Obesity cardiomyopathy is a cardiomyopathy that occurs in obese individuals and cannot be explained by hypertension, diabetes mellitus, coronary artery disease, and other known diseases. This cardiomyopathy results in impaired left ventricular function, manifesting as systolic or diastolic heart failure, and has a broad clinical spectrum ranging from asymptomatic subclinical cardiac dysfunction to halo rehypoplasia grade IV dilated cardiomyopathy. A variety of structural changes in the heart occur in obese individuals, including left atrial enlargement, left ventricular eccentric hypertrophy, and left ventricular dilatation. Right ventricular hypertrophy and dilatation are partially present, independent of obstructive respiratory sleep disorder and pulmonary hypertension caused by obesity. The development of obesity cardiomyopathy is influenced by several factors, with hemodynamic abnormalities as the initiating factor. The circulating blood volume and cardiac output increase in obese people, and the left ventricular wall becomes eccentric hypertrophy under the effect of continuous high pressure, and the ventricular systolic function decreases when the wall thickening cannot compensate for the ventricular expansion. Myocardial remodeling gradually occurs, with cardiomyocyte hypertrophy, fibrosis and interstitial collagen deposition. Long-term left heart failure can lead to increased pulmonary venous pressure and eventually pulmonary hypertension and right heart failure. Various metabolic disorders are also involved in the development of cardiomyopathy. Obese people often have insulin resistance, so that the cardiomyocytes to fatty acid uptake is excessive, myocardial oxygen consumption increases, fatty acid metabolic intermediate products such as long-chain non-esterified fatty acids, ceramide and other accumulation will damage the cardiomyocytes. Studies such as the brewing bad early burial increase dry bad noise found that the content of triacylglycerol in cardiomyocytes is positively correlated with the monthly brewing meteor, and the fatty degeneration of cardiomyocytes can also lead to dilated cardiomyopathy. Upregulation of gene expression of chronic inflammatory mediators in obese patients, inhibition of myocardial protective lipocalin, and dysfunctional mitochondrial biosynthesis in cardiomyocytes are also involved in the development of cardiomyopathy. Abnormalities in microvascular and endothelial cell function are also associated with the development of obese cardiomyopathy. Abnormal endothelial function in obese individuals causes abnormal constriction of small blood vessels and microthrombosis, and infarction and reperfusion injury of microscopic myocardial tissues cause progressive development of cardiomyopathy. Abnormalities in microvascular and endothelial cell function are also associated with the development of obese cardiomyopathy. In obese individuals, abnormal endothelial function causes abnormal constriction of small blood vessels and microthrombosis, and infarction and reperfusion injury of microscopic myocardial tissues lead to progressive development of myocardial lesions.