Myocardial abscess
Introduction
Introduction Myocardial abscess is one of the main clinical symptoms of dilated cardiomyopathy. Cardiomyopathy (DDM) is a group of lesions that are progressively impaired by cardiac function due to structural changes in the subventricular chamber (ie, the ventricle) and impaired myocardial wall function.
Cause
Cause
1. Infection: Coxsackie virus and encephalomyocarditis virus can not only cause viral myocarditis in animal experiments, but also cause lesions similar to dilated cardiomyopathy. Clinically, patients with acute viral myocarditis have been converted to dilated cardiomyopathy during long-term follow-up. The chance of the disease is significantly larger than that of the general population. The virus in the living specimens of this disease has inflammatory manifestations. Many patients with this disease have higher levels of Coxsackie virus B neutralizing antibody than normal people. In recent years, molecular biology techniques have been used. Intestinal virus or cytomegalovirus RNA is found in the myocardial biopsy specimens of patients with this disease. All of the above indicate that the disease is closely related to viral myocarditis. This disease may be the persistence of infection.
2. Gene and autoimmunity: The study found that the disease is associated with histocompatibility antigen. Compared with patients without this disease, HLAB27, HLAA2, HLADR4, and HLADQ4 points increased, while HLADRw6 sites decreased, and HLA changes. It is related to autosomal recessive inheritance and can explain the familial tendency of some patients with this disease. On the other hand, there may be changes in the immune response, increasing the susceptibility to viral infection, leading to myocardial autoimmune damage.
3. Cellular immunity: The activity of natural killer cells in the patient is reduced, the body's defense ability is weakened, and the number and function of inhibitory T lymphocytes are reduced, thereby causing a cell-mediated immune response, causing blood vessel and myocardial damage.
In summary, it is believed that the possible pathogenesis of this disease may be that the Coxsackie virus first erodes the myocardium, proliferates in the myocardium and causes myocardial cell necrosis. In the second stage, no virus can be found in the myocardium, but lymphocytes increase. Such cells are sensitized to cardiomyocytes, causing an immune response and causing necrosis of cardiomyocytes. Later, inflammatory cell infiltration is reduced or disappeared, becoming fibrosis, intermingled with hypertrophic or reduced cardiomyocytes, and constitutes a lesion of dilated cardiomyopathy. Although the theory of viral infection and immune response is the main cause of the disease, there are still many problems that have not been clarified and further research is needed.
Examine
an examination
Related inspection
Cardiovascular electrocardiogram selective angiography balance radionuclide angiography (ERNA)
It can occur in all ages, but it is mostly in middle age. The onset was slow, and the heart was enlarged at the initial examination, and the heart function was compensated without conscious discomfort. Symptoms gradually appear after a period of time, sometimes more than 10 years. Symptoms are mainly congestive heart failure, with air urgency and edema being the most common. Initially, after anxious labor or exhaustion, there will be shortness of breath during mild activities or rest, or a paroxysmal urgency at night. Because of low blood output, patients often feel weak.
Physical examination sees the heart rate accelerate, the apex beats to the left and down, there may be a lifting pulsation, the heart sounds the sound to the left to expand, often can hear the third or fourth sound, when the heart rate is fast, the horse is running. Due to the enlargement of the heart chamber, there may be a systolic murmur caused by a relative mitral or tricuspid regurgitation, which is alleviated after the improvement of cardiac function. Most of the blood pressure is normal, but the blood pressure is lower in the advanced cases, the pulse pressure is small, and the diastolic blood pressure can be slightly increased in the presence of heart failure. The appearance of alternating veins suggests left heart failure. The pulse is often weak. In heart failure, there may be rales in the base of the second vein. In the case of right heart failure, the liver enlarges, and the appearance of edema starts from the lower limbs. Pleural effusion and ascites are not common in patients with advanced disease. A variety of arrhythmia can occur, for the first time or the main performance, and a variety of arrhythmia combined to form a more complex heart rhythm, can occur repeatedly, sometimes stubborn. High atrioventricular block, ventricular fibrillation, sinus block or pause can lead to A-S syndrome, which is one of the causes of death. In addition, there are still embolizations in the brain, kidney, lungs, etc.
Diagnosis
Differential diagnosis
Differential diagnosis
Myocardial infarction: refers to the interruption of coronary blood flow on the basis of coronary artery disease, causing severe and long-lasting acute ischemia in the corresponding myocardium, eventually leading to myocardial ischemic necrosis.
Myocardial hypoxia: The heart is deprived of oxygen due to insufficient blood supply. The main manifestations are: palpitations, heart discomfort, sometimes heart pain or appreciation of colic; shortness of breath, exercise, fullness or agitation is more serious, the body is weak; in severe cases, short-term shock.
Myocardium is gray and relaxed: it is a kind of myocardial damage, which may be related to immune myocardial damage after viral infection, and is generally seen in ultrasound examination of dilated cardiomyopathy. Can be used as a differential diagnosis with other cardiomyopathy.
Myocardial stunning, also known as myocardial dysfunction after ischemia, means that myocardial transient ischemia has not caused myocardial necrosis, but mechanical resilience after reperfusion returns to normal blood flow requires hours, days or weeks. The phenomenon of complete recovery.
Cardiac hypertrophy: This is a slower but more effective compensatory function, mainly in the case of long-term stress overload, increased myocardial volume, increased contractility, allowing the heart to maintain a normal blood circulation, and at the same time Reserve power. However, this compensatory function also has its disadvantages, mainly because of hypertrophic myocardial aerobic increase, and the coronary blood supply is often unable to be met, resulting in myocardial ischemia, which will eventually lead to a decline in myocardial contractility. Hypertrophic cardiomyopathy is characterized by cardiac hypertrophy. It is characterized by ventricular muscle hypertrophy, typically in the left ventricle, with interventricular septum, occasionally concentric hypertrophy.
