Risk factors for coronary heart disease change accordingly due to aging, and in addition to coronary artery disease itself, there may be an increase in the number of risk factors affecting coronary heart disease due to older individuals: 1. Hypertension is the most important independent risk factor for coronary heart disease in the elderly. 2, Cholesterol is an independent risk factor. The corresponding changes in blood lipids with increasing age are characterized as follows: men start earlier, total cholesterol (TC) rises, its peak age is about 50 years old, and continues to 70 years of age and begins to decline; women rise only at about 45 years of age, the peak age of 60 years old, and declines after the age of 70 years. HDL-C is higher in women than in men before menopause, and declines in women after menopause. 3. Smoking is certainly a major risk factor for coronary heart disease in the prime of life, but the research data to date have not revealed any definite conclusion that smoking is associated with the occurrence of total coronary heart disease events and mortality in the elderly. 4. Diabetes mellitus increases in prevalence and complications with aging. Older people have less activity, muscle atrophy, fat increase, especially the occurrence of centripetal obesity, hypertrophy fat cells on the insulin receptor reduction, density and affinity reduction (to the organization of insulin sensitivity decline), produced insulin resistance, and at the same time, due to the insufficiency of compensatory secretion of insulin response to the old age and lead to a reduction in glucose tolerance, diabetes mellitus prevalence increases with aging and increase since the age of 45 years old, a significant rise, to 60 years of age to reach the peak. The prevalence of diabetes mellitus increases with age and rises significantly after the age of 45, reaching its peak at 60. 5, left ventricular hypertrophy, such as no other risk factors for left ventricular hypertrophy exists, old age due to aging occurred in the cardiac anatomical changes, that is, the thickness of the ventricular wall increases, connective tissue increases, so that the diastolic function is impaired, at the same time there are coronary microcirculatory changes in the aging, so the left ventricular hypertrophy tends to be earlier than the emergence of coronary artery disease clinical symptoms. Coronary artery disease patients due to myocardial ischemia, cardiac microstructural changes, myocardial stiffness increases, left ventricular diastolic myocardial compliance decreases, early disease first appeared diastolic function is impaired. With the aggravation of coronary artery disease and the increase in the number of affected coronary arteries, the diastolic and systolic hypoplasia of the left heart gradually decreases. Characteristic changes in two-dimensional cardiac ultrasound are a decrease in EF slope with or without a decrease in EF, which is accelerated with age. Possible mechanisms are: with the increase of age, the gradual accumulation of myocardial interstitial fibers, as well as the gradual increase in the accumulation of non-enzymatic glycosylation end-products (AGEs) in vivo, resulting in cross-linking of myocardial collagen in situ; AGEs are stable compounds formed in vivo by the combination of macromolecules, such as proteins and nucleic acids, with aldehyde or ketone groups of glucose and reducing sugars, and are formed through chemical rearrangement, which increases accordingly in vivo with the increase of age. It increases with age in the human body. With the aggregation of AGEs, the total collagen in the myocardial interstitium increases, and the increased collagen becomes the target protein for the aggregation of AGEs. This process leads to covalent modification of collagen and proliferation of collagen fibers, resulting in decreased LV compliance, increased stiffness, myocardial fibrosis, slower early LV filling rates, and decreased diastolic function. At the same time, structural changes occur: increased thickness of the left ventricle, thickening of the atrial wall, and enlargement of the atrial cavity. As fibrosis progresses, EF decreases and cardiac contractility declines. Therefore, the changes in cardiac structure and function in elderly patients with coronary artery disease are not only related to the number of branches of coronary vascular disease, but age is also an important factor. The correlation between the content of AGEs and the changes in cardiac structure and function needs to be further investigated.