Loeffler's endocarditis

Introduction to Lefler Endocarditis Löffler's endocarditis is also known as eosinophilic endocarditis or eosinophilic endocardial disease. basic knowledge The proportion of illness: the incidence rate is about 0.004%-0.008% Susceptible people: no special people Mode of infection: non-infectious Complications: endocarditis

Causes of Lefler endocarditis

(1) Causes of the disease

The reason is not clear, scholars have put forward a lot of doctrines, according to the disease in the backward areas of Africa and the living customs of local people, some people think that excessive intake of serotonin (local people eat more bananas, but plantains, bananas It is rich in serotonin), malnutrition, vitamin E and tryptophan deficiency, and tropical, subtropical filariasis, malaria, and schistosomiasis are widely spread, so some people have proposed this disease and the above parasitic diseases. Related, but lack of specificity, so the cause of this disease has not been known so far, pending further study.

(two) pathogenesis

1. The occurrence of this disease is thought to be related to eosinophilia, but the mechanism by which eosinophils cause endocardial or myocardial damage has not been elucidated. Some people think that it may be called eosinophils. It is related to the eosinophil cationic protein, which can affect myocardial mitochondrial respiratory function and cause myocardial damage; others believe that it may be the result of subendocardial myocardial necrosis caused by round cells and eosinophils in myocardial infiltration. Degranulated eosinophil and eosinophil granulebasic protein also play an important role in the occurrence and development of this disease.

2. The main pathological features of this disease are endocardial and inner myocardial fibrosis, thickening of the intima, decreased myocardial compliance, massive thrombus formation in the heart, subendocardial myocardial necrosis and eosinophil infiltration, clinical Upper left ventricular involvement is more common, left ventricle can also be affected, but the lesion is generally lighter than the right ventricle. The ventricular lesion mainly invades the apex and inflow tract, while the outflow tract is not affected. In severe cases, the apex can be occluded, and the papillary muscle can also be involved. , chordae and atrioventricular ring, can produce valve insufficiency, the relationship between this disease and endocardial fibrosis (emdomyocardial fibrosis (EMF) has been a long-term debate, most scholars believe that this disease may be early lesions of EMF, Later, it can be evolved into EMF, so some people have divided the pathological changes of this disease into three phases:

(1) Necrotic phase: mainly manifested as eosinophil infiltration and inflammatory changes in the endocardial and subendocardial myocardium, subendocardial myocardial injury and necrosis.

(2) Thrombosis period: As the endocardial and subendocardial myocardium inflammation subsides, thrombus formation in the wall of the heart cavity, once the thrombus falls off can cause arterial embolism.

(3) Fibrosis stage: inflammatory cells such as eosinophils completely disappear, mainly characterized by extensive proliferation of collagen fibers, and its pathological changes are difficult to distinguish from EMF.

Lefler endocarditis prevention

Generally no need to prevent

Lefler endocarditis complications Complications endocarditis

Bacterial endocarditis

Lefler endocardial inflammation symptoms Common symptoms of heart and socket pain, thrombus, leukocytosis, hepatosplenomegaly, superficial lymph node enlargement, pulmonary congestion, lymphadenopathy, gastrointestinal symptoms, edema, systolic reflux murmur

Most of the affected people are tropical, middle-aged people in poor subtropical areas, the onset of disease is concealed, and the disease progresses relatively slowly. The clinical manifestation depends on the severity of the affected heart and lesions. The right heart is mainly affected, similar to constrictive pericarditis and three The mitral regurgitation may be found in the tricuspid auscultation area, and the systolic reflux murmur and systemic congestion may be found. The lower extremity edema is mild, and the left heart is mainly affected. The mitral regurgitation and pulmonary congestion may occur. Simultaneous involvement of the biventricular can produce signs of total heart failure, but clinically, most of the right heart failure, in addition to the wall thrombus can cause symptoms of arterial embolism, the disease can still produce splenomegaly, lymphadenopathy and digestive system Affected, anemia, systemic symptoms such as eosinophilia in the blood and bone marrow.

Loughe endocarditis examination

Peripheral blood eosinophilia and leukocytosis, eosinophils>15×1008/L, proliferating myeloid granules, and the proportion of eosinophils increased.

X-ray inspection

Right ventricular involvement may be characterized by a marked enlargement of the right atrium, and a right ventricular outflow tract dilatation resulting in a slight bulging of the upper left margin of the pulmonary artery below the heart. The heart shadow may be spherical or flask-shaped, with reduced pulmonary blood, which may resemble pericardial effusion. Or the performance of Ebstein malformation, because the disease often has endocardial fiber thickening and / or wall thrombosis calcification, so some cases in the apex pointing to the outflow tract to see visible calcification, right ventricular angiography and cardiac function tests often show right ventricular apex Occlusion and diastolic dysfunction, inflow and diastolic dysfunction, the outflow tract function is basically normal, the characteristic changes of the disease, left ventricular involvement-based X-ray performance can be similar to rheumatic mitral regurgitation, but the heart is generally only Mild increase, may have left atrium, mild left ventricular enlargement and pulmonary congestion and pulmonary hypertension, left ventricular angiography can be found in the filling defect caused by the wall thrombus, endocardial surface is not smooth and uneven, more cardiac function determination Left ventricular diastolic dysfunction was observed, and the X-ray findings of both ventricles were combined with the above two types, but the right ventricular lesion was often heavier.

2. Echocardiography

Due to thickening of the endocardium, the submucosal myometrial fibrosis enhances the echogenic echo. Sometimes a wall thrombus can be found. The systolic phase can show apical occlusion. The inner diameter of the ventricular chamber can be normal, enlarged or reduced, and the atrium often has different The degree of expansion, in addition to the tricuspid and / or mitral regurgitation ultrasound signs, cardiac function tests often show diastolic dysfunction, and some cases may have signs of pericardial effusion.

3. ECG

ECG changes are not specific, may have atrial enlargement, non-specific ST-T changes, in addition, there may be various types of arrhythmias.

4. Endomyocardial biopsy

It has great value in the diagnosis of this disease, and it can be found that endocardial eosinophil infiltration, endocardial fibrosis and subendocardial necrosis and other pathological changes.

Diagnosis and identification of Lefler endocarditis

Diagnostic criteria

According to the clinical manifestations of the disease combined with relevant laboratory tests, most cases can be diagnosed. In case of the following conditions, the disease should be considered:

1. Unexplained progressive heart failure with second, tricuspid regurgitation murmur and third heart sound, heart enlargement but hemodynamic changes resemble constrictive pericarditis.

2. Leukocytosis, eosinophils> 15 × 100 8 / L, proliferating myeloid granules, the proportion of eosinophils increased.

3. Associated with organs other than the cardiovascular system, such as hepatosplenomegaly, gastrointestinal symptoms, superficial lymphadenopathy, anemia, etc., which are not commensurate with the degree of heart failure.

4. X-ray, ULG and other examinations showed occlusion of the apex, involvement of the inflow, expansion of the outflow tract, endocardial and endocardial thickening and wall thrombosis, and cardiac function tests were mainly diastolic dysfunction.

5. Endocardial myocardial biopsy showed endocardial collagen fibrosis, myocardial necrosis and eosinophil infiltration and other pathological changes.

Differential diagnosis

The disease mainly needs to be differentiated from Ebstein malformation, rheumatic mitral regurgitation and constrictive pericarditis.

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