Dilated cardiomyopathy is one of the diseases with the greatest impact on cardiac function of all cardiomyopathies, and most patients have a low 5-10 year survival rate (30-40%) after the onset of the disease. The psychological and financial burden of patients is exacerbated by the fact that low cardiac function severely affects their quality of life, work capacity and life expectancy, and the need for long-term drug therapy, which accelerates the disease progression process. As far as the current treatment methods worldwide are concerned, there is no complete cure for this disease, which is basically a palliative therapy focusing on the protection of cardiac function, and even surgical heart transplantation has benefited only a few patients due to its high price and lack of donor sources. Therefore, in terms of the current treatment status, we should seriously consider whether the theoretical basis of our past and current treatment is indeed consistent with the etiology, pathology and pathophysiological development of the patient, and whether there are more ideal treatment options to be thought about and explored. 1.Theoretical system of pathogenesis of dilated cardiomyopathy According to the viewpoint of modern medicine, the pathogenesis of dilated cardiomyopathy is due to abnormalities in the control genes of cardiomyocytes, viral infections and immune system dysfunction, which lead to gradual degeneration, necrosis, fibrosis and interstitial edema of cardiomyocytes, resulting in gradual spherical enlargement of the heart, gradual reduction of cardiac function and finally heart failure and death. According to this theory, the current clinical treatment mainly adopts measures to nourish myocardium, improve metabolism, reduce cardiac anterior and posterior loads, increase myocardial contractility and correct cardiac function. Improvement of cardiac remodeling is the result of recent research, mainly the application of β-blockers and angiotensin-converting enzyme inhibitors, after many large clinical trials confirmed that these two types of drugs are effective but have limited effect on the improvement of cardiac function, the actual clinical treatment effect is not satisfactory, most of the patients’ cardiac function improvement is short-term, and soon return to the original state, or even heavier than the original. Some scholars apply heart pump assist devices to reduce cardiac load and improve cardiac function, but still cannot fundamentally solve the essential problem of the disease. For this reason, most researchers put more effort into researching new treatments in order to improve the outcome and prognosis of patients, but after decades of efforts, there is still no complete and effective cure, resulting in high long-term mortality in these patients. 2, dilated cardiomyopathy poor efficacy of the possible causes of modern medical treatment is mainly taken to nourish the myocardium, improve metabolism and correct cardiac function measures, while auxiliary angiotensin-converting enzyme inhibitors and β-blockers to prevent myocardial remodeling. This treatment is mainly an adjunctive treatment for increased myocardial load and altered metabolic levels, which reduces the pre and afterload and remodeling effects of the heart but does not interrupt the progressive myocardial damage process and improve cardiac function. Although this treatment protocol has basically fully satisfied the theoretical basis of treatment in modern medicine, why did this unsatisfactory result occur? What exactly is the essence of the problem? Is it a defect in the theoretical basis of treatment on which we rely? What is the basis for the development of this disease? Are there any changes in structural tissues other than myocardial cell damage? Is there damage to the myocardium first or to the fibrous scaffolding structures of the heart? All these questions are directly related to whether the current medical treatment basis for dilated cardiomyopathy is consistent with the objective pathogenesis of the patient. 3. New hypothesis of the pathogenesis of dilated cardiomyopathy Based on the analysis of the above-mentioned issues and the characteristics of the actual clinical pathological changes, we envisage that the initial factors in the pathogenesis of dilated cardiomyopathy are altered eukaryotic gene expression in cardiomyocytes, viral infection and defective and dysfunctional immune system, which first lead to damage of the fibrous scaffold stromal cells of the ventricular wall, followed by gradual degeneration, necrosis and extracellular interstitial edema of cardiomyocytes. Finally, whole heart enlargement, reduced cardiac function and heart failure occur. This hypothesis is based on the fact that in the early stage of dilated heart disease, most patients have enlarged heart chambers without significant cardiac insufficiency; secondly, the results of tissue biopsy and ultrasound and nuclear scans confirm that the early stage of dilated heart disease is not characterized by massive myocardial cell necrosis, but by fibrosis and myocardial cell degeneration and apoptotic changes; thirdly, the treatment with simple nutritional protection of the myocardium does not completely stop the progression of the disease in almost all patients. The third basis is that the simple nutritional protection of the myocardium can not completely stop the process of disease development, but can only delay the progress of the disease can not cure the patient. The reality of these situations suggests to us that our cognitive process and depth of this disease may be defective, and we need to strengthen our research on the pathogenesis and deeper cognition of cardioplegia in order to improve or refine our therapeutic measures and methods, and further enhance our therapeutic standards for the betterment of mankind. 4. Prospects of dilated cardiomyopathy cognition and treatment The initiating factors of dilated cardiomyopathy pathogenesis may be related to genetic mutations, viral infections, immune defects and the lack of certain biological elements induced. From the epidemiological statistics in recent years, the incidence of dilated cardiomyopathy is significantly lower in urban areas than in rural areas, and the young-adult population is significantly higher than the middle-aged and elderly population. The treatment of dilated heart disease aimed solely at nutrition of the myocardium, improvement of myocardial metabolism and ventricular remodeling is the main reason for the current poor effect of medical treatment. If the treatment of dilated heart disease is based on the principle of strengthening and improving the prevention and control of the enlargement of the skeletal structure of the ventricle and inhibiting the dilatation of the ventricular wall, supplemented by the nutrition of the myocardium and improvement of myocardial metabolism, it may produce better results. As far as the current state of medical development is concerned, the measures to inhibit ventricular dilatation are mainly composed of three aspects: drug therapy, stem cell therapy and biomechanical therapy. Pharmacological treatment is mainly the application of immunomodulators and angiotensin-converting enzyme inhibitors and β-blockers that improve ventricular remodeling, which are effective but cannot replace etiologic treatment. Biomechanical treatments are mainly for ventricular enlargement and heart failure after causing relative valve closure insufficiency and increasing cardiac function, including interventional annulus reduction and surgical annulus narrowing and triple-chamber pacemaker implantation, which are under investigation. Stem cell tissue engineering therapy is a hot research topic in recent years, mainly to increase the number of cardiomyocytes and stabilize the skeletal structure of the heart through implantation, which has the potential to revolutionize the current treatment status as research progresses, significantly improve the treatment effect of heart enlargement, improve the quality of life, and prolong the survival of patients.