at the proper level. There is also an increased rate of oxygen recovery in tissues with a change in the hemoglobin dissociation curve.

Additional mechanisms that triggered the development of ZKMP:

• Neurohormonal activation. Reduced cardiac output stimulates the adrenergic nervous system, as well as the renin-angiotensin-aldosterone system. In the course of their activation, arginine vasopressin is released and secretion of natriuretic peptides is performed. As a result, vasodilation and sodium thrombosis develop.
• Circulation of cytokines. These substances can provoke myocardial damage. In particular, TNF-alpha, which participates in all necrosis processes, works. The presence of this factor impairs the function of the left ventricle, and also gradually die cardiomyocytes. Also, some interleukins contribute to hypertrophy of the ventricle, which is confirmed by an increase in their number in the blood of patients with CHF.

Over time, the compensatory mechanisms are weakened, which contributes to further damage to the heart muscle, dysfunction and geometric remodeling of the heart (concentric or eccentric).

Video Dilatational cardiomyopathy. Pathogenesis. Dilated Cardiomyopathy 3D

Reasons

Congestive cardiomyopathy develops for various reasons, including heredity, infection and toxic effects.A systemic approach to the definition of etiology is needed to select the most effective treatment strategy.

The most common causes of congestive cardiomyopathy are:

• Heredity
• Secondary connection with other diseases of the heart and vessels (ischemia, hypertension, valve dysfunction, induced by tachycardia)
• Infectious factors of influence (viral, rickettsia, bacterial, fungal, metazol, protozoal)
• Metabolic disorders (endocrine pathologies such as hyperthyroidism, hypothyroidism, acromegaly, myxedema, hypoparathyroidism, hyperparathyroidism, as well as diabetes mellitus, pheochromocytoma and imbalances of such electrolytes as potassium, phosphate, magnesium)
• Rheumatologic / connective tissue disorders (scleroderma, rheumatoid arthritis, systemic lupus erythematosus)
• Disturbances of diet such as thiamine deficiency (beriberi disease), protein deficiency, fasting, insufficient carnitine
• Toxic effects of drugs, poisons, food products, anesthetics, heavy metals, ethanol
• Infiltrative diseases (hemohromatosis, amyloidosis, hemogenic disorder)
• Granulomatosis (sarcoidosis, giant cell myocarditis)
• Physical factors (extreme temperatures, ionizing radiation, electric shock, non-penetrating thoracic trauma)
• Neuromuscular diseases (muscular dystrophy, Duchenne dystrophy, fascioculogumeral dystrophy of the Landusi-Deherin, Friedreich's disease, myotonic dystrophy)
• Primary cardiac tumor (myxoma)
• Physiological aging of the body
• Immunological effects (post-vaccination, wheezing, transplant rejection)
• Stress-induced cardiomyopathy (Tacosci Cardiomyopathy)

Toxic effects are an important reason for the development of ZKMP.Almost a third of the cases of the pathology are caused by serious abuse of ethanol ( 90 g / day, or from 7 to 8 beverages per day) for more than 5 years in a row.

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In many cases, the cause of congestive cardiomyopathy remains unexplained. However, some idiopathic diseases may be the result of inability to identify etiological factors associated with infections or toxins.

Clinic

Symptoms indicate the severity of congestive cardiomyopathy and may include the following:

• Fatigue
• Sweat at physical activity or cough
• rthopnea, paroxysmal shortness of breath at night
• Pronounced swelling, weight gain or abdominal girth

In the physical examination, signs of heart failure can be determined. Additionally, vital signs that can be expressed in:

• Tahipnoe
• Tachycardia
• Hypertension or hypotension

Some clinical signs may indicate the presence of cardiac compensation or decompensation:

• Symptoms of hypoxia (eg cyanosis, fainting)
• Pulmonary edema (cracks and / or wheezing)
• A three-part rhythm of the heart
• Enlarged liver
• Ascites or peripheral edema

When looking at the neck attracts attention:

• Increase in jugular veins
• Hepatigular reflux (swelling of the cervical veins under pressure on the right hypochondrium)
• Changes in central venous pressure

The auscultation of the heart allows you to determine the following features:

• Cardiomegaly (increase in heart size)
• Noise (with corresponding changes)
• The accent of the second tone at the base (paradoxical splitting)
• Triple and four-part rhythm
• Irregular rhythm
• The rhythm of the gallop
• Tachycardia

Video Dilatational cardiomyopathy. Symptoms, Symptoms and Treatment Methods

Diagnostics

Examination of patients with suspected congestive cardiomyopathy may include the following:

• Echocardiography
• Complete blood test
• Heart biomarkers
• Electrocardiography (ECG)
• Tests of the thyroid gland function
• X-ray of the chest organs
• Analysis of B-type natriuretic peptide
• Magnetic resonance imaging of the heart (MRI)
• Integrated metabolism panel

In some cases, the diagnosis of congestive cardiomyopathy is based on an endomyocardial biopsy. Indications for such a study are as follows:

• The recent onset of the disease and rapid deterioration of the cardiac function
• The patient receives chemotherapy with doxorubicin
• The patient is ill with systemic diseases with possible cardiac insufficiency (eg hemohromatosis, sarcoidosis, amyloidosis, Leffler's endocarditis, endomyocardial fibroelastosis)

Treatment

Congestive cardiomyopathy is treated in the same way as chronic heart failure (CHF). Some therapeutic effects relate to symptomatic treatment, while others affect the effects of:

In the treatment of congestive cardiomyopathy, the following classes of drugs are used:

• Angiotensin converting enzyme (ACE inhibitors) inhibitors
• Angiotensin II receptor blockers
• Beta-blockers
• Antagonists of aldosterone
• Cardiac glycosides
• Diuretics
• Vasodilators
• Antiarrhythmic
• Inotropic agents
• Nitrates
• Anticoagulants can be used in individual patients.

Surgical treatment of patients suffering from refractory to the ongoing medical therapy include the following methods:

• Temporary mechanical circulatory support
• Auxiliary devices for the left ventricle
• Cardiac resynchronous therapy (biventricular stimulation)
• Gastrointestinal Surgery
• Heart transplantation

Forecast

With prolonged decompensation of congestive cardiomyopathy, mechanical support for circulatory or cardiac transplantation may be required.

For patients with complicated cardiomyopathy, the prognosis depends on several factors:

• Etiology of the disease
• Age (less favorable prognosis is more often male patients)
• Severe Congestive Heart Failure (CHF).

he Hearting Framingham study found that approximately 50% of patients diagnosed with CHF died within 5 years. Patients with severe heart failure are twice as likely to be at risk of death. With the presence of mild heart failure, better predictions are made, especially if the patient is treated with optimal medical therapy.

In determining the prognosis for ZKMP, a cardiopulmonary load test is performed, which is to analyze respiratory gases (volume of oxygen and volume of carbon dioxide). The VO2 peak reflects the functional capacity and heart reserve.  With its decrease, they suspect an early decompensation of cardiac activity.

Prevention

It is concluded in the conduct of non-pharmacological effects. In particular, the instructions for a sodium diet with salt restriction of up to 2 g / day are given. Its significance is very important and in some cases it can eliminate the need for diuretics or reduce their therapeutic dose. You should also adhere to fluid restrictions that necessarily complements a low-sodium diet. Patients may be involved in cardiovascular rehab with aerobic exercise.