**4.1 After achieving LDL-C target**

Based on the close association between hypercholesterolemia, especially LDL-C, with the incidence and mortality of ASCVD, the current treatment guidelines mainly focus on on lowering LDL-C levels [9, 11]. However, numerous clinical trials of statins, non-statin LDL-C lowering agents, and combination therapy have shown that the risk of ASCVD persists despite positive LDL-C reduction [14, 86, 87]. Accumulating evidence from epidemiological and genetic studies, as well as randomized clinical trials, suggests that TRLs [29, 41, 88], Lp(a) [77, 79, 82], inflammatory phenomenon [89–91] and thrombosis risk [92–95] are associated with risk of ASCVD in individuals with active LDL-C control and interventions to these factors yield promising results promise in improving the incidence of CV events [96].

Non-HDL-C dyslipidemia plays an important role in the residual risk of CVD. Recent recommendations for the quantification of atherogenic lipoproteins in addition to LDL-C for lipid-lowering strategies have been published [97].
