What is myocardial hypertrophy? History, prevalence and types. What to do if hypertrophic cardiomyopathy is detected. Myocardial hypertrophy of the intestinal tract, what

Prevalence and causes of hypertrophy

Geographically, the prevalence of HCM is variable. In addition, different regions take different age categories. It is difficult to provide precise epidemiological data because a disease such as hypertrophic cardiomyopathy does not have specific clinical symptoms. It is safe to say that the disease is more often detected in men. The third part of cases is represented by a familial form, the remaining cases are related to HCM, which has no connection with a hereditary factor.

The reason that leads to hypertrophy of the interventricular septum (IVS) is a genetic defect. This defect can occur in one of ten genes, each of which is involved in encoding information regarding the functioning of the contractile protein in the muscle fibers of the heart. To date, about two hundred such mutations are known, as a result of which hypertrophic cardiomyopathy develops.

2 Pathogenesis

What happens with hypertrophy of the interventricular septum? There are several interrelated pathological changes that occur during myocardial hypertrophy. First, thickening of the myocardium occurs in the specified area separating the right and left ventricles. The thickening of the interventricular septum is not symmetrical, so such changes can occur at any site. The most unfavorable option is thickening of the septum in the outflow tract of the left ventricle.

This causes one of the leaflets of the mitral valve, which separates the left atrium and ventricle, to come into contact with the thickened IVS. As a result, the pressure in this area (outflow section) increases. At the moment of contraction, the myocardium of the left ventricle has to work with greater force so that blood from this chamber enters the aorta. Under conditions of continued increased pressure in the outflow tract and in the presence of hypertrophy of the IVS of the heart, the myocardium of the left ventricle loses its former elasticity and becomes stiff or rigid.

Losing the ability to adequately relax during diastole or filling, the left ventricle begins to perform its diastolic function worse. The chain of pathological changes does not end here; diastolic dysfunction entails a deterioration in the blood supply to the myocardium. Ischemia (oxygen starvation) of the myocardium occurs, which is subsequently supplemented by a decrease in the systolic function of the myocardium. In addition to the IVS, the thickness of the walls of the left ventricle may also increase.

3 Classification

Currently, a classification is used that is based on echocardiographic criteria that makes it possible to distinguish hypertrophic cardiomyopathy into the following options:

1. Obstructive form. The criterion for this variant of hypertrophic cardiomyopathy is the difference in pressure (pressure gradient) that occurs in the area of ​​the left ventricular outflow tract and ranges from 30 mm Hg. and higher. This pressure gradient is created at rest.
2. Latent form. At rest, the pressure gradient is below 30 mm Hg. When performing a stress test, it increases and is more than 30 mm Hg.
3. Non-obstructive form. The pressure gradient at rest and during a stress test does not reach 30 mmHg.

4 Symptoms

The presence of hypertrophy of the interventricular septum and left ventricle does not always have any clinical signs. Patients can live quite a long time, and only after the age of seventy do they begin to show the first signs. But this statement does not apply to everyone. After all, there are forms of IVS hypertrophy that manifest themselves only under conditions of intense physical activity. There are options that make themselves felt with minimal physical activity. And all of the above is connected with the part in which the interventricular septum is thickened. In another case, the only manifestation of the disease may be sudden cardiac death.

First of all, symptoms will appear with the obstructive form of hypertrophy. The most common complaints of patients with IVS hypertrophy in the area of ​​the outflow tract are the following:

• dyspnea,
• chest pain,
• dizziness,
• fainting states,
• weakness.

All of these symptoms tend to progress. As a rule, they first appear during physical activity. As the disease progresses, symptoms become apparent even at rest.

5 Diagnosis and treatment

Despite the fact that standard diagnosis should begin with the patient’s complaints, for the first time, hypertrophy of the IVS and left ventricle can be detected using an echocardiographic study (EchoCG, cardiac ultrasound). In addition to physical methods for diagnosing hypertrophy of the IVS and left ventricle, carried out in the doctor’s cabin, laboratory and instrumental methods are used. The following instrumental diagnostic methods are used:

1. Electrocardiography (ECG). The main ECG signs of myocardial hypertrophy of the interventricular septum and left ventricle are: signs of overload and enlargement of the left heart, negative T waves in the chest leads, deep atypical Q waves in leads II, III aVF; disturbance of rhythm and conduction of the heart.
2. X-ray of the chest organs.
3. 24-hour Holter ECG monitoring.
4. Ultrasound of the heart. Today, this method is the leading one in diagnostics and represents the “gold standard”.
5. Magnetic resonance imaging Coronary angiography.
6. Genetic diagnosis uses a mapping method. DNA analysis of mutant genes is used.

All of these diagnostic methods are not only used to make a diagnosis of HCM, but to carry out differential diagnosis in relation to a number of similar diseases.

Treatment of hypertrophic cardiomyopathy has several goals: to reduce the manifestations of the disease, slow down the progression of heart failure, prevent life-threatening complications, etc. Like most, if not all cardiac diseases, HCM requires non-drug measures that contribute to the progression of the disease. The most important are normalizing body weight, giving up bad habits, and normalizing physical activity.

The main groups of drugs for the treatment of IVS and left ventricular hypertrophy are beta-blockers, calcium channel blockers (verapamil), anticoagulants, angiotensin-converting enzyme inhibitors, angiotensin receptor antagonists, diuretics, class 1A antiarrhythmics (disopyramide, amiodarone). Unfortunately, HCM is difficult to treat with medication, especially if there is an obstructive form and insufficient effect of drug therapy.

Today, there are the following options for surgical correction of hypertrophy:

• excision of hypertrophied cardiac muscle in the area of ​​the IVS (myoseptectomy),
• mitral valve replacement, mitral valve repair,
• removal of hypertrophied papillary muscles,
• alcohol septal ablation.

6 Complications

Despite the fact that this disease, hypertrophic cardiomyopathy, can be completely asymptomatic, it can have the following complications:

1. Heart rhythm disturbance. Non-fatal (non-fatal) rhythm disturbances such as sinus tachycardia may occur. In other situations, HCM can be complicated by more dangerous types of arrhythmias - atrial fibrillation or ventricular fibrillation. It is the last two variants of arrhythmias that occur with IVS hypertrophy.
2. Impaired cardiac conduction (blockade). About a third of cases of HCM can be complicated by blockades.
3. Sudden cardiac death.
4. Infectious endocarditis.
5. Thromboembolic complications. Blood clots formed in a certain place in the vascular bed can spread through the bloodstream and clog the lumen of the vessel. The danger of such a complication is that these microthrombi can enter the vessels of the brain and lead to impaired cerebral circulation.
6. Chronic heart failure. The progression of the disease steadily leads to the fact that first the diastolic and then the systolic function of the left ventricle decreases with the development of signs of heart failure.

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It is important to know! An effective means for normalization heart function and blood vessel cleansing exists! ...

Despite its prevalence (IVS hypertrophy is observed in more than 70% of people), it is most often asymptomatic and is detected only during very intense physical activity. After all, hypertrophy of the interventricular septum itself is its thickening and the resulting reduction in the useful volume of the chambers of the heart. As the thickness of the cardiac walls of the ventricles increases, the volume of the heart chambers also decreases.

Symptoms and causes of hypertrophic cardiomyopathy

chest pain; shortness of breath with increased physical activity (for example, climbing stairs); dizziness and fainting; increased fatigue; tachyarrhythmia that occurs for short periods of time; heart murmur on auscultation; labored breathing.

The causes of this pathology lie not only in an incorrect lifestyle. Smoking, alcohol abuse, excess weight - all this becomes a factor contributing to the increase in severe symptoms and the manifestation of negative processes in the body with an unpredictable course.

Possible complications of IVS hypertrophy

What complications are possible with the development of cardiopathy of the type under discussion? Everything will depend on the specific case and individual development of the person. After all, many will never know throughout their lives that they have this condition, and some may experience significant physical ailments. We list the most common consequences of thickening of the interventricular septum. So:

1. Heart rhythm disturbances such as tachycardia. Such common types as atrial fibrillation, ventricular fibrillation and ventricular tachycardia are directly associated with IVS hypertrophy. 2. Disorders of blood circulation in the myocardium. Symptoms that occur when the outflow of blood from the heart muscle is disrupted include chest pain, fainting and dizziness. 3. Dilated cardiomyopathy and the associated decrease in cardiac output. The walls of the heart chambers, under conditions of pathologically high load, become thinner over time, which is the cause of the appearance of this condition. 4. Heart failure. The complication is very life-threatening and in many cases ends in death. 5. Sudden cardiac arrest and death.

Of course, the last two conditions are terrifying. But, nevertheless, with a timely visit to the doctor, if any symptom of cardiac dysfunction occurs, a timely visit to the doctor will help you live a long and happy life.

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• Hypertrophic cardiomyopathy (HCM)

Hypertrophic cardiomyopathy is most often defined as severe hypertrophy of the left ventricular myocardium for no apparent reason. The term “hypertrophic cardiomyopathy” is more precise than “idiopathic hypertrophic subaortic stenosis”, “hypertrophic obstructive cardiomyopathy” and “muscular subaortic stenosis”, since it does not necessarily imply left ventricular outflow tract obstruction, which occurs in only 25% of cases.

Course of the disease

Histologically, hypertrophic cardiomyopathy reveals a disordered arrangement of cardiomyocytes and myocardial fibrosis. Most often, in descending order, the interventricular septum, apex and middle segments of the left ventricle undergo hypertrophy. In a third of cases, only one segment undergoes hypertrophy. The morphological and histological diversity of hypertrophic cardiomyopathy determines its unpredictable course.

The prevalence of hypertrophic cardiomyopathy is 1/500. It is often a familial disease. Hypertrophic cardiomyopathy is probably the most common inherited cardiovascular disease. Hypertrophic cardiomyopathy is detected in 0.5% of patients referred for echocardiography. It is the most common cause of sudden death in athletes under 35 years of age.

Symptoms and complaints

Heart failure

Dyspnea at rest and during exercise, nocturnal attacks of cardiac asthma and fatigue are based on two processes: increased diastolic pressure in the left ventricle due to diastolic dysfunction and dynamic obstruction of the left ventricular outflow tract.

Increased heart rate, decreased preload, shortened diastole, increased left ventricular outflow tract obstruction (eg, with exercise or tachycardia), and decreased left ventricular compliance (eg, with ischemia) aggravate complaints.

In 5-10% of patients with hypertrophic cardiomyopathy, severe systolic dysfunction of the left ventricle develops, dilation and thinning of its walls occurs

Myocardial ischemia

Myocardial ischemia in hypertrophic cardiomyopathy can occur regardless of obstruction of the right ventricular outflow tract.

Myocardial ischemia manifests itself clinically and electrocardiographically in the same way as usual. Its presence is confirmed by myocardial scintigraphy with 201 Tl, positron emission tomography, and increased lactate production in the myocardium with frequent atrial stimulation.

The exact causes of myocardial ischemia are unknown, but it is based on a discrepancy between the need for oxygen and its delivery. The following factors contribute to this.

• Damage to small coronary arteries with impairment of their ability to expand.

• Increased tension in the myocardial wall, resulting from delayed relaxation in diastole and obstruction of the left ventricular outflow tract.

• Decrease in the number of capillaries in relation to the number of cardiomyocytes.

• Decreased coronary perfusion pressure.

Fainting and presyncope

Fainting and presyncope occur due to decreased cerebral blood flow as cardiac output falls. They usually occur during exercise or arrhythmias.

Sudden death

The one-year mortality rate for hypertrophic cardiomyopathy is 1-6%. Most patients die suddenly. The risk of sudden death varies from patient to patient. In 22% of patients, sudden death is the first manifestation of the disease. Sudden death most often occurs in older and younger children; It is rare under 10 years of age. Approximately 60% of sudden deaths occur at rest, the rest after heavy physical activity.

Rhythm disturbances and myocardial ischemia can trigger a vicious circle of arterial hypotension, shortened diastolic filling time and increased left ventricular outflow tract obstruction, which ultimately leads to death.

Physical examination

When examining the jugular veins, a pronounced A wave may be clearly visible, indicating hypertrophy and intractability of the right ventricle. A cardiac impulse indicates right ventricular overload and may be noticeable with concomitant pulmonary hypertension.

The apex beat is usually shifted to the left and diffuse. Due to left ventricular hypertrophy, a presystolic apical impulse may appear, corresponding to the IV sound. A triple apical impulse is possible, the third component of which is caused by late systolic bulging of the left ventricle.

The pulse in the carotid arteries is usually bifurcated. A rapid rise in the pulse wave, followed by a second peak, is due to increased contraction of the left ventricle.

Auscultation

The first tone is usually normal, preceded by the IV tone.

The second sound may be normal or paradoxically split due to prolongation of the ejection phase of the left ventricle as a result of obstruction of its outflow tract.

The rough fusiform systolic murmur of hypertrophic cardiomyopathy is best heard along the left sternal border. It is carried out in the area of ​​the lower third of the sternum, but is not carried out on the vessels of the neck and in the axillary region.

An important feature of this noise is the dependence of its volume and duration on pre- and post-load. As venous return increases, the noise shortens and becomes quieter. As the filling of the left ventricle decreases and its contractility increases, the noise becomes rougher and longer lasting.

Tests that influence pre- and afterload make it possible to differentiate hypertrophic cardiomyopathy from other causes of systolic murmur.

Table. The influence of functional and pharmacological tests on the loudness of systolic murmur in hypertrophic cardiomyopathy, aortic stenosis and mitral regurgitation

EDLV - end-diastolic volume of the left ventricle; CO - cardiac output; ↓ - reduction in noise volume; - increase in noise volume.

Mitral regurgitation is common in hypertrophic cardiomyopathy. It is characterized by a pansystolic, blowing noise conducted in the axillary region.

A quiet, diminishing early diastolic murmur of aortic insufficiency is heard in 10% of patients with hypertrophic cardiomyopathy.

Heredity

Familial forms of hypertrophic cardiomyopathy are inherited in an autosomal dominant manner; they are caused by missense mutations, that is, substitutions of single amino acids, in the genes of sarcomeric proteins (see table)

Table. Relative frequency of mutations in familial forms of hypertrophic cardiomyopathy

Familial forms of hypertrophic cardiomyopathy should be distinguished from such phenotypically similar diseases as apical hypertrophic cardiomyopathy and hypertrophic cardiomyopathy of the elderly, as well as from hereditary diseases in which disordered cardiomyocytes and left ventricular systolic dysfunction are not accompanied by hypertrophy.

The least favorable prognosis and the highest risk of sudden death are observed with certain mutations of the myosin heavy beta chain (R719W, R453K, R403Q). With mutations of the troponin T gene, mortality is high even in the absence of hypertrophy. There is not yet enough data to use genetic analysis in practice. The available information relates mainly to familial forms with a poor prognosis and cannot be extended to all patients.

Diagnostics

Although in most cases there are pronounced changes on the ECG (see table), there are no ECG signs pathognomonic for hypertrophic cardiomyopathy.

EchoCG is the best method, it is highly sensitive and completely safe.

The table shows echocardiographic criteria for hypertrophic cardiomyopathy for M-modal and two-dimensional studies.

Sometimes hypertrophic cardiomyopathy is classified depending on the location of the hypertrophy (see table).

Doppler imaging can identify and quantify the effects of anterior systolic motion of the mitral valve.

About a quarter of patients with hypertrophic cardiomyopathy have a pressure gradient in the right ventricular outflow tract at rest; For many, it appears only during provocative tests.

Obstructive hypertrophic cardiomyopathy is defined as an intraventricular pressure gradient of more than 30 mmHg. Art. at rest and more than 50 mm Hg. Art. against the background of provocative tests. The magnitude of the gradient corresponds well to the onset time and duration of contact between the interventricular septum and the mitral valve leaflets; the earlier the contact occurs and the longer it is, the higher the pressure gradient.

If there is no obstruction of the left ventricular outflow tract at rest, it can be provoked by medications (inhalation of amyl nitrite, administration of isoprenaline, dobutamine) or functional tests (Valsalva maneuver, physical activity), which reduce preload or increase contractility of the left ventricle.

The anterior systolic movement of the mitral valve is explained by the suction effect of accelerated blood flow through the narrowed outflow tract of the left ventricle, the so-called Venturi effect. This movement further narrows the outflow tract, increasing its obstruction and increasing the gradient.

Although the clinical significance of left ventricular outflow tract obstruction has been questioned, its surgical or drug removal improves the condition of many patients. Therefore, identifying left ventricular outflow tract obstruction is very important.

Detection of mitral regurgitation and mitral valve changes can significantly influence the tactics of surgical and medical treatment of patients with hypertrophic cardiomyopathy.

Approximately 60% of patients with hypertrophic cardiomyopathy have mitral valve pathology, including excessive leaflet length, calcification of the mitral annulus, and, rarely, abnormal attachment of the papillary muscles to the anterior mitral valve leaflet.

If the structure of the mitral valve is not changed, the severity of mitral regurgitation is directly proportional to the severity of obstruction and the degree of non-closure of the leaflets

The main advantages of MRI for hypertrophic cardiomyopathy are high resolution, absence of radiation and the need for administration of contrast agents, the ability to obtain a three-dimensional image, and assess the structure of the tissue. Disadvantages include high cost, length of examination, and the inability to perform MRI in some patients, such as those with implanted defibrillators or pacemakers.

Cine-MRI allows you to examine the apex of the heart, the right ventricle, and study the functioning of the ventricles.

MRI with myocardial marking is a relatively new method that makes it possible to trace the path of certain points of the myocardium during systole and diastole. This makes it possible to assess the contractility of individual areas of the myocardium and thereby identify areas of predominant damage

Cardiac catheterization and coronary angiography

Cardiac catheterization and coronary angiography are performed to evaluate the coronary artery before myectomy or mitral valve surgery and to determine the cause of myocardial ischemia. Characteristic signs determined during an invasive hemodynamic study are shown in the table and figure.

*Arises as a result of obstruction of the left ventricular outflow tract
**Can occur both due to mitral regurgitation and due to increased pressure in the left atrium.

Even with unchanged coronary arteries, patients may have classic angina. Myocardial ischemia in hypertrophic cardiomyopathy may be based on a sharp increase in myocardial oxygen demand, compression of large coronary arteries by myocardial bridges, as well as systolic compression of the septal branches; in the coronary arteries with hypertrophic cardiomyopathy, reverse systolic blood flow can be determined.

Left ventriculography usually shows a hypertrophied ventricle with a noticeable bulging of the interventricular septum into its cavity, almost complete collapse of the ventricular cavity in systole, anterior systolic movement of the mitral valve and mitral regurgitation. In the apical form of hypertrophic cardiomyopathy, the ventricular cavity takes on the shape of a card peak.

Drawing. Pressure curves in the chambers of the heart in hypertrophic cardiomyopathy
Up. Pressure gradient between the outflow tract (LVOT) and the rest of the left ventricle (LV) Ao - aortic pressure curve
At the bottom. Peak-dome pressure curve in the aorta

Myocardial scintigraphy and positron emission tomography

In hypertrophic cardiomyopathy, myocardial scintigraphy has some features, but in general its importance in diagnosing ischemia is the same as usual. Persistent storage defects indicate scarring after myocardial infarction and are usually accompanied by decreased left ventricular function and poor exercise tolerance. Reversible storage defects indicate ischemia caused by decreased coronary reserve in normal arteries or coronary atherosclerosis. Reversible defects are often silent but appear to increase the risk of sudden death, especially in younger patients with hypertrophic cardiomyopathy.

Isotope ventriculography can reveal delayed filling of the left ventricle and a prolongation of the period of isovolumic relaxation.

Positron emission tomography is a more sensitive method; in addition, it allows one to take into account and eliminate interference associated with signal attenuation.

Fluorodeoxyglucose positron emission tomography confirms the presence of subendocarial ischemia caused by decreased coronary reserve.

Treatment should be aimed at the prevention and treatment of heart failure, which is based on systolic and diastolic dysfunction, arrhythmias and ischemia, as well as the prevention of sudden death.

LVOT - left ventricular outflow tract

Treatment for hypertrophic cardiomyopathy is as varied as its clinical manifestations.

Drug treatment

There is no evidence that beta blockers reduce mortality in hypertrophic cardiomyopathy, however, these drugs are used primarily regardless of the presence of left ventricular outflow tract obstruction.

Beta-blockers eliminate angina, shortness of breath and fainting; According to some reports, their effectiveness reaches 70%. Beta blockers with alpha blocking properties, carvedilol and labetalol, have vasodilatory effects and should probably not be used.

Beta blockers have negative inotropic and chronotropic effects due to suppression of sympathetic stimulation. They reduce myocardial oxygen demand and thereby alleviate or eliminate angina pectoris and improve diastolic filling of the left ventricle, which reduces obstruction of its outflow tract.

Contraindications to beta-blockers are bronchospasm, severe AV block without pacemaker and decompensated left ventricular failure.

Calcium antagonists are second-line drugs. They are quite effective and are used when beta-blockers are contraindicated or when they are ineffective.

Calcium antagonists have a negative inotropic effect and reduce heart rate and blood pressure. In addition, they may improve diastolic function through a rapid filling phase, although they may increase left ventricular end-diastolic pressure.

Apparently, only non-dihydropyrndine calcium antagonists - verapamil and diltiazem - are effective for hypertrophic cardiomyopathy. (see table)

*If well tolerated, doses may be higher.

The effect of calcium antagonists on hemodynamics is unpredictable due to their vasodilatory effect, therefore, in cases of severe obstruction of the left ventricular outflow tract and pulmonary hypertension, they should be prescribed very carefully. Contraindications to calcium antagonists - conduction disorders without pacemaker and systolic
left ventricular dysfunction.

Disopyramide, a Class Ia antiarrhythmic agent, may be prescribed instead of or in addition to a beta blocker or calcium antagonist. Due to its pronounced negative inotropic properties in combination with an antiarrhythmic effect against ventricular and supraventricular arrhythmias, disopyramide is effective for severe obstruction of the left ventricular outflow tract and rhythm disturbances. The disadvantages of disopyramide include its anticholinergic effect, accumulation in the blood during renal or hepatic failure, the ability to improve AV conduction in atrial fibrillation, and the weakening of its antiarrhythmic effect over time. Because of its side effects, disopyramide is usually used only in severe cases, pending more radical treatment: myectomy or destruction of the interventricular septum with ethanol. Disopyramide is not used for long-term treatment of hypertrophic cardiomyopathy.

Non-drug treatment

In very severe patients without left ventricular outflow tract obstruction, the only option is heart transplantation. If there is obstruction and symptoms persist despite drug treatment, dual-chamber pacemaker, myectomy, including mitral valve replacement, and destruction of the interventricular septum with ethanol may be effective.

Dual-chamber pacemaker

The first studies on dual-chamber pacemaker showed that it improves well-being and reduces left ventricular outflow tract obstruction, but these results are now being questioned. The pacemaker may impair ventricular filling and reduce cardiac output. Randomized crossover studies have shown that the improvement is largely due to the placebo effect.

Destruction of the interventricular septum with ethanol

Destruction of the interventricular septum with ethanol is a relatively new method, which is currently being compared with myectomy.

In the cardiac catheterization laboratory, a guidewire is placed in the trunk of the left coronary artery to catheterize the first, second, or both septal branches. A catheter is installed at the mouth of the septal branch, through which an echo contrast agent is injected. This allows you to assess the size and location of a future infarction. A heart attack is induced by injecting 1–4 ml of absolute ethanol into the septal branch.

The akinesia and thinning of the interventricular septum resulting from the procedure reduces or completely eliminates left ventricular outflow tract obstruction. Possible complications include AV block, intimal detachment of the coronary artery, large anterior infarction, and arrhythmias due to post-infarction scar. Long-term results are still unknown.

Surgical treatment of hypertrophic cardiomyopathy

Surgical treatment of hypertrophic cardiomyopathy has been performed for more than 40 years.

In experienced hands, mortality after myectomy (Morrow procedure) does not exceed 1-2%. This operation eliminates the intraventricular gradient at rest in more than 90% of cases; most patients experience long-term improvement. The resulting dilation of the left ventricular outflow tract reduces anterior systolic motion of the mitral valve, mitral regurgitation, left ventricular systolic and diastolic pressure, and intraventricular gradient.

Mitral valve replacement (with low-profile prostheses) eliminates obstruction of the left ventricular outflow tract, but it is indicated mainly for minor septal hypertrophy, after ineffective myectomy, and for structural changes in the mitral valve itself.

Selected issues of diagnosis and treatment

Atrial fibrillation

Atrial fibrillation occurs in approximately 10% of patients with hypertrophic cardiomyopathy and causes severe consequences: shortening of diastole and lack of atrial pumping can lead to hemodynamic disturbances and pulmonary edema. Due to the high risk of thromboembolism, all patients with atrial fibrillation in hypertrophic cardiomyopathy should receive anticoagulants. It is necessary to maintain a low frequency of ventricular contraction; an attempt must be made to restore and maintain sinus rhythm.

For paroxysms of atrial fibrillation, electrical cardioversion is best. To maintain sinus rhythm, disopyramide or sotalol is prescribed; if they are ineffective, amiodarone is used in low doses. With severe obstruction of the left ventricular outflow tract, a combination of a beta-blocker with disopyramide or sotalol is possible.

Persistent atrial fibrillation may be tolerated fairly well if the ventricular rate is kept low with beta blockers or calcium antagonists. If atrial fibrillation is poorly tolerated and sinus rhythm cannot be maintained, destruction of the AV node with implantation of a dual-chamber pacemaker is possible.

Prevention of sudden death

Prophylactic measures such as implantation of a defibrillator or administration of amiodarone (the effect of which has not been proven on long-term prognosis) are possible only after identifying risk factors with sufficiently high sensitivity, specificity and predictive value.

There is no convincing data on the relative importance of risk factors for sudden death. The main risk factors are listed below.

• History of circulatory arrest

• Sustained ventricular tachycardia

• Sudden death of close relatives

• Frequent paroxysms of unsustained ventricular tachycardia during Holter ECG monitoring

• Recurrent fainting and presyncope (especially during physical exertion)

• Decrease in blood pressure during exercise

• Massive left ventricular hypertrophy (wall thickness > 30 mm)

• Myocardial bridges over the anterior descending artery in children

• Left ventricular outflow tract obstruction at rest (pressure gradient > 30 mm Hg)

The role of EPI in hypertrophic cardiomyopathy has not been determined. There is no convincing evidence that it allows assessing the risk of sudden death. When performing EPS according to the standard protocol, it is often not possible to induce ventricular arrhythmias in survivors of circulatory arrest. On the other hand, the use of a non-standard protocol can cause ventricular arrhythmias even in patients with a low risk of sudden death.

Clear recommendations for the implantation of defibrillators in hypertrophic cardiomyopathy can only be developed after the completion of appropriate clinical studies. It is currently believed that implantation of a defibrillator is indicated after rhythm disturbances that could result in sudden death, with sustained paroxysms of ventricular tachycardia and with multiple risk factors for sudden death. In the high-risk group, implanted defibrillators are activated in approximately 11% per year among those who have already experienced circulatory arrest, and in 5% per year among those in whom defibrillators were implanted for primary prevention of sudden death.

Sports heart

Differential diagnosis with hypertrophic cardiomyopathy

On the one hand, playing sports with undiagnosed hypertrophic cardiomyopathy increases the risk of sudden death, on the other hand, an erroneous diagnosis of hypertrophic cardiomyopathy in athletes leads to unnecessary treatment, psychological difficulties and unreasonable restrictions on physical activity. Differential diagnosis is most difficult if the thickness of the left ventricular wall in diastole exceeds the upper limit of normal (12 mm), but does not reach the values ​​​​characteristic of hypertrophic cardiomyopathy (15 mm), and there is no anterior systolic movement of the mitral valve and obstruction of the left ventricular outflow tract .

Hypertrophic cardiomyopathy is supported by asymmetric myocardial hypertrophy, end-diastolic size of the left ventricle less than 45 mm, thickness of the interventricular septum more than 15 mm, enlargement of the left atrium, diastolic dysfunction of the left ventricle, and a family history of hypertrophic cardiomyopathy.

An athletic heart is indicated by a left ventricular end-diastolic dimension of more than 45 mm, an interventricular septal thickness of less than 15 mm, an anteroposterior dimension of the left atrium of less than 4 cm, and a decrease in hypertrophy upon cessation of training.

Exercise for hypertrophic cardiomyopathy

The restrictions remain in place despite medical and surgical treatment.

With hypertrophic cardiomyopathy under the age of 30, regardless of the presence of obstruction of the left ventricular outflow tract, one should not engage in competitive sports that require heavy physical exertion.

After age 30, restrictions may be less stringent because the risk of sudden death likely decreases with age. Sports activities are possible in the absence of the following risk factors: ventricular tachycardia with Holter ECG monitoring, sudden death in close relatives with hypertrophic cardiomyopathy, fainting, intraventricular pressure gradient more than 50 mm Hg. Art., decreased blood pressure during exercise, myocardial ischemia, anteroposterior size of the left atrium more than 5 cm, severe mitral regurgitation and paroxysms of atrial fibrillation.

Infective endocarditis

Infective endocarditis develops in 7-9% of patients with hypertrophic cardiomyopathy. Its mortality rate is 39%.

The risk of bacteremia is high during dental procedures, intestinal and prostate operations.

Bacteria settle on the endocardium, which is subject to constant damage due to hemodynamic disturbances or structural damage to the mitral valve.

All patients with hypertrophic cardiomyopathy, regardless of the presence of left ventricular outflow tract obstruction, are given antibacterial prophylaxis for infective endocarditis before any interventions accompanied by a high risk of bacteremia.

Apical left ventricular hypertrophy (Yamaguchi disease)

Characterized by chest pain, shortness of breath, and fatigue. Sudden death is rare.

In Japan, apical left ventricular hypertrophy accounts for a quarter of cases of hypertrophic cardiomyopathy. In other countries, isolated apical hypertrophy occurs in only 1-2% of cases.

Diagnostics

The ECG shows signs of left ventricular hypertrophy and giant negative T waves in the precordial leads.

EchoCG reveals the following signs.

• Isolated hypertrophy of the sections of the left ventricle located apical to the origin of the chordae tendineae

• Myocardial thickness in the apical region is more than 15 mm or the ratio of myocardial thickness in the apical region to the thickness of the posterior wall is more than 1.5

• Absence of hypertrophy of other parts of the left ventricle

• Absence of left ventricular outflow tract obstruction.

MRI allows you to see limited hypertrophy of the apical myocardium. MRI is used mainly when echocardiography is uninformative.

With left ventriculography, the cavity of the left ventricle in diastole has the shape of a card peak, and in systole its apical part completely collapses.

The prognosis is favorable compared to other forms of hypertrophic cardiomyopathy.

Treatment is aimed only at eliminating diastolic dysfunction. Beta-blockers and calcium antagonists are used (see above).

Hypertensive hypertrophic cardiomyopathy of the elderly

In addition to the symptoms inherent in other forms of hypertrophic cardiomyopathy, arterial hypertension is characteristic.

The exact incidence is unknown, but the disease is more common than one might think.

According to some data, the basis of hypertrophic cardiomyopathy in the elderly is the late expression of the mutant gene for myosin-binding protein C.

Compared to young patients (under 40 years of age), older patients (65 years of age and older) have their own characteristics.

General signs

• Intraventricular gradient at rest and during exercise

• Asymmetric hypertrophy

• Anterior systolic movement of the mitral valve.

Signs common to older people

• Less pronounced hypertrophy

• Less severe right ventricular hypertrophy

• Oval rather than slit-shaped cavity of the left ventricle

• Noticeable bulging of the interventricular septum (it takes on an S-shape)

• A more acute angle between the aorta and the interventricular septum due to the fact that the aorta unfolds with age

Treatment of hypertrophic cardiomyopathy in the elderly is the same as for its other forms.

The prognosis is relatively favorable compared to hypertrophic cardiomyopathy at a younger age.

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Literature
B. Griffin, E. Topol "Cardiology" Moscow, 2008

If asymptomatic, this disease can result in sudden cardiac arrest. It's scary when this happens to seemingly healthy young people who play sports. What happens to the myocardium, why such consequences arise, whether hypertrophy is treated - remains to be figured out.

What is myocardial hypertrophy

This autosomal dominant disease is characterized by hereditary traits of gene mutation and affects the heart. It is characterized by an increase in the thickness of the walls of the ventricles. Hypertrophic cardiomyopathy (HCM) has a classification code according to ICD 10 No. 142. The disease is often asymmetric, with the left ventricle of the heart more susceptible to damage. This happens:

• chaotic arrangement of muscle fibers;
• damage to small coronary vessels;
• formation of areas of fibrosis;
• obstruction of blood flow - an obstacle to the ejection of blood from the atrium due to displacement of the mitral valve.

With heavy loads on the myocardium caused by diseases, sports, or bad habits, the body’s protective reaction begins. The heart needs to cope with increased work volumes without increasing the load per unit of mass. Compensation begins to occur:

• increased protein production;
• hyperplasia – increase in the number of cells;
• increase in myocardial muscle mass;
• wall thickening.

Pathological myocardial hypertrophy

With prolonged work of the myocardium under loads that are constantly increased, a pathological form of HCM occurs. A hypertrophied heart is forced to adapt to new conditions. Myocardial thickening occurs at a rapid pace. In this situation:

• growth of capillaries and nerves lags behind;
• blood supply is disrupted;
• the influence of nervous tissue on metabolic processes changes;
• myocardial structures wear out;
• the ratio of myocardial sizes changes;
• systolic and diastolic dysfunction occurs;
• repolarization is disrupted.

Myocardial hypertrophy in athletes

Abnormal development of the myocardium—hypertrophy—occurs unnoticed in athletes. During high physical activity, the heart pumps large volumes of blood, and the muscles, adapting to such conditions, increase in size. Hypertrophy becomes dangerous, causing stroke, heart attack, sudden cardiac arrest, in the absence of complaints and symptoms. You should not suddenly stop training to avoid complications.

Sports myocardial hypertrophy has 3 types:

• eccentric - muscles change proportionally - typical for dynamic activities - swimming, skiing, long-distance running;
• concentric hypertrophy - the ventricular cavity remains unchanged, the myocardium increases - observed in gaming and static types;
• mixed - inherent in activities with the simultaneous use of immobility and dynamics - rowing, cycling, skating.

Myocardial hypertrophy in a child

It is possible that myocardial pathologies may appear from the moment of birth. Diagnosis at this age is difficult. Hypertrophic changes in the myocardium are often observed during adolescence, when cardiomyocyte cells actively grow. Thickening of the anterior and posterior walls occurs until the age of 18, then stops. Ventricular hypertrophy in a child is not considered a separate disease - it is a manifestation of numerous ailments. Children with HCM often have:

• heart disease;
• myocardial dystrophy;
• hypertension;
• angina pectoris.

Causes of cardiomyopathy

It is customary to distinguish between primary and secondary causes of hypertrophic development of the myocardium. The first ones are influenced by:

• viral infections;
• heredity;
• stress;
• alcohol consumption;
• physical overload;
• excess weight;
• toxic poisoning;
• changes in the body during pregnancy;
• drug use;
• lack of microelements in the body;
• autoimmune pathologies;
• malnutrition;
• smoking.

Secondary causes of myocardial hypertrophy are provoked by the following factors:

Left ventricular hypertrophy

More often, the walls of the left ventricle are susceptible to hypertrophy. One of the causes of LVH is high pressure, which forces the myocardium to work at an accelerated rhythm. Due to the resulting overloads, the left ventricular wall and IVS increase in size. In this situation:

• the elasticity of the myocardial muscles is lost;
• blood circulation slows down;
• normal heart function is disrupted;
• there is a danger of a sudden load on it.

Left ventricular cardiomyopathy increases the heart's need for oxygen and nutrients. Changes in LVH can be noticed during instrumental examination. Low output syndrome appears - dizziness, fainting. Among the signs accompanying hypertrophy:

• angina pectoris;
• pressure changes;
• heartache;
• arrhythmia;
• weakness;
• high blood pressure;
• bad feeling;
• shortness of breath at rest;
• headache;
• fatigue;

Right atrial hypertrophy

Enlargement of the wall of the right ventricle is not a disease, but a pathology that appears when there is overload in this department. It occurs due to the receipt of a large amount of venous blood from large vessels. The cause of hypertrophy can be:

• birth defects;
• atrial septal defects, in which blood enters the left and right ventricles simultaneously;
• stenosis;
• obesity.

Right ventricular hypertrophy is accompanied by symptoms:

• hemoptysis;
• dizziness;
• night cough;
• fainting;
• chest pain;
• shortness of breath without exertion;
• bloating;
• arrhythmia;
• signs of heart failure - swelling of the legs, enlarged liver;
• malfunction of internal organs;
• cyanosis of the skin;
• heaviness in the hypochondrium;
• dilation of veins in the abdomen.

Hypertrophy of the interventricular septum

One of the signs of the development of the disease is hypertrophy of the IVS (interventricular septum). The main cause of this disorder is gene mutations. Hypertrophy of the septum provokes:

• ventricular fibrillation;
• atrial fibrillation;
• mitral valve problems;
• ventricular tachycardia;
• impaired blood flow;
• heart failure;
• cardiac arrest.

Dilation of the heart chambers

Hypertrophy of the interventricular septum can provoke an increase in the internal volume of the heart chambers. This expansion is called myocardial dilatation. In this position, the heart cannot perform the function of a pump, and symptoms of arrhythmia and heart failure occur:

• fast fatiguability;
• weakness;
• dyspnea;
• swelling of the legs and arms;
• rhythm disturbances;

Cardiac hypertrophy - symptoms

The danger of myocardial disease in asymptomatic progression for a long time. It is often diagnosed accidentally during medical examinations. As the disease progresses, signs of myocardial hypertrophy may be observed:

• chest pain;
• heart rhythm disturbance;
• shortness of breath at rest;
• fainting;
• fatigue;
• labored breathing;
• weakness;
• dizziness;
• drowsiness;
• swelling.

Forms of cardiomyopathy

It should be noted that the disease is characterized by three forms of hypertrophy, taking into account the systolic pressure gradient. All together the obstructive form of HCM corresponds. Stand out:

• basal obstruction – resting state or 30 mmHg;
• latent – ​​calm state, less than 30 mm Hg – it characterizes the non-obstructive form of HCM;
• labile obstruction – spontaneous intraventricular gradient fluctuations.

Myocardial hypertrophy - classification

For convenience of work in medicine, it is customary to distinguish between the following types of myocardial hypertrophy:

• obstructive – at the top of the septum, over the entire area;
• non-obstructive – symptoms are mild, diagnosed by chance;
• symmetrical – all walls of the left ventricle are affected;
• apical - the heart muscles are enlarged only from above;
• asymmetrical - affects only one wall.

Eccentric hypertrophy

With this type of LVH, the ventricular cavity expands and at the same time a uniform, proportional compaction of the myocardial muscles occurs, caused by the growth of cardiomyocytes. With a general increase in heart mass, the relative thickness of the walls remains unchanged. Eccentric myocardial hypertrophy can affect:

• interventricular septum;
• top;
• side wall.

Concentric hypertrophy

The concentric type of disease is characterized by maintaining the volume of the internal cavity while increasing the mass of the heart due to a uniform increase in wall thickness. There is another name for this phenomenon - symmetrical myocardial hypertrophy. The disease occurs as a result of hyperplasia of myocardiocyte organelles, provoked by high blood pressure. This development of events is typical for arterial hypertension.

Myocardial hypertrophy – degrees

To correctly assess the patient’s condition with HCM, a special classification has been introduced that takes into account myocardial thickening. According to how much the size of the walls increases during heart contraction, cardiology distinguishes 3 degrees. Depending on the thickness of the myocardium, the stages are determined in millimeters:

• moderate – 11-21;
• average – 21-25;
• pronounced – over 25.

Diagnosis of hypertrophic cardiomyopathy

At the initial stage, with a slight development of wall hypertrophy, it is very difficult to identify the disease. The diagnostic process begins with interviewing the patient, finding out:

• presence of pathologies in relatives;
• the death of one of them at a young age;
• past diseases;
• fact of radiation exposure;
• external signs during visual inspection;
• blood pressure values;
• indicators in blood and urine tests.

A new direction is being used – genetic diagnosis of myocardial hypertrophy. The potential of hardware and radiological methods helps to establish the parameters of HCM:

• ECG - determines indirect signs - rhythm disturbances, hypertrophy of sections;
• X-ray - shows an increase in the contour;
• Ultrasound – assesses myocardial thickness, blood flow disturbances;
• echocardiography – records the location of hypertrophy, diastolic dysfunction;
• MRI – gives a three-dimensional image of the heart, determines the degree of myocardial thickness;
• ventriculography – examines contractile functions.

How to treat cardiomyopathy

The main goal of treatment is to return the myocardium to its optimal size. Activities aimed at this are carried out in a comprehensive manner. Hypertrophy can be cured when diagnosed early. An important part in the system of myocardial health is played by lifestyle, which implies:

• diet;
• giving up alcohol;
• smoking cessation;
• weight loss;
• drug exclusion;
• limiting salt intake.

Drug treatment of hypertrophic cardiomyopathy includes the use of drugs that:

• reduce blood pressure - ACE inhibitors, angiotensin receptor antagonists;
• regulate heart rhythm disturbances - antiarrhythmics;
• drugs with a negative ionotropic effect relax the heart - beta blockers, calcium antagonists from the verapamil group;
• remove fluid - diuretics;
• improve muscle strength - ionotropes;
• if there is a threat of infective endocarditis, antibiotic prophylaxis.

An effective method of treatment that changes the course of excitation and contraction of the ventricles is dual-chamber pacing with a shortened atrioventricular delay. More complex cases - severe asymmetric hypertrophy of the IVS, latent obstruction, lack of effect of the drug - require the participation of surgeons for regression. Help save a patient's life:

• installation of a defibrillator;
• pacemaker implantation;
• transaortic septal myectomy;
• excision of part of the interventricular septum;
• transcatheter septal alcohol ablation.

Cardiomyopathy - treatment with folk remedies

On the recommendation of the treating cardiologist, you can supplement the main course with herbal remedies. Traditional treatment for left ventricular hypertrophy involves the use of viburnum berries without heat treatment, 100 g per day. It is useful to consume flax seeds, which have a positive effect on heart cells. Recommend:

• take a spoonful of seeds;
• add boiling water - liter;
• hold in a water bath for 50 minutes;
• filter;
• drink per day - dose 100 g.

Oat infusion for regulating the functioning of the heart muscles has good reviews in the treatment of HCM. According to the healers' prescription, it is required:

• oats – 50 grams;
• water – 2 glasses;
• heat to 50 degrees;
• add 100 g of kefir;
• pour in radish juice - half a glass;
• stir, stand for 2 hours, strain;
• put 0.5 tbsp. honey;
• dosage – 100 g, three times a day before meals;
• course – 2 weeks.

Video: hypertrophy of the heart muscle

The information presented in the article is for informational purposes only. The materials in the article do not encourage self-treatment. Only a qualified doctor can make a diagnosis and make recommendations for treatment based on the individual characteristics of a particular patient.

One of the characteristic symptoms of hypertrophic cardiomyopathy is hypertrophy of the IVS (interventricular septum). When this pathology occurs, thickening of the walls of the right or left ventricle of the heart and the interventricular septum occurs. This condition itself is a derivative of other diseases and is characterized by an increase in the thickness of the walls of the ventricles.

Despite its prevalence (IVS hypertrophy is observed in more than 70% of people), it is most often asymptomatic and is detected only during very intense physical activity. After all, hypertrophy of the interventricular septum itself is its thickening and the resulting reduction in the useful volume of the chambers of the heart. As the thickness of the cardiac walls of the ventricles increases, the volume of the heart chambers also decreases.

In practice, this all leads to a reduction in the volume of blood that is released by the heart into the vascular bed of the body. To provide the organs with a normal amount of blood under such conditions, the heart must contract stronger and more often. And this, in turn, leads to its early wear and tear and the occurrence of diseases of the cardiovascular system.

A large number of people around the world live with undiagnosed IVS hypertrophy, and only with increased physical activity does their existence become known. As long as the heart can ensure normal blood flow to the organs and systems, everything proceeds hidden and the person will not experience any painful symptoms or other discomfort. But you should still pay attention to some symptoms and contact a cardiologist if they occur. These symptoms include:

• chest pain;
• shortness of breath with increased physical activity (for example, climbing stairs);
• dizziness and fainting;
• increased fatigue;
• tachyarrhythmia that occurs for short periods of time;
• heart murmur on auscultation;
• labored breathing.

It is important to remember that undiagnosed IVS hypertrophy can cause sudden death even in young and physically strong people. Therefore, a medical examination by a therapist and/or cardiologist should not be neglected.

The causes of this pathology lie not only in an incorrect lifestyle. Smoking, alcohol abuse, excess weight - all this becomes a factor contributing to the increase in severe symptoms and the manifestation of negative processes in the body with an unpredictable course.

And doctors call gene mutations the reason for the development of IVS thickening. As a result of these changes at the level of the human genome, the heart muscle becomes abnormally thick in some areas.

The consequences of the development of such a deviation become dangerous.

After all, additional problems in such cases will be disturbances in the conduction system of the heart, as well as weakening of the myocardium and the associated decrease in the volume of blood ejected during cardiac contractions.

Hypertrophy of the left or right parts of the heart occurs due to damage to the muscles, valves of the organ, due to disruption of blood flow. This often happens with congenital developmental anomalies, due to increased blood pressure, lung diseases, and significant physical activity. Most often, hypertrophy of the left ventricle of the heart is detected. This is due to the greater functional load in this area.

Reasons for appearance

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Reasons for appearance

The disease occurs as a result of various disorders that interfere with the normal functioning of the organ. The myocardium begins to contract with increased load, its metabolism increases, tissue volume and cell mass increase.

At the initial stage of the disease, the heart maintains normal blood flow due to an increase in its mass. But later the myocardium is depleted, and hypertrophy gives way to atrophy - the cells significantly decrease in size.

There are two types of pathology: concentric - the heart enlarges, its walls thicken, the atria/ventricles decrease, and eccentric (the organ is enlarged, but the cavities are expanded).

Cardiac hypertrophy can affect healthy people involved in physical labor and athletes. Against the background of such changes, acute heart failure may occur. When engaging in bodybuilding, hockey, or heavy physical labor, you need to monitor the condition of the myocardium.

Due to its occurrence, ventricular hypertrophy is divided into 2 types:

• working – due to increased load on a healthy body;
• substitution is the result of adaptation to work with another disease.

Causes of left ventricular damage

Most often, the muscle of the left ventricle undergoes changes. If its thickness is more than 1.2 cm, this violation occurs. In this case, hypertrophy of the IVS (interventricular septum) of the heart is also observed. In severe cases, the thickness can reach 3 cm and the weight can reach 1 kg.

Poor blood pumping into the aorta is provoked, therefore blood supply throughout the body is disrupted. Weight gain leads to a lack of oxygen and nutrients. As a result, hypoxia and sclerosis occurs.

Causes of changes in the left ventricle: arterial hypertension; cardiomyopathy; narrowing (stenosis) of the aortic valve; increased physical activity; hormonal disorders; obesity; kidney disease with secondary hypertension.

Causes of left atrium damage:

• Arterial hypertension;
• Hypertrophic cardiomyopathy;
• Congenital pathologies of the heart/aorta;
• General obesity, especially in children and adolescents;
• Stenosis/insufficiency of the aortic or mitral valve.

Causes of right ventricular damage

Changes in the right atrium are usually associated with pulmonary pathologies and disturbances in the pulmonary circulation of blood flow. Blood enters the right atrium through the vena cava from tissues and organs. From there it enters the ventricle through the tricuspid valve and further into the pulmonary artery and lungs.

In the latter, gas exchange occurs. It is for this reason that it disrupts the normal structure of the right sections due to various diseases of the respiratory system.

The main factors provoking atrial hypertrophy of right-sided localization:

• Congenital developmental pathologies (eg tetralogy of Fallot, IVS defect);
• Chronic obstructive pulmonary diseases, for example, emphysema, pneumosclerosis, bronchial asthma, bronchitis;
• Tricuspid valve stenosis/insufficiency, pulmonary valve changes, right ventricular enlargement.

Chronic lung pathology provokes damage to the vessels of the small circle, proliferation of connecting tissues, gas exchange and microcirculation decreases. As a result, blood pressure in the vessels of the lungs increases, so the myocardium begins to contract with greater force, which leads to hypertrophy.

Narrowing or incomplete closure of the tricuspid valve leads to the same disruption of blood flow as in a similar case with mitral pathology.

Causes of changes in the right ventricle: congenital malformations, chronic pulmonary hypertension, narrowing of the pulmonary valve, increased venous pressure with congestive insufficiency.

Hypertrophy of the right ventricle of the heart occurs if the thickness of its wall is more than 3 mm. It leads to expansion of the departments and poor blood circulation. As a result, venous return through the vena cava is disrupted, and stagnation occurs. Patients develop swelling, shortness of breath, bluish skin, and then complaints about the functioning of internal organs.

It should be noted that if the left ventricle is damaged, the left atrium will also be affected. Then the right sections are also subject to changes.

Symptoms of hypertrophy of the left and right ventricle of the heart

When the myocardium of the left half is damaged, the following occur: fainting, dizziness, shortness of breath, arrhythmias, pain in this area, weakness, and fatigue.

When the right half is affected, the following symptoms occur: cough, shortness of breath, difficulty breathing; swelling; cyanosis, pale skin; rhythm disturbance.

How is hypertrophy of both ventricles of the heart diagnosed?

The simplest and at the same time effective methods are ultrasound (US) and echocardiography (ECG). In the process, the thickness of the walls and the size of the organ are determined.

Indirect symptoms of changes detected on the ECG:

• When the right sections change, the electrical conductivity changes, the rhythm is disrupted, and a deviation of the electrical axis to the right is observed;
• Changes in the left sections are indicated by deviation of the axis to the left, respectively, and voltage signs are recorded.

It is also possible to confirm or refute the diagnosis using the results of a chest x-ray.

Treatment of various forms of cardiac hypertrophy

All efforts to eliminate the disease are directed primarily at the cause that caused it.

For example, if a disorder occurs due to a respiratory disease, the course of treatment is aimed at compensating lung function. Anti-inflammatory therapy is prescribed. Bronchodilators and a number of others are used, depending on the underlying cause.

In case of damage to the left side caused by arterial hypertension, treatment only involves taking antihypertensive medications of different groups, as well as diuretics.

If severe valve defects are detected, they may resort to surgery and even prosthetics.

Treatment of hypertrophy of the left and right ventricle of the heart in all cases of the disease includes eliminating the symptoms of myocardial damage. For this purpose, antiarrhythmic therapy is used, as well as cardiac glycosides.

It is possible that drugs will be prescribed that improve the metabolic process in the heart muscle (eg riboxin, ATP, etc.). Patients are advised to adhere to a special diet, limit fluid and salt intake. In case of obesity, efforts are directed towards normalizing body weight.

In case of congenital heart disease, the pathology is eliminated surgically, if possible. In very severe cases, when the structure is severely damaged and hypertrophic cardiomyopathy develops, the only option is an organ transplant.

As can be judged from the above, the approach to patients is carried out purely individually. Doctors take into account all existing manifestations of organ dysfunction, the general condition of the patient, and the presence of concomitant diseases.

It should be noted that timely detected myocardial pathology can be corrected in the vast majority of cases. If you feel the first alarming symptoms, you should immediately seek advice from a specialist - a cardiologist. After the examination, he will identify the cause of the disease and prescribe adequate treatment.

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Causes

The causes of hypertrophic cardiomyopathy were established after an ultrasound scan of the patients' relatives. It turned out that 65% of members of the same family have similar changes in the heart muscle.

There are 2 forms of the disease based on etiology.

Primary or idiopathic

Primary is the hereditary form of cardiomyopathy. The development of genetics has made it possible to establish the exact gene responsible for the development of the disease in half of the cases. In 50% of families, an exact indication of the altered genes has not been established.

The type of inheritance is autosomal dominant. This means that the disease necessarily manifests itself in the heirs, regardless of the gender of the child. Hypertrophic cardiomyopathy in children occurs with a 50% probability if one of the parents is healthy and the other is a carrier of the mutant gene. If both parents have genetic changes, then the probability reaches 100%.

Scientists believe that gene mutation can occur under the influence of unfavorable conditions in the external environment (smoking, past infections, radiation) affecting the expectant mother during pregnancy.

Secondary

Secondary changes form after the age of 60 in patients with hypertension who had changes in the structure of muscle tissue in the prenatal period.

It has been established that 1/5 of patients who survive to old age may develop systole weakness and dilation of the left ventricular cavity. In such cases, hypertrophic cardiomyopathy does not differ from the dilated type.

The mechanism of pathology development

As a result of genetic mutations, “wrong” main protein molecules that ensure the contraction process, actin and myosin, appear in muscle tissue. They do not produce the required amount of calories due to a sharp decrease in the content of necessary enzymes. In 90% of patients, muscle cells lose their direction. In the myocardial tissue, areas incapable of contraction are formed.

In response, other fibers take over the work functions. Their muscle mass increases (hypertrophies) because they have to contract with increased load. The thickness of the left ventricle increases, although no data are available on congenital or acquired defects or hypertension. At the same time, thickening of the interventricular septum occurs. This leads to a narrowing of the blood ejection pathways into the aorta.

Areas of hypertrophy may be localized in patches (usually at the exit to the aorta) or affect a large part of the left ventricle. Less commonly, they spread to the right side of the heart muscle. Damage occurs to the valve leaflets (mitral and aortic), and to the vessels supplying the myocardium.

During diastole, the atria have to work harder to fill the ventricles, because the tissues become dense, hard, and lose elasticity. The pressure in the pulmonary circulation increases.

Increased muscle mass requires more oxygen. The discrepancy between the growth of myocardial demands and capabilities leads to the development of ischemia. This is also facilitated by mechanical compression of the mouth of the left coronary artery.

Types of heart damage

Due to the uniformity and symmetry of the development of areas of myocardial hypertrophy, the following forms are distinguished:

• symmetrical (concentric) - the thickness of the walls of the left ventricle increases to the same extent along the anterior, posterior surfaces and in the area of ​​the septum, less often hypertrophy of the right ventricle is added;
• asymmetric - areas of thickening form in the upper or lower part of the interventricular septum, it becomes one and a half to three times thicker than the posterior wall of the left ventricle (in a normal heart they are equal), in 2/3 of patients these changes are combined with hypertrophy of the region of the anterior, lateral wall of the left ventricle or apex, without changes in the posterior wall.

Based on the strength of the obstruction to the flow of blood from the left ventricle to the aorta, it is customary to distinguish:

• obstructive hypertrophic cardiomyopathy (subaortic or subvalvular) - changes in anatomical relationships create a barrier to blood exit;
• non-obstructive - there is no barrier.

Clinical picture

Symptoms of hypertrophic cardiomyopathy first appear between the ages of 20 and 25. The most typical are the following:

• Pain behind the sternum of a pressing nature, very similar to angina attacks, has a similar irradiation to the left shoulder, neck, and shoulder blade. Unlike angina pectoris, they are not relieved by medications containing Nitroglycerin. There are atypical pains of aching or stabbing type.


• An important sign is increased shortness of breath when changing the horizontal position of the body to a vertical one. Over time, increased shortness of breath leads to cardiac asthma and pulmonary edema.
• Arrhythmias, increased heart rate.
• Dizziness that reaches the point of fainting is associated with a malnutrition of the brain. It intensifies during physical activity, straining, after a heavy meal, and when getting up quickly.

For hypertrophic cardiomyopathy, a characteristic manifestation is the sudden death of a person (the classification specifies that no more than 1 hour should pass from the moment of loss of consciousness, the case cannot have any signs of violence).

How to identify the disease

Diagnosis of the disease is very difficult. The doctor needs to know the family history (cases of confirmed disease in relatives or sudden death at a young age), the course of pregnancy in the mother, connections with industrial toxic substances, previous infectious diseases, stay in areas with high radiation.

During the examination, the doctor pays attention to the pallor of the skin, cyanosis of the lips and fingers. High or normal blood pressure is recorded.

On auscultation, a characteristic murmur is heard over the projection of the aorta.

In order to exclude possible pathology of the heart and blood vessels, a general analysis of blood, urine, biochemical tests for metabolic products, glucose, and the blood coagulation system are checked.

Additional examination methods

Hardware diagnostics allows you to accurately identify disease problems.

• An ECG study records information on disturbed rhythm, hypertrophy of the heart, and the development of blockades.
• The phonocardiogram records noise from certain points, which makes it possible to establish a connection between the audible noise and the aorta.
• An x-ray shows an increase in the contours of the cardiac shadow, but the size may be normal if hypertrophy develops inside the cavity.
• Ultrasound is the main method in making a diagnosis. The size of the heart chambers, wall thickness, condition of the valve apparatus, interventricular septum are assessed, and blood flow disturbances are observed.
• Magnetic resonance imaging allows you to obtain a three-dimensional image of the heart, identify obstruction, and the degree of wall thickness.
• Genetic research is a method of the future, but it is not yet developed enough.
• By inserting catheters into the cavities of the heart, the pressure in the atria and ventricles and the speed of blood flow are studied and measured. The technique allows you to take material for a biopsy.
• Coronary angiography of the heart vessels is performed in patients over 40 years of age for differential diagnosis with ischemic lesions of the heart vessels.

A biopsy is permissible only if all other diseases are excluded and there is no help from other diagnostic methods. Under a microscope, altered muscle fibers become visible.

Treatment

Specific elimination of gene mutations has not yet been achieved. Treatment of hypertrophic cardiomyopathy is carried out with medications that affect all aspects of the pathogenesis of the disease.

If signs of the disease are detected, it is necessary to limit physical activity and stop playing sports.

If the patient has any chronic infectious diseases, prophylactic antibiotics are prescribed.

Groups of medications that block adrenergic receptors, calcium antagonists are used, and agents that reduce thrombus formation in the cavities of the heart are added.

Surgical methods

The method of choice for open heart surgery is myotomy - removal of part of the interventricular septum from the inside or through the aorta. The mortality rate of these operations reaches 5%, which is comparable to the overall mortality rate.

A more gentle technique is carried out - concentrated alcohol is injected into the septal area through a puncture of the chest and heart under ultrasound control. Cell death and thinning of the septum are artificially caused. The obstacle to the passage of blood is reduced.

To treat the disturbed rhythm, an electrical stimulator or defibrillator is implanted (depending on the type of disorder).

Modern data suggest that survival after surgical treatment for 10 years is 84%, and with continuous conservative treatment - 67%.

In case of obstruction, an operation is used to replace the mitral valve with an artificial one, this eliminates its contact with the septum and “clears” the passage for blood flow.

Course of the disease

Hypertrophy is possible from the moment of birth. But in most patients it begins to appear during adolescence. Over three years, the thickness of the myocardial wall increases by 2 times. However, no symptoms of the disease are found in 70% of patients. By the age of 18 (less often until 40), the progression of thickening of the heart wall stops.

Subsequently, clinical manifestations develop with an obstructive variant of the pathology. In cases of non-obstructive forms, the course is favorable and is detected by chance during an ECG examination.

The annual incidence of sudden death from hypertrophic cardiomyopathy and its complications among adults is up to 3%, among children – from 4 to 6%. The main cause is considered to be ventricular fibrillation.

What are the possible complications?

Hypertrophic cardiomyopathy does not occur in isolation; the disease affects all aspects of the heart’s activity and causes serious complications.

• Arrhythmias and impaired conduction are observed in almost every patient. Depending on the severity, they may come out on top in terms of threat to the patient’s life. They are the direct cause of cardiac arrest or fibrillation.
• The addition of infection of the mitral and aortic valves leads to the development of endocarditis with subsequent insufficiency of the valve apparatus.
• The separation of a blood clot and the introduction of an embolus into the vessels of the brain (up to 40% of cases), into internal organs, and into the arteries of the extremities occurs with atrial fibrillation, a paroxysmal form.
• The development of chronic heart failure is possible during a long course of the disease, when part of the myocardial muscle fibers are replaced by scar tissue.

Forecast

Treatment can lead to temporary stabilization of hypertrophy. Average life expectancy does not directly depend on the form of the disease. The most favorable prognosis is considered to be with a long asymptomatic course, as well as with apical localization and the absence of cases of sudden death among relatives.

The main sign that aggravates the prognosis among patients from 15 to 50 years old is considered to be fainting, ischemia, and ventricular tachycardia detected on the ECG. The appearance of shortness of breath and chest pain in a patient sharply increases the risk of sudden death.

Statistical studies show, from the moment of detection, a five-year survival rate of 82 to 98%, a ten-year survival rate of 64 to 89%, with an average annual mortality rate of 1%.

Complexities in the etiological factors of the disease make any kind of prevention almost impossible. With this pathology, the main attention should be paid to identifying it, starting from adolescence, and carrying out symptomatic therapy.

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What is myocardial hypertrophy

This autosomal dominant disease is characterized by hereditary traits of gene mutation and affects the heart. It is characterized by an increase in the thickness of the walls of the ventricles. Hypertrophic cardiomyopathy (HCM) has a classification code according to ICD 10 No. 142. The disease is often asymmetric, with the left ventricle of the heart more susceptible to damage. This happens:

• chaotic arrangement of muscle fibers;
• damage to small coronary vessels;
• formation of areas of fibrosis;
• obstruction of blood flow - an obstacle to the ejection of blood from the atrium due to displacement of the mitral valve.

With heavy loads on the myocardium caused by diseases, sports, or bad habits, the body’s protective reaction begins. The heart needs to cope with increased work volumes without increasing the load per unit of mass. Compensation begins to occur:

• increased protein production;
• hyperplasia – increase in the number of cells;
• increase in myocardial muscle mass;
• wall thickening.

Pathological myocardial hypertrophy

With prolonged work of the myocardium under loads that are constantly increased, a pathological form of HCM occurs. A hypertrophied heart is forced to adapt to new conditions. Myocardial thickening occurs at a rapid pace. In this situation:

• growth of capillaries and nerves lags behind;
• blood supply is disrupted;
• the influence of nervous tissue on metabolic processes changes;
• myocardial structures wear out;
• the ratio of myocardial sizes changes;
• systolic and diastolic dysfunction occurs;
• repolarization is disrupted.

Myocardial hypertrophy in athletes

Abnormal development of the myocardium—hypertrophy—occurs unnoticed in athletes. During high physical activity, the heart pumps large volumes of blood, and the muscles, adapting to such conditions, increase in size. Hypertrophy becomes dangerous, causing stroke, heart attack, sudden cardiac arrest, in the absence of complaints and symptoms. You should not suddenly stop training to avoid complications.

Sports myocardial hypertrophy has 3 types:

• eccentric - muscles change proportionally - typical for dynamic activities - swimming, skiing, long-distance running;
• concentric hypertrophy - the ventricular cavity remains unchanged, the myocardium increases - observed in gaming and static types;
• mixed - inherent in activities with the simultaneous use of immobility and dynamics - rowing, cycling, skating.

Myocardial hypertrophy in a child

It is possible that myocardial pathologies may appear from the moment of birth. Diagnosis at this age is difficult. Hypertrophic changes in the myocardium are often observed during adolescence, when cardiomyocyte cells actively grow. Thickening of the anterior and posterior walls occurs until the age of 18, then stops. Ventricular hypertrophy in a child is not considered a separate disease - it is a manifestation of numerous ailments. Children with HCM often have:

• heart disease;
• myocardial dystrophy;
• hypertension;
• angina pectoris.

Causes of cardiomyopathy

It is customary to distinguish between primary and secondary causes of hypertrophic development of the myocardium. The first ones are influenced by:

• viral infections;
• heredity;
• stress;
• alcohol consumption;
• physical overload;
• excess weight;
• toxic poisoning;
• changes in the body during pregnancy;
• drug use;
• lack of microelements in the body;
• autoimmune pathologies;
• malnutrition;
• smoking.

Secondary causes of myocardial hypertrophy are provoked by the following factors:

Left ventricular hypertrophy

More often, the walls of the left ventricle are susceptible to hypertrophy. One of the causes of LVH is high pressure, which forces the myocardium to work at an accelerated rhythm. Due to the resulting overloads, the left ventricular wall and IVS increase in size. In this situation:

• the elasticity of the myocardial muscles is lost;
• blood circulation slows down;
• normal heart function is disrupted;
• there is a danger of a sudden load on it.

Left ventricular cardiomyopathy increases the heart's need for oxygen and nutrients. Changes in LVH can be noticed during instrumental examination. Low output syndrome appears - dizziness, fainting. Among the signs accompanying hypertrophy:

• angina pectoris;
• pressure changes;
• heartache;
• arrhythmia;
• weakness;
• high blood pressure;
• bad feeling;
• shortness of breath at rest;
• headache;
• fatigue;

Right atrial hypertrophy

Enlargement of the wall of the right ventricle is not a disease, but a pathology that appears when there is overload in this department. It occurs due to the receipt of a large amount of venous blood from large vessels. The cause of hypertrophy can be:

• birth defects;
• atrial septal defects, in which blood enters the left and right ventricles simultaneously;
• stenosis;
• obesity.

Right ventricular hypertrophy is accompanied by symptoms:

• hemoptysis;
• dizziness;
• night cough;
• fainting;
• chest pain;
• shortness of breath without exertion;
• bloating;
• arrhythmia;
• signs of heart failure - swelling of the legs, enlarged liver;
• malfunction of internal organs;
• cyanosis of the skin;
• heaviness in the hypochondrium;
• dilation of veins in the abdomen.

Hypertrophy of the interventricular septum

One of the signs of the development of the disease is hypertrophy of the IVS (interventricular septum). The main cause of this disorder is gene mutations. Hypertrophy of the septum provokes:

• ventricular fibrillation;
• atrial fibrillation;
• mitral valve problems;
• ventricular tachycardia;
• impaired blood flow;
• heart failure;
• cardiac arrest.

Dilation of the heart chambers

Hypertrophy of the interventricular septum can provoke an increase in the internal volume of the heart chambers. This expansion is called myocardial dilatation. In this position, the heart cannot perform the function of a pump, and symptoms of arrhythmia and heart failure occur:

• fast fatiguability;
• weakness;
• dyspnea;
• swelling of the legs and arms;
• rhythm disturbances;

Cardiac hypertrophy - symptoms

The danger of myocardial disease in asymptomatic progression for a long time. It is often diagnosed accidentally during medical examinations. As the disease progresses, signs of myocardial hypertrophy may be observed:

• chest pain;
• heart rhythm disturbance;
• shortness of breath at rest;
• fainting;
• fatigue;
• labored breathing;
• weakness;
• dizziness;
• drowsiness;
• swelling.

Forms of cardiomyopathy

It should be noted that the disease is characterized by three forms of hypertrophy, taking into account the systolic pressure gradient. All together the obstructive form of HCM corresponds. Stand out:

• basal obstruction – resting state or 30 mmHg;
• latent – ​​calm state, less than 30 mm Hg – it characterizes the non-obstructive form of HCM;
• labile obstruction – spontaneous intraventricular gradient fluctuations.

Myocardial hypertrophy - classification

For convenience of work in medicine, it is customary to distinguish between the following types of myocardial hypertrophy:

• obstructive – at the top of the septum, over the entire area;
• non-obstructive – symptoms are mild, diagnosed by chance;
• symmetrical – all walls of the left ventricle are affected;
• apical - the heart muscles are enlarged only from above;
• asymmetrical - affects only one wall.

Eccentric hypertrophy

With this type of LVH, the ventricular cavity expands and at the same time a uniform, proportional compaction of the myocardial muscles occurs, caused by the growth of cardiomyocytes. With a general increase in heart mass, the relative thickness of the walls remains unchanged. Eccentric myocardial hypertrophy can affect:

• interventricular septum;
• top;
• side wall.

Concentric hypertrophy

The concentric type of disease is characterized by maintaining the volume of the internal cavity while increasing the mass of the heart due to a uniform increase in wall thickness. There is another name for this phenomenon - symmetrical myocardial hypertrophy. The disease occurs as a result of hyperplasia of myocardiocyte organelles, provoked by high blood pressure. This development of events is typical for arterial hypertension.

Myocardial hypertrophy – degrees

To correctly assess the patient’s condition with HCM, a special classification has been introduced that takes into account myocardial thickening. According to how much the size of the walls increases during heart contraction, cardiology distinguishes 3 degrees. Depending on the thickness of the myocardium, the stages are determined in millimeters:

• moderate – 11-21;
• average – 21-25;
• pronounced – over 25.

Diagnosis of hypertrophic cardiomyopathy

At the initial stage, with a slight development of wall hypertrophy, it is very difficult to identify the disease. The diagnostic process begins with interviewing the patient, finding out:

• presence of pathologies in relatives;
• the death of one of them at a young age;
• past diseases;
• fact of radiation exposure;
• external signs during visual inspection;
• blood pressure values;
• indicators in blood and urine tests.

A new direction is being used – genetic diagnosis of myocardial hypertrophy. The potential of hardware and radiological methods helps to establish the parameters of HCM:

• ECG - determines indirect signs - rhythm disturbances, hypertrophy of sections;
• X-ray - shows an increase in the contour;
• Ultrasound – assesses myocardial thickness, blood flow disturbances;
• echocardiography – records the location of hypertrophy, diastolic dysfunction;
• MRI – gives a three-dimensional image of the heart, determines the degree of myocardial thickness;
• ventriculography – examines contractile functions.

How to treat cardiomyopathy

The main goal of treatment is to return the myocardium to its optimal size. Activities aimed at this are carried out in a comprehensive manner. Hypertrophy can be cured when diagnosed early. An important part in the system of myocardial health is played by lifestyle, which implies:

• diet;
• giving up alcohol;
• smoking cessation;
• weight loss;
• drug exclusion;
• limiting salt intake.

Drug treatment of hypertrophic cardiomyopathy includes the use of drugs that:

• reduce blood pressure - ACE inhibitors, angiotensin receptor antagonists;
• regulate heart rhythm disturbances - antiarrhythmics;
• drugs with a negative ionotropic effect relax the heart - beta blockers, calcium antagonists from the verapamil group;
• remove fluid - diuretics;
• improve muscle strength - ionotropes;
• if there is a threat of infective endocarditis, antibiotic prophylaxis.

An effective method of treatment that changes the course of excitation and contraction of the ventricles is dual-chamber pacing with a shortened atrioventricular delay. More complex cases - severe asymmetric hypertrophy of the IVS, latent obstruction, lack of effect of the drug - require the participation of surgeons for regression. Help save a patient's life:

• installation of a defibrillator;
• pacemaker implantation;
• transaortic septal myectomy;
• excision of part of the interventricular septum;
• transcatheter septal alcohol ablation.

Cardiomyopathy - treatment with folk remedies

On the recommendation of the treating cardiologist, you can supplement the main course with herbal remedies. Traditional treatment for left ventricular hypertrophy involves the use of viburnum berries without heat treatment, 100 g per day. It is useful to consume flax seeds, which have a positive effect on heart cells. Recommend:

• take a spoonful of seeds;
• add boiling water - liter;
• hold in a water bath for 50 minutes;
• filter;
• drink per day - dose 100 g.

Oat infusion for regulating the functioning of the heart muscles has good reviews in the treatment of HCM. According to the healers' prescription, it is required:

• oats – 50 grams;
• water – 2 glasses;
• heat to 50 degrees;
• add 100 g of kefir;
• pour in radish juice - half a glass;
• stir, stand for 2 hours, strain;
• put 0.5 tbsp. honey;
• dosage – 100 g, three times a day before meals;
• course – 2 weeks.

sovets.net

Definition. Left ventricular myocardium (LVMH) is an excess of the mass of the left ventricle relative to its proper value due to thickening (proliferation) of the myocardium (heart muscle).

Methods for diagnosing LVMH. Currently, 3 instrumental methods are used to diagnose LVMH:

— Standard ECG. When verifying LVMH, a conventional ECG is generally characterized by low sensitivity - no more than 30%. In other words, of the total number of patients who objectively have LVMH, an ECG allows it to be diagnosed in only a third. However, the more pronounced the hypertrophy, the higher the likelihood of recognizing it using a regular ECG. Severe hypertrophy almost always has ECG markers. Thus, if the ECG correctly diagnoses LVMH, this most likely indicates its severe degree. Unfortunately, in our medicine, a conventional ECG is given too much importance in diagnosing LVMH. Often, using low-specific ECG criteria for LVMH, doctors speak affirmatively about the phenomenon of hypertrophy where it actually does not exist. You should not expect more from a standard ECG than it actually shows.

— Ultrasound of the heart. It is the “gold standard” in the diagnosis of LVMH, as it allows real-time visualization of the walls of the heart and the necessary calculations. To assess myocardial hypertrophy, it is customary to calculate relative values ​​that reflect myocardial mass. However, for simplicity, it is permissible to know the value of only two parameters: the thickness of the anterior (interventricular septum) and posterior wall of the left ventricle, which makes it possible to diagnose hypertrophy and its degree.

— Magnetic resonance imaging (MRI)). An expensive method of layer-by-layer scanning of the “zone of interest”. To assess LVMH, it is used only if for some reason ultrasound of the heart is not feasible: for example, in a patient with obesity and pulmonary emphysema, the heart will be covered on all sides by lung tissue, which will make its ultrasound visualization impossible (extremely rare, but this does occur).

The thickness of the IVS and LVSD is directly related to hypertrophy of the left ventricular myocardium (the clinical significance of the EDR during hypertrophy will be discussed in the following). If the normal value of even one of the two presented parameters is exceeded, we can speak of “hypertrophy”.

Causes and pathogenesis of LVMH. Clinical conditions that can lead to LVMH (in order of decreasing frequency):

1. Diseases leading to increased afterload on the heart:

— Arterial hypertension (hypertension, secondary hypertension)

— Heart defect (congenital or acquired) - aortic stenosis.

Afterload is understood as a set of physical and anatomical parameters of the cardiovascular body that create an obstacle to the passage of blood through the arteries. Afterload is determined mainly by the tone of the peripheral arteries. A certain basic value of arterial tone is the norm and one of the obligate manifestations of homeostasis, maintaining the level of blood pressure, according to the current needs of the body. An excessive increase in arterial tone will mark an increase in afterload, which is clinically manifested by an increase in blood pressure. So, with spasm of the peripheral arteries, the load on the left ventricle increases: it needs to contract more strongly in order to “push” blood through the narrowed arteries. This is one of the main links in pathogenesis in the formation of a “hypertensive” heart.

The second common cause that leads to an increase in afterload on the left ventricle, and therefore creates an obstacle to arterial blood flow, is aortic stenosis. With aortic stenosis, the aortic valve is affected: it shrinks, calcifies, and becomes deformed. As a result, the aortic opening becomes so small that the left ventricle must contract significantly more to ensure that an adequate volume of blood passes through the critical bottleneck. Currently, the main cause of aortic stenosis is senile (senile) valve damage in the elderly.

Microscopic changes during myocardial hypertrophy include thickening of the cardiac fibers and some proliferation of connective tissue. At first, this is compensatory in nature, but with a long-term increased afterload (for example, with long-term untreated hypertension), hypertrophied fibers undergo dystrophic changes, the architectonics of the myocardial syncytium is disrupted, and sclerotic processes in the myocardium are predominant. As a result, hypertrophy turns from a compensation phenomenon into a mechanism for the manifestation of heart failure - the heart muscle cannot work under tension for an indefinitely long time without consequences.

2. Congenital cause of LVMH: hypertrophic cardiomyopathy. Hypertrophic cardiomyopathy is a genetically determined disease, which is characterized by the appearance of unmotivated LVMH. The manifestation of hypertrophy occurs after birth: as a rule, in childhood or adolescence, less often in adults, but in any case no later than 35-40 years. Thus, in hypertrophic cardiomyopathy, LVMH occurs against a background of complete well-being. This disease is not very rare: according to statistics, 1 person out of 500 suffers from it. In my clinical practice, I annually see 2-3 patients with hypertrophic cardiomyopathy.

Unlike a hypertensive heart, with hypertrophic cardiomyopathy, LVMH can be very pronounced (severe) and often asymmetrical (more on this in more detail). Only with hypertrophic cardiomyopathy does the thickness of the wall of the left ventricle sometimes reach “exorbitant” values ​​of 2.5-3 cm or more. Microscopically, the architecture of the cardiac fibers is grossly disrupted.

3. LVMH as a manifestation of systemic pathological processes.

— Obesity. Excess body weight is not solely a cosmetic problem. This is a deep pathophysiological process affecting all organs and systems, during which biochemical processes, psychodynamics of thinking, human selfhood, etc. change. With obesity, adipose tissue is deposited in excess not only under the skin, but also in almost all organs. The heart is forced to provide blood to “the body with all its excess mass.” Such an increased load cannot but affect cardiac functionality - it certainly increases: the heart contracts more often and stronger. Thus, in obesity, LVMH can develop in the absence of persistent arterial hypertension.

In obesity, the myocardium thickens not only due to the proliferation of cardiac fibers and connective tissue, but also due to the deposition of excess fat.

— Amyloidosis(primary or secondary) - a pathology in which a special amyloid protein is deposited in the internal organs, leading to the development of diffuse sclerosis and organ failure. Despite the possibility of developing LVMH due to amyloidosis, it rarely comes to the fore in the clinical picture of the disease: other organs (for example, kidneys) are more significantly affected, which will determine the specific picture of the disease.

4. Relatively natural causes of LVH.

— Elderly age. Senile age is characterized by slow but steadily progressive degradation (dystrophy) of all organs and systems. The specific gravity of water and parenchymal components in organs decreases; on the contrary, sclerotic processes intensify. The heart of an old man is no exception: the muscle fibers become thinner and loosen, at the same time, the connective tissue develops powerfully, due to which LVMH primarily occurs in old age. What is important to know is that senile LVMH, in the absence of other causes, never reaches significant values. It does not exceed the degree of “insignificant” and is more often only an age-related phenomenon, without any particular clinical significance.

— The heart of an athlete. We are talking about people who have been involved in professional sports for a long time. LVMH in such subjects can be called purely compensatory (working), as well as the concomitant hypertrophy of skeletal muscles. After the end of a sports career, LVMH undergoes complete or partial regression.

The following diseases (conditions) lead to concentric LVMH:

S-hypertrophy has no particular clinical significance, being more often a marker of an “age-related” heart. Occasionally, this type of hypertrophy occurs in middle-aged people.

Clinical significance of LVMH. Diseases leading to the development of LVMH can be asymptomatic for a long time (years, decades) or have nonspecific manifestations: for example, headache due to arterial hypertension. The earliest symptom of LVH (which, by the way, can appear after years of hypertrophy) is dyspnea with usual physical activity: walking, climbing stairs. Mechanism of shortness of breath: диастолическая SЃРµСЂРґРµС‡РЅР°СЏ недостаточРШость. It is known that blood filling of the heart occurs during diastole (relaxation): blood moves along a concentration gradient from the atria to the ventricles. With hypertrophy, the left ventricle becomes thicker, stiffer, denser - this leads to the fact that the process of relaxation and stretching of the heart becomes more difficult and incomplete; Accordingly, the blood supply to such a ventricle is disrupted (decreased). Clinically, this phenomenon manifests itself as shortness of breath. Symptoms of diastolic heart failure in the form of shortness of breath and weakness may be the only manifestation of LVMH for many years. However, in the absence of adequate treatment of the underlying disease, the symptoms will gradually increase, leading to a progressive decrease in exercise tolerance. The final outcome of advanced diastolic heart failure will be the development of systolic heart failure, the treatment of which is even more difficult. So, LVMH is a direct path to heart failure, which means a high risk of early cardiac death.

The next common complication of LVMH is development of paroxysmal atrial fibrillation (atrial fibrillation). Impaired relaxation (diastole) of the hypertrophied left ventricle inevitably entails an increase in blood pressure in it; this in turn causes the left atrium to contract more strongly in order to “push” the required volume of blood into the “container” with increased pressure. However, the left atrium is a thin-walled cardiac chamber that cannot operate in super mode for a long time; As a result, the left atrium dilates (widens) to accommodate the excess blood. Dilatation of the left atrium is one of the most important risk factors for the development of atrial fibrillation. As a rule, damage to the left atrium for a long time is manifested only by atrial extrasystole; subsequently, when the atrium “dilates sufficiently” to “maintain” fibrillation, atrial fibrillation occurs: first paroxysmal, then constant. The risks that atrial fibrillation brings into a patient’s life are described in detail in a separate chapter.

Obstructive syncope. A rare variant of the course of LVMH. It is almost always a complication of the asymmetric variant of hypertrophic cardiomyopathy, when the thickness of the interventricular septum is so great that there is a threat of transient obstruction (blocking) of blood flow in the area of ​​the outflow tract of the left ventricle. Paroxysmal obstruction (cessation) of blood flow in this “critical place” will inevitably lead to fainting. As a rule, the risk of developing obstruction occurs when the thickness of the interventricular septum exceeds 2 cm.

Ventricular extrasystole- another possible satellite for LVMH. It is known that any micro- and macroscopic changes in the heart muscle can theoretically be complicated by extrasystole. Hypertrophied myocardium is an ideal arrhythmogenic substrate. The clinical course of ventricular extrasystole against the background of LVMH is variable: more often, its role is limited to a “cosmetic arrhythmic defect”. However, if the disease leading to LVMH is not treated (ignored), and the regimen for limiting intense physical activity is not followed, life-threatening ventricular arrhythmias triggered by extrasystole may develop.

Sudden cardiac death. The most severe complication of LVMH. Most often, LVMH due to hypertrophic cardiomyopathy leads to this outcome. There are two reasons. Firstly, in this disease, LVMH can be particularly massive, which makes the myocardium extremely arrhythmogenic. Secondly, hypertrophic cardiomyopathy very often has an asymptomatic course, which does not allow patients to take preventive measures in the form of limiting intense physical activity. Sudden cardiac death in other nosologies complicated by LVMH is generally a rare phenomenon, if only because the manifestation of these diseases begins with symptoms of heart failure, which in itself forces the patient to see a doctor, which means there is a real opportunity to take the disease under control.

Possibility of regression of LVMH. The likelihood of a decrease in the mass (thickness) of the left ventricular myocardium during treatment depends on the cause of hypertrophy and its degree. A classic example is the athletic heart, the walls of which can decrease to normal thickness after the end of a sports career.

LVMH due to arterial hypertension or aortic stenosis can successfully regress with timely, complete and long-term control of these diseases. However, it is considered this way: only mild hypertrophy undergoes absolute regression; when treating moderate hypertrophy, there is a chance of reducing it to mild; and heavy can “become medium”. In other words, the more advanced the process, the less likely it is to return everything completely to its original state. However, any degree of regression of LVMH automatically means correctness in the treatment of the underlying disease, which in itself reduces the risks that hypertrophy introduces into the subject’s life.

With hypertrophic cardiomyopathy, any attempts at drug correction of the process are pointless. There are surgical approaches for the treatment of massive hypertrophy of the interventricular septum, which is complicated by obstruction of the left ventricular outflow tract.

The likelihood of regression of LVMH due to obesity, in older people, and with amyloidosis is practically absent.

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Content

Thickening of the wall of the myocardium (the muscular lining of the heart) is a pathological condition. In medical practice, there are various types of cardiomyopathy. Morphological changes in the main organ of the circulatory system lead to a decrease in the contractility of the heart, and insufficient blood supply occurs.

What is hypertrophic cardiomyopathy

A disease characterized by thickening (hypertrophy) of the wall of the left (rarely right) ventricle of the heart is called hypertrophic cardiomyopathy (HCM). The muscle fibers of the myocardium are located chaotically - this is a characteristic feature of the disease. In most cases, asymmetric thickening is observed, and hypertrophy of the interventricular septum develops.

The pathology is characterized by a decrease in ventricular volume and impaired pumping function. The heart has to beat frequently to deliver enough blood to the organs. The consequence of these changes is heart rhythm disturbances and the appearance of heart failure. 30–50 years is the average age of patients diagnosed with hypertrophic cardiomyopathy. The disease is more common in men. The pathological condition is recorded in 0.2–1.1% of the population.

Causes

HCM is a hereditary disease. Occurs as a result of gene mutation. The type of transmission of altered hereditary structures is autosomal dominant. Pathology is not only congenital. In some cases, mutations occur under the influence of unfavorable environmental factors. The consequences of changing the genetic code are as follows:

• the biological synthesis of myocardial contractile proteins is disrupted;
• muscle fibers have an incorrect location and structure;
• muscle tissue is partially replaced by connective tissue, myocardial fibrosis develops;
• altered cardiomyocytes (muscular membrane cells) work uncoordinated, with increased load;
• muscle fibers thicken, myocardial hypertrophy occurs.

Thickening of the muscle membrane (compensatory hypertrophy) is caused by one of two pathological processes:

1. Violation of diastolic myocardial function. During the period of relaxation of the heart (diastole), the ventricle is not filled with blood enough due to poor distensibility of the myocardium. This leads to an increase in diastolic pressure.
2. Obstruction (impaired patency) of the left ventricular outflow tract. Myocardial hypertrophy of the interventricular septum occurs. Blood flow is hampered due to impaired mobility of the mitral valve leaflet. At the moment of blood ejection, a difference in systolic pressure occurs between the cavity of the left ventricle and the initial part of the aorta. For this reason, some of the blood is retained in the heart. As a result, left ventricular end-diastolic pressure increases. Myocardial hypertrophy, dilatation (expansion) of the left atrium are consequences of compensatory hyperfunction.

Classification

The criteria underlying the classification of the disease are different. The following types of illness are distinguished:

Criterion		Common diagnoses: asymmetric hypertrophy of the interventricular septum; hypertrophic obstructive cardiomyopathy; asymmetric hypertrophy of the apex of the heart (apical)
Localization	Right ventricular or left ventricular hypertrophy
Features of thickening formation	Asymmetrical, concentric (or symmetrical)
Changed structures	Hypertrophy of the interventricular septum, apex of the heart, anterolateral wall, posterior wall
The presence of a gradient (difference) of systolic pressure in the left ventricle	Obstructive, non-obstructive
Degree of myocardial thickening	Moderate – 15-20 mm, average – 21-25 mm, pronounced – more than 25 mm

Taking into account the prevailing complaints of patients, nine forms of pathology are distinguished. While there are general symptoms, each variant of HCM has specific symptoms. The clinical forms are as follows:

• lightning;
• pseudovalvular;
• arrhythmic;
• cardialgic;
• low-symptomatic;
• vegetodistonic;
• infarct-like;
• decompensatory;
• mixed.

The clinical and physiological classification identifies four stages of disease development. The main criterion is the difference in systolic pressure in the left ventricular outflow tract (LVOT) and in the aorta:

• The first stage is a pressure indicator in the LVOT no more than 25 mm Hg. Art. The patient has no complaints about the deterioration of his condition.
• The second stage is a pressure gradient of about 36 mmHg. Art. The condition worsens with physical activity.
• The third stage – the pressure difference is up to 44 mm Hg. Art. Shortness of breath is observed and angina develops.
• The fourth stage is a systolic pressure gradient in the LVOT of more than 88 mmHg. Art. Blood circulation is impaired and sudden death is possible.

Symptoms of hypertrophic cardiomyopathy

The disease may not manifest itself for a long time. Hypertrophic cardiomyopathy is the main cause of death among young athletes who were unaware of the presence of a hereditary disease. 30% of patients with GTCS have no complaints and do not experience a deterioration in their general condition. The symptoms of the pathology are as follows:

• fainting, dizziness, shortness of breath, cardialgia, angina pectoris and other conditions associated with low blood output syndrome;
• left ventricular heart failure;
• heart rhythm disturbances (extrasystoles, paroxysms, arrhythmias);
• sudden death (in the absence of symptoms);
• the occurrence of complications - infective endocarditis, thromboembolism.

Diagnostics

The first signs of the disease appear in childhood, but in most cases it is diagnosed in adolescence or in patients 30–40 years old. Based on a physical examination (assessment of external condition), the doctor makes a primary diagnosis. The examination helps to identify the expansion of the borders of the heart, listen to the characteristic systolic murmur, if there is an obstructive form of the disease, the emphasis of the second tone may be on the pulmonary artery. When examining the jugular veins for hypertrophy, poor contractility of the right ventricle is indicated by a well-defined A wave.

Additional diagnostic methods include:

• Electrocardiography. In the presence of pathology, the ECG is never normal. The study allows us to determine the enlargement of the heart chambers, disturbances in conduction and contraction frequency.
• Chest X-ray. Helps identify changes in the size of the atria and ventricles.
• Echocardiography. The main method for identifying the location of thickening of the heart wall, the degree of blood flow obstruction, and diastolic dysfunction.
• Electrocardiogram monitoring throughout the day, with the use of physical activity. The method is important for preventing sudden death, prognosis of the disease, and identifying heart rhythm disturbances.
• Radiological methods. Ventriculography (examination of the heart with the introduction of a contrast agent) and magnetic resonance imaging (MRI) are performed. They are used in complex cases to identify and accurately assess pathological changes.
• Genetic diagnostics. The most important method for assessing the prognosis of the disease. Genotype analysis is carried out on the patient and his family members.

Treatment of hypertrophic cardiomyopathy

If a patient has symptoms of hypertrophic cardiomyopathy, a wide range of medications are used. If drug therapy is ineffective in the case of an obstructive form of pathology, surgical and alternative interventional methods of correction are used. A special treatment regimen is prescribed for patients with a high risk of sudden death or the last stage of the disease. The goals of therapy are:

• reducing the severity of symptoms and clinical manifestations of pathology;
• increasing the patient’s “quality of life”, improving functional ability;
• ensuring a positive prognosis of the disease;
• prevention of cases of sudden death and progression of the disease.

Drug therapy

In patients with symptoms of HCM, restriction of physical activity is recommended. This rule should be strictly followed by patients with an obstructive form of the disease. Loads provoke the development of arrhythmias, fainting, and an increase in the LVOT pressure gradient. To alleviate the condition with moderate symptoms of HCM, drugs of different pharmacological groups are prescribed:

• Beta blockers (Propranolol, Metoprolol, Atenolol) or calcium channel blockers (Verapamil). They reduce heart rate, lengthen diastole (relaxation phase), improve filling of the ventricles with blood, and reduce diastolic pressure.
• Calcium antagonists (Finoptin, Amiodarone, Cardil). Medicines reduce the amount of calcium in the coronary arteries, improve relaxation of structures (diastole), and stimulate myocardial contractility.
• Anticoagulants (Phenindione, Heparin, Bivalirudin). Medicines reduce the risk of thromboembolism.
• Diuretics (Furosemide, Indapamed), ACE inhibitors (Captopril, Ramipril, Fosinopril). The drugs are recommended for patients with heart failure.
• Antiarrhythmic drugs (Disopyramide, Amiodarone).

In case of HCM, the use of cardiac glycosides, nifedipine, and nitrites is contraindicated. These drugs contribute to the development of obstruction.

Surgery

Cardiac surgical treatment is advisable in the absence of effectiveness of taking pharmacological drugs. Surgery is indicated for patients in whom the pressure difference between the left ventricle (LV) and the aorta is more than 50 mm Hg. Art. at rest and during physical activity. To alleviate the patient's condition, the following surgical techniques are used:

• Transaortic septal myectomy (TSM). It is recommended for patients who experience fainting, shortness of breath, or chest pain during physical activity. The essence of the operation is to remove part of the interventricular septum. This manipulation ensures good LV contractility and free movement of blood into the aorta.
• Percutaneous alcohol ablation. The operation is prescribed for patients with contraindications to EMS, elderly patients who have inadequate blood pressure under stress conditions. Sclerosing substances (for example, alcohol solutions) are injected into the hypertrophied interventricular septum.
• Dual-chamber pacing. The technique is used for patients with contraindications to surgery. The manipulation improves heart function and increases cardiac output.
• Implantation of an artificial mitral valve. Prosthetics are recommended for patients in whom poor blood flow is not due to thickening of the interventricular septum, but as a result of inversion of the valve into the aortic lumen.
• Installation of ICD (implantable cardioverter-defibrillator). Indications for such a procedure are a high risk of sudden death, previous cardiac arrest, and persistent ventricular tachycardia. To install an ICD, an incision is made in the subclavian region, the electrodes are inserted through a vein (there can be 1-3, depending on the pacemaker model) and installed under x-ray control inside the heart.
• Heart transplantation. Prescribed to patients with the last stage of heart failure, in the absence of effect from drug treatment.

Surgical operations significantly improve the condition of patients and increase tolerance to physical activity. Surgical treatment does not protect against further development of pathological thickening of the myocardium and complications. In the postoperative period, the patient must undergo regular examinations using hardware diagnostic techniques and take pharmacological medications prescribed by the doctor for life.

Forecast

Hypertrophic cardiomyopathy has different development options. The non-obstructive form is stable, without pronounced symptoms. The consequence of prolonged development of the disease is heart failure. In 5–10% of cases, the thickening of the myocardial wall stops on its own; the same percentage is likely to transform hypertrophic cardiomyopathy into dilated cardiomyopathy (stretching of the heart cavities).

Mortality in the absence of treatment is observed in 3–8% of cases. In half of the patients, sudden death occurs, caused by severe ventricular arrhythmias, complete heart block, or acute myocardial infarction. In 15–25%, coronary atherosclerosis develops. Infectious endocarditis, which affects the mitral and aortic valves, occurs as a complication of the pathology in 9% of patients.

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Hypertrophy of various parts of the heart is a fairly common pathology that occurs as a result of damage not only to the heart muscle or valves, but also when blood flow in the pulmonary circle is disrupted due to lung diseases, various congenital anomalies in the structure of the heart, due to increased blood pressure, as well as in healthy people experiencing significant physical activity.

Causes of left ventricular hypertrophy

Among causes of hypertrophy LV the following can be distinguished:

• Arterial hypertension;
• Stenosis (narrowing) of the aortic valve;
• Hypertrophic cardiomyopathy;
• Increased physical activity.

• So, with hypertrophy of the right heart, the ECG will show a change in electrical conductivity, the appearance of rhythm disturbances, an increase in the R wave in leads V 1 and V 2, as well as a deviation of the electrical axis of the heart to the right.
• With left ventricular hypertrophy, the ECG will show signs of deviation of the electrical axis of the heart to the left or its horizontal position, a high R wave in leads V 5 and V 6, and others. In addition, voltage signs (changes in the amplitudes of the R or S waves) are also recorded.

Changes in the configuration of the heart due to the enlargement of certain parts of the heart can also be judged by the results radiography chest organs.

Schemes: ventricular and atrial hypertrophy on the ECG

Hypertrophy of the left ventricle (left) and right ventricle of the heart (right)

Hypertrophy of the left (left) and right (right) atria

Treatment of cardiac hypertrophy

Treatment of hypertrophy of various parts of the heart comes down to influencing the cause that caused it.

In the case of the development of cor pulmonale due to diseases of the respiratory system, they try to compensate for lung function by prescribing anti-inflammatory therapy, bronchodilators and others, depending on the underlying cause.

Treatment of left ventricular hypertrophy in arterial hypertension is reduced to the use of antihypertensive drugs from various groups.

In the presence of severe valve defects, surgical treatment up to prosthetics is possible.

In all cases, they fight the symptoms of myocardial damage - antiarrhythmic therapy is prescribed according to indications, drugs that improve metabolic processes in the heart muscle (ATP, riboxin, etc.). It is recommended to follow a diet with limited amount of salt and fluid intake, normalization of body weight in case of obesity.

For congenital heart defects, if possible, the defects are eliminated surgically. In case of severe disturbances in the structure of the heart, the development of hypertrophic cardiomyopathy, the only way out of the situation may be.

In general, the approach to the treatment of such patients is always individual, taking into account all existing manifestations of cardiac dysfunction, general condition and the presence of concomitant diseases.

In conclusion, I would like to note that Acquired myocardial hypertrophy detected in time is quite amenable to correction. If you suspect any disturbances in the functioning of the heart, you should immediately consult a doctor, he will identify the cause of the disease and prescribe treatment that will give you a chance for many years of life.

Video: left ventricular hypertrophy in the program “About the Most Important Thing”