What is left ventricular overload? Ventricular systolic overload

The left ventricle of the heart (LV) plays a significant role in organizing blood flow. This is where the large circle of blood circulation begins. Blood, saturated with oxygen and nutrients, is released from it into the aorta - a powerful arterial highway that feeds the entire body.

If the load on the heart muscle is constantly increased for any reason, left ventricular hypertrophy (cardiomyopathy) may develop. The pathology is expressed in thickening and compaction of the walls of the LV.

The occurrence of hypertrophy

The walls of the ventricular chambers consist of three layers:

Endocardium is an inner layer with a smooth surface that facilitates blood flow.
Myocardium is muscle tissue, the most powerful part of the wall.
The epicardium is the outer layer that protects the muscle.

Since the LV bears the main responsibility for pumping blood, nature has provided it with a certain margin of safety. The left chamber is larger than the right (the size of the LV is one third of the total volume of the cardiac cavities), its muscle tissue is noticeably more powerful. The average myocardial thickness in different parts of the LV ranges from 9 to 14 mm.

If the muscles of the chamber undergo increased stress (increased pressure or a significant volume of blood), the organ is forced to adapt to these conditions. The compensatory reaction of the LV consists of the proliferation of cardiomyocytes (heart muscle cells). The walls of the left ventricle become denser and gradually lose their elasticity.

The danger of left ventricular hypertrophy is a change in the normal process of muscle contraction. The result of this is insufficient blood supply to the internal organs. The threat of coronary artery disease, strokes, and myocardial infarction increases.

Types of hypertrophy

The proliferation of cardiomyocytes can spread throughout the entire chamber, or can be localized in different places. This is mainly the interventricular septum, the transition of the atrium to the LV, and the aortic opening. Depending on the places where the muscle layer thickened, several types of anomalies are distinguished:

Concentric hypertrophy of the left ventricular myocardium

The main reason is that the chamber is overloaded with blood pressure. With hypertension or narrowing of the aortic valve, the myocardium thickens evenly, sometimes thereby reducing the LV cavity. The muscle layer of the ventricle gradually increases in order to be able to push the entire volume of blood into the narrow opening of the main artery, and in case of hypertension - into the vessels compressed by spasm.

Eccentric left ventricular hypertrophy

Here the main role is played by the overload of the ventricular chamber with the amount of blood. As a result of insufficiency of the heart valves, the volume of ejection into the aortic opening is reduced. The chamber fills with blood, stretching the walls, causing the total mass of the LV to increase.

Obstructive cardiomyopathy

Obstruction is a bulging of an already enlarged wall into the lumen of the chamber. The ventricle is often divided in two, like an hourglass. If the myocardium is also enlarged in the area of blood ejection into the aorta, the uniformity of systemic blood flow is further disrupted.

The severity of the pathology is determined by the thickness of the overgrown tissue:

Severe LV hypertrophy - more than 25 mm.
Average - from 21 mm to 25 mm.
Moderate - from 11 to 21 mm.

Moderate left ventricular hypertrophy is not life-threatening. It is observed in athletes and people with physical labor who experience high stress.

Factors causing the disease

Excessive load on the LV is based on congenital or acquired heart disease.

Hereditary anomalies include:

Genetic defects. They arise as a result of mutation of one of the genes responsible for the synthesis of heart proteins. In total, about 70 persistent changes were found in these genes that cause proliferation of the LV myocardium.
Congenital defects: decreased aortic diameter (coarctation), ventricular septal defect, closed or absent pulmonary artery. It is with hereditary defects of the heart muscle that left ventricular hypertrophy in children is associated. Here, the main type of therapy is surgery.
Congenital narrowing of the aortic valve (the outlet of the left ventricle through which blood is ejected into the artery). Normally, the valve area is 3-4 square meters. cm, with stenosis it narrows to 1 square. cm.
Mitral regurgitation. A defect in the valve leaflets causes blood to flow back into the atrium. Each time during the relaxation phase, the ventricle becomes filled with blood (volume overload).

Acquired left ventricular myocardial hypertrophy can develop under the influence of certain diseases and factors:

Arterial hypertension. Holds first place among pathologies causing myocardial compaction (90% of cases). Muscle tissue grows due to the fact that the organ constantly works under pressure overload;
Atherosclerosis of the aorta. Cholesterol plaques are deposited on the walls of the aorta and in its valve, which later become calcified. The walls of the main artery lose elasticity, which interferes with the free flow of blood. The LV muscle tissue, experiencing increasing tension, begins to increase its volume;
Cardiac ischemia;
Diabetes;
Overeating, high weight, obesity;
Prolonged stress;
Alcoholism, smoking;
Adynamia;
Insomnia, emotional instability;
Hard physical work.

All of the above causes of left ventricular hypertrophy cause the heart to work more intensely. The reason for this is the thickening of the myocardium.

Signs of the disease

Cardiac pathology does not manifest itself for a long time. But over time, increased muscle mass begins to have an effect on systemic blood flow. The first signs of illness appear. They are usually associated with heavy physical activity. As the disease progresses, manifestations bother the patient even at rest.

Symptoms of left ventricular hypertrophy:

Shortness of breath, heart palpitations, lack of air.
Dizziness, fainting.
Anginal (squeezing, pressing) pain behind the sternum.
Changes in blood pressure.
High blood pressure, difficult to respond to therapeutic measures.
Swelling of the limbs and face in the evening.
Attacks of suffocation, causeless coughing when lying down.
Blueness of nails, nasolabial triangle.
Drowsiness, headaches of unknown origin, weakness.

If you notice such signs in yourself, you should rush to see a cardiologist.

Diagnosis of LV hypertrophy

At the first appointment, the doctor collects anamnesis (patient complaints, information about family diseases). If there are endocrine diseases, hypertension, or heart defects in the family, then hypertrophy of the walls of the left ventricle becomes more than likely.

To clarify the diagnosis, the following procedures are prescribed:

Chest X-ray. The x-ray will show enlarged shadows of the heart and shadows of the aorta;
Electrocardiogram;
Daily ECG monitoring;
Echocardiography;
Stress echocardiography (ultrasound of the heart before and after exercise);
Doppler test (checking cardiac blood flow also using stress);
Laboratory blood test;
Blood test for hormones;
Analysis of urine.

To determine the extent of the disease, the doctor will prescribe coronary angiography (an X-ray examination with the injection of contrast fluid into the cardiac bloodstream). This is how they determine how free the lumen of the coronary arteries is.

To accurately visualize intracardiac pathologies, cardiac MRI is performed.

Forms of treatment

Eccentric, obstructive and concentric left ventricular hypertrophy are difficult to treat. But modern medical technologies make it possible to significantly stabilize the patient’s condition. Treatment tactics are mainly complex.

Drug therapy

To restore the natural rhythm of the heart muscle, beta blockers (Propranolol, Anaprilin, Metapropol, Atenolol) are prescribed.

Calcium channel blockers (Verapamil, Procardia) correct the blood supply to the heart and central systems of the body and have a vasodilating effect.

ACE inhibitors - Capoten, Zestril, Enalapril. Reduce blood pressure.

Anticoagulants (Warfarin, Indandione derivatives) prevent the formation of blood clots in the ventricle.

Sartans (Lorista, Valsartan) are first-line drugs for the treatment of hypertension and the prevention of cerebral strokes.

Diuretics (Indal, Navidrex) are used in combination with the above-mentioned drugs if LV myocardial hypertrophy is pronounced.

Surgery

If drug therapy is ineffective, surgical techniques are used. The following surgical interventions are indicated:

Morrow operation - fragmentary removal of the myocardium in the area of the interventricular septum;
Mitral valve replacement;
Aortic valve replacement or transplant;
Commissurotomy - separation of adhesions at the mouth of the main artery, fused as a result of stenosis (narrowing);
Stenting of coronary vessels (introduction of an expander implant into the lumen of the artery).

In cases where the treatment of left ventricular hypertrophy does not give the expected results, a cardioverter-defibrillator or pacemaker is sewn in. The devices are designed to restore the correct heart rhythm.

ethnoscience

If the cardiologist approves, you can use the following means:

Infusions of cornflower, lily of the valley, hawthorn flowers;
Infusion of St. John's wort with honey;
A mixture of garlic and honey in equal parts;
Mixed decoction of wild rosemary, motherwort and cucumber;
Decoction of parsley stems in red wine.

Long-term consumption of baked milk with strawberry jam, grated cranberries with sugar, dried fruits, raisins, and dried apricots gives a good effect.

Finally

Increasingly, LV hypertrophy is being found in people under 35 years of age. Hoping for the compensatory capabilities of the young body, patients avoid going to the clinic.

But heart pathologies are dangerous because without medical treatment and control they steadily progress.

Only 5-10% of patients experience reverse development of cardiomyopathy. The rest fall into the high-risk group. Only persistent treatment and compliance with the cardiologist’s recommendations will allow a person not to change the usual rhythm of life.

Left ventricular hypertrophy, or cardiomyopathy, is a very common heart disorder in patients diagnosed with hypertension. This is a rather dangerous disease, since its final stage is often death in 4% of all cases.

1. What is it?

Hypertrophy implies thickening of the walls of the left ventricle and this does not occur due to the characteristics of the internal space. The septum between the ventricles changes, and tissue elasticity is lost.

The thickening is not necessarily uniform, but can occur only in some areas of localization.

Hypertrophy itself is not a diagnosis, but is one of the symptoms of any disease of the cardiovascular system. This is mainly hypertension. In addition, we can distinguish various types of heart defects, frequent and heavy loads on the heart muscle.

In order for the heart muscle to begin to increase in size, the following conditions are necessary:

A large load, which leads to expansion of the internal cavity of the heart. At the same time, during systole, the myocardium begins to contract more strongly.
Pressure load on the heart, which is characterized by the fact that in order to expel blood, muscle contraction must occur much more often and stronger.

Both of these provoking factors will contribute to the thickening of contractile fibers - myofibrils of cardiomyocytes. At the same time, mechanisms for increasing connective tissue are launched. The heart needs to increase its ability to expand more and more, so collagen development will occur faster.

Therefore, it turns out that hypertrophy in almost all cases leads to disruption of the structure of the myocardium. The more intense the process of hypertrophy, the faster the ratio of collagen and myocytes decreases.

The most dangerous situation is intense and sudden physical activity. This applies to people who smoke, abuse alcohol, or sedentary individuals whose physical activity increases sharply. If a modification of the left ventricle did not lead to death, this does not mean that it is safe for health. It can lead to quite serious disorders - it could be a myocardial infarction or stroke.

Left ventricular hypertrophy is a signal that indicates a worsening of the conditions in which the myocardium is located at that time. This is like a warning, indicating to a person the need to stabilize his blood pressure and correctly distribute the load.

2. Causes of hypertrophy

One of the main causes of left ventricular hypertrophy is heredity. A genetic predisposition has been observed in those people who have a history of heart disease in their family. Thickening of the walls of the left ventricle in such people is observed quite often.

The reasons also include the following:

hypertonic disease;
cardiac ischemia;
diabetes;
atrial fibrillation;
atherosclerosis;
aortic valve stenosis;
heavy weight;
diseases of the peripheral system;
great physical activity;
emotional instability;
anxiety, excitement, stress;
muscular dystrophy;
insufficient sleep and rest;
inactivity;
smoking;
alcoholism;
Farby's disease.

Long and intense sports and frequent training can also cause left ventricular hypertrophy. All of the above factors contribute to an increase in blood pulsation, as a result of which the heart muscle thickens. And this leads to thickening of the walls of the left ventricle.

3. Symptom

Hypertrophy provokes changes not only in the area of the walls of the left ventricle. This expansion also extends outward. Very often, along with thickening of the inner wall, the septum between the ventricles becomes thicker.

The symptoms of the disease are heterogeneous. In some cases, patients do not even know for several years that they have left ventricular hypertrophy. It is also possible that at the very beginning of the disease the state of health becomes simply unbearable.

Angina is the most common symptom indicating ventricular hypertrophy. Its development occurs due to compression of the blood vessels that provide nutrition to the heart muscle. Atrial fibrillation also occurs, atrial fibrillation and myocardial starvation are observed.

Very often a person has a condition in which the heart seems to freeze for a moment and does not beat at all. This leads to loss of consciousness. Sometimes the appearance of shortness of breath may indicate hypertrophy.

There are a number of additional symptoms of left ventricular hypertrophy:

high blood pressure;
pressure changes;
headache;
arrhythmia;
poor sleep;
general weakness and poor health;
heartache;
chest pain.

The list of diseases in which hypertrophy is one of the symptoms is as follows:

congenital heart defect;
swelling in the lungs;
glomerulonephritis in the acute stage;
myocardial infarction;
atherosclerosis;
heart failure.

4. Treatment

In order to carry out qualified treatment, it is necessary not only to diagnose the disease, but also to determine its nature of occurrence and the characteristics of its course. Based on the examination data obtained, the most optimal method of treating hypertrophy is selected, the purpose of which is to normalize myocardial function and provide adequate medical or surgical treatment.

Treatment of hypertrophy involves the use of the drug verampil along with beta blockers. Their combined use reduces the symptoms of the disease and improves the general condition of the patient. As additional therapy, it is recommended to follow a certain diet and give up unhealthy habits. Physical activity should be moderate.

The possibility of surgical intervention should not be ruled out. Its essence is to eliminate a section of the heart muscle that has been hypertrophied.

If symptoms relevant to this disease appear, you should consult a cardiologist. Do not delay treatment, as the disease can cause serious complications and death.

Drugs

Correctly prescribed therapy includes drugs that normalize blood pressure and reduce heart rate. ACE inhibitors are also used to prevent the progression of hypertrophy. Thanks to them, the symptoms of the disease gradually decrease.

All medications are primarily aimed at improving myocardial nutrition and restoring normal heart rhythm. These include: Verapamil, beta blockers and antihypertensive drugs (Ramipril, Enalaprim and others).

Treatment with folk remedies

Traditional methods of treating traditional medicine in the treatment of hypertrophy are used, but not often. The exception is those substances that have antioxidant properties, as well as some plants that have a calming effect.

Plants that can strengthen the walls of blood vessels and cleanse the blood of atherosclerotic plaques are also used. Taking vitamins and dietary supplements containing potassium, omega, calcium, magnesium and selenium is useful.

As additional remedies for hypertrophy, decoctions and infusions of the following medicinal herbs are used:

Mix 3 tablespoons of motherwort herb, 2 tablespoons of dried rosemary and wild rosemary, 1 spoon of kidney tea. Pour a large spoonful of this mixture into one and a half glasses of cold water and boil for 5 minutes. Wrap the broth in a warm cloth and leave for 4 hours. After straining, take half a glass warm three times a day before meals. The interval between taking the decoction and eating should be a quarter of an hour.
Pounded cranberries with sugar, a small spoonful three times a day after meals, is considered very healthy.

Diet

A therapeutic diet is an integral part of the treatment of hypertrophy. You should eat up to 6 times a day in small portions.

You should avoid salt, fried, fatty and smoked foods. The diet should always include dairy and fermented milk products, fresh fruits and vegetables, seafood, and lean meats. Flour products should be limited, as well as reduce the consumption of sweet foods to a minimum, and limit animal fats.

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Symptoms

LVH usually develops gradually. A patient in the early stages may not experience any symptoms. As LVH progresses, you may experience:

dyspnea;
fatigue;
chest pain, often after exercise;
a feeling of rapid or fluttering heartbeat;
dizziness or fainting.

You should seek immediate medical attention in the following cases:

chest pain lasts more than a few minutes;
severe shortness of breath;
severe, recurring dizziness or loss of consciousness.

If a person has mild shortness of breath or other symptoms (such as palpitations), they should visit their doctor.

Causes

Myocardial hypertrophy can occur when certain factors make the heart work harder. These include:

High blood pressure (arterial hypertension). This is the most common cause of myocardial hypertrophy. More than a third of people with LVH are diagnosed with hypertension.
Aortic valve stenosis. This is a narrowing of the opening of the valve that separates the aorta from the left ventricle. To pump blood through this narrowed opening, the left ventricle needs to contract harder.
Hypertrophic cardiomyopathy. This genetic disease develops when the heart muscle becomes abnormally thick. Sometimes this pathology occurs in children.
Sports training. Intense and long-term strength training can lead to the development of adaptation of the heart to increased stress. It is not yet clear whether such myocardial hypertrophy can lead to impaired elasticity of the heart muscle and the development of the disease.

In addition, there are the following risk factors for the development of LVH:

elderly age;
overweight;
family history;
diabetes;
Gender – Women with hypertension have a higher risk of developing LVH than men with the same blood pressure.

Why is LVH dangerous?

With left ventricular hypertrophy, the structure and function of the heart changes. An enlarged left ventricle may:

weaken the force of your contractions;
lose elasticity, which interferes with the proper filling of the ventricle with blood and increases pressure in the heart;
compress the coronary arteries that supply blood to the heart itself.

How is LVH diagnosed?

Upon examination, the doctor may detect increased blood pressure, the borders of the heart shifted to the left and the apex beat, and the presence of murmurs above the heart. You can clarify the diagnosis using the following methods:

Electrocardiogram (ECG) - with its help, a cardiologist can detect voltage signs, which are manifested by an increase in the amplitude of the waves. LVH is often associated with impaired myocardial repolarization processes, which can also be detected on the ECG.
Echocardiography (ultrasound of the heart) - can show thickened walls of the left ventricle and help detect cardiac pathology leading to LVH (for example, aortic valve stenosis).
Magnetic resonance imaging.

How to treat LVH?

Treatment for LVH depends on its cause and involves medication or surgery.

LVH associated with hypertension is treated with blood pressure control measures. These include lifestyle changes (weight loss, regular exercise, diet, smoking cessation) and medications (angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, beta blockers, calcium channel blockers and diuretics).
Sports-related LVH usually does not require treatment. A person with this problem needs to stop exercising for 3 to 6 months. After this time, a repeat echocardiogram should be performed to determine the thickness of the heart muscle and see if it has decreased.
Hypertrophic cardiomyopathy is a rare disease that must be treated under the close supervision of an experienced cardiologist. Therapy can be conservative or surgical.
LVH caused by aortic stenosis may require surgical treatment (valve repair or valve replacement).

If you have LVH, it is very important to carry out the correct treatment and follow the doctor’s recommendations. Although this condition can be successfully controlled, there is a risk of developing heart failure.

Prevention

The best way to prevent the development of myocardial hypertrophy is to maintain normal blood pressure. To do this you need:

Measure your blood pressure regularly and often.
Make time for physical exercise.
Follow a diet - avoid salty and fatty foods, eat more fruits and vegetables, do not drink alcoholic beverages (or drink them in moderation).
Quit smoking.

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Causes of left ventricular hypertrophy

Myocardial thickening in the left ventricular area is not a separate disease, but rather a consequence of serious cardiovascular pathologies:

Hypertension and symptomatic hypertension. In these conditions, the left ventricle constantly works with maximum force, so the myocardial muscle fibers in this part of the heart grow and increase in volume.
Heart defects, especially aortic valve stenosis. It becomes an obstacle to the normal flow of blood from the left ventricle and causes the muscles of the latter to contract more intensely.
Atherosclerosis of the aorta, in which the left ventricle is also under constant increased tension.

In addition, the left ventricle quite often hypertrophies in young people involved in sports, as well as loaders. In these categories of patients, the main cause of changes in the myocardium is systematic severe physical activity, during which the heart works to wear out.

Obese people also suffer from hypertrophic changes in the left ventricle; their hearts have to pump blood in large volumes and for a long duration of the vascular bed. It is also worth highlighting the possibility of a hereditary predisposition to thickening of the walls of the heart.

What is the danger of left ventricular hypertrophy?

The problem with this pathology is that with it, only the myocardium grows in the heart wall, other important structures (vessels, elements of the conduction system) remain in place, and the wall itself loses its elasticity. This leads to ischemia of muscle cells (they all simply do not have enough oxygen), disruption of rhythm, contractility and blood filling of the left ventricle. Therefore, patients have an increased risk of developing a heart attack, heart failure, ventricular arrhythmias, and blockades. Well, the most dangerous complication is sudden death.

Signs of left ventricular hypertrophy

You can suspect the presence of left ventricular hypertrophy based on the following signs:

pain in the heart, it can have a different nature and duration;
dizziness and weakness;
shortness of breath;
a feeling of sudden sinking of the heart, followed by a strong palpitation;
repeated fainting;
swelling of the limbs;
sleep disturbance;
physical inability to do heavy work.

It is worth noting that in half of patients, hypertrophy can occur unnoticed at first, this is especially true for athletes.

Basic principles of treatment

Cardiologists recommend that all patients with myocardial hypertrophy, first of all, give up smoking and alcohol and try to normalize weight. In addition, switch to a diet that is beneficial for the myocardium and helps normalize blood pressure. In the diet it is necessary to limit salt (it is better not to add enough salt to dishes at all), animal fats from meat and dairy products, easily digestible carbohydrates, all offal, smoked and preserved foods, as well as caffeinated drinks. Instead, you should diversify your diet with healthy vegetable oils, fresh vegetables, fruits, seafood, low-fat cottage cheese and kefir, and cereals.

After consultation with a cardiologist, it is recommended to expand your physical activity with walks and jogging in the park, swimming, and physical therapy. In this case, all loads should be moderate. Also, for myocardial hypertrophy, drug therapy is used aimed at normalizing blood pressure, restoring rhythm and improving myocardial function. For this purpose, drugs of the following groups are used: ACE inhibitors, calcium antagonists, sartans and other drugs.

If drug therapy does not help, the pathology progresses, the normal functioning of the heart septa and valves is disrupted, and various types of surgical operations are performed.

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Causes of left ventricular hypertrophy

The main pathogenetic mechanism in the development of myocardial hypertrophy is a long-term disruption of the ejection of blood from the ventricular cavity into the aorta.

An obstacle to normal release may be:

narrowing of the aortic opening (part of the blood remains in the LV cavity due to stenosis of the aortic valve);
insufficiency of the aortic valves (due to incomplete closure of the semilunar valves, after completion of contraction of the LV myocardium, part of the blood returns to its cavity).

Stenosis can be congenital or acquired. In the latter case, its formation is caused by infective endocarditis (as a result of calcification of the leaflets), rheumatism, senile vascular calcification (usually after 65 years), systemic lupus erythematosus, etc.

The causes of aortic valve insufficiency can also be congenital pathologies and hereditary pathologies of connective tissue, infectious diseases, syphilis, SLE, etc.

In this case, the ability of the arteries to stretch under the pressure of the blood flow is impaired. An increase in arterial stiffness leads to an increase in the pressure gradient, an increase in the load on the heart muscle and contributes to an increase in the number and mass of cardiomyocytes in response to overload.

Other common causes of left ventricular hypertrophy are:

increased physical activity, especially in combination with a low-calorie diet;
atherosclerosis;
arterial hypertension;
obesity;
endocrinopathies.

In the first case, the so-called “athletic heart” is formed - this is a complex of adaptive mechanisms leading to left ventricular hypertrophy in response to volume overload. That is, due to increased physical activity, the heart is forced to pump large volumes of blood, which leads to an increase in the number of muscle fibers.

As a result, the “performance” of the heart increases and adaptation to intense training occurs. However, long-term overload, especially in combination with fashionable low-calorie diets, contributes to the rapid depletion of compensatory mechanisms and the appearance of symptoms of heart failure (HF).

Endocrine disorders, obesity, atherosclerosis and arterial hypertension (hereinafter referred to as hypertension) can be either interconnected links in one chain or individual risk factors. Excess body weight leads to the formation of resistance (addiction) to insulin in peripheral tissues and the development of type 2 diabetes, metabolic disorders, hyperlipidemia, atherosclerosis and increased blood pressure.

As a consequence of hypertension, an overload of blood volume is created, and atherosclerotic plaques create obstacles in the path of the blood wave, disrupting its hemodynamic properties, and contribute to increased rigidity of the vascular wall. Left ventricular hypertrophy develops in response to increased workload on the heart.

Among the endocrinological causes of LVH, the “thyrotoxic heart” should also be distinguished. This refers to left ventricular hyperfunction as a result of increased contractility of the heart muscle due to increased influence of the sympathetic nervous system and high output syndrome.

This leads to a sequential chain of pathogenetic mechanisms:

hyperfunction,
depletion of compensatory mechanisms and dystrophy,
cardiosclerosis,
outcome in heart failure.

Also, diseases of the kidneys and adrenal glands, leading to arterial hypertension, can lead to the formation of LVH.

Hereditary risk factors for the development of left ventricular hypertrophy also include syncope, severe arrhythmias, and sudden death syndrome in relatives of the patient. These data are important for excluding the familial form of hypertrophic cardiomyopathy.

Types of LVH

Left ventricular hypertrophy can be asymmetrical or symmetrical (concentric).

With asymmetric, pathological changes are observed in individual segments or walls of the LV.

According to the localization of the pathological process, the following are distinguished:

LVH with involvement of the interventricular septum (about 90 percent of cases);
midventricular;
apical;
combined lesion of the free wall and septum.

Symmetric hypertrophy of the left ventricle is characterized by the spread of the pathological process to all walls.

Based on the presence of outflow tract obstruction, it is classified:

obstructive cardiomyopathy, also called idiopathic hypertrophic subaortic stenosis (occurs in 25 percent of cases);
non-obstructive cardiomyopathy (diagnosed in 75% of cases)

According to the course and outcome, LVH is distinguished with:

stable, benign course;
sudden death;
progressive course;
development of atrial fibrillation and complications;
progressive heart failure (end stage).

Symptoms of the disease

The insidiousness of the disease lies in its gradual development and slow appearance of clinical symptoms. The initial stages of myocardial hypertrophy may be asymptomatic or accompanied by vague, nonspecific complaints.

Patients suffer from headaches, dizziness, weakness, insomnia, increased fatigue and decreased overall performance. Subsequently, chest pain and shortness of breath develop, increasing with physical activity.

Arterial hypertension is both one of the provoking factors in the development of LVH and one of the important symptoms of this disease. When the body's compensatory capabilities are depleted, complaints of unstable blood pressure arise, ranging from elevated numbers to a sharp drop, even to severe hypotension.

The severity of complaints depends on the form and stage, the presence of obstruction, heart failure and myocardial ischemia. Symptoms also depend on the underlying disease.

With aortic valve stenosis, the classic picture of the disease is manifested by a triad of symptoms: chronic heart failure, exertional angina and syncope (sudden fainting).

Syncope is associated with a decrease in cerebral blood flow as a result of a decrease in blood pressure, due to insufficient cardiac output during decompensation of the disease. The second cause of syncope is baroreceptor dysfunction and the vasodepressor response to a marked increase in left ventricular systolic pressure.

In young people and children, LVH can be detected completely accidentally during an examination.

What is the danger of hypertrophy?

Decompensation of the pathological process leads to:

obstruction of the excretory compartment;
progressive heart failure (HF);
severe rhythm disturbances, up to ventricular fibrillation (VF);
coronary heart disease;
cerebrovascular accident;
myocardial infarction;
sudden death syndrome.

Sometimes left ventricular myocardial hypertrophy can be asymptomatic and lead to premature death. This course is typical for hereditary forms of cardiomyopathies.

Stages of hypertrophy and energy processes

There are three stages during the course of the disease:

The stage of initial changes and adaptation (provoking factors lead to an increase in the number and mass of cardiomyocytes and increased consumption of energy reserves in cells). May be asymptomatic or with minimal, nonspecific complaints;
Stage of compensated course (characterized by the appearance and progression of clinical symptoms due to the gradual depletion of energy reserves in cells, oxygen deficiency, and ineffective heart function).
Hypertrophy of the left ventricular myocardium with decompensated course and severe heart failure.

The last stage is characterized by:

dystrophic changes in the myocardium,
ischemia,
dilatation of the LV cavity,
cardiosclerosis,
interstitial fibrosis,
extremely poor prognosis for survival.

Diagnostics

Genetic testing is performed to exclude hereditary forms of HCM.

To clarify the stage of the disease, markers of chronic heart failure are examined.

Of the instrumental studies, the following are mandatory:

LVH on ECG,
daily ECG monitoring,
transthoracic resting cardiography (ECHO-CG) and stress ECHO-CG,
tissue Doppler study.

Echo-KG allows you to evaluate:

location of the site of myocardial hypertrophy,
wall thickness,
LV ejection fraction,
dynamic obstruction,
condition of the valve apparatus,
volume of the ventricles and atria,
systolic pressure in the LA,
diastolic dysfunction,
mitral regurgitation, etc.

Chest x-ray allows you to assess the degree of left ventricular enlargement.

If necessary, MRI and CT of the heart are performed.

To identify atherosclerotic changes in the coronary vessels, coronary angiography is performed.

Treatment of LVH

Treatment tactics depend on the severity and stage of the disease, the degree of heart failure and the LV ejection fraction.

The basis of therapy is the elimination of the provoking factor and treatment of concomitant diseases.

Patients with systolic dysfunction and ejection fraction less than 50% are treated according to the chronic HF treatment protocol.

The main drugs used for treatment are:

beta blockers,
ACE inhibitors,
calcium channel blockers,
angiotensin receptor blockers,
antiarrhythmic drugs,
diuretics.

Surgical treatment is indicated for patients with an obstructive form.

Forecast

The prognosis of the disease depends on the cause of LVH, the type of course of the disease (stable or progressive), the functional class of heart failure, the stage of the disease, the presence of obstruction and aggravating conditions (arterial hypertension, endocrine disorders).

Syncope attacks also indicate a decompensated course and a poor prognosis for survival.

However, in patients with an uncomplicated family history and a stable course of the disease, with complex timely treatment, six-year survival rates are about 95%.

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What to do if you have heart failure

If the right atrium (RA) is overfilled with blood or pressure overload, myocardial hypertrophy subsequently occurs. Signs of this condition are shortness of breath, dizziness, fainting, and irregular contractions. Treatment requires an impact on the disease that caused overstrain of the heart muscle (lung disease, valvular heart disease).

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Causes of increased load on the right atrium of the myocardium

In order for the load on the cardiac muscle of the RA to increase when blood is ejected into the ventricle, the pressure in it must increase due to an obstruction (tricuspid valve stenosis) or the blood volume must increase. This situation occurs with reverse reflux (valvular insufficiency), high pressure in the right ventricle (). Diseases leading to overload, and subsequently hypertrophy of the PP, may differ in adulthood and childhood.

In adults

The most common pathologies accompanied by a large load on the right atrium:

All these processes disrupt the ejection of blood from the right ventricle into the lungs, which leads to its overstrain and subsequent hypertrophy, and the RA is affected for the second time. Also causes of pathological changes include rheumatism, endocarditis involving the tricuspid valve. Excessive load on the RA occurs with tricuspid stenosis, insufficiency and combined acquired.

The child has

The first place among the factors of PP overload is taken by heart defects, in which circulatory disorders occur in the pulmonary circulation:

(underdevelopment of the valve in the right side of the heart) and (septal defect and aortic displacement);
narrowed pulmonary or;
chronic;
displacement of the great vessels (transposition);
congenital malformations of the tricuspid valve.

Right atrium overload

The addition of hypertrophy of the right parts of the heart occurs with decompensation of circulatory failure of the left ventricular type. This is due to the increase in congestion in the lungs, which over time complicates the work of the right atrium.

Signs and symptoms of stress

If overstrain of the PP occurs against the background of acute inflammatory processes or exacerbation of bronchial asthma, bronchitis, then there are no characteristic symptoms, or the overload is manifested by an excessive increase in shortness of breath during physical activity. If the underlying diseases are heart defects, then the signs are:

Is it dangerous

Increased load on the right atrium does not have negative consequences if it is possible to eliminate its cause - through medical or surgical treatment of the underlying disease. With unoperated heart defects, heart failure and congestive processes in the internal organs develop quite early, many of which have irreversible consequences.

In the later stages, fluid accumulates in the abdominal cavity (ascites), chest (hydrothorax), pericardial sac (hydropericardium), liver cirrhosis and severe rhythm disturbances occur.

ECG readings of load on the right atrium

Short-term manifestations of PP overload can be detected by recording an ECG at the time of an asthma attack, thromboembolism, or extensive pneumonia:

pulmonary (pulmonary) P wave;
increase in the first (right atrial part) P;
high and pointed P in leads 2 and 3, aVF.

These symptoms disappear after the patient’s condition normalizes, or their severity decreases significantly. With hypertrophy, the P waves are high-amplitude, pointed, and have a normal duration.

A decrease in the manifestations of heart failure occurs with the use of (Diroton, Enap), beta blockers (Corvitol), angiotensin antagonists (Lorista, Diovan).

High load on the right atrium occurs in diseases of the lungs and heart. It can be temporary or permanent, leading to myocardial hypertrophy. Often appears secondary to overstrain of the right ventricle.

Clinical symptoms (shortness of breath, cyanosis, edema, liver enlargement) occur when heart failure occurs. To identify it, it is enough to conduct an ECG, but to find the cause, additional examination is required. Treatment depends on the underlying pathological condition.

Useful video

Watch the video about atrial hypertrophy on the ECG:

Basic ECG concepts for the left ventricle

The rhythmic work of the heart muscle creates an electric field with electrical potentials having a negative or positive pole. The difference between these potentials is recorded in leads - electrodes attached to the patient’s limbs and chest (indicated “V” on the graph). The electrocardiograph records changes in signals that arrive over a certain time range and displays them as a graph on paper.

A fixed time period is reflected on the horizontal line of the graph. Vertical angles (teeth) indicate the depth and frequency of impulse changes. Teeth with a positive value are displayed upward from the time line, with a negative value - downward. Each tooth and lead are responsible for recording the functionality of a particular cardiac section.

Indicators of the left ventricle are: waves T, S, R, segment S-T, leads – I (first), II (second), III (third), AVL, V5, V6.

The T-wave is an indicator of the recovery stage of the muscle tissue of the ventricles of the heart between contractions of the middle muscular layer of the heart (myocardium);
Q, R, S - these teeth show agitation of the cardiac ventricles (excited state);
ST,QRST, TP are segments indicating the horizontal distance between adjacent teeth. Segment + tooth = interval;
Leads I and II (standard) – display the anterior and posterior walls of the heart;
III standard lead – fixes I and II according to a set of indicators;
V5 – lateral wall of the left ventricle in front;
AVL – lateral cardiac wall anterior to the left;
V6 – left ventricle.

Schematic representation of S-T segment elevation in V1 and V2, indicating LVH

The electrocardiogram evaluates the frequency, height, degree of jaggedness and location of the teeth relative to the horizontal in the leads. The indicators are compared with the norms of cardiac activity, changes and deviations are analyzed.

Left ventricular hypertrophy on the cardiogram

When compared with the norms, the signs of left ventricular hypertrophy on the ECG will have the following differences.

Prong/segment	Standard indicators	Deviations in hypertrophy
R (standard leads)	acute-angled, high in leads II and AVF	high in I and AVL, serrated
R(chest leads)	in V3, V4 – high	in V5, V6 – high
T left (I, AVL, V5, V6)	always positive	negative, consists of two parts
S-wave	in leads II and V3 equal in height to R	lowest in I, AVL, V5, V6, and deepest in III, AVF, V1, V2
S-T (segment) in the left leads	always in line with the horizontal line	sloping lower in relation to the horizontal line in V5, V6, located opposite to the left in V1, V2

Learn more about changing tine values

Left ventricular hypertrophy is visually determined by the height and width of the R wave in leads V5 V6 (increased wave parameters), compared to leads V1, V2. Transformation of the T-wave in leads V5, V6 indicates left-sided pathology in the case of:

negative tooth value;
doublings (two parts of one tooth);
the first half “looks” down, and the second half looks up.

A slight displacement of the S-T segment up or down relative to the horizontal line is a sign of thickening of the walls of the left ventricle. Significant displacement is an indicator of myocardial infarction or ischemic heart disease (coronary heart disease).

The S-wave in the presence of a hypertraffiated ventricle changes as follows:

in leads: III, AVF, V1, V2 – increased depth of the tooth;
in leads: AVL, V5, V6, I – weakly expressed;
jaggedness is observed.

Deviations from the norm of the parameters of the Q, R, S waves are called the voltage of the cardiogram. If the teeth are located below normal by more than 0.5 mV, a low-voltage potential will be recorded on the cardiogram. Voltage changes always indicate the presence of cardiac pathology.

Electrocardiogram of the heart with LVH (signs of pathology are circled in red)

Causes of hypertrophy

Left ventricular hypertrophy detected during an ECG means the presence of excessive load on the heart and myocardial diseases:

narrowing of the aortic lumen in the valve area (aortic stenosis). Due to the transformation of the valve leaflets, blood flow is disrupted, and the heart is forced to work in emergency mode;
change in the volume of the left ventricular wall towards thickening (hypertrophic cardiomyopathy). The thickness of the walls impedes blood circulation, which increases the load on the myocardium;
persistently high blood pressure (hypertension).

Deformation can occur due to reasons that depend directly on the patient himself. First of all, these are the following factors: eating habits leading to obesity, irrational physical activity. LVH is common to many athletes, since excessive load on the heart during training provokes an increase in the volume and mass of the organ, systematic psycho-emotional overload (state of stress), and an unhealthy lifestyle (smoking, alcohol, lack of fresh air, unhealthy foods).

In addition, the culprit of ventricular pathology may be a hereditary predisposition or a congenital anatomical anomaly. In patients aged 65+, the cause is often atherosclerosis.

Dangerous consequences

The left ventricle is responsible for oxygen saturation and movement of arterial blood into the aorta and further through all small vessels to nourish the organs. As the volume increases, the blood presses on the walls, the connective tissue displaces the muscle tissue, and the ventricle ceases to cope with its functional duties.

Pathology can even lead to death

What such changes threaten is determined by the following diagnoses:

coronary heart disease - a violation of the blood supply to the heart due to thickening of the walls of the gastric chamber;
myocardial infarction – death (necrosis) of part of the heart muscle;
ventricular extrasystole (arrhythmia) – failure of the heart rhythm;
atrioventricular or ventricular block - cessation of the passage of electrical impulses between the atria and ventricles, leading to hemodynamics;
heart failure is a low contractility of the heart muscle, often leading to death.

Timely detection of LVH will help prevent serious complications. The most informative in terms of diagnosing pathology is the electrocardiographic examination method.

Prevention of LVH

The main preventive measures include:

elimination of bad habits (alcohol and nicotine addiction);
a healthy diet (eliminating foods containing low-density lipoproteins, the so-called bad cholesterol, while increasing the intake of high-density lipoproteins, the “good cholesterol”);
body weight control (obesity always negatively affects heart function);
balanced physical activity appropriate for age;
regular exposure to fresh air (active oxygen stimulates proper cardiac activity).

Ventricular systolic overload in congenital heart defects, it is observed with isolated pulmonary artery stenosis (for the right ventricle), stenosis of the aortic mouth and coarctation of the aorta (for the left ventricle), diastolic - with blood discharge from left to right: atrial and interventricular septal defect, patent ductus arteriosus, transposition of the great vessels. With the development of pulmonary hypertension in these defects, systolic overload is added to the diastolic overload of the ventricles.

Due to heart overload(systolic or diastolic), hyperfunction and hypertrophy of the myocardium of all parts of the heart develop early, but mainly of the ventricle on which the maximum load falls (L. D. Krymsky, 1962, 1963).

G. F. Lang proposed to distinguish between the following causes of heart failure: I - causing overwork of the heart muscle (heart defects, hypertension); II - disorders of the blood supply to the myocardium (diseases of blood vessels, anemia); III - direct chemical effect on the myocardium (intoxication, starvation, vitamin deficiencies, infections); IV - neurotrophic and hormonal (endocrine diseases).

Sometimes at the same sick there is a combination of several reasons. For example, in most patients with congenital heart defects, overwork of the hypertrophied heart muscle is accompanied by circulatory disturbances caused by infection (pneumonia, childhood infections), which leads to an earlier development of clinically pronounced heart failure. In cyanotic heart defects, impaired blood supply to the myocardium also plays a role, due to the fact that mixed blood, poor in oxygen, enters the coronary arteries.

All types of heart failure are characterized by the following changes in intracardiac hemodynamics: an increase in residual systolic volume, blood; increased end-diastolic pressure; dilatation of the heart; decrease in cardiac output; an increase in pressure in those parts of the circulatory system from where blood flows.

These shifts lead to clinical manifestations of heart failure and metabolic disorders in various organs and tissues: disturbances of water and electrolyte metabolism, liver damage in the form of cardiac cirrhosis, damage to the kidneys and adrenal glands, in particular increased secretion of aldosterone, leading to an even greater increase in edema.
Clinical picture of heart failure diverse. This depends on the rate of development of heart failure (acute or chronic) and the location of congestion.

G. F. Lang distinguishes four types of heart failure depending on the location of pulmonary congestion (left ventricular); in a large circle, with enlarged liver and edema (right ventricular); in the portal vein system, usually due to the development of liver cirrhosis; in the area of the head, neck and upper extremities (with compressive and effusion pericarditis).
Foreign authors heart failure is divided into right ventricular, left ventricular and mixed forms.

Classification of heart failure, which is currently used by most therapists and pediatricians, was proposed by G. F. Lang (1934) and developed by N. D. Strazhesko and V. X. Vasilenko (1949). Heart failure is divided into three stages:

I - latent: there are no symptoms of heart failure at rest; during physical activity, palpitations and fatigue appear; hypertrophy and tonogenic dilatation of one or another part of the heart are noted;

II - severe: shortness of breath and tachycardia that occurs during light physical exertion. The heart enlarges due to myogenic dilatation. Congestion develops in a large or small circle, depending on which part of the heart is decompensated.

This stage usually divided into two periods:
1) symptoms of heart failure are not pronounced;
2) a pronounced clinical picture of heart failure occurring in the systemic and pulmonary circulation: enlarged liver, congestion in the lungs, edema;

III - dystrophic: symptoms of heart failure are accompanied by irreversible dysfunction of internal organs and metabolic disorders.