Acute Left Ventricular Aneurysm

Myocardial infarction is a focus of ischemic necrosis of the heart muscle, which develops as a result of acute disturbance of coronary circulation. It is clinically manifested by burning, pressing or compressing pains behind the sternum, giving to the left hand, collarbone, scapula, jaw, shortness of breath, fear, cold sweat. The developed myocardial infarction serves as an indication for emergency hospitalization in cardiological resuscitation. Failure to provide timely assistance may result in death.

At the age of 40-60 years, myocardial infarction is 3-5 times more often observed in men due to the earlier (10 years earlier than in women) development of atherosclerosis. After 55-60 years, the incidence among both sexes is approximately the same. The mortality rate for myocardial infarction is 30–35%. Statistically, 15-20% of sudden deaths are due to myocardial infarction.

Violation of the blood supply to the myocardium for 15-20 minutes or more leads to the development of irreversible changes in the heart muscle and cardiac upset. Acute ischemia causes the death of part of the functional muscle cells (necrosis) and their subsequent replacement with connective tissue fibers, i.e., the formation of a post-infarction scar.

In the clinical course of myocardial infarction, five periods are distinguished:

  • 1 period – preinfarction (prodromal): increased and intensified angina attacks, may last several hours, days, weeks;
  • 2 period – the most acute: from the development of ischemia to the appearance of myocardial necrosis, lasts from 20 minutes to 2 hours;
  • 3 period – acute: from the formation of necrosis to myomalacia (enzymatic melting of necrotic muscle tissue), duration from 2 to 14 days;
  • 4 period – subacute: the initial processes of scar organization, the development of granulation tissue in place of necrotic tissue, duration 4-8 weeks;
  • 5 period – post-infarction: maturation of the scar, adaptation of the myocardium to new conditions of functioning.

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Keeping of

Aneurysm of the heart (aneurysma cordis) – pathological protrusion of a thinned section of the heart wall. For the first time A. s. described by Gunther (W. Hunter, 1757).

The most frequent reason A. with. (95%) is myocardial infarction: according to domestic and foreign authors, A. p. observed in 20-40% of patients after myocardial infarction. More rare species A. of page. are congenital, infectious and traumatic (including postoperative).

In most cases A. with. formed in the wall of the left ventricle; more than 60% of left ventricular aneurysms are located on the antero-lateral wall and apex. Localization A. with. in the right ventricle and atrium is 1%. A. s. rarely seen on the posterior wall and interventricular septum.

Usually A. s. are single, although the presence of 2-3 aneurysms at the same time is not so rare.

Postinfarction A. of page have the greatest clinical value, to-rye are divided into acute, subacute and chronic; this division is conditional and determines the phase of development of A. s.

In the form of A. s. can be diffuse (flat), bag-shaped, mushroom-shaped; there is also the so-called. aneurysm in aneurysm (Fig. 1). Diffuse are called flat aneurysms, with to-ryh the outer contour of the protrusion is gentle, and a cup-shaped recess is determined from the side of the cardiac cavity. The saccular aneurysm is a kind of hemisphere with a rounded bulge on a relatively wide base.

Mushroom aneurysm – a large sack-like formation, the diameter of the bottom of the cut is larger than the diameter of the neck. Sometimes in the area of ​​the bottom of the aneurysm one or several small protrusions can be observed with sharply thinned walls, prone to rupture – “aneurysm in the aneurysm”. Most often diffuse A. with. Meets, less bag-shaped and even less mushroom-shaped and “aneurysm in an aneurysm”.

Causes of myocardial infarction

Myocardial infarction is an acute form of IHD. In 97–98% of cases, the basis for the development of myocardial infarction is atherosclerotic lesion of the coronary arteries, causing a narrowing of their lumen. Often, atherosclerosis of the arteries is joined by acute thrombosis of the affected area of ​​the vessel, causing a complete or partial cessation of blood supply to the corresponding region of the heart muscle. The increased blood viscosity observed in patients with coronary heart disease contributes to thrombosis. In some cases, myocardial infarction occurs against a background of spasm of the branches of the coronary arteries.

The development of myocardial infarction is promoted by diabetes, hypertension, obesity, mental stress, alcohol addiction, smoking. A sharp physical or emotional stress on the background of coronary heart disease and angina pectoris can trigger the development of myocardial infarction. More often, left ventricular myocardial infarction develops.

Almost 95% of cases of cardiac aneurysm occur as a result of myocardial infarction, mainly when it developed in the left ventricle. Such a ventricular aneurysm does not always develop immediately (we will consider the classification of the disease below), it can be provoked by such phenomena in the post-infarction period as:

  • arterial hypertension;
  • smoking;
  • a large amount of fluid used;
  • physical activity causing tachycardia;
  • recurrent myocardial infarction.

Etiology and pathogenesis

The main determining factor in the education of A. s. is a massive transmural myocardial infarction (see), which leads to the destruction of all structures of the heart wall. The force of intracardiac pressure stretches and thins the necrotic wall of the heart. All circumstances, which increase the work of the heart and intraventricular pressure (early rising, tachycardia, arterial hypertension, etc.), play a significant role in the formation of A. s. On the frequency of occurrence A. with. localization of a heart attack and repeated heart attacks also affects.

So, infarction of the posterior wall of the left ventricle is almost as common as infarction of the anterior wall, and aneurysm of the posterior wall is much less common. Diameter A. s. can range from 2-3 to 18-20 cm.

To Art. Aneurysm of the heart. Fig. 1. Chronic aneurysm of the anterior wall of the left ventricle, apex, and interventricular septum. Sharp thinning of the wall in the area of ​​the aneurysm

Wall acute A. with. It is a site of necrotic myocardium, stretched and swelling under the influence of intraventricular pressure. In under the acute period (3-8 weeks. Illness) A.’s wall of page. consists of a thickened endocardium (there are accumulations of histiocytes and fibroblasts in it, there are also newly formed reticular, collagen and elastic fibers), and the place of the destroyed smooth muscle cells is occupied by elements of connective tissue of different maturity.

Wall of chronic A. with. formed by fibrous tissue; the larger the A. page, the thinner its wall, sometimes its thickness does not exceed 2 mm (tsvetn. tab., Fig. 1). Under a microscope, three layers of the wall of the fibrous sac can be distinguished, which correspond to the endocardial, intramural and epicardial layers of the heart wall. Endocardium of a wall of chronic A. with. always thickened, whitish. It reveals the proliferation of fibrous, often hyalinized, connective tissue.

To Art. Aneurysm of the heart. Fig. 2. Aneurysm of the anterior wall of the left ventricle, apex and part of the posterior wall. Massive parietal thrombi performing aneurysm cavity

Characteristic for chronic A. with. there is the presence of a parietal thrombus of various sizes, to-ry or only lining its inner surface, or fulfills almost completely the entire aneurysmal sac (tsvetn. tab., Fig. 2).

Fig. 1. Aneurysm of the heart: 1 – diffuse

Blood clots in long-existing aneurysms are usually of a dense consistency, in the section they have a hyaline or layered, lamellar appearance; often lime salts are deposited in them. Parietal thrombosis in aneurysm occurs at the very beginning of the formation of protrusion of the heart wall and is associated with a change in hemodynamics, increased thrombogenic properties of the blood and a reactive process that occurs in the endocardium when the latter is involved in the ischemic zone. Loose thrombi are easily fragmented and are a source of thromboembolic complications.

Fig. 1. Aneurysm of the heart: 2 – saccular

Congenital aneurysms of the heart are rare. Usually this is a diverticulum protrusion, communicating with the cavity of the left ventricle and simultaneously contracting with it. In contrast to other aneurysms, they do not lead to heart failure and blood clots in the aneurysmal protrusion.

Fig. 1. Aneurysm of the heart: 3 – mushroom

Traumatic aneurysms of the heart can be true and false. They are extremely rare with closed or open injuries. This group includes postoperative aneurysms. The last often arise after operations on the “infundibular” part of the right ventricle concerning Fallot’s tetrad or with a closed valvulotomy in people with pulmonary stenosis (see Congenital heart defects). Aneurysms of the right ventricle are most often traumatic.

Fig. 1. Aneurysm of the heart: 4 – “aneurysm in aneurysm”

Infectious heart aneurysms (syphilitic, rheumatic, aneurysms caused by bacterial ulcerative endocarditis and embolic processes in septic conditions) are very rare.

Classification of myocardial infarction

Aneurysm of the heart is a formation that can have different localization, wall structure, size, shape and mechanism of formation. If the disease developed as a result of a heart attack, then the timing of its occurrence is also important. Therefore, the classification of the disease is very extensive. It is carried out on the basis of ultrasound of the heart (echocardiography).

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a) sharp. Formed in the initial 14 days from the appearance of myocardial cell death; the wall consists of a dead myocardium. If the protrusion is small, there is a chance that the body itself will “smooth it out” with the help of a dense scar. But if the formation is large, then it is very dangerous: from any increase in intraventricular pressure can quickly increase and even burst.

b) Subacute, occurring at 3-8 post-infarction week. The wall consists of a thickened endocardium, there are also cells of connective tissue of varying degrees of maturity. These aneurysms are more predictable, since the tissue performing them has almost formed and is more dense (less responsive to intraventricular pressure fluctuations).

c) Chronic, which form after 8 weeks after the formation of myocardial necrosis. The wall consists of three layers: the endocardium and the epicardium, between which the former muscle layer is located.

Chronic aneurysms, having, although a thinned, but rather dense wall, slowly grow and rarely burst, but other complications are typical for them:

  • blood clots that form due to stagnation;
  • rhythm disturbances, the reason for which is that a normal myocardium is interrupted by an aneurysm consisting of tissue that does not conduct impulses.
  1. True. Consist of the same walls as the heart. Intradermally may contain different amounts of connective tissue. This type we are considering.
  2. False. The wall of such aneurysms consists of a leaf of a heart bag or adhesions. Blood in such an artificial “bag” gets through a defect in the heart wall.
  3. Functional. The myocardium – the wall of such an aneurysm – is quite viable, but has low contractility. It swells only in systole.

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By localization

Most often, an aneurysm of the heart develops in the left ventricle, because its oxygen demand, like wall thickness and internal pressure, is higher. In the right ventricle, aneurysm can also develop, but its appearance in the atria is almost unrealistic.

Other possible localization of aneurysm:

  • the top of the heart;
  • front heart wall;
  • interventricular septum. In this case, a true saccular protrusion is not formed, and the septum is shifted towards the right ventricle. This condition is life-threatening, as heart failure quickly forms here;
  • rarely, the posterior heart wall.

By size

Ultrasound of the heart indicates the size of the aneurysm. The patient’s prognosis also depends on this parameter: the greater the protrusion of the heart wall, the worse it is.

According to the form

This characteristic, determined by echocardiography, makes it possible to judge how fast the aneurysm is growing and how dangerous it is in terms of rupture.

Unlike the previous parameter, the form of the aneurysm is described in different terms:

  • Diffuse. It has a small volume, its bottom is on the same level with the rest of the myocardium. Her chance to burst is small, and blood clots rarely form in her. But due to the fact that the tissue of the walls of the aneurysm is not involved in conducting the pulse and contractions, it becomes a source of arrhythmias. Diffuse aneurysm can grow and change its shape.
  • Mushroom-shaped. It is formed from scars or necrosis of small diameter. It looks like an inverted jug: from the site where there are no cardiomyocytes, a small mouth leaves, which further ends with a “sac”, the cavity of which gradually expands. Such an aneurysm is dangerous rupture and thrombosis.
  • Baggy. Here the wide base, the “mouth” and the cavity are not very different in diameter. Moreover, the “pouch” is more capacious than in the case of diffuse aneurysm. These formations are dangerous with a tendency to tear and accumulate blood clots.
  • “Aneurysm in aneurysm.” This is the most explosive species. Here an additional aneurysm appears on the wall of the diffuse or saccular formation. This species is less common than the rest.

This classification is based on what tissue performs the protrusion wall: muscle, connective, their combination. It coincides with the separation of aneurysms in time and because of education. So, if an aneurysm formed after a heart attack, scar tissue will prevail in its wall. The expansion of the area of ​​the heart formed as a result of myocarditis contains not only connective tissue fibers – some of the muscle cells remain intact.

The composition of the wall also affects the prognosis of the disease, and this criterion distinguishes:

  1. Muscle aneurysms. These defects appear when there is congenital weakness of the muscle fibers in a separate area of ​​the myocardium, or did not stop, but the nutrition or nervous regulation in a limited area was disturbed. As a result, under the action of intraventricular pressure, the wall bends, but the scarring process does not start here. Muscular aneurysms rarely occur, for a long time they do not manifest themselves with any symptoms.
  2. Fibrous. These are mainly post-infarction aneurysms, where connective tissue replaces the site of dead normal myocardial cells. Such defects are weak, they gradually stretch under the influence of blood pressure. This is the most unfavorable type of aneurysm.
  3. Fibro-muscular. They are formed after myocarditis, ionizing radiation, toxic damage to the myocardium, sometimes after a heart attack, when the myocardium has not died out over the entire thickness of the wall.

The structure of the wall is judged by the medical history and ultrasound of the heart. A biopsy is not performed to find out the exact structure, as this will lead to the formation of a defect in the wall of the heart.

So, based on all the above classifications, cardiac aneurysms are considered the most prognostically unfavorable:

  • sharp;
  • mushroom shape;
  • “Aneurysm in aneurysm”;
  • fibrous;
  • gigantic.

In accordance with the size of the focal lesion of the heart muscle, myocardial infarction is distinguished:

Small focal myocardial infarction accounts for about 20% of clinical cases, but often small foci of necrosis in the heart muscle can transform into large focal myocardial infarction (in 30% of patients). Unlike large-focal, with small-focal heart attacks, aneurysm and cardiac rupture do not occur, the course of the latter is less often complicated by heart failure, ventricular fibrillation, thromboembolism.

Depending on the depth of necrotic damage to the heart muscle, myocardial infarction is distinguished:

  • transmural – with necrosis of the entire thickness of the muscular wall of the heart (usually large-focal)
  • intramural – with necrosis in the thickness of the myocardium
  • subendocardial – with myocardial necrosis in the area adjacent to the endocardium
  • subepicardial – with myocardial necrosis in the area adjacent to the epicardium

According to the changes recorded on the ECG, distinguish:

  • “Q-infarction” – with the formation of a pathological Q wave, sometimes the ventricular complex QS (usually large-focal transmural myocardial infarction)
  • “Not a Q-heart attack” – is not accompanied by the appearance of a Q wave, is manifested by negative T-waves (usually small focal myocardial infarction)

According to the topography and depending on the lesion of certain branches of the coronary arteries, myocardial infarction is divided into:

  • right ventricular
  • left ventricular: anterior, lateral and posterior walls, interventricular septum

According to the frequency of occurrence, myocardial infarction is distinguished:

  • primary
  • recurrent (develops within 8 weeks after the primary)
  • repeated (develops 8 weeks after the previous one)

According to the development of complications, myocardial infarction is divided into:

By the presence and localization of pain, the forms of myocardial infarction are distinguished:

  1. typical – with localization of pain behind the sternum or in the precardial region
  2. atypical – with atypical pain manifestations:
  • peripheral: left-scapular, left-handed, laryngeal-pharyngeal, mandibular, upper vertebral, gastralgic (abdominal)
  • painless: collaptoid, asthmatic, edematous, arrhythmic, cerebral
  • low symptom (obliterated)
  • combined

In accordance with the period and dynamics of the development of myocardial infarction, there are:

  • stage of ischemia (acute period)
  • necrosis stage (acute period)
  • stage of organization (subacute period)
  • scarring stage (post-infarction period)
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The clinical picture of post-infarction

The clinical picture of post-infarction aneurysm of the heart until recent years seemed fuzzy and its recognition was available in isolated cases. The first intravital diagnosis of A. with. in our country was delivered by the Kazan clinician A.N. Kazem-Beck in 1896. He also described the clinic of this disease. In the future, a great contribution to the study of the clinic A. s. contributed by F. I. Yakovlev, D. D. Pletnev, A. L. Myasnikov, etc.

More often A. s. occurs in men (68%) aged 40 to 70 years. For acute and subacute postinfarction A. with. characteristic: 1) a history of myocardial infarction; 2) the development and progression of heart failure from the first days of the disease; 3) the expansion of the borders of the heart to the left and less often to the right; 4) long-lasting leukocytosis;

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5) a long febrile period; 6) the appearance of precordial pulsation (a symptom of Kazem-Beck); 7) “frozen” electrocardiographic picture of acute myocardial infarction. These symptoms are not always found, and some of them, including a symptom of precordial pulsation, can be observed with myocardial infarction without aneurysm. At a number of patients A. page. the noise of pericardial friction is heard.

At acute A. with. noise, in contrast to that observed with myocardial infarction, is more prolonged, is heard for several days (sometimes weeks) and is characterized by a rougher timbre. It usually occurs during the formation of acute A. s., When fibrous inflammation of the pericardium develops, leading to the formation of pleuropericardial adhesions. Timely and correct diagnosis of acute A. with. allows you to determine further therapeutic tactics.

The clinical picture of chronic postinfarction A. with. largely depends on the degree of atherosclerotic lesion of the coronary arteries and the compensatory capabilities of the cardiovascular system. Most patients complain of pain in the region of the heart or behind the sternum and shortness of breath, which are more often observed during physical exertion.

The most obvious clinical sign of chronic A. with. is a precordial pulsation, determined by palpation, and sometimes even by eye. This symptom is characteristic of aneurysm of the anterior-lateral wall of the left ventricle. Suprapercussive pulsation – a specific symptom of chronic A. with. Pathological pulsation in the region of the apex of the heart must be differentiated from the apical impulse.

Aneurysmal pulsation is usually extended in time, more diffuse and sometimes reaches the level of the third intercostal space. In some cases, it is possible to separately determine the pulsation of the aneurysm and the apical impulse. Subsequently, the precordial pulsation may increase or decrease until it completely disappears with the formation of parietal thrombi in the aneurysmal sac.

In 1896, Kazem-Bek noted in patients with A. s. pulse of small filling with increased pulsation in the region of the heart. This symptom is observed infrequently, as a rule, in severe patients with severe heart failure. Listened at A. with. noise is characterized by great variability. They meet both in an acute, and in a chronic stage of development of A. with.

and depend on many reasons: the size and shape of the aneurysm, the presence of blood clots in the aneurysmal sac, the functional state of the heart muscle and valvular apparatus. Characteristic for chronic A. with. is systolodiastolic murmur – a sharp, high timbre, “squeaking noise” (A. L. Myasnikov), but it is not observed in all patients (absent in aneurysms accompanied by pericarditis, as well as in aneurysms that pulsate poorly as a result of filling the aneurysmal sac with thrombotic masses, and disappears with weakening of cardiac activity).

Very often at A. with. deaf heart sounds are heard, but this symptom has a small diagnostic value, because it also occurs with cicatricial changes in the myocardium without aneurysm. Heart rhythm disturbances or impaired conduction may be observed. The most common ventricular extrasystole (cm).

Appearance of atrial fibrillation (see) and paroxysmal tachycardia (see) at A. with. worsens the prognosis; often followed by cardiac decompensation, leading to death. Often the gallop rhythm is heard, which occurs as a result of a sharp violation of the period of diastolic tension of the ventricles (increased III cardiac sound).

One of characteristic clinical manifestations of A. with. is persistent cardiovascular failure observed in 70% of patients. Initially, left-ventricular failure develops, as evidenced by an increase in the final diastolic pressure, a decrease in shock and minute discharge, the presence of stagnation in the pulmonary circulation. Clinically, this is manifested by tachycardia, shortness of breath, and then attacks of cardiac asthma. Later signs of right ventricular failure join.

The reasons of development of heart failure at chronic A. with. complex and diverse. They depend not only on the size and location of the aneurysm, but also on the functional state of the myocardium. Often at chronic A. with. thromboembolic complications and repeated myocardial infarction are observed.

Breaks of chronic A. of page, in contrast to acute, are extremely rare.

Fig. 2. Aneurysm of the left ventricle. Semi-ovarian protrusion along the left contour of the left ventricle. A “notch” is visible on the upper border of the aneurysm (radiograph)

Symptoms of aneurysm of the heart

Clinical manifestations depend on the size and location of the aneurysm.

Subacute aneurysm of the heart is manifested by rapidly progressive symptoms of circulatory failure.

Chronic aneurysm of the heart is characterized by:

  • pronounced signs of heart failure (shortness of breath, rest angina and tension, a feeling of interruption in the work of the heart, in the later stages – swelling of the veins of the neck, swelling, etc.)
  • fibrous pericarditis, causing adhesions in the chest cavity.

Bot Adr ug - Acute Left Ventricular Aneurysm

With chronic aneurysm of the heart, thromboembolic syndrome may develop (the iliac and femoral-popliteal segments, brachiocephalic trunk, arteries of the brain, kidneys, lungs, intestines are more often affected.

Among the dangerous complications of chronic heart aneurysm can be called gangrene of the limb, stroke, kidney infarction, pulmonary embolism, repeated myocardial infarction.

In some cases, a rupture of a chronic aneurysm of the heart is possible. It occurs 2-9 days after myocardial infarction and leads to instant death. Clinical manifestations of rupture of aneurysm of the heart: sudden sharp pallor (which is quickly replaced by cyanosis of the skin), cold sweat, overflow of neck veins with blood, loss of consciousness, cold extremities, noisy, hoarse, shallow breathing.

Preinfarction (prodromal) period

About 43% of patients report a sudden development of myocardial infarction, while in the majority of patients, a period of unstable progressive angina pectoris that is different in duration is observed.

Acute period

Typical cases of myocardial infarction are characterized by extremely intense pain syndrome with localization of pain in the chest and radiating to the left shoulder, neck, teeth, ear, collarbone, lower jaw, interscapular region. The nature of the pain can be compressive, bursting, burning, pressing, acute (“dagger”). The larger the area of ​​myocardial damage, the more pronounced the pain.

The pain attack proceeds in waves (sometimes intensifying, then weakening), lasts from 30 minutes to several hours, and sometimes even days, it does not stop by repeated administration of nitroglycerin. Pain is associated with severe weakness, agitation, a sense of fear, shortness of breath.

Perhaps an atypical course of the acute period of myocardial infarction.

Patients have a sharp pallor of the skin, a sticky cold sweat, acrocyanosis, anxiety. Blood pressure during the attack period is increased, then moderately or sharply decreases compared to the initial (systolic lt; 80 rt Art., pulse lt; 30 mmHg Art.), noted tachycardia, arrhythmia.

During this period, acute left ventricular failure (cardiac asthma, pulmonary edema) may develop.

Acute period

In the acute period of myocardial infarction, the pain syndrome usually disappears. Preservation of pain is caused by a pronounced degree of ischemia of the near-infarction zone or by the attachment of pericarditis.

As a result of the processes of necrosis, myomalacia and perifocal inflammation, a fever develops (from 3-5 to 10 or more days). The duration and height of temperature rise during fever depend on the area of ​​necrosis. Arterial hypotension and signs of heart failure persist and increase.

Subacute period

There is no pain, the patient’s condition improves, and body temperature normalizes. Symptoms of acute heart failure become less pronounced. Tachycardia, systolic murmur disappears.

Post-infarction period

In the post-infarction period, clinical manifestations are absent, laboratory and physical data with practically no deviations.

Atypical forms of myocardial infarction

Sometimes there is an atypical course of myocardial infarction with localization of pain in atypical places (in the throat, fingers of the left hand, in the area of ​​the left shoulder blade or cervico-thoracic spine, in the epigastrium, in the lower jaw) or painless forms, the leading symptoms of which can be cough and severe suffocation, collapse, swelling, arrhythmias, dizziness and dizziness.

Atypical forms of myocardial infarction are more common in elderly patients with severe signs of cardiosclerosis, circulatory failure, against the background of repeated myocardial infarction.

However, usually only the most acute period usually occurs atypically; further development of myocardial infarction becomes typical.

The erased course of myocardial infarction is painless and is accidentally detected on an ECG.

Signs of a cardiac aneurysm can vary significantly: this is due to its size, localization, and cause of formation. It is generally difficult for a person who has had myocardial infarction to navigate in his condition, so the disease changes him. Meanwhile, an aneurysm is formed in almost one in ten people in the post-infarction period, and it is impossible to predict its appearance. Therefore, the task of each patient is to pay attention to the slightest change in health, and inform the attending cardiologist about it.

There are several main signs of any cardiac aneurysm, we will consider them in detail.

Chest pain

It is localized behind the sternum or slightly to the left. Paroxysmal: at rest does not bother, but is provoked by physical exertion, smoking, stress, drinking alcohol. It occurs due to various reasons:

  • connective tissue overgrowth of the branches of the coronary arteries, which fed not only the dead area, but also neighboring ones. The pain arises due to the fact that the nutrition of these zones adjacent to the aneurysm is disturbed, but gradually it passes, since the larger artery directs its newly grown branches to these areas;
  • heart overload. In the cavity of the aneurysm after a contraction of the heart, a small amount of blood remains. Then the muscle relaxes, and the heart cavity is replenished with new blood. Both – residual and functional – volumes create an increased load on the myocardium, and this is manifested by heart pain;
  • squeezing aneurysm of other tissues. This happens if the pathological cavity in the heart has grown to gigantic proportions.

The aneurysm itself, especially post-infarction, does not hurt, since it is formed by connective tissue, in which there are no nerve endings.


It occurs due to insufficient oxygen delivery to the muscles and nervous system. The reason for the trophic disturbance is that the volume that remains in the aneurysm that cannot contract is turned off from the blood circulation.


Rhythm disturbances occur because the tissue performing the walls of the aneurysm does not conduct an electrical impulse, due to which the heart contracts. The second cause of the condition is an organ overload with a blood volume.

Arrhythmias with aneurysm usually appear with stress or physical exertion. They pass quickly, but can also cause a prolonged sensation of a “pounding” heart. The latter case requires urgent correction by a cardiologist.


Its cause is congestion in the cavity of the aneurysm, when the increased pressure inside the heart is gradually transmitted to the vessels of the lungs. This leads to a deterioration in oxygen metabolism, due to which the respiratory rhythm is disturbed.


It appears first on the face and limbs, then covers the whole body. In parallel, people note rapid freezing of the limbs, “goosebumps” on the skin and a decrease in its sensitivity.

All this happens because, due to the deposition of volume in the aneurysm cavity, oxygen delivery to tissues is reduced. The skin does not belong to those organs whose life support the body will support in any way. Her diet is “cut” to provide blood to the brain, kidneys and the heart itself.


It is dry, appears seizures, is not accompanied by fever or sore throat. The reason for this condition can be one of two things: either congestion in the vessels of the lungs (as in the case of shortness of breath), or squeezing of lung tissue with a large aneurysm.

Normally, a person does not feel the work of his own heart. But if rhythm disturbances occur, or if the heart with an aneurysm tries to push through a larger volume of blood, a feeling of its beating appears.

Other symptoms

For cardiac aneurysm are also characteristic:

  • a feeling of heaviness in the chest;
  • increased sweating;
  • dizziness;
  • swelling of the limbs and face;
  • hoarseness.


Possibilities of diagnosis of chronic A. with. expanded with the use of electrocardiography and X-ray examination, including cinema ventriculography and coronary angiography. Electrocardiographic picture of chronic A. with. represented by a frozen monophasic curve characteristic of transmural myocardial infarction.

Accordingly, a deep Q wave is noted at the lesion site. R wave is low or more often completely absent. The QRS complex takes the form of QS. The S – T segment arches above the contour, turning into a negative T wave. Aneurysms of the anterior wall of the left ventricle are characterized by ECG changes in the I standard and corresponding chest leads.

At apical localization A. with. ECG changes are observed in IV chest assignment; with localization on the side wall – in the left chest leads, with localization on the front wall and front of the septum – in the right chest leads. For aneurysm of the posterior wall of the left ventricle, changes in II, III standard ECG leads and in unipolar lead from the left leg are characteristic.

Fig. 3. The same patient as in fig. 2. Right oblique position

Radiodiagnosis of aneurysm of the heart began to develop in the twenties of the 20th century. [Christian, Frick (HA Christian, H. Frick), 1922] and continues to improve, enriched with new techniques, and yet the recognition of this disease presents significant difficulties. For diagnosis A. with. Multiprojection fluoroscopy with a thorough study of the features of cardiac contractions is needed to identify areas of akinesia (“silent zones”) and dyskinesia (paradoxical pulsation) characteristic of aneurysms.

In addition to radiographs in a direct and oblique projections, radiographs with a slight rotation of the patient (20-30 °) in both the right and left oblique positions are recommended. In the same projections, X-ray diffraction and electro-Kimography are performed. The most important sign of saccular A. with. serves as a semi-oval protrusion on the contour of the left ventricle (Fig.

2 and 3), delimited on both sides by notches. For large A. s. a sharp increase in the diameter of the heart shadow is characteristic. In this case, the left heart contour often has rectangular outlines (Fig. 4.). These gross morphological features are inconsistent and often absent in diffuse aneurysms. Therefore, the symptom of the wavy contour, i.e.,

weakly expressed, sometimes hardly noticeable flat protrusions. The role of these signs increases dramatically if, accordingly, such a protrusion is observed and violations of the contractile properties of the myocardium in the form of a motionless contour or paradoxical pulsation. It should be noted that tracking the phenomenon of paradoxical pulsation along the posterior contour of the left ventricle in the second oblique and lateral positions can also be observed normally due to systolic transformation of the heart shape. Sometimes, along the contour of the left ventricle, small angular deformations of the contour (pericardial fusion) are visible.

Fig. 4. Aneurysm of the left ventricle. An increase in the diameter of the heart to the left. Rectangular outlines of the left contour of the heart (radiograph)

bot menu sep - Acute Left Ventricular Aneurysm

In recognition of functional signs A. with. fluoroscopy is of great importance, but for a detailed study, a graphical recording of the movements of the heart contour is needed – fluoroscimography and electrocymography.

On X-ray diffraction patterns, zones of akinesia, their localization and extent are clearly defined. When comparing X-ray images of the aorta and the heart, untimely – paradoxical (in systole – outward) displacement of the contour in the region of A. s., And sometimes also signs of sharp passive displacements of the thinned fibrous wall of A. s.

in the form of “torn segments” of the heart shadow or paradoxical transverse striping of the heart shadow (M. A. Ivanitskaya, 1950). The advantage of electrochemography is the possibility of a more accurate analysis of violations of the myocardial counter-activity: when recording the movements of the left ventricular contour in the A. region. the rise of the curve during systole is determined instead of lowering it to normal, moreover, the simultaneous recording of an electro- or phonocardiogram allows you to accurately determine the time of occurrence of this paradoxical movement, its duration and amplitude with respect to the total amplitude of the curve.

Distinguish between a complete paradoxical pulsation of the contours of the aneurysm, when the movement in the systole outward occupies the entire systole (these are especially sharp violations of the myocardial contractility), and partial paradoxical pulsation, when this movement occupies only a part of the systole; in this case, the tooth of both the electro-Kimographic and X-ray curve acquires an additional vertex.

Of great importance for recognition A. with. X-ray diffraction has a simultaneous study of morphological and functional features. Functional radiological signs facilitate the diagnosis of flat, diffuse aneurysms that do not give an expressive morphological picture. For revealing apical A. with.

!  Characteristic signs and consequences of anterior heart attack

The most accurate morphological and functional characteristics of A. s. in a crust, time is provided by kinoventriculography [Gorlin (R. Gorlin), 1967], by means of a cut aneurysms of any localization come to light. Comparison of the data of a comprehensive X-ray examination of the heart before and after the operation allows an objective assessment of the results of surgical treatment of A. s.

Complications of myocardial infarction

Aneurysm is dangerous for its thromboembolic consequences. Blood clots that accumulate in the pathological cavity can “fly off” and clog vessels of the limbs (usually the legs), the brachiocephalic trunk (this can lead to the development of a stroke), kidneys, intestines, or lungs. Therefore, aneurysm can cause:

  • thrombotic embolism of the pulmonary artery – a deadly disease if large branches of this vessel become clogged;
  • gangrene of the limb;
  • mesenteric thrombosis (blockage of the intestinal vessels by a thrombus, which leads to its death);
  • cerebral stroke;
  • kidney infarction;
  • recurrence of myocardial infarction.

The second dangerous complication of aneurysm is its rupture. It mainly accompanies only acute postinfarction aneurysm, developing 2-9 days after the death of a section of the heart muscle. Symptoms of aneurysm rupture:

  • sharp pallor, which is replaced by blue skin;
  • cold sweat;
  • the veins of the neck “fill up” and pulsate;
  • loss of consciousness;
  • breathing becomes hoarse, shallow, noisy.

If the aneurysm was large, death occurs within a few minutes.

Arrhythmias are considered the third complication. Moreover, important organs do not receive the amount of oxygen they need.

The fourth and most common consequence of aneurysm is heart failure, usually of the left ventricular type. Signs of this complication: weakness, fear of cold, pallor, dizziness. Over time, shortness of breath, cough, swelling on the extremities appears.

Complications often arise already in the first hours and days of myocardial infarction, making it harder. In most patients, in the first three days, various types of arrhythmias are observed: extrasystole, sinus or paroxysmal tachycardia, atrial fibrillation, complete intraventricular block. The most dangerous is ventricular fibrillation, which can go into fibrillation and lead to the death of the patient.

Left ventricular heart failure is characterized by congestive rales, cardiac asthma, pulmonary edema and often develops in the acute phase of myocardial infarction. An extremely severe degree of left ventricular failure is cardiogenic shock, which develops with extensive heart attack and usually leads to death. Signs of cardiogenic shock is a fall in systolic blood pressure below 80 mm Hg. Art., impaired consciousness, tachycardia, cyanosis, decreased diuresis.

A rupture of muscle fibers in the area of ​​necrosis can cause cardiac tamponade – hemorrhage in the pericardial cavity. In 2-3% of patients, myocardial infarction is complicated by thromboembolism of the pulmonary artery system (can cause pulmonary infarction or sudden death) or a large circle of blood circulation.

Patients with extensive transmural myocardial infarction in the first 10 days may die from rupture of the ventricle due to acute cessation of blood circulation. With extensive myocardial infarction, scar tissue failure may occur, its swelling with the development of acute cardiac aneurysm. Acute aneurysm can transform into a chronic one, leading to heart failure.

Deposition of fibrin on the walls of the endocardium leads to the development of parietal thromboendocarditis, which is dangerous because of the possibility of embolism of the vessels of the lungs, brain, and kidneys from detached thrombotic masses. In a later period, a post-infarction syndrome may develop, manifested by pericarditis, pleurisy, arthralgia, eosinophilia.


Treatment for heart aneurysm is usually two-stage. Initially, drug therapy is carried out aimed at diluting the blood, reducing the myocardial oxygen demand, and correcting the heart rhythm. After that – according to strict indications – they begin surgical intervention.

It is carried out at the stage of preparation for the operation, as well as for life if the aneurysm is small or a person consciously refuses the operation.

The purpose of prescribing medications is to reduce the load on the left ventricle, the prevention of thrombosis and life-threatening arrhythmias. To do this, use:

  • Beta-blockers: Corvitol, Nebivolol, Metoprolol. These drugs reduce myocardial oxygen demand.
  • Blood thinners: Warfarin, salicylic acid preparations;
  • Diuretics are needed to reduce the blood load on the heart. Appointed with concomitant hypertension. List of diuretics.
  • Nitrates: Cardicet, Isoket, Nitroglycerin. They expand the coronary arteries, improving heart nutrition.

Specific drugs and their dosage are selected only by a cardiologist. Self-medication is dangerous by rupture of the aneurysm, respiratory arrest or blood circulation.

Operative therapy

The operation of the aneurysm of the heart is performed according to the following indications:

  • arrhythmias (especially their ventricular types), poorly amenable to medical treatment;
  • aneurysm growth;
  • rapidly progressing heart failure;
  • the risk of “exit” the thrombus from the cavity of the aneurysm;
  • repeated limb thrombosis, microstrokes or strokes;
  • false aneurysm;
  • when a heart aneurysm is diagnosed in a newborn;
  • rupture of the wall of the ventricle;
  • rupture of aneurysm.

The last 2 points are indications for emergency surgery.

The operation to excise pathologically enlarged walls with subsequent suturing of the heart within healthy tissues is performed under general anesthesia in conditions of cardiopulmonary bypass. Then the heart, which is essentially a pump, deliberately stops with a special drug. Its function of providing oxygen to organs is carried out by a special apparatus (AIK – a cardiopulmonary bypass), which consists of several pumps connected to large vessels and working smoothly.

During the operation of the AIC, the heart stops contracting, which allows cardiac surgeons to precisely dissect the aneurysm and put in neat but tight sutures (often with simultaneous strengthening of the heart wall with polymeric materials). At the same time, doctors examine the coronary arteries and, if necessary, restore the normal diameter of their lumen – to prevent recurrent myocardial infarction.

When the main stage of the operation ends, the heart is triggered by a direct electric discharge. The cardiac surgeon, together with the anesthetist, monitors the restoration of the contractility of the heart, and only after making sure that it works without interruptions, turn off the AIC. If necessary, an artificial pacemaker is implanted – a pacemaker. He will prevent dangerous rhythm failures, “imposing” the correct sequence of heart contractions.

After the operation, medications are required:

  • blood thinners;
  • improving coronary blood flow;
  • antiarrhythmics;
  • antibiotics.

Conservative methods of treating heart aneurysm cannot be eliminated, and when the first signs of heart failure appear, the question is about surgery. The main method for treating heart aneurysm is surgical excision and suturing of a heart wall defect. In some cases, aneurysm wall is reinforced with polymer materials.

In the preoperative period, cardiac glycosides, anticoagulants, antihypertensive drugs, oxygen therapy, oxygen barotherapy are prescribed. Patients are advised to strictly limit physical activity.

The Cardiology Department of MedicCity has all the necessary equipment for the comprehensive diagnosis of a wide range of cardiac diseases. Reception is conducted by highly qualified cardiologists who have undergone professional internships in Russia and abroad.

With myocardial infarction, emergency hospitalization to cardiological resuscitation is indicated. In the acute period, the patient is prescribed bed rest and mental rest, fractional, limited in volume and calorie nutrition. In the subacute period, the patient is transferred from resuscitation to the cardiology department, where treatment of myocardial infarction continues and the regime is gradually expanding.

Relief of pain is carried out by a combination of narcotic analgesics (fentanyl) with antipsychotics (droperidol), intravenous administration of nitroglycerin.

Therapy for myocardial infarction is aimed at preventing and eliminating arrhythmias, heart failure, cardiogenic shock. Prescribe antiarrhythmic drugs (lidocaine), ß-blockers (atenolol), thrombolytics (heparin, acetylsalicylic acid), antagonists of Ca (verapamil), magnesia, nitrates, antispasmodics, etc.

In the first 24 hours after the development of myocardial infarction, perfusion can be restored by thrombolysis or emergency balloon coronary angioplasty.

The use of modern special research methods has made it possible to increase the frequency of intravital diagnosis of A. s., Which is of great practical importance in connection with the success of the surgical treatment of this disease.

A. s. refers to prognostically unfavorable complications of myocardial infarction. Numerous domestic and foreign statistics show that 5 years after myocardial infarction complicated by aneurysm, no more than 12% of patients remain alive. In the first 3 years after a heart attack complicated by an aneurysm, 73% die, and after 5 years – 88% of patients, including 70% from heart failure and 30% from thromboembolic complications, although there are separate indications of patients’ life expectancy of up to 10 and more years.

The following are subject to surgical treatment: 1) patients with chronic A. with. Complicated by heart failure, angina pectoris, arrhythmia, not amenable to conservative therapy; 2) patients with A. of page, complicated by a bag thrombosis or its progressive increase, threatening a gap. Only in some patients with a small uncomplicated diffuse or saccular A. s.

in a stable state, the operation can be postponed under the condition of clinical observation until the clinical picture changes. Resection of saccular A. s. should be done no earlier than 3-4 months. after a heart attack, i.e. when a strong scar tissue is formed, which prevents the failure of the sutures along the excision line of the aneurysmal sac.

In connection with a serious condition of patients and complexity of operations of intervention at A. with. worn until the mid 50s of the 20th century. random character. In 1931, Sauerbruch (E. F. Sauerbruch), during an operation on the chest, mistakenly opened the right ventricular aneurysm, which he mistook for a mediastinal tumor, sutured it at the base and excision. In 1942, Beck (S. S.

Beck) strengthened with a free piece of the wide fascia of the thigh the wall of the post-infarction left ventricular aneurysm diagnosed before surgery. Since 1944, with the surgical treatment of chronic A. a number of interventions are used: 1) strengthening the thinned wall of the aneurysm with various autografts: pectoral muscle [D’Allen (GD

Allen), 1956], a large omentum (V. I. Kazansky, 1964), a skin flap [Nidner (FF Niedner), 1955] and others; 2) sinking of the aneurysm with sutures (B.V. Petrovsky, F.G. Uglov, A.A. Vishnevsky, 1954-1957); 3) immersion of the aneurysm with sutures using the intercostal muscle on the leg [Shpachek (V. Spacek), 1954]; 4) resection of the aneurysm in a closed manner using a needle clamp [Bailey (S. P.

The operation of strengthening the aneurysm wall with various tissues is used in the crust, time only with diffuse aneurysm. With a bag-shaped aneurysm, it is insufficient ^, because it does not eliminate the paradoxical pulsation and the threat of rupture of the aneurysm.

Operation of immersion A. with. sutures can be used only for small saccular aneurysms of the ventricle or atrium, accidentally identified during surgery for compressive pericarditis or rheumatic heart diseases; with aneurysms complicated by thrombosis, it can not be used because of the danger of embolism.

Cover and immersion A. s. using intercostal muscle has not found wide application: eliminating paradoxical pulsation, this intervention does not improve the nutrition of the heart muscle. As shown by the experience of thoracoplasty according to Abrajanov, the muscles used for plastic purposes are always scarred; in addition, embolism due to parietal thrombi is possible.

Resection of the aneurysmal sac in a closed way refers to radical interventions. This method was developed by Bailey, who in 1954 performed a similar operation, having pressed the base of the aneurysm with special terminals. Later, he clamped the base of the aneurysm to prevent embolism only after its dissection and removal of parietal thrombi.

Particular attention is paid to washing the thrombotic masses with a blood stream, which, independently of Bailey, B.V. Petrovsky proposed to remove blood clots from the ear and atrium during operations for mitral stenosis and A. s. The advantage of this method is that it does not require sophisticated equipment, it is simple and effective, and the use of washing blood clots to some extent serves to prevent thromboembolism.


According to the history of the disease (heart attack, severe flu, frequent drinking of alcohol, and so on) and characteristic symptoms, a cardiologist may suspect an aneurysm. Upon examination, he will not always be able to confirm his assumption: a seal in the region of the heart above which the noise is heard can only be detected if it is large and located in the region of the apex of the heart (there it is closest to the ribs).

Suspect the presence of aneurysm indirectly by ECG. So, it should change after a heart attack, and when a defect is formed at the site of necrosis, the cardiogram “freezes”, stops changing. This study also allows you to evaluate the work of the myocardium, to establish the type of arrhythmia (this helps to choose a treatment).

The main method for detecting cardiac aneurysm is ultrasound with dopplerography. So you can not only clearly localize the aneurysm, but also measure intracardiac pressure, estimate the thickness of the heart wall, measure how much blood leaves the heart in 1 contraction, see blood clots or thinning the bottom of the aneurysmal sac, which may indicate its predisposition to rupture. Echocardioscopy also helps to distinguish true from false aneurysm, to evaluate the operation of the valves.

If it makes sense to treat the aneurysm promptly, myocardial scintigraphy is performed when a radioisotope is introduced into the blood, which accumulates selectively in the myocardial cells. Next, a special apparatus is examined, which makes it possible to obtain a clear image of the heart. And if scintigraphy is carried out with a load, then this makes it possible to calculate what load will be extremely permissible for a person.

Laboratory diagnosis in the detection of aneurysm of the heart is not informative.

In 50% of patients, pathological precordial pulsation is detected.

ECG signs are nonspecific – a “frozen” picture of acute transmural myocardial infarction is detected, there may be rhythm disturbances (ventricular extrasystole) and conduction (blockade of the left bundle branch block).

ECHO-KG allows you to visualize the cavity of the aneurysm, determine its size and localization, to identify the presence of a parietal thrombus.

Myocardial viability in the zone of chronic aneurysm of the heart is determined by stress echocardiography and PET.

With the help of chest x-ray it is possible to detect cardiomegaly, stagnant processes in the blood circulation.

Radiocontrast ventriculography, MRI and MSCT of the heart are also used to determine the size of the aneurysm of the heart, to identify thrombosis of its cavity.

For the purpose of differential diagnosis of a disease from a coelomic pericardial cyst, mitral heart disease, mediastinal tumors, cardiac sounding, coronarography can be prescribed.

The most important diagnostic criteria for myocardial infarction are the medical history, characteristic ECG changes, and serum enzyme activity indicators. Complaints of a patient with myocardial infarction depend on the form (typical or atypical) of the disease and the extent of damage to the heart muscle. Myocardial infarction should be suspected with a severe and prolonged (longer than 30-60 minutes) attack of chest pains, impaired conduction and heart rate, acute heart failure.

Characteristic ECG changes include the formation of a negative T wave (for small focal subendocardial or intramural myocardial infarction), a pathological complex of QRS or Q wave (for large focal transmural myocardial infarction). Echocardiography reveals a violation of locally contractile ventricle, thinning of its wall.

In the first 4-6 hours after a pain attack in the blood, an increase in myoglobin is determined – a protein that transport oxygen inside the cells. An increase in the activity of creatine phosphokinase (CPK) in the blood by more than 50% is observed after 8-10 hours from the development of myocardial infarction and decreases to normal in two days. The determination of the level of CPK is carried out every 6-8 hours. Myocardial infarction is ruled out with three negative results.

To diagnose myocardial infarction at a later date, they resort to the determination of the enzyme lactate dehydrogenase (LDH), the activity of which increases later than CPK – 1-2 days after the formation of necrosis and comes to normal values ​​after 7-14 days. Highly specific for myocardial infarction is an increase in the isoforms of the myocardial contractile protein troponin – troponin-T and troponin-1, which also increase with unstable angina. In the blood, an increase in ESR, leukocytes, aspartate aminotransferase (AsAt) and alanine aminotransferase (AlAt) is determined.

Coronary angiography (coronarography) allows you to establish thrombotic occlusion of the coronary artery and a decrease in ventricular contractility, as well as assess the possibilities of coronary artery bypass grafting or angioplasty – operations that help restore blood flow in the heart.

Prognosis for myocardial infarction

Myocardial infarction is a serious, associated with dangerous complications of the disease. Most deaths develop on the first day after myocardial infarction. The pumping ability of the heart is associated with the localization and volume of the infarct zone. If more than 50% of the myocardium is damaged, as a rule, the heart cannot function, which causes cardiogenic shock and death of the patient. Even with less extensive damage, the heart does not always cope with stresses, as a result of which heart failure develops.

After an acute period, the prognosis for recovery is good. Adverse prospects in patients with complicated myocardial infarction.

In general, the prognosis is poor, it improves only during the operation. The quality of life worsens and its duration decreases under the following factors:

  • the aneurysm is large;
  • its mushroom shape or “aneurysm in aneurysm”;
  • it formed in the period up to 2 weeks after myocardial infarction;
  • localized in the left ventricle;
  • the patient’s age is older than 45 years;
  • there are severe concomitant diseases: diabetes mellitus, renal pathology

Tatyana Jakowenko

Editor-in-chief of the Detonic online magazine, cardiologist Yakovenko-Plahotnaya Tatyana. Author of more than 950 scientific articles, including in foreign medical journals. He has been working as a cardiologist in a clinical hospital for over 12 years. He owns modern methods of diagnosis and treatment of cardiovascular diseases and implements them in his professional activities. For example, it uses methods of resuscitation of the heart, decoding of ECG, functional tests, cyclic ergometry and knows echocardiography very well.

For 10 years, she has been an active participant in numerous medical symposia and workshops for doctors - families, therapists and cardiologists. He has many publications on a healthy lifestyle, diagnosis and treatment of heart and vascular diseases.

He regularly monitors new publications of European and American cardiology journals, writes scientific articles, prepares reports at scientific conferences and participates in European cardiology congresses.