Medical expert of the article
New publications
Causes and pathogenesis of dilated cardiomyopathy
Last reviewed: 06.07.2025
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
Various hypotheses have been put forward regarding the origin of dilated cardiomyopathy; however, in recent years, the opinion has increasingly been expressed about the multifactorial genesis of the disease.
The development of dilated cardiomyopathy is based on the disruption of systolic and diastolic functions of the myocardium with subsequent dilation 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.).
A number of studies have demonstrated a connection between myocardial damage and metabolic disorders in it. In children, cases of dilated cardiomyopathy caused by a deficiency of carnitine, taurine, and selenium have been described.
The role of genetic mechanisms in the origin of dilated cardiomyopathy is evidenced by familial forms of dilated cardiomyopathy, their share, according to some authors, is 20-25%. Molecular genetic studies have revealed significant genetic heterogeneity of the familial form of dilated cardiomyopathy. Four possible types of inheritance have been discovered: autosomal dominant, autosomal recessive, X-linked, and through mitochondrial DNA.
Based on the virus-immunological hypothesis of the development of dilated cardiomyopathy, the assumption of a genetically determined disorder of immunological reactivity, which determines the susceptibility of the myocardium to viral infection, seems more justified. It is assumed that persistent viruses induce autoimmune processes that arise both against viruses and against their own proteins. The change in the antigenic properties of cardiomyocytes caused by the virus leads to the activation of cellular and humoral effectors of the immune system aimed at their elimination.
In recent years, the inflammatory theory of the origin of dilated cardiomyopathy has become most widespread. The disease is considered a sluggish and latent chronic myocarditis resulting from the interaction of a myocardial viral infection and a disturbed immune response.
Along with chronic inflammation due to viral persistence, an autoimmune mechanism with viral-induced neoantigens and cross-reacting antibodies is discussed. Among the numerous cardiac antigens to which antibodies can be formed, antimyolemmal and antimyosin antibodies play the most significant role.
Apoptosis of cardiomyocytes is considered as a fundamental mechanism leading to irreversible impairment of myocardial contractility in DCM.
[