Hypercholesterolemia is one of the major modifiable cardiovascular risk factors, while current guidelines mark the low-density lipoprotein cholesterol (LDL-C) levels as the primary target of treatment to reduce ASCVD risk. Yet, clinical trials demonstrate a persistent residual risk despite aggressive LDL-C lowering, mainly by non-HDL-C and triglyceride-rich particles levels, attributed by high triglycerides (TG) levels, as well as high apolipoprotein B (apo B) or lipoprotein (a) levels and inflamation processes [1–3].
