Dose-dependent, effective in 2 weeks, It reaches its peak in 4-6 weeks, and long-term application can maintain the efficacy.

(1) Competitively inhibit HMG-CoA reductase and reduce Ch synthesis. (2) Compensatory increase in the number and activity of LDL receptors. (3) Reduce the synthesis and release of VLDL in the liver

Hyperlipoproteinemia: Mainly used for heterozygous familial and non-familial lla, Ilb and Sichuan type hyperlipoproteinemia. It can also be used for hypercholesterolemia caused by type 2 diabetes and nephrotic syndrome.

Prevention of acute cardiovascular and cerebrovascular events: used for primary and secondary prevention of coronary heart disease, significantly reducing morbidity and mortality. Reduce the occurrence of stroke, angina pectoris and myocardial infarction.

Nephrotic syndrome: regulates blood lipids, inhibits glomerular mesangial cell proliferation, and delays renal arteriosclerosis.

Inhibit restenosis after angioplasty

Commonly seen are GI, skin flushing, and headache. About 0.5% causes transaminase 1, which is dose-related and can be recovered after 2 to 3 months of drug withdrawal. Myopathic syndrome, myalgia, and CK↑ occur in <1%. In severe cases, rhabdomyolysis may cause acute renal failure or even death. Be careful when combined with fibrates (10%-30%).

Cholestyramine (cholestyramine) colestipol (colestipol)

Mechanism of action

clinical application

adverse reactions

Mechanism of action

Adjust blood lipids: Reduce TG by 20%~60%, VLDL-C by 63%, TC 6%-25%, LDL-C26% Increase HDL-C10%~30%

Anti-inflammatory, anticoagulant, antithrombotic

1. Activate the peroxisome proliferatoractivated receptor PPARa (peroxisome proliferatoractivated receptora) and regulate the expression of apoCII, LPL, apoAI and other genes. 2. Inhibit the activity of certain coagulation factors and reduce the production of plasminogen activator inhibitor (PAI-1).

Type 11b, III, and IV hyperlipoproteinemia. Bezafibrate can improve glucose metabolism and can be used for patients with diabetes and high TG.

Combined use with statins increases the risk of myopathy.

(1) Large doses lower TG and VLDL by 20%~60%; lowering LDL-C slowly (5~7 days) and weakly (10%~25%) Increase HDL by 15%~30%; decrease Lp(a)

(2) Inhibit the production of TXA2, increase the production of PGI2 to prevent platelet aggregation and expand blood vessels.

Reduce cellular cAMP levels, inhibit hormone-sensitive lipase, inhibit the release of free fatty acids from adipose tissue, reduce liver triglyceride synthesis, and reduce the synthesis and release of VLDL.

Broad spectrum, effective for both 116 and type IV hyperlipidemia. Suitable for mixed type, high TG, low HDL and high Lp(a)emia. Combined with statins or fibrates, the efficacy can be improved.

Liver damage, hyperuricemia, hyperglycemia, etc. can cause and aggravate gastrointestinal ulcers.

1. Adjust blood lipids: reduce TG, VLDL, increase HDL-C, apoAl/apoA ll

2. Anti-platelet aggregation, anti-thrombosis, and blood vessel dilation.

3. Inhibit the proliferation and migration of VSMCs.

4. Improve the plasticity of RBCs and improve microcirculation.

5. Inhibit the expression of various cytokines in the early inflammatory response of As.

High TG hyperlipidemia and diabetes complicated with hyperlipidemia. Significant improvement in prognosis for patients with myocardial infarction