Post-infarction Dressler syndrome. Dressler's syndrome: treatment and post-infarction complications

Cardial pathologies are of a threatening nature not only in themselves. Significant risks arise after apparent prosperity and complete cure from illness.

Many conditions of the described profile can lead to autoimmune processes in the body. Such phenomena are relatively rare; according to various estimates, the probability of a reaction occurring is no more than 3-10%.

Dressler's syndrome is a pronounced autoimmune response to necrosis of cardiomyocytes (post-infarction syndrome). As a result of the destruction of cellular structures, a large number of special protein compounds are released, to which an immune response occurs.

This is a delayed result of damage to the cardiovascular system. Becomes the result of a heart attack, inflammatory diseases, other pathologies.

Restoration is carried out in outpatient setting. Complications are formidable, but, fortunately, they occur no more often than in 4% of situations.

The syndrome extremely rarely provokes death; isolated cases of such a result have been described. However, the quality of life drops significantly. The disease is prone to chronicity and frequent relapses.

The phenomenon under consideration is heterogeneous in nature. What is worth knowing about him. During inflammation, heart attack and other destructive phenomena, the death of cardiomyocyte cells is detected.

A large number of protein compounds enter the blood. The immune system reacts to them as dangerous invaders, producing special antibodies. Gradually the answer gets out of control and becomes stereotypical.

All similar protein structures of cell membranes are attacked by their own immunity. This is not only healthy heart tissue, but also tissue of joints, pulmonary structures and other anatomical formations.

Typically, Dressler syndrome develops as a result of extensive damage to the heart, in particular the myocardium. Clinical variations depend on predisposition.

Also, the course and risks are aggravated by a history of concomitant autoimmune pathological processes. For example, rheumatoid arthritis, systemic lupus erythematosus and others.

WITH high probability the localization of the syndrome will correspond to the main focus. One condition causes another.

Reasons for the formation

There are relatively few development factors. They always have a strictly cardiac origin and are associated with damage to cardiac tissue.

An approximate list of phenomena:

Myocardial infarction

Most common pathological process. Leads among the culprits in the onset of the described autoimmune condition. The essence is the death, necrosis of active, functional tissues.

The larger the affected area, the more intense the disease. This is understandable given the amount of protein compounds released. The strength of the immune response corresponds to the state of affairs.

The development of Dressler syndrome is not early, but delayed. It is impossible to immediately notice any changes. Approximate timeframe - 2-7 weeks, plus or minus.

The disease occurs acutely, symptoms appear immediately and in full. Moreover, it is not necessary that the signs will be from the heart. Joints, lungs and other structures are under attack.

The number of cases of post-infarction Dressler syndrome is defined as 95-97%.

Chest injuries

From bruises to fractures, including ribs and others. Heart damage does not always occur, so cases are considered on an individual basis.

If involvement of cardiac structures is suspected, ECG echocardiography is performed, and, if possible, magnetic resonance imaging. Consultation with a specialized specialist is required.

The likelihood of developing Dressler's syndrome due to injury is minimal. Except for cases of extensive myocardial damage (this is possible, for example, in a traffic accident with severe damage, etc.).

Radiofrequency ablation

Minimally invasive cardiac surgery. Prescribed to eliminate foci of pathological electrical excitation in the myocardium.

It is carried out in extreme cases, as a method of restoring normal rhythm. Complications are always possible, the patient should be aware of this.

The probability of the described outcome is insignificant, approximately 1-3% of total number situations ends with Dressler's syndrome. Even in such a case, everything is usually limited to a single episode in a lifetime.

Other types of operations performed

Any. From prosthetics to implantation of a stimulator, defibrillator and others. Each surgery is a traumatic experience for the heart. Therefore, it is impossible to avoid damage to myocytes.

The release of specific proteins does not always end so badly, depending on the extent of the damage.

Risk factors

The main culprit remains a heart attack. The question arises, why, in this case, Dressler syndrome after a heart attack is not observed in all patients? Indeed, according to statistics, the approximate number of patients with a diagnosed autoimmune process ranges from 4 to 20%, according to various estimates. It's a group of high-risk factors.

Research shows that most patients had at least one of the following in their anamnesis:

Hypersensitization of the body. Usually against the background of the current allergic reaction. It doesn’t matter how it manifests itself: urticaria, Quincke’s edema, bronchial asthma or other phenomena.
Autoimmune pathologies. Rheumatoid arthritis, Hashimoto's thyroiditis, vasculitis, systemic lupus erythematosus, psoriasis. Doesn't matter. Any factor is defined as a moment of increased risk.
Weakened immunity. Against the background of frequently transmitted infectious and inflammatory pathologies and other conditions.

All patients are similar in these indicators. The disease does not have any gender or age specific characteristics.

Symptoms, depending on location

In total, there are 6 pathological processes caused by the described disease. Approximate time the appearance of the first manifestations - 2-7 weeks.

Possible late onset of the condition. Then the clinical picture develops after almost a year, but this is relative rare option. What localizations are we talking about:

Heart

Presented with pericarditis. We are talking about inflammation of a special connective tissue sac in which a muscle organ is located. It protects it from displacement and keeps it in one place.

The condition is accompanied by a group of signs:

Intense pulsating, pressing or burning pain in the chest. Moreover, they are not similar to those during a heart attack, as the patients themselves say. The strength of the discomfort becomes different when changing body position, especially after a deep breath.
Temperature rise. Up to 38-39 degrees Celsius. This is the result of an autoimmune lesion.
An increase in venous pressure is manifested by swelling of the cervical vessels. Fall arterial indicator(usually minor, within 10-20 mmHg of normal).

Arrhythmias are possible due to the accumulation of effusion in the pericardium; this is the first sign of incipient tamponade. A terrible phenomenon.

Skin localization

Presented autoimmune dermatitis or hives.

Symptoms:

Intense, painful itching.
The formation of a reddish or bright rash throughout the body or in specific areas, depending on the strength of the immune response.
The formation of papules, that is, small blisters filled with serous (transparent) exudate.
Increase in local temperature.

At the same time, the connection between a heart attack or injury is so unobvious that it is difficult to think about the cardiogenic nature of the pathological process; a long examination is required.

Maybe, we're talking about about a match or a response to a reception medicines. Diagnostics will put an end to the issue. Moreover, the blood picture against the background of an autoimmune process is quite specific.

Abdominal localization of Dressler's syndrome

It is defined by peritonitis, inflammation of the internal lining of the cavity. Has a clear clinical picture:

Excruciating, intense pain in the abdomen. The severity of discomfort becomes lower when you find the correct, comfortable body position. Usually lying on your side with your legs bent.
Diarrhea or constipation.
Increase in temperature (up to 39 degrees, sometimes less).

Specific reactions are also present. Special tests make it possible to detect peritonitis.

In this case, it is urgent to distinguish the autoimmune form from the infectious-inflammatory form. The second is often the result of advanced appendicitis or other pathologies gastrointestinal tract.

Therapeutic tactics depend on the diagnostic results. With an aseptic form not associated with the penetration of bacteria, conservative treatment is required.

Attention:

Characteristic feature lesions provoked by pathogenic agents - temperature above 39 degrees.

Pleural localization

The outer lining of the lungs becomes inflamed. Manifestations are not very specific:

Dry nonproductive cough not for several days.
Pain in the chest at the back, dull, aching in nature.
Increased body temperature to 39 degrees Celsius or lower.

Pulmonary localization

Alveolitis (also called pneumonitis, not to be confused with a similar disease). It is non-infectious in nature, but the symptoms are approximately the same:

Intense discomfort when breathing, inability to take in air, dissatisfaction with the process.
Blueness of the skin due to insufficient gas exchange throughout the body.
Weakness, drowsiness.
Cough with a small amount of sputum.
Intolerance to even minimal physical activity.

Differential diagnosis is pneumonia. Spirography is indicated, if possible bronchoscopy or at least radiography chest or MRI/CT.

Articular shape

Arthritis. It usually affects large joints: shoulder, knee, hip, on one or both sides at once.

Signs resemble manifestations of rheumatoid inflammation:

Severe pain at the site of involvement in the pathological process.
Violations motor activity.
Feeling of stiffness.
Redness, swelling and swelling of the joint.
Inability to carry out basic actions.

A complication is additional damage to the periosteum. It is observed in long-term untreated cases.

There are also some common symptoms:

Stable high temperature body at a febrile level (but not higher than 39 degrees Celsius).
Weakness, drowsiness, malaise.
Inflammation of the mucous membranes. genitals, oral cavity and others. Possibly in a complex. This clue allows one to suspect the described autoimmune process.

Dressler's syndrome in cardiology is variable: cardiac forms account for no more than 15% of all recorded situations. This is paradoxical.

Recovery is carried out in an inpatient or outpatient setting.

Diagnostics

Examination under the supervision of a cardiologist and group specialized specialists. Which ones exactly are determined by the clinical picture.

Approximate scheme of events:

Oral questioning of the patient. The symptoms described above speak volumes about the process.
Anamnesis collection. As a rule, within 2 months, less than a year, a chest injury or heart attack, or myocarditis was observed. It is even worse if no treatment was carried out at all.
Measurement blood pressure, heart rate.
Electrocardiography, ECHO-CG.

Also MRI of the chest. These are the main methods for identifying Dressler syndrome, localized in the connective tissue bursa.

Additionally shown:

General blood test. In the background normal amount leukocytes and ESR (excludes acute infectious process) an increase in the level of eosinophils is detected. A clear indication of an autoimmune origin.
Chest X-ray, MRI or CT scan if necessary.
Bronchoscopy. In extreme cases.
Assessing the condition of the joint using ultrasound or puncture.
Sputum analysis.
Ultrasound examination of the abdominal cavity.

The diagram is approximate. In reality, more or fewer positions may be required. In any case, Dressler's syndrome, given its relative rarity and nonspecific symptoms, poses a difficult challenge to the leading physician.

Treatment

Mostly conservative. Involves taking medications from several pharmaceutical groups:

Anti-inflammatory non-steroidal origin. Ketorolac, Ibuprofen, Nise and others. To stop the process.
Glucocorticoids. For the same purposes, but if the first ones are ineffective. Dexamethasone or Prednisolone courses. In case of resistant course, it is recommended to take certain regimens throughout the patient’s life.
Alkaloids. Colchicine. Relieves inflammation, prevents tissue breakdown under the influence of immune factors.
Drugs to protect the gastrointestinal tract. Omeprazole and others.

Attention:

If there are significant doubts about the origin, it is permissible to use antibiotics as an experimental method. There will be no effect against the background of the syndrome.

Surgical therapy is used extremely rarely. The goal of such treatment is to eliminate complications that may arise. Basically we are talking about pericarditis.

Puncture, excision of the pericardial sac, and other techniques are performed. Assessing the condition and developing radical tactics falls on the shoulders of the doctor.

Post-infarction Dressler syndrome is treated conservative methods, surgical method indicated in extreme cases, against the background of the development of potentially fatal processes.

Possible consequences

The likelihood of complications occurring is minimal.

Among them:

. The release of fluid into the pericardium with compression of the muscular organ itself.

Hepatitis. Inflammation of the liver structures. It leads to cirrhosis relatively rarely, but it’s not worth the risk.
Vasculitis. Defeats vascular walls. The result is scarring, closure of the lumen, formation of blood clots and other issues.

Glomerulonephritis. Inflammatory and degenerative kidney damage of an autoimmune nature. Destruction leads to failure, rapid fatal outcome.

It is possible to develop multiple, combined forms of Dressler's syndrome. Potentially, this type is much worse treated.

Forecast

Determined individual characteristics body. According to statistics, survival rate is close to 95-98%.

Death from the described condition is extremely rare. Isolated cases have been described in the literature. This is casuistry.

The main causes of death are heart failure, stopping the functioning of a muscular organ due to tamponade. However, the quality of life with Dressler syndrome drops significantly.

The prognosis is generally favorable. Maintaining work activity is unlikely; the ability to take care of oneself at home decreases significantly.

In conclusion

Autoimmune consequences of heart attack and other lesions of cardiac structures are rare. But they tend to early chronicity and resistance (immunity) to treatment. Therefore, the patient has to put up with new living conditions.

With proper therapy, the duration of biological existence is indistinguishable from that without the described syndrome. The prognosis is good in any case. But we cannot turn a blind eye to the situation.

Moreover, it can aggravate, lead to complication of heart failure and indirect development of death.

- a serious cardiovascular catastrophe that can be complicated by various clinical situations. One of them is Dressler's syndrome (in cardiology - post-infarction autoimmune syndrome).

This complication develops up to 10-14 days after heart attack. The insidiousness and danger of the pathology lies in the damage to blood vessels, internal organs, joints, serous and mucous membranes.

Dressler's syndrome is a complication of myocardial infarction

The incidence of the described pathology has decreased today. This can be explained by the use of adequate treatment regimens immediately from the moment of diagnosis of myocardial infarction.

In addition, the use non-steroidal drugs and high-quality reperfusion reduces the risk of developing autoaggression.

It has been noted that post-infarction autoimmune syndrome is typical for extensive, large-focal necrosis of the heart muscle. The likelihood of developing this complication increases with recurrent or repeated infarction.

The disease can occur in several clinical forms, which will be discussed below. Maybe chronic course with alternating exacerbations and periods of remission.

Resumption clinical symptoms worsens the quality of life and its prognosis. Therefore, it is important to treat a heart attack and its complications promptly and adequately.

Forms

They approach the classification of Dressler syndrome from various positions:

Systematicity of the lesion.
The onset of development of clinical signs of post-infarction autoimmune syndrome relative to the onset of a heart attack.
The severity of the disease picture.

Early forms develop 2–3 weeks after a heart attack has occurred. Late Dressler syndrome can only be diagnosed after 2 or more months. The low-symptomatic form is identified separately by cardiologists. Once detected, the prognosis for the disease is relatively favorable.

The two largest groups of variants of the course of the disease include typical and atypical. The difference is that the forms from the first group are characterized by the involvement of only the serous membranes. Atypical variants of Dressler's syndrome occur with damage to the skin, joint membranes, renal and bronchial structures.

More often than others, the pericardial form is diagnosed. In this case, antibodies are formed that are directed to the tissues and structures of the cardiac membrane -.

The pleural form occurs less frequently. In this clinical situation, the pleura is involved in the pathological process. This option may be complicated by damage to the lung tissue with the development of pneumonitis and pleuropulmonitis. This form is more difficult to treat and requires hormonal therapy.

Among mixed forms Various combinations of the following situations occur:

Pericardial-pleural lesion (after inflammation of the pleural layers, the pleural membrane becomes involved in the process).
The pericardial-pneumonic variant of Dressler's syndrome in cardiology marks the transition of autoaggression from the pericardium to the pulmonary tissue, while the pleural layers are intact.
The pericardial-pleuro-pneumonic form of the pathology differs from the one described above in the development of pleurisy.
Pleuro-pneumonitis is a complication of Dressler's syndrome without involvement of the pericardium, but with inflammation of the pleural layers and pulmonary structures.

Mixed forms require integrated approach in treatment, since not one organ is affected, but several at once. Atypical variants include lesions shoulder joint, skin, peritoneum, vascular walls, periarticular structures. Post-infarction autoimmune glomerulonephritis is rare.

Reasons

The cause of Dressler's syndrome is myocardial infarction

Main etiological factor development of the syndrome is. Necrosis of cardiac fibers is accompanied by the release of destroyed particles into the general bloodstream.

It is basically denatured protein. Protein structures recognized by the human immune system as foreign. Therefore, protective mechanisms inevitably come into play.

Cells called lymphocytes produce antibodies aimed at eliminating particles of dead cells and tissues. Immunoglobulins have an affinity for the epithelial lining of the serous membranes.

For this reason, typical forms of the disease are manifested by inflammation of the pleura and pericardium. Sometimes immunoglobulins settle on articular surfaces(synovia), skin, vascular endothelium and renal glomeruli.

The described mechanism is realized due to the phenomenon of antigenic mimicry. That is, particles of necrotic myocardium resemble the structures described above. Therefore, antibodies fall not only on denatured protein elements, but also on the mesothelium of the serous membranes, the lining of blood vessels and joints.

In addition to myocardial infarction, Dressler syndrome in cardiology can be caused by invasive interventions on the valves or cavities of the heart. For example, prosthetics, changing valves, commissurotomy, .

All these operations are associated with the death of a certain number of cardiomyocytes. Decay products enter the bloodstream and cause autoaggression.

The second possible mechanism is that during heart surgery the integrity of tissues is disrupted. The protective barrier is opened, so the cells and fibers are vulnerable to immunoglobulins, which have a high affinity for the structures of the serous cavities, joints, and glomeruli of the kidneys.

For this reason, another name for Dressler syndrome is postcardiotomy or postcommissurotomy syndrome. Its prevention and early detection is extremely important and is the task of cardiologists and cardiac surgeons.

Watch a video about myocardial infarction:

Symptoms

Dressler syndrome has no specific symptoms; most patients complain of general weakness

Clinical manifestations of the disease are not specific. Patients complain of general weakness and fatigue. In the evening, body temperature rises, but it almost never reaches febrile levels.

Pleurisy is manifested clinically by pain in the left side, sometimes in the back. In this case, a cough (dry pleurisy) is possible. Large quantity exudate (inflammatory fluid) in pleural cavity leads to progression of respiratory failure.

Pneumonitis occurs with cough and chest pain. Sometimes the sputum of a patient with Dressler syndrome contains pinkish streaks. The involvement of the pericardium in the pathological process explains the appearance of and, which decrease when bending forward or in a horizontal position.

Chest-shoulder syndrome, which occurs less frequently nowadays, is characterized by pain in the right shoulder. These symptoms are accompanied by “pins and needles” crawling along the outer surface of the forearm and hands, and a change in sensitivity.

Swelling and puffiness in the projection of the left claviosternal joint is also caused by the described disease and is often mistaken for Tietze syndrome or manifestations of spinal chondrosis.

Diagnostics

ECG is one of the methods used in the diagnosis of Dressler syndrome

Anamnestic data are of great importance in making a correct diagnosis. If you have suffered a myocardial infarction, surgery on the cavities or valve apparatus of the heart, it becomes clear in which direction to continue the diagnostic search.

Objectively pay attention to the presence of wheezing in the lungs, their sonority, dependence on body position, cough and others important factors. For pericarditis (dry), an auscultatory phenomenon such as a pericardial friction rub is pathognomonic. This sound phenomenon has clear musical characteristics, does not depend on phase cardiac cycle or breathing.

With pleurisy, a pleural friction noise is heard, reminiscent of the crunch of snow or the crack of cellophane. If the cause of Dressler's syndrome is myocardial infarction, then auscultation reveals muffled or completely dull heart sounds.

The laboratory and instrumental minimum includes the following studies:

Blood test with determination of leukemia formula and erythrocyte sedimentation rate
Urine analysis with qualitative protein determination, sediment microscopy
Serum biochemical profile
Cardiac-specific markers of inflammation
and the dynamics of its change
X-ray of the chest and shoulder joints
Ultrasound examination of internal organs

Determine in blood increased amount leukocytes due to the lymphocytic germ. Among granulocytes, the content of eosinophils is increased (more than 7%). With Dressler's syndrome, almost all cases are accompanied by an acceleration of ESR.

The biochemical profile shows the presence of acute phase reactants - C-reactive protein. Cardiac enzymes are elevated during relapse or in the case of repeated myocardial infarction. If there is a suspicion of post-infarction autoimmune syndrome, these indicators are determined over time.

The ECG film shows a pathological Q wave. Sometimes, with diffuse effusion pericarditis, the Spodic sign is determined, as well as specific T-P changes interval.

Echocardioscopy will reveal hypokinesis of areas of the heart during a heart attack and the presence of effusion. X-ray is designed to confirm pneumonitis and pleurisy. In unclear situations, computed tomography or MRI is indicated.

The puncture must be performed in case of life-threatening insufficiency of heart or lung function, as well as for diagnostic purposes.

Treatment

Thromboass is used in the treatment of Dressler syndrome to prevent blood clots

Dressler's syndrome should be supervised in a specialized cardiology hospital. Therapy of the disease has several objectives, so a number of groups of drugs are used.

The drugs of choice for symptomatic damage to the pleura and pericardium are non-steroidal anti-inflammatory drugs. The use of Ibuprofen, Indomethacin, Diclofenac in full therapeutic dosages is effective.

If NSAIDs do not have the desired effect, hormones are added to the treatment regimen. This may be Prednisolone, Dexamethasone and their analogues. Important both at the inpatient stage and subsequent outpatient treatment it is correct to reduce the dose and discontinue these drugs.

Used to treat the underlying disease standard set drugs:

Statins to reduce the concentration of its atherogenic fractions
ThromboASS or Acecardol - prevention of thrombosis
Lisinopril or Perindopril to reduce the risk of cardiac remodeling
Bisoprolol or Egilok to improve life prognosis and prevent sudden cardiac death

Ineffective treatment with medications dictates the need for a puncture. In this case, it is of a therapeutic and diagnostic nature.

Lifestyle, complications, prognosis

Post-infarction syndrome is a reason for modifying the mode of physical activity and nutrition. Bad habits must remain in the past. Dietary recommendations include limiting easily digestible carbohydrates, fatty and salty foods.

Dressler's syndrome is complicated by constructive and restrictive. But such a situation is rare. The disease has a favorable prognosis. The estimated period of incapacity for work does not exceed 5 months.

Dressler's syndrome (or post-infarction syndrome) is an autoimmune complication of myocardial infarction, in which immune system the patient begins to produce antibodies that destroy their own connective tissue in different parts body. Such autoimmune attacks may include various organs and tissues: pleura, lungs, pericardium, internal articular membranes.

Typically, this post-infarction complication occurs 2-8 (sometimes 11) weeks after the attack and is expressed by a characteristic triad - pericarditis, pneumonitis and pleurisy. In addition to these three manifestations of the disease, damage to the synovial membranes of the joints or skin may occur. This syndrome lasts about 3-20 days and its danger lies in the fact that after remission, periodic exacerbations may occur, which significantly affect the general well-being of the patient and complicate his life.

In this article we will introduce you to the causes, forms, symptoms, methods of diagnosis and treatment of Dressler syndrome. This information will help you suspect the development of the disease in time and take timely measures to treat it.

Dressler's syndrome is an autoimmune process in which antigens are modified proteins formed in response to the entry of myocardial cell necrosis products into the blood

The primary cause of the development of post-infarction syndrome is the death of myocardial cells and the release of tissue necrosis products. In response to these processes, altered proteins are formed in the body, and the immune system begins to produce antibodies against them. With increased immune sensitivity to denatured protein, the produced substances begin to attack their own proteins located on the connective tissue membranes lining the surface of the heart, lungs, chest cavity or joints. As a result of such autoimmune aggression, aseptic inflammatory processes occur in these organs and tissues.

Such disruptions in the functioning of the immune system can occur not only with transmural or large-focal infarction, but also in response to cardiac surgery. The development of such autoimmune reactions can be provoked by reconstructive operations on mitral valve– postcommissurotomy syndrome, or heart surgery accompanied by dissection of the outer lining of the heart – postcardiotomy syndrome. Such syndromes are in many ways similar to Dressler's syndrome, and they are often grouped under this name. In addition, heart damage resulting from injuries can trigger such autoimmune processes.

In more in rare cases Dressler's syndrome is caused by viral infections. In this case, an increased amount of antiviral antibodies is detected in the patient’s blood.

The risk of post-infarction syndrome increases under the influence of the following factors:

the patient has a history of autoimmune diseases;
late onset of motor activity after suffered a heart attack.

Forms

Depending on the combination of certain autoimmune lesions connective tissue There are several forms of Dressler syndrome.

Typical shape

With this course of the syndrome, the following types of lesions are identified:

pericardial – autoimmune damage to the outer lining of the heart (pericardium);
pneumonic – autoimmune damage to lung tissue;
pleural – autoimmune damage to the membranes covering the chest and lungs (pleura);
pericardial-pleural – autoimmune damage to the pericardium and pleura;
pericardial-pneumonic – autoimmune damage to the pericardium and lung tissue;
pleuro-pneumonic – autoimmune damage to the pleura and lung tissue;
pericardial-pleural-pneumonic - autoimmune damage to the pericardium, pleura and lung tissue.

Atypical form

With this course of post-infarction syndrome, the following options are possible:

articular – autoimmune damage to the synovial membranes of the joints;
cutaneous - an autoimmune skin lesion, manifested by rashes and redness.

Low-symptomatic forms

This course of Dressler syndrome can be expressed by the following manifestations:

prolonged low-grade fever;
increase ESR level in combination with leukocytosis and eosinophilia;
persistent joint pain (arthralgia).

Symptoms

In addition to pain in the heart area, a person with Dressler syndrome is bothered by general weakness, fever, chills and a number of other symptoms

For the first time, signs of Dressler's syndrome appear 2-8 (sometimes 11) weeks after an attack of myocardial infarction. The patient experiences squeezing or pressing, a feeling of weakness and weakness, fever (sometimes up to 39°C, but more often 37-38°C). After this, the clinical picture is complemented by symptoms of hydrothorax.

Chest pain may radiate to left hand or a spatula. They are usually not relieved by taking Nitroglycerin and last 30 to 40 minutes or more. When examining the patient, pale skin, rapid pulse, and decreased blood pressure are determined. Listening to heart sounds reveals a “gallop rhythm” and dullness of tones. With an atypical course of post-infarction syndrome, rashes and redness on the skin and joint pain may appear.

Classic triad of Dressler syndrome

The most typical manifestations of this disease are: pericarditis, pleurisy and pneumonitis.

Pericarditis

The intensity of pain in the heart with this syndrome can be different and vary from moderate to paroxysmal or painful. As a rule, in a standing position it is less pronounced, and in a supine position it becomes most noticeable. Its manifestations can be aggravated by coughing or attempts to breathe deeply. The pain may occur periodically or be constant.

In addition to pain, post-infarction syndrome is manifested by the following symptoms:

heartbeat;
fever and chills;
signs of general intoxication: weakness, pain in muscles and joints, malaise;

At the left edge of the sternum, when listening to the heart, a pericardial friction rub is detected. It is especially noticeable when the patient bends forward. After fluid accumulates in the pericardial sac, the noise becomes less pronounced.

A blood test reveals an increase in the level of ESR, eosinophils and leukocytes.

At severe course syndrome, the patient develops the following symptoms:

with episodes of shallow and rapid breathing;
swelling of the veins in the neck;
swelling in the legs;
increase in liver size;
ascites.

Signs of pericarditis are mandatory components Dressler syndrome and often have a mild course. Usually after a few days the pain becomes less intense, the fever disappears, and general health the patient is improving.

Pleurisy

In post-infarction syndrome, inflammation of the pleura can occur independently or be accompanied by other signs of pathology (pericarditis, pneumonitis, etc.). Pleurisy is manifested by the following complaints and symptoms:

pain or scratching sensation in the chest;
difficulty breathing;
fever;
pleural friction noise.

Pain in autoimmune pleurisy increases with deep breathing or cough. As a rule, they go away on their own after a few days.

In post-infarction syndrome, pleurisy can be dry, wet, one- or two-sided.

Pneumonitis

Autoimmune inflammation of the lung tissue is detected somewhat less frequently than pleurisy or pericarditis. Pneumonitis is manifested by the following symptoms:

dry or wet cough(there may be blood in the sputum);
chest pain;

As a rule, with Dressler syndrome, it is the lower lobes of the lungs that are most often affected. When tapped, their inflammation manifests itself as a shortening of the percussion sound, and when auscultated, it manifests itself as fine-bubbly moist rales.

Other symptoms

In some cases, post-infarction syndrome occurs in the form of autoimmune inflammation of the synovial membranes of the joints, skin rashes, or asymptomatic.

Joint lesions

With autoimmune damage to the inner articular membrane, the patient experiences signs of arthritis:

fever;
pain in the affected joint;
redness and swelling of the skin over the joint;
mobility restrictions;
paresthesia.

Dressler syndrome can affect one or more joints at once.

Skin lesions

Post-infarction syndrome can manifest itself as skin lesions. In such cases, on skin areas of redness and rash elements appear, similar to erythema, urticaria, eczema or dermatitis.

Asymptomatic course

With an asymptomatic variant of the course of Dressler's syndrome, the patient develops atralgia and persistent, prolonged and unjustified subfebrile condition. In a clinical blood test in such cases long time the following deviations are detected:

increase in ESR;
eosinophilia;
leukocytosis.

Course of post-infarction syndrome

When Dressler's syndrome occurs for the first time, it can last from 3 to 20 days. After this, remission occurs, which is periodically replaced by exacerbations.

Typically, remission is achieved with treatment. However, cessation of therapy can provoke relapses of the syndrome, the duration of which can range from 1-2 to 8 weeks.

Diagnostics

In diagnostics great value have evidence of a recent myocardial infarction

It is possible to suspect the development of Dressler's syndrome by the appearance characteristic symptoms and patient complaints, suffered a heart attack myocardium 2-3 months ago. To clarify the diagnosis, the following instrumental and laboratory examinations are prescribed:

expanded clinical analysis blood;
clinical urine analysis;
biochemical, immunological tests blood and rheumatic tests;
chest x-ray;
x-ray of joints;
MRI or CT scan of the chest.

Treatment

Depending on the severity of symptoms, patients with Dressler syndrome may be offered outpatient or inpatient treatment.

Drug and conservative treatment

The following drugs can be used to eliminate signs of autoimmune inflammation:

non-steroidal anti-inflammatory drugs - Indomethacin, Aspirin, Diclofenac;
glucocorticoids – Dexamethasone, Prednisolone.

If the syndrome is not severe, it may be sufficient to prescribe only non-steroidal anti-inflammatory drugs. If they are ineffective or the disease is more severe, the patient is recommended glucocorticoid drugs, which are more short terms eliminate the inflammatory autoimmune reaction. After taking them, within 2-3 days the patient’s condition improves significantly. As a rule, for post-infarction syndrome it is recommended long-term use such hormonal drugs.

Surgical treatment

When acute effusion pericarditis or pleurisy occurs, a large volume of fluid may accumulate in the pericardial sac or pleural cavity. To remove it, the following surgical procedures can be performed:

pericardial puncture;
pleural puncture.

Dressler's syndrome is almost always autoimmune complication myocardial infarction and is much less likely to be provoked by other factors. Its manifestations are usually expressed in a characteristic triad: pericarditis, pleurisy, pneumonitis. Non-steroidal anti-inflammatory or glucocorticoid drugs are used to treat this disease, which worsens the quality of life of the patient.

A specialist talks about Dressler's syndrome (English):

Version: MedElement Disease Directory

Dressler's syndrome (I24.1)

General information

Brief description

Dressler's syndrome (DS)) is one of the many complications of myocardial infarction (MI), manifested by pericarditis, pleurisy, pneumonitis, arthritis, fever, leukocytosis, increased erythrocyte sedimentation rate and antimyocardial antibody titers

Etiology and pathogenesis

The main cause of diabetes is MI. It is believed that diabetes often develops after large-focal and complicated infarctions, as well as after bleeding into the pericardial cavity. Diabetes, or more precisely post-cardiac injury syndrome, can develop after cardiac surgery (postpericardiotomy syndrome, postcommissurotomy syndrome). Besides this, typical signs Diabetes can appear after other injuries to the heart (wound, contusion, non-penetrating blow to the chest, catheter ablation).

Currently, diabetes is considered as an autoimmune process caused by autosensitization to myocardial and pericardial antigens. Certain importance is also attached to the antigenic properties of blood entering the pericardial cavity. In post-infarction syndrome, antibodies to heart tissue are constantly detected, although they are often found in patients with MI without any signs of this syndrome, although in smaller quantities

The etiological factor of diabetes may be an infection, in particular a viral one, since in patients who developed this syndrome after cardiac surgery, an increase in the titer of antiviral antibodies is often recorded

Pathological anatomy

Even in severe cases, post-infarction syndrome does not lead to death. If such patients die from other complications of acute myocardial infarction, pathologists usually detect fibrinous, serous, or serous-hemorrhagic pericarditis. Unlike epistenocardial pericarditis, inflammation of the pericardium in diabetes is diffuse.

Epidemiology

Sign of prevalence: Rare

Post-infarction syndrome usually develops between the 2nd and 6th weeks of myocardial infarction, sometimes at earlier and later dates. The frequency of typical post-infarction syndrome is 3 - 5.8%, but when taking into account atypical or asymptomatic forms it increases to 14.7 - 22.7%.

Clinical picture

Clinical diagnostic criteria

Low-grade fever, pericarditis, pleurisy, pneumonitis, joint pain,

Symptoms, course

Classically, the syndrome develops in the 2-4th week of MI, but these periods can decrease - “early DM” and increase to several months, “late DM”. Sometimes the course of diabetes becomes aggressive and protracted; it can last months and years, occur with remissions and exacerbations

Basic clinical manifestations syndrome: fever, pericarditis, pleurisy, pneumonitis and joint damage. Simultaneous damage to the pericardium, pleura and lungs in post-infarction syndrome is not often observed. More often, pericarditis is combined with pleurisy or pneumonitis. In some cases, only pericarditis or pleurisy, or pneumonitis occurs.

Fever with diabetes does not have any strict pattern. As a rule, it is low-grade, although in some cases it may be febrile or absent altogether.

Pericarditis is a mandatory element of the SD. Clinically, it manifests itself as pain in the pericardial zone, which can radiate to the neck, shoulder, back, abdominal cavity. The pain can be acute, paroxysmal (pleuritic) or pressing, squeezing (ischemic). It may get worse with breathing, coughing, swallowing and get better when standing upright or lying on your stomach. As a rule, it is long-lasting and disappears or weakens after the appearance of inflammatory exudate in the pericardial cavity. The main auscultatory sign of pericarditis is a pericardial friction noise: on the first day of illness, with careful auscultation, it is detected in the absolute majority (up to 85%) of patients. The murmur is best heard at the left edge of the sternum, when the patient holds his breath and bends his torso forward. In the classic version, it consists of three components - atrial (determined in systole) and ventricular (systolic and diastolic). Like pain, the pericardial friction noise decreases or disappears altogether after the appearance of effusion in the pericardial cavity, pushing apart the rubbing pericardial sheets. Typically, pericarditis is not severe: after a few days the pain subsides, and exudate in the pericardial cavity almost never accumulates in such quantities as to impair blood circulation, although sometimes signs of severe cardiac tamponade may appear. Sometimes inflammatory process in the pericardium with diabetes takes on a protracted relapsing character and ends with the development of constrictive pericarditis.

When anticoagulants are used against the background of diabetes, the development of hemorrhagic pericarditis is also possible, although a similar complication can occur in the absence of anticoagulant therapy.

Pleurisy. It manifests itself as pain in the lateral parts of the chest, aggravated by breathing, difficulty breathing, pleural friction noise, dullness of percussion sound. It can be dry and exudative, unilateral and bilateral. Often, pleurisy is interlobar in nature and is not accompanied by typical physical symptoms.

Pneumonitis. Pneumonitis in diabetes is detected less frequently than pericarditis and pleurisy. If the focus of inflammation is large enough, dullness of percussion sound, weakened or hard breathing, the appearance of a focus of fine bubbling wheezing. Coughing and sputum production are possible, sometimes mixed with blood, which always causes certain diagnostic difficulties.

Joint damage. Diabetes is characterized by the appearance of the so-called “shoulder syndrome”: painful sensations in the area of the glenohumeral joints, most often on the left, there is limited mobility of these joints. Involvement of the synovial membranes in the process often leads to pain in the large joints of the limbs.

Other manifestations. A manifestation of post-infarction syndrome may be heart failure due to diastolic dysfunction, hemorrhagic vasculitis and acute glomerulonephritis.

Diagnostics

Electrocardiography(ECG). In the presence of pericarditis, the ECG shows diffuse ST segment elevation and, periodically, PR segment depression, with the exception of lead aVR, in which ST depression and PR elevation are observed. As exudate accumulates in the pericardial cavity, the amplitude of the QRS complex may decrease.

Echocardiography. When fluid accumulates in the pericardial cavity, separation of its leaves is detected and signs of cardiac tamponade may appear. It should be emphasized that diabetes is not characterized by a large volume of fluid in the pericardial cavity - as a rule, the separation of the pericardial layers does not reach 10 mm in diastole.

Radiography. An accumulation of fluid in the pleural cavity, interlobar pleurisy, expansion of the boundaries of the cardiac shadow, and focal shadows in the lungs are detected.

Computed tomography or magnetic resonance imaging also reveals pleural or pericardial fluid and pulmonary infiltration.

Pleural and pericardial puncture. Exudate extracted from the pleural cavity or pericardium can be serous or serous-hemorrhagic. A laboratory study reveals eosinophilia, leukocytosis and high level C-reactive protein.

Laboratory diagnostics

Often (but not always!) There is an increase in ESR and leukocytosis, as well as eosinophilia. Very characteristic sharp increase C-reactive protein level.

In patients with diabetes, normal levels markers of myocardial damage (MB-fraction of creatine phosphokinase (MB-CPK), myoglobin, troponins), although sometimes there is a slight increase in them, which requires differential diagnosis with recurrent myocardial infarction

Differential diagnosis

DM is differentiated from recurrent or repeated MI, bacterial pneumonia, thromboembolism pulmonary artery, pericarditis or pleurisy of another etiology and some other more rare diseases. In addition to clinical and instrumental data, great importance in differential diagnosis have laboratory tests: determination of markers of myocardial damage (myoglobin, MB-CK, troponins) and fibrin degradation products (D-dimer).

Complications

Cardiac tamponade, hemorrhagic or constrictive pericarditis, occlusion (compression) of a coronary artery bypass graft and rarely anemia.

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Treatment

Nonsteroidal anti-inflammatory drugs(NSAIDs). Ibuprofen (400-800 mg/day) is traditionally considered the drug of choice for diabetes. Aspirin is used less frequently. Other NSAIDs are not used because of their negative influence to the peri-infarction zone.

Glucocorticoids usually used for diabetes refractory to NSAID therapy. Typically, prednisolone is used, although other drugs can be used.

After achieving a clinical effect, glucocorticoids are discontinued gradually over 6-8 weeks, since rapid withdrawal may result in relapse of diabetes.

Sometimes small doses of glucocorticoids (prednisolone at a dose of 15 mg/day) are used in combination with NSAIDs. In severe cases, glucocorticoids are administered parenterally. The rapid disappearance of the manifestations of diabetes when glucocorticoids are prescribed is so characteristic that it has a certain differential diagnostic value.

Long-term use of glucocorticosteroids is undesirable, since, in addition to the complications characteristic of this group of drugs (gastroduodenal ulcers, fluid retention, osteoporosis), they can contribute to the formation of aneurysm and myocardial rupture, since they inhibit the process of scarring and cause thinning of the developing scar. Naturally, gastroprotection is necessary during therapy with NSAIDs and glucocorticoids.

Other drugs. For severe recurrent diabetes refractory to NSAID and glucocorticoid therapy, other drugs such as colchicine and methotrexate can be used. In particular, colchicine (1.0 mg/day) is especially effective in postpericardiotomy syndrome

Anticoagulants

Due to the threat of developing hemopericardium and cardiac tamponade, the use of anticoagulants in diabetes should be avoided. If this is not possible, then they are prescribed in subtherapeutic doses.

Pericardiocentesis used for cardiac tamponade

Pericardiectomy. Due to the threat of worsening or relapse of diabetes, pericardiectomy is rarely used (for constrictive pericarditis)

Forecast

The prognosis for diabetes is usually favorable. However, its course sometimes takes on a protracted, relapsing character. In addition, there is evidence that 5-year survival among survivors of this syndrome, although slightly, is reduced.

Prevention

The use of NSAIDs and glucocorticoids to prevent the development of diabetes is ineffective. The COPPS (COlchicine for the Prevention of Post-pericardiotomy Syndrome) study is currently underway to study the effectiveness of colchicine in preventing the development of this complication after cardiac surgery

Information

Lectures on cardiology / Under. ed. L.A. Boqueria, E.Z. Golukhova. In 3 volumes - T.2. - M.: Publishing house NTsSSKh im. A.N. Bakuleva RAMS, 2001. - 288 p.
Alpert J., Francis G. Treatment of myocardial infarction. Per. from English - M.: Praktika, 1994. - 255 p.
Diseases of the circulatory system: A guide for doctors. Chazov E.I. ed. M.: Medicine, 1997
Heart diseases. Moiseev V.S., Sumarokov A.V. M.: Universum Publishing, 2001
Groer K., Cavallaro D. Cardiopulmonary resuscitation. Pocket guide. - M.: Praktika, 1996. - 128 p.
Gurevich M.A. Issues of pathogenesis and treatment of heart failure during myocardial infarction // Klin. Med.- 2002.- T.74, No. 4.- P. 15-20.
International Guide to Myocardial Infarction. Ed. V. Ronald and F. Campbell. - 1997. - Moscow.
Emergency treatment in cardiology: reference book by Fomin I.G. M.: Medicine, 1997
Okorokov A.N. Diagnosis of diseases of internal organs: T. 6. Diagnosis of diseases of the heart and blood vessels. - M.: Medical literature, 2002. - 464 p.
Optimization and standards of treatment of diseases of internal organs. Collection of articles ed. prof. R.S. Bogacheva, prof. A.I. Borokhova. - 1999.- Smolensk. - 145 p.
Orlov V.N. Guide to electrocardiography. - M.: Medical Information Agency LLC, 1997.- 528 p.
Savchenko A.P., Matchin Yu.G. Endovascular treatment acute heart attack myocardium // Heart.- 2002.- T.1, No. 1.- P. 20-22.
Fried M., Grines S. Cardiology in tables and diagrams. - Trans. from English - M.: Praktika, 1996. - 736 p.

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Dressler's syndrome - rare autoimmune disease, arising against the background of a previous myocardial infarction. The first symptoms of the pathology develop only several weeks or months after the formation of ischemic changes in the muscle tissue of the heart. Clinical signs are associated with the occurrence of pericarditis, inflammation of the serous membranes of the chest cavity and lungs. Manifestations include shortness of breath, general weakness, cough and painful sensations. Treatment is based on the use of hormonal agents that suppress the immune response. Prevention involves preventing the development of myocardial infarction, which is the main etiological factor of the disease.

Causes

The disease is an autoimmune process. This means that the problem is formed due to inadequate functioning of the body’s defense mechanisms. It has been established that the occurrence of Dressler's syndrome after a heart attack is provoked by the following cascade of reactions:

Ischemic processes in the myocardium lead to changes normal structure muscle tissue. At oxygen starvation cells die, that is, necrosis occurs.
Post-infarction syndrome develops in cases where the immune system does not react correctly to dead elements of cardiac structures. Normally, individual areas of necrosis are surrounded by inflammation, but pathological antigen-antibody complexes are not formed.
The occurrence of the disease can be compared to an allergy. The body rejects dead cells, that is, it reacts to the protein contained in the tissues. However, in the case of Dressler syndrome, immune complexes are formed in response to damage to the body's own cells. Their deposition leads to worsening inflammation, which affects not only muscle tissue, but also the pericardium, as well as serous membranes, lungs and even joints.

Most common cause A similar autoimmune process is ischemic myocardial damage. That is why Dressler's syndrome is called post-infarction syndrome. However, other factors can also provoke the development of the disease. The disorder occurs as a complication of cardiac surgery, traumatic injury to the heart, as well as infection with certain viral infections.

Thus, for Dressler syndrome to occur, a damaging effect on heart tissue is required, which is accompanied by the development of inflammation. And a change in the normal immune response to this process leads to the formation of a characteristic clinical picture.

On initial stage studying the disease, Dressler made an assumption about the prevalence of the lesion. He hypothesized that an immunological disorder would occur in approximately 3–4% of patients with a previous myocardial infarction. However, today the problem is diagnosed much less frequently. Doctors associate this pattern with significant progress in the medical field. Important role in this case, not only the therapy of Dressler syndrome itself plays a role, but also the assistance provided to patients with acute ischemia hearts.

Modern methods of dealing with heart attack, as well as its accelerated diagnosis, have significantly reduced the rate of complications.

The risk of developing a pathological immune response remains in patients who suffer from multiple disorders at the same time, as well as in people who become infected infectious pathologies during the rehabilitation period. There is also data about high probability the occurrence of Dressler's syndrome in the post-infarction state in people who have previously undergone long-term therapy Prednisolone and other corticosteroids. Presumably, patients with a third blood group and a negative Rh factor are more likely to encounter a similar complication.

Characteristic symptoms

Several forms of the disease are described in cardiology:

The typical course of Dressler's syndrome is associated with the development of inflammation in the cavity of the heart sac, lungs and joints. The pleura is also involved in the pathological process. This type problems occur most often.
The atypical form of the disease is accompanied by joint damage, development skin manifestations allergies, as well as the occurrence of asthma and peritonitis in the patient. In some cases, symptoms of Dressler syndrome include inflammation of the kidneys, inner surface vessels and periosteum.
In rare cases clinical signs pathologies include hyperthermia against the background of an increase in the number of leukocytes in the blood, as well as an increase ESR indicator. At the same time, the classic manifestations of the disease are often not recorded, which greatly complicates the diagnosis of the problem. Then they talk about a low-symptomatic form of the disease.

The main clinical signs of Dressler syndrome that occur during the typical course of the disease include:

The development of pericarditis, which occurs due to the accumulation of immune complexes in the heart sac. In the background this process noted severe inflammation leading to severe pain. In addition, complaints of shortness of breath are recorded, as well as visible enlargement of the veins in the neck. Pericarditis is often accompanied by swelling of the extremities and ascites. In the absence of adequate medical care there is a high risk of developing cardiac tamponade.
Pleurisy is the second characteristic symptom of Dressler's syndrome. It is customary to differentiate two types of pathology: dry and wet. In the first case, a characteristic friction noise is diagnosed, which is felt by patients when breathing. Both halves of the chest or only one can be affected. If exudate accumulates between the serous leaves, the pain becomes less intense. There is a muffled heartbeat, cyanosis of the integument and a significant deterioration in health.
Pneumonitis in Dressler syndrome is less common than pleurisy or pericarditis. Defeat is characteristic lower sections lungs. Patients experience severe cough, resulting in the discharge of sputum, often mixed with blood. During auscultation respiratory system Moist rales are heard.

In most cases, there is a combination of several characteristic symptoms. This is what allows doctors to suspect an autoimmune pathology.

Necessary diagnostics

The development of Dressler's syndrome is indicated by a previous myocardial infarction, as well as surgery on the heart or its traumatic injuries. To confirm the presence of a problem, the patient is examined, auscultation and percussion of the chest are performed, during which characteristic features diseases. The formation of exudate in the cardiac sac and between the serous layers of the chest cavity can be diagnosed using x-rays.

The images visualize characteristic darkening, and also show signs of enlargement of the borders of the heart. In some cases, in order to confirm the disease, it is also used computed tomography, which gives a clearer image.

Diagnosis of Dressler's syndrome involves an ECHO. Ultrasound reveals a characteristic accumulation of fluid, as well as thickening of the pericardial layers and the development adhesive processes. To assess the nature of the exudate, a puncture is performed and the contents are collected for analysis. Laboratory tests are used to determine the involvement of other internal organs in the process.

Therapeutic measures

Although Dressler's syndrome is not one of the emergency conditions, unlike a heart attack, it also requires timely medical care. In most cases, the disease is treated with conservative therapy using various groups drugs. If there is no effect from such methods, they resort to the use of surgical techniques. Recommendations also include balanced diet, rest and giving up bad habits.

Drug therapy

The following means are used to combat the disease:

Nonsteroidal anti-inflammatory drugs are prescribed when the patient's condition is stable. This group includes medications such as Ibuprofen and Diclofenac. They help reduce the intensity of clinical manifestations.
The basis of treatment for Dressler syndrome is glucocorticoids, such as Dexamethasone and Prednisolone. These compounds inhibit pathological defensive reactions, due to which the formation of immune complexes stops and a visible improvement in the patient’s well-being occurs. If the problem recurs hormone therapy used throughout life.
To maintain the functioning of the heart muscle, medications containing elements such as potassium and magnesium are prescribed. Such products include “Panangin” and “Asparkam”.
If there is a pronounced pain syndrome the use of potent analgesics is justified.
To prevent the development of a secondary infection, antibiotics are prescribed, for example, Clarithromycin. They are used in combination with steroids and prevent the proliferation of pathogenic bacteria.

Surgical intervention

If there is no effect from conservative therapy More radical methods are used:

Pericardiectomy is a procedure that involves resection of the heart sac. Serous sheets are removed completely or partially. This operation is used to relieve pressure from cardiac structures.
Puncture of the pericardial cavity. It is performed with both diagnostic and therapeutic purpose. Pumping out exudate from the cavity of the heart sac leads to a significant improvement in the patient's condition.

Forecast at timely treatment favorable. Early consultation with a doctor prevents the development of life-threatening complications.