In recent years, there is a wealth of evidence in evidence-based medicine regarding the irreplaceable role of statins in the prevention and control of atherosclerotic disease and its treatment. The role of statins in reducing venous thromboembolism in the prevention of venous thrombotic events is controversial. The JUPITER study, a large prospective trial of statin primary prevention in a “healthy population” published this year, showed that statin use prevented venous thromboembolism at 1.9 years of follow-up. Venous thromboembolism is common, difficult to diagnose, costly, and has a poor prognosis, so prevention and treatment is important. hsCRP >5 mg/L in the JUPITER study showed a trend toward increased venous thromboembolism, but the predictive value of hsCRP is limited. The antivenous thromboembolic effect of statin is not related to its anti-inflammatory effect. The mechanism of statin prevention of venous thromboembolism may be that statin inhibits isoprenoid signaling proteins, delays fibrinogen clearance by reducing tissue factor expression and thrombin production, and activates factors V and VII, among other pathways, to exert antithrombotic effects. Statin also increases the transcriptional activity of the transcription factor KLF-2 and promotes the expression of endothelial cell thrombomodulin, which in turn enhances the activity of the protein C anticoagulation pathway. However, the JUPITER study only used symptomatic venous thromboembolism as an endpoint event, when in fact clinically asymptomatic individuals are more common, and the results may underestimate the incidence of venous thromboembolic events. The study was conducted on an underlying healthy population, can the preventive effect in the low-risk population be extended to the high-risk population? What are the dose-effect and benefit-risk ratios of statins? What is the difference in the mechanism of statin against arterial thrombosis and venous thrombosis? Further clarification is needed. Prevention of perioperative infarction Perioperative myocardial infarction is an important complication of PCI, with an incidence of 30% and a serious impact on patient prognosis. 2005, the American College of Cardiology/American Heart Association (ACC/AHA) guidelines included vascular surgery as an indication for statin therapy. Numerous studies have confirmed that intensive statin therapy during the peri-interventional or peri-operative period can significantly reduce the incidence of adverse endpoint events and benefit patients. Additional evidence of plaque reversal was added to the ASTEROID and COSMOS [IVUS Evaluation of Statin Effects on Coronary Atherosclerosis in a Japanese Population] studies, which confirmed that aggressive lipid-modifying therapy in ethnically diverse populations can reverse plaque progression. Another small clinical study, the first to apply VH-IVUS to evaluate the effect of statins on non-incident coronary atherosclerotic plaque progression, was a non-randomized, double-blind study with a relatively small number of cases, and those with high lipid levels were excluded due to ethical issues, and its findings have yet to be validated. The ARBITER 6-HALTS study reaffirms the importance of reducing the risk of vascular residuals. Previous studies have shown that even with aggressive LDL-C interventions, 2/3 of cardiovascular events are still not prevented. Atherogenic lipoprotein profile (including elevated TG levels, increased small and dense LDL, and decreased HDL-C levels) is a risk factor for vascular residual risk. Niacin elevates HDL-C levels, and its combination with statin reverses plaque and reduces cardiovascular events. Whether the combination of statin and ezetimibe in an intensive LDL-C regimen is beneficial in the management of cardiovascular events will be answered in the ongoing Acute Coronary Syndrome (IMPROVE-IT) study. Can renal failure dialysis patients benefit? The 4D trial (Deutsche Diabetes Dialysis Study) showed that statins did not reduce adverse cardiovascular events in patients on dialysis with diabetes.The AURORA study (Assessment of Survival and Cardiovascular Events in Patients on Conventional Hemodialysis with Statins) included 2,776 patients with ESRD on hemodialysis and found that statins did not prevent cardiac events in these patients at a mean follow-up of 3.5 years . The relationship between dyslipidemia and cardiovascular disease in patients with CKD is complex The dyslipidemia in patients with CKD is mainly characterized by elevated TG and decreased HDL-C, and LDL is dominated by small and dense LDL particles and oxidized LDL, while LDL-C levels are not elevated when patients have no proteinuria, so the lipid profile of ESRD patients is different from that of cardiovascular disease alone in terms of harm to the vessel wall. In addition, many other cardiovascular risk factors (such as anemia, inflammation, vascular calcification, oxidative stress, endothelial dysfunction, etc.) are present in CKD patients. Under the combined factors, the cardiovascular pathological basis of CKD and ESRD patients is different from that of coronary heart disease, and the heart and vessel walls are often severely calcified. The limited effect of statin on calcified plaque may explain the limited benefit of statin lipid modulation in ESRD patients, so the importance of early prevention and treatment of cardiovascular disease in CKD patients should be emphasized. The effect of statin on the heart and kidney of CKD patients is more controversial Several studies (e.g. ALLIANCE, HPS, CARE, etc.) have shown that statin can protect renal function [delay the decline of GFR and reduce proteinuria], which may be related to its pleiotropic effects, such as statin can improve endothelial cell function, increase renal perfusion, reduce LDL-C levels, mitigate direct damage to glomerular basement membrane by hyperlipidemia , attenuate the damage of inflammatory response to the kidney, or participate in renal protection by antioxidant, affecting fibrinolytic activity, reducing extracellular matrix production, immunomodulation, etc. However, the ALLHATLLT (Antihypertensive and Lipid-Lowering Therapy for the Prevention of Cardiac Events) study confirmed that statins at 40 mg/d did not reduce cardiovascular events in patients with CKD and did not improve GFR significantly, and both the ALLIANCE study and the 4D study showed that intensive statin therapy did not reduce cardiovascular events in patients with CKD. Therefore, there are still questions about the safety and effectiveness of statins for cardiorenal protection in patients with progressive CKD. To date, no randomized clinical studies have been conducted directly in patients with CKD. What is the role of statin in CKD? For which etiology or stage of CKD is a statin indicated? What is the mechanism of action? These questions will be answered in the ongoing prospective studies (PLANET II, SHARP and LORD), the results of which are expected. Overall, in the decade since the introduction of statins, their role in both primary and secondary prevention of coronary heart disease is irreplaceable. Intensive reduction of LDL-C levels is the basis for the prevention of cardiovascular events and cardiovascular deaths, but statins have limited protective effect on chronic heart failure, ESRD and other end-state diseases. Therefore, the concept of “prevention is better than cure” should be implemented in clinical practice.