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Causes and pathogenesis of dilated cardiomyopathy
Last reviewed: 23.04.2024
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Various hypotheses of the origin of dilated cardiomyopathy have been put forward, nevertheless, in recent years, the opinion about the multifactorial genesis of the disease has been increasingly expressed.
At the heart of the development of dilated cardiomyopathy is the disruption of the systolic and diastolic functions of the myocardium, followed by dilatation of the heart cavities, caused by damage to cardiomyocytes and the formation of replacement fibrosis under the influence of various factors (toxic substances, pathogenic viruses, inflammatory cells, autoantibodies, etc.).
In a number of works, the relationship between myocardial damage and metabolic abnormalities was demonstrated. Children described cases of dilated cardiomyopathy, due to a deficiency of carnitine, taurine, selenium.
The role of genetic mechanisms in the origin of dilated cardiomyopathy is evidenced by family forms of dilated cardiomyopathy, their share, according to some authors, is 20-25%. In molecular genetic studies, a significant genetic heterogeneity of the family form of dilated cardiomyopathy was revealed. There are four possible types of inheritance: autosomal dominant, autosomal recessive, linked to the X chromosome, and also through mitochondrial DNA.
Relying on the virus-immunological hypothesis of the development of dilated cardiomyopathy, it seems more reasonable to assume a genetically conditioned violation of immunological reactivity, which causes myocardial susceptibility to a viral infection. It is suggested that persistent viruses induce autoimmune processes that arise both against viruses and against native proteins. The change in antigenic properties of cardiomyocytes caused by the virus leads to activation of cellular and humoral immune system effectors aimed at their elimination.
In recent years, the most widespread inflammatory theory of the origin of dilated cardiomyopathy. The disease is treated as sluggish and hidden by the current chronic myocarditis, which is the result of the interaction of myocardial viral infection and an impaired immune response.
Along with chronic inflammation due to the persistence of viruses, an autoimmune mechanism with a virus-mediated appearance of neoantigens and cross-reacting antibodies is discussed. Among the numerous cardiac antigens to which antibodies can form, the most important role is played by antimyomemic and anti-myosin antibodies.
As a fundamental mechanism leading to an irreversible violation of myocardial contractility in DCM, apoptosis of cardiomyocytes is considered.
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