Primary dilated cardiomyopathy

Many people have rarely heard of the disease called primary dilated myocardium, and do not understand its symptoms, harmfulness, etc. In fact, from the literal meaning, we can know that the symptoms of this disease should be the enlargement of the myocardial chambers, which leads to the contraction of some original cardiopulmonary functions and causes the disease. Therefore, once this phenomenon is discovered, it must be treated in time to avoid worsening of the condition. So today I will give you a brief introduction to primary dilated cardiomyopathy.

Dilated cardiomyopathy (DCM) is a primary myocardial disease of unknown cause. The disease is characterized by left or right ventricular enlargement or bilateral ventricular enlargement, accompanied by ventricular systolic dysfunction, with or without congestive heart failure. Ventricular or atrial arrhythmias are common. The disease is progressive and death can occur at any stage of the disease.

1. Infection

In animal experiments, viruses can not only cause viral myocarditis, but also cause lesions similar to dilated cardiomyopathy. In recent years, molecular biology techniques have been used to find enterovirus or cytomegalovirus RNA in myocardial biopsy specimens of patients with this disease, indicating that this disease is closely related to viral myocarditis.

2. Genes and autoimmunity

In the past, it was believed that most DCM cases were sporadic or idiopathic, but now it is found that familial cases account for at least 40% to 60%. Family analysis showed that most DCM families were inherited by autosomal dominant inheritance, while a few were inherited by autosomal recessive inheritance, mitochondrial inheritance, and X-linked inheritance. On the other hand, changes in immune response can increase susceptibility to disease and may also lead to myocardial autoimmune damage.

3. Cellular Immunity

In patients with this disease, the activity of natural killer cells is reduced, which weakens the body's defense ability and reduces the number and function of suppressor T lymphocytes, resulting in a cell-mediated immune response and causing vascular and myocardial damage.

Clinical manifestations

Most of them are middle-aged people. The onset is usually slow, sometimes lasting more than 10 years. The main symptoms are congestive heart failure, among which shortness of breath and edema are the most common. Initially, shortness of breath occurs after labor or fatigue, and later shortness of breath also occurs during light activity or rest, or there are paroxysmal dyspnea at night. Patients often feel fatigued.

Physical examination shows accelerated heart rate, apex beat shifted to the lower left, there may be a lifting beat, the boundary of cardiac dullness expanded to the left, the third or fourth sound can often be heard, and the heart rate is a gallop rhythm when fast. Due to the enlargement of the heart chamber, there may be a systolic blowing murmur caused by relative mitral or tricuspid regurgitation, which will be alleviated as heart function improves. In late-stage cases, blood pressure is low, pulse pressure is small, and diastolic blood pressure may be slightly elevated when heart failure occurs. The presence of pulse alternans suggests left heart failure. The pulse is often weak.

There may be rales in both lungs in heart failure. When right heart failure occurs, the liver is enlarged and edema appears starting from the lower limbs. In the late stage, there may be pleural and abdominal effusion, and various arrhythmias may occur. High-degree atrioventricular block, ventricular fibrillation, and sinoatrial block can lead to Adams-Stokes syndrome, which is one of the causes of death. In addition, there may be embolism in the brain, kidneys, lungs, etc.