What are the causes of dilated cardiomyopathy

Many people do not understand dilated cardiomyopathy. Dilated cardiomyopathy will cause the ventricles to continue to expand, leading to more complications. There are actually several causes of dilated cardiomyopathy, including viral infection and genetic problems. Understanding the causes of dilated cardiomyopathy is very helpful in preventing the disease.

1. Etiology In animal experiments, Coxsackievirus and encephalomyocarditis virus can not only cause viral myocarditis, but also cause lesions similar to dilated cardiomyopathy. Clinically, long-term follow-up of patients with acute viral myocarditis found that the chance of developing dilated cardiomyopathy was significantly greater than that of the general population. Virus examination of myocardial live specimens of patients with this disease showed inflammatory manifestations, and the titer of coxsackievirus B neutralizing antibodies in the blood of many patients with this disease was higher than that of normal people. In recent years, molecular biology techniques have been used to find enterovirus or cytomegalovirus RNA in myocardial biopsy specimens of patients with this disease. All of the above indicate that this disease is closely related to viral myocarditis and may be the persistence of infection.

2. Genetic and autoimmune studies have found that this disease is related to tissue compatibility antigens. Compared with non-disease patients, the HLAB27, HLAA2, HLADR4, and HLADQ4 loci in this disease are increased, while the HLADRw6 locus is decreased. The changes in HLA are related to autosomal recessive inheritance, which can explain the familial tendency of some patients with this disease. On the other hand, there may be changes in the immune response, increasing susceptibility to viral infection and leading to autoimmune damage to the myocardium.

3. Cellular immunity: The activity of natural killer cells in patients with this disease is reduced, which weakens the body's defense ability and reduces the number and function of suppressor T lymphocytes. As a result, a cell-mediated immune response occurs, causing vascular and myocardial damage.

In summary, it is currently believed that the possible pathogenesis of this disease may be that the Coxsackie virus first invades the myocardium, proliferates in the myocardium and causes myocardial cell necrosis. In the second stage, the virus cannot be found in the myocardium, but there is an increase in lymphocytes. These cells sensitize myocardial cells, cause an immune response and cause myocardial cell necrosis. In the later stage, the infiltration of inflammatory cells decreases or disappears, becoming fibrosis, which is intertwined with the hypertrophic or reduced myocardial cells to constitute the lesions of dilated cardiomyopathy. Although viral infection and immune response theories are currently the main theories of the disease, there are still many unclear issues that require further research.