Libman-Sachs endocarditis. Other types of endocarditis Atypical verrucous endocarditis of Liebmann-Sachs

Libman-Sachs endocarditis (otherwise known as verrucous, maranthic, or abacterial thrombotic endocarditis) is the most characteristic cardiac manifestation of the autoimmune disease systemic lupus erythematosus (SLE). Libman and Sacks were the first to describe atypical sterile verrucous endocarditis in 1924. This endocarditis usually affects the mitral valve and rarely the aortic valve. However, observations of damage to all four valves and the endocardial surface of the ventricles are known.

Previous autopsy studies have described grape-like or wart-like vegetations on the ventricular surface of the posterior mitral leaflet, often with adherence of the mitral leaflet and chordae to the mural endocardium.

Vegetations typically consist of accumulations of immune complexes and mononuclear cells. The use of steroid therapy for systemic lupus erythematosus has significantly changed the spectrum of valvular lesions.

If atypical Libman-Sachs warty endocarditis was previously detected in children only during pathological examination, now, thanks to echocardiography, it is diagnosed intravitally, but relatively rarely (in 13% of patients), as well as its outcome (in 4% of patients) in severe valve insufficiency .

Liebman-Sachs endocarditis can be combined with primary or secondary antiphospholipid syndrome. However, the role of antiphospholipid antibodies in the pathogenesis of endocarditis remains controversial.

In addition to the valvular endocardium, the parietal endocardium is also affected in patients with SLE (5%). The nature of endocarditis has changed in recent years. Against the background of early and actively carried out therapy, manifestations of endocarditis are rarely pronounced and undergo rapid reverse development against the background of modern complex therapy. According to A.A. Baranova, L.K. Bazhenova (2002), the formation of valvular defects is not typical for SLE in children.

Diagnostics
Clinically, Libman-Sachs endocarditis is difficult to suspect. Mitral valve valvulitis may be detected, which does not cause hemodynamic disturbances and does not create conditions for the occurrence of organic noise. Sometimes mitral valve valvulitis is combined with damage to the aortic or tricuspid valves. In typical cases, auscultation reveals a distinct systolic murmur or a combination of systolic murmur and diastolic murmur. However, systolic murmur at the apex or elsewhere occurs in 2/3 of patients with systemic lupus erythematosus and is often associated with mitral valve regurgitation or associated fever and anemia.

Transthoracic echocardiography has low sensitivity (63%) and specificity (58%) in the diagnosis of Liebman-Sachs endocarditis compared with transesophageal echocardiography. Three-dimensional echocardiography has high sensitivity in diagnosing Libman-Sachs endocarditis.

The combination of Libman-Sachs endocarditis and infective endocarditis in children is very rare, but possible at older ages (>18 years), mainly in women. The authors made the following conclusions: 1) with Libman-Sachs endocarditis, a mask of IE is possible; 2) approximately 10% of patients with Libman-Sachs endocarditis are at risk of developing secondary IE; 3) prevention of IE is advisable in hemodynamically expressed forms of Libman-Sachs endocarditis.

Treatment
Treatment of the underlying disease (SLE) is usually effective and prevents the formation of Libman-Sachs endocarditis.

Forecast
In children and adolescents, the prognosis of the disease is relatively favorable.

Lupus endocarditis - endocardial damage in systemic lupus erythematosus - is very peculiar; It is still rarely diagnosed during life.

Lupus endocarditis it is more correct to consider it only as one of the manifestations, as with rheumatism, and partly with prolonged septic endocarditis, although this latter disease has long been considered as an isolated endocardial lesion.

Only in 1924 did Libman and Sacks describe a peculiar atypical warty endocarditis, different from rheumatic and septic, as the main manifestation of heart damage in 4 patients who suffered, which was more definitely established later. Later, such endocardial damage became known as Libman-Sachs endocarditis.

Later, lupus endocarditis was described by Baehr et al (1931, 1935) and Gross (1932). In 1940, Gross gave a summary analysis of the characteristics of lupus endocarditis. Lupus verrucous endocarditis is undoubtedly characterized by multiple lesions of the valves and widespread lesions of the parietal endocardium. The mitral valve is most often affected, often in combination with the aortic, pulmonary, and tricuspid valves; Much less often, the lesion is single - in the form of vegetations spreading in islands along the parietal endocardium or isolated on the pulmonary artery and tricuspid valves.

The lesions are located on the free edge of the valves with spread over both surfaces and to the adjacent endocardium of the atria and ventricle. Gross drew attention to the characteristic localization of vegetations accumulating on the underside of the valve, at the junction of it with the ventricular endocardium (pocket lesion); Further from the valves, the lesion takes on the character of flat plaques.

Lupus endocarditis never leads to disfigurement of the valves, chords, and trabeculae; Only superficial ulcerations are possible, which do not contribute to the development of severe hemodynamic disturbances, turbulence of the blood flow, or separation of emboli.

The incidence of endocarditis varies widely according to individual authors. In part, this may depend on the inclusion of endocarditis cases of minimal growths on the valves or even thrombotic overlays, perhaps terminal and lacking specificity for the disease. Most authors register only significant lesions of the valves as Libman-Sachs type lesions, in the presence of parietal endocarditis as an obligatory sign.

Baggenstoss (1952) found typical warty lupus endocarditis (namely valvulitis with tissue necrosis and exudative reaction, usually stronger than in rheumatism) in 40% of cases, Harvey - in ⅓ of sectional cases (mainly mitral valve endocarditis).

Lupus endocarditis rarely gives obvious intravital auscultation and other manifestations, so reliable diagnosis is possible only on a dissection table. As Armas-Cruz and co-workers write (1958), such endocarditis actually exists only on the anatomical table rather than in the clinic.

Systolic murmur for recognizing Libman-Sachs syndrome is only of relative importance, which is obvious from the observations of a number of authors. Harvey, of 7 patients with apical systolic murmur, found endocarditis in only 4, and, conversely, of 6 patients with lupus endocarditis, only 2 had systolic murmur. Similar comparisons are made by Griffith and Vural (1951), who out of 7 patients with a systolic murmur found mitral endocarditis on section in only 2, while at the same time, out of 6 patients with proven endocarditis, only 2 had an apical systolic murmur heard during life.

Previously, endocarditis was observed more often in systemic lupus erythematosus; now it develops less frequently, apparently delayed by modern, more active therapy. The distribution and location of endocarditis has also changed in that damage to many valves, especially the pulmonary, tricuspid, and aortic valves, has become less common. Nowadays, they often find damage only to the mitral valve and, to some extent, to a parietal lesion, which, one might say, somewhat smoothes out the difference between lupus endocarditis and rheumatic endocarditis. However, in advanced and late cases treated with hormones, multiple lesions can now be observed, for example, three valves simultaneously.

Phonocardiogram of a patient with acute systemic lupus erythematosus. Mitral valve insufficiency.

Lupus endocarditis can be recognized more quickly by indirect signs: a long-term active disease with high fever and damage to other parts of the heart with a relatively low severity of other visceritis. Of course, sound phenomena, especially changing diastolic murmurs, retain a certain significance. A thorough dynamic clinical phonocardiographic study capturing the variability of auscultatory data may help in solving this problem.

Lupus endocarditis only rarely gives rise to bacterial endocarditis type endocarditis tape. Thus, in all 4 cases of Libman and Sacks, the blood culture was negative. Klemperer and colleagues (1941) discovered prolonged septic endocarditis in 4 cases, Tareev E.M. in my early observations - only in 1 case.

Apparently, minor hemodynamic disturbances do not contribute to infection of the affected valves. Patients with systemic lupus erythematosus, moreover, already in the early stages of the disease, even if it has not yet been correctly recognized, usually receive intensive treatment with antibiotics due to fever and other manifestations of the disease. Thus, presumably, the addition of streptococcal infection is prevented. In addition, with modern treatment with steroid hormones, the development of endocarditis in general is more reliably prevented.

Data from Tareev E.M. confirm the complexity of intravital diagnosis of lupus endocarditis.

Thus, in an early series of observations of Libman-Sachs endocarditis, Tareev E.M. and his colleagues observed in 22 patients out of 50, including damage to the mitral valve during life was established in 10 patients (in 5 there were even signs of stenosis), damage to the mitral and aortic valves - in another 2 patients; in the rest, endocarditis was discovered only at autopsy. Of the mitral valve lesions diagnosed intravitally, in 7 cases, autopsy revealed changes in the form of warty endocarditis or focal sclerosis of the mitral and other valves, as well as the parietal endocardium. Among 10 patients in whom lupus endocarditis was not diagnosed during life, 6 people had clinical signs that were clearly underestimated by clinicians, and in 4 patients there were no symptoms of valvular damage, however, on section, warty endocarditis of the aortic valves (in one) and focal sclerosis of various valves (in the other three).

Phonocardiogram of a patient with acute systemic lupus erythematosus. Libman-Sachs endocarditis.

According to a late series of observations, endocardial damage was recognized in 29 patients out of 85. In 17 of them, a thorough targeted clinical and instrumental study revealed current (active) endocarditis predominantly of the mitral valve with the possible formation of its insufficiency in 5 (see figure); for the remaining 12, it was possible to think about eliminating the current process without the formation of a defect (see figure). In 6 patients in this group, an intense but very dynamic independent murmur was also detected, localized on the pulmonary artery, possibly due to damage to the pulmonary valves.

Let us take the following observation as an example.

A 21-year-old patient had a hemorrhagic rash on the face, fever, arthralgia, abdominal pain, and increasing weakness. Later, the rash resembled erysipelas and spread to the trunk, limbs and oral mucosa with the formation of necrosis. Confluent pneumonia developed in the lungs, kidney infarction progressed. There was an increase in the left border of the heart, a systolic murmur at the apex, an accent of the second tone on the pulmonary artery, tachycardia - up to 130 beats per minute, blood pressure 100/50 mmHg. The electrocardiogram shows right type, sinus tachycardia, mild changes in the myocardium. The patient died 3 months after the onset of the disease.

An autopsy revealed verrucous endocarditis of the mitral, tricuspid and pulmonary valves, focal mural endocarditis of the left ventricle, and moderate sclerosis of the mitral valve.

Histologically, sclerosis of the mitral valve and its hyalinosis with areas of fibrinoid swelling were revealed; large round cell infiltrates under the endocardium; gentle perivascular sclerosis of the myocardium, connective tissue in places with phenomena of fibrinoid swelling, dull swelling of muscle fibers.

Atypical warty Liebman-Sachs endocarditis

Endocarditis in systemic lupus erythematosus was first described by E. Libman and B. Sacks in 1924, long before it was established that this pathology belonged to systemic connective tissue diseases. Endocarditis is detected at autopsy in 20-60 % such patients, on average 40%, and after widespread use in the treatment of systemic redness

In case of glucocorticosteroids for lupus, its frequency decreased slightly. Macroscopically, on both surfaces of the leaflets of any of the four valves, most often the mitral valve, small warty growths are detected, which can spread to the valve ring, chords, papillary muscles and parietal endocardium. Only rarely do they reach 10 mm in length, becoming overgrown with thrombotic masses and can interfere with the closure of the valves. Valve dysfunction usually does not develop. Only a small proportion of patients may experience valve insufficiency, mainly mitral, which very rarely reaches significant severity. Microscopic examination reveals endothelial proliferation with thrombotic overlays, inflammatory infiltration, foci of necrosis with hematoxylin bodies - analogues of lupus cells - and fibrosis. The immune pathogenesis of endocarditis is evidenced by the detection of immunoglobulins and complement on the endothelium of small vessels growing into warty growths. During healing, a fibrous plaque forms. Moreover, in some patients, local deformation of the valves can cause persistent mitral or aortic insufficiency.

Clinical manifestations of Libman-Sachs endocarditis are often absent. Its most common sign is a murmur (in approximately 50% of patients), in most cases systolic, usually low-intensity, short and unstable. In the presence of anemia, fever, tachycardia and signs of myocarditis, it is often impossible to confidently attribute it to endocarditis. A more specific sign of lupus endocarditis is the protodiastolic murmur of aortic regurgitation, which, however, is mild in most cases. There are isolated reports of the occurrence of stenosis of the mitral and aortic valves as a result of occlusion of the orifices by large vegetations with thrombotic overlays.

Diagnosis is based primarily on the identification of valve leaflet overlaps, thickening, and regurgitant flows on two-dimensional Doppler echocardiography. Due to the impossibility of visualizing small-sized vegetations, on the one hand, and the nonspecific thickening of the valve leaflets,

Panov as a sign of endocarditis - on the other hand, the accuracy of intravital diagnosis of Libman-Sachs endocarditis in the absence of significant valve dysfunction is low.

Complications of atypical warty endocarditis are rare. These include systemic emboli from fragments of vegetation, mainly thrombotic masses, the addition of infective endocarditis and heart failure. Infectious endocarditis was identified by N. Doherty et al (1985) in 4.9% of deceased patients with warty endocarditis at autopsy and in 1.3% of patients in the clinic. The development of heart failure is associated mainly with myocarditis concomitant with lupus endocarditis and, in some cases, with pericarditis.

In most patients, atypical warty endocarditis does not require special treatment. This also applies to pathogenetic therapy with glucocorticosteroids, the dose of which is determined, as a rule, based on the nature and severity of other manifestations of systemic lupus erythematosus. There is no data on the possibility of accelerated healing of affected valves and a decrease in their residual dysfunction under the influence of glucocorticosteroids in such patients. In rare cases of the development of hemodynamically significant valve insufficiency, valve replacement is resorted to, guided by generally accepted indications. These operations are, however, associated with a significant increase in risk.

Most experts consider it advisable to carry out primary antibiotic prophylaxis of infective endocarditis in patients with systemic lupus erythematosus with the presence, according to echocardiography, of overlaps on the valves and their thickening. These recommendations are, however, empirical in nature, since special studies of the effectiveness of such prophylaxis for Libman-Sachs endocarditis have not been conducted,

Abacterial thrombotic endocarditis

Abacterial thrombotic endocarditis develops mainly in patients with severe chronic diseases, most often malignant tumors, especially of the stomach, pancreas and lungs. Second place

The most common type is severe congestive heart failure. Less commonly, abacterial thrombotic endocarditis occurs in patients with stroke and infectious diseases - osteomyelitis, tuberculosis, pneumonia, etc. Since a significant part of such patients are elderly, as well as with significant loss of body weight associated with the underlying disease, this form of endocarditis was previously called marantic or cachectic. Both of these terms cannot be considered successful, since neither old age nor cachexia are obligatory signs of this disease. The mitral valve is most often affected, less often the aortic valve or both valves.

The etiology and pathogenesis of abacterial thrombotic endocarditis have not been established. It is believed that disseminated intravascular coagulation plays an important role, the activation of which is often observed in all diseases associated with abacterial thrombotic endocarditis. In a significant proportion of such patients, nonspecific degenerative changes in the valvular endocardium can also be detected. Focal exposure of collagen fibers and connective tissue ground substance causes platelet adhesion and thrombus formation. Since microscopic examination of the affected leaflets always shows no signs of inflammation, the question arises about the legality of using the term endocarditis. The resulting vegetations do not cause valve dysfunction, but can serve as sources of thromboembolism, primarily in the brain, kidneys, spleen, sometimes with serious consequences, including death. They can also become infected and cause the development of infective endocarditis.

In the clinic, abacterial thrombotic endocarditis often remains unrecognized or this diagnosis is made only tentatively. Heart murmurs are heard in no more than 1/3 of such patients and have no characteristic signs. In this regard, in most cases they are attributed to background degenerative changes in the valves that develop with age, or anemia and fever, which are often observed in patients with nonbacterial thrombotic

endocarditis due to the underlying disease. This diagnosis can be assumed by the occurrence of systemic thromboembolism, especially recurrent, in patients with malignant tumors or other serious diseases in the absence of other possible causes, such as atrial fibrillation or post-infarction left ventricular aneurysm with thrombosis. Aseptic thrombotic endocarditis can also be accompanied by an unreasonable increase in body temperature, sometimes to febrile levels, not inferior to antibacterial therapy. After a few days, body temperature usually returns to normal spontaneously. Therefore, this disease must be remembered as a possible cause of temperature reaction in patients with severe chronic diseases of internal organs.

There are no methods for verifying the diagnosis of abacterial thrombotic endocarditis. Suspicion of its occurrence in the case of causeless thromboembolism allows in some cases to identify a previously undiagnosed curable tumor.

There are no specific treatment methods.

In 50%, lupus is diagnosed at autopsy. In 43% it is detected by echocardiographic examination.
In 6-10%, echocardiographic examination reveals antiphospholipid antibody syndrome.
Most often, the disease affects women living in Africa and the Caribbean.

Pathology

In the classic form, warty vegetations form on the ventricular surface of the valve leaflets. Diffuse thickening of the valve leaflets is considered a chronic stage of healing.
Characterized by valvular insufficiency; stenosis is observed in rare cases.
It is not entirely clear whether antiphospholipid antibodies are the cause of the disease. Antigens are negatively charged phospholipids of endothelial cell membranes. The prevalence and severity of valvular disease is the same regardless of whether antibodies are present or not.
Sites of endothelial damage may serve as sites of thrombosis or further damage due to the presence of turbulent flows and slower flow rates.
Thickening of the valve wall and its insufficiency are typical for patients in old age and after glucocorticoid therapy.

Symptoms and signs

The disease is in most cases asymptomatic and is not detected during examination of the cardiovascular system.
Standard manifestations of lupus include malar rash, arthritis, sweating and alopecia.
Repeated miscarriages, thrombosis of arteries and veins, thrombocytopenia indicate antiphospholipid syndrome.
Heart failure and valvular pathology.

Imaging evidence for systemic lupus erythematosus

Valve damage occurs in 28-74% of cases. Vegetation in 4-43% of cases, especially in the presence of antiphospholipid antibodies. Thickening of the valve leaflets occurs in 19-52%, accompanied by insufficiency in 73% of cases.
Pericardial effusion or thickening, left ventricular hypertrophy (due to hypertension), left ventricular dilatation and segmental dysfunction.

Imaging Findings in Primary Antiphospholipid Syndrome

Valve damage occurs in 30-32% of cases, in particular with thrombosis of peripheral arteries. Vegetation in 6-10% and thickening of valve flaps in 10-24%.
Valve insufficiency is 10-24%.

Blood test

Blood cultures are performed to rule out infective endocarditis.
Complete blood count, coagulogram, antibody screening.

Treatment

There is no specific therapy.
Symptomatic treatment and treatment of complications are carried out.
Antibiotic prophylaxis when performing interventions that cause bacteremia.

Prognosis for systemic lupus erythematosus

Death from cardiovascular diseases is in third place among patients.
Combined morbidity: heart failure, valve replacement, thromboembolism and infective endocarditis in 22% of cases.

In this case, signs indicating a deterioration in the condition of the myocardium are often observed (in particular, the height of the T wave on the ECG decreases), and a pericardial friction noise occurs less frequently.

It should be remembered that pericarditis and myocarditis can develop with systemic lupus erythematosus and without endocarditis. All these circumstances complicate the recognition of endocarditis, as a result of which it is often detected only by a pathologist.

When diagnosing endocarditis, it is important to correctly interpret heart murmurs. Systolic murmur at the apex or at other points occurs in 2/3 of patients with systemic lupus, and, of course, it is often associated with muscular insufficiency of the mitral valve and sometimes with fever and anemia. These same factors may also be responsible for diastolic murmur, which is much less common in lupus.

Particularly great diagnostic difficulties arise in cases where symptoms of endocardial damage appear early and the diagnosis of the underlying disease - systemic lupus erythematosus - is not yet clear. In such cases, the possibility of rheumatism, prolonged septic endocarditis, rheumatoid arthritis is usually discussed; due to the presence of fever, lymphadenopathy, and sometimes splenomegaly, a diagnosis of lymphogranulomatosis is suggested.

According to the observations of V.A. Nasonova (1971), for correct early recognition of systemic lupus erythematosus, it should be borne in mind that the disease often begins with arthralgia, which often recurs in the future.

“Recognition of heart diseases”, A.V. Sumarokov

This information is for your information only; please consult your doctor for treatment.

Liebman Sachs endocarditis

Vasospastic angina (Prinzmetal's angina) or variant angina is a form of unstable angina. It affects older people.

Heart failure is a condition in which the heart fails to act as a pump to circulate blood.

In most cases, acute heart failure occurs at night, when the patient suddenly wakes up from a feeling of suffocation and sits up in bed. Cold profuse sweat appears, shortness of breath increases, the skin becomes ashy blue.

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Other types of endocarditis

Atypical warty Liebman-Sachs endocarditis

Panov as a sign of endocarditis - on the other hand, the accuracy of intravital diagnosis of Libman-Sachs endocarditis in the absence of significant valve dysfunction is low.

Abacterial thrombotic endocarditis

Abacterial thrombotic endocarditis develops mainly in patients with severe chronic diseases, most often malignant tumors, especially of the stomach, pancreas and lungs. Second place

Liebman Sachs endocarditis

There may be symptoms of myocardial deterioration, and rarely a pericardial friction rub may occur.

It must be borne in mind that myocarditis and pericarditis can occur as a result of systemic lupus erythematosus without the occurrence of endocarditis. This makes recognizing endocarditis challenging, and it can often only be detected by a pathologist.

When diagnosing endocarditis, correct interpretation of heart murmurs is important. In 2/3 of those examined with a diagnosis of systemic lupus erythematosus, a systolic murmur occurs at the apex or at other points, and it may be associated with insufficiency of the mitral valve muscle, and sometimes with anemia and fever. These factors can also cause diastolic murmur, which is much less common in lupus.

Diagnosis is especially difficult in cases of early onset of symptoms of endocardial damage, when the diagnosis of the underlying disease - systemic lupus erythematosus - has not yet been made. Usually in this case, the presence of rheumatism, rheumatoid arthritis, prolonged septic endocarditis is assumed, due to the presence of fever and lymphadenopathy.

To recognize systemic lupus erythematosus in the early stages of the disease, you need to remember that the first symptoms of the disease are often arthralgia, which often recurs later.

In treatment, the main attention is paid to suppressing the activity of the process using a rational combination of cytostatics and glucocorticoids.

Libman-Sachs disease

Systemic lupus erythematosus (Libman-Sachs disease) is a systemic disease with severe autoimmunization, which has an acute or chronic course and is characterized by predominant damage to the skin, blood vessels and kidneys.

Systemic lupus erythematosus (SLE) occurs in 1 in 2,500 healthy people. Young women (90%) aged 20-30 years are affected, but the disease also occurs in children and elderly women.

Etiology. The cause of SLE is unknown. At the same time, a lot of data has accumulated that indicate a deep breakdown of the immunocompetent system under the influence of a viral infection (presence of virus-like inclusions in the endothelium, lymphocytes and platelets; persistence of a viral infection in the body, determined using antiviral antibodies; frequent presence of measles and parainfluenza viruses in the body , rubella, etc. A contributing factor in the development of SLE is a hereditary factor. It is known that in patients with SLE the HLA-DR2, HLA-DR3 antigens are most often detected, the disease develops in identical twins, and in patients and their relatives the function of the immunocompetent system is reduced by nonspecific provoking factors. The development of SLE are a number of medications (hydrazine, D-penicillamine), vaccination for various infections, ultraviolet irradiation, pregnancy, etc.

Pathogenesis. It has been proven that in patients with SLE there is a sharp decrease in the function of the immunocompetent system, leading to a distortion of its function and the formation of multiple organ autoantibodies. The main issue concerns the processes of regulation of immunological tolerance due to a decrease in T-cell control - Autoantibodies and effector cells are formed to the components of the cell nucleus (DNA, RNA, histones, various nucleoproteins, etc. in total there are more than 30 components). Toxic immune complexes and effector cells circulating in the blood affect the microcirculatory bed, in which predominantly slow-type hypersensitivity reactions occur, and multiple organ damage to the body occurs.

Pathological anatomy. The morphological nature of changes in SLE is very diverse. Fibrinoid changes in the walls of microvasculature vessels predominate; nuclear pathology manifests itself as vacuolization of nuclei, karyorrhexis, and the formation of so-called hematoxylin bodies; characterized by interstitial inflammation, vasculitis (microvasculature), polyserositis. A typical phenomenon for SLE is lupus cells (phagocytosis of the cell nucleus by neutrophil leukocytes and macrophages) and antinuclear, or lupus, factor (antinuclear antibodies). All these changes are combined in various relationships in each specific observation, determining the characteristic clinical and morphological picture of the disease.

The skin, kidneys and blood vessels are most severely affected in SLE.

A red “butterfly” is noted on the skin of the face, which is morphologically represented by proliferative-destructive vasculitis in the dermis, swelling of the papillary layer, and focal perivascular lymphohistiocytic infiltration. Immunohistochemically, deposits of immune complexes are detected in the walls of blood vessels and on the basement membrane of the epithelium. All these changes are regarded as subacute dermatitis.

Lupus glomerulonephritis occurs in the kidneys. Characteristic signs of SLE in this case are “wire loops”, foci of fibrinoid necrosis, hematoxylin bodies, hyaline thrombi. Morphologically, the following types of glomerulonephritis are distinguished: mesangial (mesangioproliferative, mesangiocapillary), focal proliferative, diffuse proliferative, membranous nephropathy. As a result of glomerulonephritis, shrinkage of the kidneys may occur. Currently, kidney damage is the leading cause of death in patients with SLE.

Vessels of different sizes undergo significant changes, especially the vessels of the microvasculature - arteriolitis, capillaritis, and venulitis occur. In large vessels, due to changes in vasa vasorum, elastofibrosis and elastolysis develop. Vasculitis causes secondary changes in organs in the form of degeneration of parenchymal elements and foci of necrosis.

In the heart of some patients with SLE, abacterial warty endocarditis (Libman-Sachs endocarditis) is observed, a characteristic feature of which is the presence of hematoxylin bodies in the foci of necrosis.

In the immunocompetent system (bone marrow, lymph nodes, spleen), phenomena of plasmatization and hyperplasia of lymphoid tissue are detected; the spleen is characterized by the development of periarterial “onion-shaped” sclerosis.

Complications of SLE are mainly caused by lupus nephritis - the development of renal failure. Sometimes, due to intensive treatment with corticosteroids and cytostatic drugs, purulent and septic processes and “steroidal” tuberculosis may occur.

Aseptic thromboendocarditis (Liebman-Sachs endocarditis)

A characteristic feature of infective endocarditis is the formation of vegetations on the valves or parietal endocardium. Typically, endocarditis develops as a result of bacterial colonization of initially sterile vegetations consisting of platelets and fibrin.

Sterile vegetations (aseptic thromboendocarditis) are formed at sites of endothelial injury due to a foreign body in the heart cavity or turbulent blood flow (for example, with valve deformation), on scars and in severe non-cardiac diseases (marantic endocarditis).

What is endocarditis

Endocarditis is a special process of inflammation that damages part of the heart. Basically, this disease does not occur on its own. It is a consequence or continuation of some other disease.

Both adults and children can suffer from endocarditis. More than a hundred microorganisms can serve as its causative agents.

This disease belongs to the ICD-10 class. That is, acute and subacute endocarditis (malignant, slow-flowing, infectious NOS, bacterial, ulcerative, septic).

With this disease, the patient may experience a state of fever, profuse sweating and chills, the skin becomes pale, and the joints begin to ache very much. Measures must be taken at an early stage, since a heart defect may form.

Reasons

It is necessary to be able to distinguish between the different causes of this heart disease. After all, the method of treating endocarditis depends on this. In addition, if you find out exactly what caused this heart disease, then in the future you can avoid the recurrence of the disease.

The main causes of endocarditis:

The endocardium is too close to almost all structures that contain connective tissue. As a result, both tissues become inflamed. And it doesn't matter which of them was affected first.
DPST can occur due to certain viruses. The most common disease of diffuse connective tissue pathologies is rheumatism. It is precisely this that causes endocarditis in this case.
Rheumatism occurs as a result of an allergy caused by a specific infectious virus. The tissues of the junction begin to become inflamed and disorganized. The cause of this disease is contact with a microbe such as streptococcus. By the way, it can serve as a microbe for infective endocarditis.
If treatment measures are not taken on time, this stage of the disease will last a couple of weeks, after which a more serious and dangerous stage will begin.
The immune system will produce special substances to begin the fight against germs. In some cases, such a struggle can be quite strong. And as a result, antibodies will begin to attack the tissue cells of the connection, which can lead to consequences.
In this case, several important cardiac structures will be affected (deep layers of the myocardium; aortic, mitral and tricuspid valves; parietal endocardium and chordae tendineae).
Thus, with rheumatic endocarditis, severe inflammatory processes begin to occur.

Sometimes there are situations in which endocarditis occurs some time after some traumatic damage to skin cells. For example, after heart surgery and not only, due to medical errors.
As a rule, traumatic endocarditis means the accumulation of a certain number of masses of blood clots in the area of the heart valves. The inflammation proceeds unnoticed.
But traumatic endocarditis can cause slow valve deformation. The fibrous ring gradually begins to narrow. If the disease is detected in time, then you can get rid of it very easily.

The development of endocarditis due to allergic manifestations of the body is a fairly rare occurrence. But still some patients suffer from it.
Such endocarditis can be caused by individual intolerance of the human body to specific chemical reagents that enter the patient’s blood. Often these chemical compounds refer to certain medications.
A patient may take some medicine and not even suspect that he is allergic to its components.
This form of endocarditis has a mild course and is not fraught with consequences. In this case, the doctor simply recommends that the patient not take medications to which he is allergic in the future.

sometimes endocarditis is caused by excessively high levels of colorless crystals in the body;
this process can be observed after specific chemicals or toxins enter the blood;
in this case, masses of blood clots collect to the left of the heart valve;
the symptoms of such endocarditis are very mild.

Causative agents of infective endocarditis include:

enterococcus;
streptococcus pneumoniae;
viridans streptococcus;
Staphylococcus aureus;
other staphylococci and streptococci;
gram-negative bacteria;
bacteria of the HACEK group;
fungal infections;
other pathogens;
combination of several pathogens.

Such a large number of infections creates difficulties for specialists in diagnosing endocarditis. After all, each bacteria is quite individual.

If the patient suffers from bacterial endocarditis, then vegetations (a collection of microbes attached to the heart valve) form on the heart valves on the left side. Consequently, a small blood clot appears, to which infections attach. These accumulations may become larger as the disease progresses.

Consequences

If a person is diagnosed with endocarditis and treatment is prescribed immediately, then there are still specific consequences of this disease. They can be either minor or serious.

The case when a blood clot breaks off and blocks an artery is called thromboembolism. Thromboembolism can cause death. A thrombus can grow quite slowly right near the parietal endocardium, or it can form near the heart valve. One way or another, it enters the bloodstream.
A thrombus formed in the sections of the ventricle located on the left enters the systemic circulation, and in the sections on the right - into the small one.
In the first case, the arteries of the internal organs become blocked because the blood clot gets stuck in one of the parts of the body. If the blockage occurs in the arm or leg area, then this part of the body must be amputated.
In the second case, everything is a little more complicated. The clot interferes with gas exchange because it gets stuck in one of the lungs. The patient's death occurs quickly if he is not helped in time.
Thrombi from the left ventricle most often lead to blockage of the cerebral, mesenteric arteries, arteries of the extremities, spleen and retina.
In such cases, specialists prescribe echocardiography to their patients, and then decide on the method of treatment.

Chronic heart failure is usually understood as a condition when the organ is unable to transfer the required volumes of blood from one valve to another.
When a person develops a disease such as endocarditis, the heart muscles contract at the wrong pace, and the heart chambers significantly decrease in volume (or, conversely, increase). All this leads to heart failure.
This problem can be solved by installing a valve implant.

During the period when the patient suffers from endocarditis and this disease develops, microorganisms originate and accumulate in the heart valve. As a result of this accumulation, bacteremia may occur.
Bacteria stay in the body for a long time and this entails unpleasant consequences. Microorganisms spread throughout the internal organs and create a feverish state. In this case, the patient gets rid of endocarditis, but still suffers from weakness, headache and joint pain for a long time.

Warty endocarditis (Libman-Sachs)

Liebman-Sachs endocarditis is associated with antiphospholipid syndrome and lupus. Acute warty endocarditis is usually understood as the presence of a thin valve leaflet and the absence of blood vessels. In this case, diffuse histiolymphocytic infiltration and the development of necrosis fibers take place.

Recurrent verrucous endocarditis involves a thickened valve leaflet. Capillary-type neoplasms arise, the endothelium under the necrosis zone is destroyed, and a mixed thrombus is attached.

Lupus is detected in half of the cases only at autopsy, and in the other half - during echocardiography. In rare cases, echocardiography shows antiphospholipid syndrome. As a rule, this disease affects women living in Africa.

Warty vegetations appear on the surface of the heart valve leaflets. There is insufficiency in the valve. Rarely, stenosis may occur.

Scientists have not yet fully determined whether antiphospholipid syndrome can cause endocarditis.

If the patient is elderly, then thickened walls of the heart valve may be characteristic of him.

The main signs of warty endocarditis include:

arterial thrombosis, thrombocytopenia;
rashes in the cheekbone area, sweating and arthritis;
valve pathology;
heart failure.

It is also worth noting that in case of endocarditis, it is mandatory to conduct blood tests of the patient. That is, take a general analysis, antibody analysis, culture, and so on. This is necessary because doctors need to find out which form of endocarditis the patient is suffering from.

There is no specific treatment for verrucous endocarditis. In such cases, prophylaxis with antibiotics and treatment of individual symptoms is carried out.

Death from such diseases is in third place in the overall ranking.

In order to avoid serious complications from endocarditis, try to consult a specialist after the first signs of this disease appear.

Inflammation in the inner layer of the lining of the heart wall (endocardium) is called endocarditis. Often, disorders develop under the influence of other bacterial diseases. The presence of bacteria in the blood is called bacteremia. This factor is the main cause of endocarditis. They also provoke illness.

Infectious endocarditis is an inflammatory process that occurs in acute or subacute form, affecting the parietal endocardium. The cause of inflammation is various infections. In adolescence and childhood, infective endocarditis often causes death. Pathology causes.

The forms of endocarditis are very diverse, its symptoms and signs have a wide range of manifestations. In clinical diagnosis, a group of symptoms is identified that indicate manifestations of heart failure and disturbances in the functioning of this organ. They manifest themselves in all forms of this disease. There are also specific ones.

The treatment program is determined depending on the type of disease and symptoms. If there is a possibility of inflammation due to infection, then emergency hospitalization is necessary to clarify the diagnosis, which is associated with a high incidence of deaths caused by complications. Treatment can be carried out in.

Endocarditis is an inflammatory process that affects the inner lining of the heart. This disease is manifested by a violation of the smoothness and elasticity of the myocardial chambers. Endocarditis can be caused by many reasons, including rheumatism. In this case, inflammation spreads to the connective tissue of the valves.

A large number of people suffer from heart disease. One of the common ailments can be considered endocarditis. This is a disease in which a pathological process occurs in the internal cavity of the heart. The entry of an infectious agent can lead to inflammation, but there are other factors, for example, already existing ones.

Eosinophilia, active carditis and multiple organ damage were described by the scientist W. Leffler in the mid-30s of the 20th century. Loeffler's endocarditis is characterized by the development of eosinophilic myocarditis and endomycardial fibrosis. Manifests clinically in the form of thromboembolism and acute heart failure. Restrictive.

Subacute septic endocarditis is an infectious infection of the heart (its inner lining) and valves. The cause of infection in most cases is viridans streptococcus, staphylococcus aureus or white staphylococcus. Other infections can also cause septic infection of the heart, but such facts are reported much less frequently.

Bacterial endocarditis, unlike other forms of pathology, is an independent disease. The disease is characterized by inflammatory damage to the parietal endocardium, heart arteries and valves. This type of endocarditis develops due to the harmful effects of microorganisms, among which they are most often found.

Infectious or bacterial endocarditis is a general infectious disease, which is characterized by the predominant localization of the pathological process at the site of the valvular or parietal endocardium. Recently, cases of the disease in childhood have increased significantly. This.