Sepa- rately, Lp(a) is a modified form of LDL that appears to possess atherogenic potential.S2.3-5 Relative indications for its measurement are family history of premature ASCVD or personal history of ASCVD not explained by major risk factors. Lp(a) increases ASCVD risk especially at higher levels. Thus, if a decision is made to measure Lp(a), an Lp(a) 50 mg/dL or 125 nmol/L, Lp(a) may be considered a risk-enhancing factor.S2.3-6 Current evi- dence shows that it should be considered in women only in the presence of hypercholesterolemia and Recommendations for Measurements of LDL-C and Non HDL-C (Continued) COR LOE Recommendations CLINICAL STATEMENTS AND GUIDELINES with the understanding that the improvement in risk prediction in adult women in a large clinical trial was In the present document, an elevation of Lp(a) is considered to be a risk-enhancing factor.S2.3-6 This is especially in those with higher Lp(a) values and, if used in women, only in the presence of hypercholes 2.4. Monitoring Response of LDL-C to Statin Therapy In large RCTs of cholesterol-lowering therapy, LDL-C lowering has been consistently shown to reduce the risk of ASCVD. One large meta-analysisS2.4-1 of statin clinical trials showed a progressive reduction in risk of major ASCVD events with lower on-treatment LDL-C levels. In another larger meta-analysisS2.4-2 of 14 statin trials, it was observed that a 38.7-mg/dL (1-mmol/L) reduction of LDL-C levels is accompanied by a 21% reduction in ASCVD risk. In clinical practice, howev- er, absolute responses in LDL-C to statin therapy de- pend on baseline LDL-C concentrations. A given dose of statins produces a similar percentage reduction in LDL-C levels across a broad range of baseline LDL- C levels. For this reason, a more reliable indicator of statin efficacy is percentage reduction. 