The high prevalence of hyperuricemia is in middle-aged and elderly men and postmenopausal women, but in recent years it is becoming increasingly younger and has become an important risk factor for metabolic and cardiovascular diseases. Blood uric acid has long been an important biochemical indicator used to diagnose and evaluate patients with gout. However, many studies in recent years have proven that hyperuricemia is not only a detection indicator of gout and concurrent kidney damage, but also closely related to cardiovascular disease and metabolic diseases. Studies have confirmed that hyperuricemia can promote atherosclerosis and platelet aggregation, accelerate the deposition of lipids in the vascular wall, and urate can damage the arterial intima and cause vascular endothelial dysfunction. According to the survey, there are about 120 million patients with hyperuricemia in China, accounting for about 10% of the total population, which needs to be paid great attention by both doctors and patients. 1. Uric acid and coronary heart disease Because of the low physical solubility of uric acid, uric acid crystals are easily precipitated in the blood, which are attached to the blood vessel wall and directly damage the coronary microvascular function of the heart. Uric acid crystals can also activate platelets, causing them to aggregate and promote thrombosis. In addition, uric acid has the effect of depositing lipids in the intima of arteries, promoting atherosclerosis and plaque formation, which leads to the development of coronary heart disease. Investigations have shown that the risk of coronary heart disease increases when the blood uric acid level is ≥357 mmol/L. The mortality rate of coronary heart disease is 2.5 times higher in the hyperuricemia group than in the hypouricemia group, and more significantly in women. 2. Uric acid and hypertension Uric acid increases blood pressure by damaging vascular endothelial function, causing vasodilatation dysfunction, increased vascular resistance, and vascular sclerosis. About 30% of the population with primary hypertension has hyperuricemia. It was found that for every 100 μmol/L increase in serum uric acid, the risk of hypertension increased by 23%. On the other hand, in hypertensive patients, increased blood pressure decreases renal blood flow, resulting in increased uric acid reabsorption from the renal tubules and promoting the development of hyperuricemia. That is, hyperuricemia can lead to hypertension, and hypertension is a contributing factor to hyperuricemia. 3. Uric acid and cardiovascular events A large body of data confirms that patients with hyperuricemia are at greatly increased risk of cardiovascular disease. Hyperuricemia is not only closely related to coronary heart disease and hypertension, but is also a high-risk causative factor for many cardiovascular diseases, such as obesity, hypertriglyceridemia, renal disease, insulin resistance, and metabolic syndrome. A 59.5 μmol/L increase in blood uric acid is associated with a 48% increased risk of death from coronary heart disease in women, and the risk of stroke is significantly higher when blood uric acid levels are >416.5 μmol/L. Patients with hyperuricemia with gout have a significantly increased risk of cardiovascular events. However, the risk of cardiovascular events from uric acid is bipartite, i.e., those with the lowest or highest uric acid levels have the highest incidence of cardiovascular events. 4. uric acid and heart failure In patients with heart failure, blood uric acid is increased due to reduced uric acid clearance due to renal hypoxia and ischemia. Hyperuricemia can affect cardiac energy metabolism and is also a cause of decreased cardiac function. Therefore, hyperuricemia and heart failure are also mutually influential and causal. Increased uric acid concentrations are associated with increased mortality in patients with heart failure. Therefore, patients with hyperuricemia should be actively prevented and treated. The main source of serum uric acid is endogenous. By adjusting dietary habits and improving lifestyle, both exogenous factors can be counteracted and the body’s metabolism of uric acid can be adjusted so that serum uric acid levels can be reduced. Patients should first of all limit the intake of high purine food, such as animal offal, red meat, fish and shrimp without scales, crab, soybean products, various kinds of broth, dairy products, etc. To promote the excretion of uric acid, we should drink more water, abstain from alcohol, limit calories, adhere to physical exercise and reduce body weight, all of which are beneficial to regulate the metabolism of uric acid in the body. All people with uric acid >535μmol/L should be treated with uric acid-lowering drugs regardless of whether they have symptoms or not. ACEI and ARB, which are commonly used to lower blood pressure, can inhibit the reabsorption of uric acid and have the effect of promoting uric acid excretion. Small doses of aspirin and lipid-regulating drugs have a strong effect on reducing blood uric acid levels. Internal sodium bicarbonate can increase the solubility of uric acid and also benefit the excretion of uric acid. Clinicians should maintain the patient’s urine pH at 6.0 to 6.5 through food and drug therapy.