LDL-C and lipoprotein(a) levels independently and additively associated with ASCVD risk: Study

The results of a recent study that was published in the journal of Circulation, suggest that low-density lipoprotein cholesterol (LDL-C) and lipoprotein(a) (Lp[a]) levels are independent and additive for atherosclerotic cardiovascular disease (ASCVD) risk, and lowering LDL-C does not completely counteract Lp(a)-mediated risk.

Lp(a), which is mostly genetically driven, has been demonstrated to be an independent predictor of calcific aortic stenosis and ASCVD risk. Numerous genetic studies have demonstrated a link between elevated Lp(a) and cardiovascular disease, and several treatments are being developed to reduce and treat it. According to US standards, Lp(a) is regarded as a "risk enhancer," a surrogate that can assist certain patients in making treatment decisions. Some guidelines, including those from the European Atherosclerosis Society and the National Lipid Association, suggest being more aggressive with LDL reduction to counter the risk associated with high Lp(a) in the absence of effective medications.

To evaluate the relationship between LDL-C and Lp(a) levels and the risk of stroke, coronary heart disease events, or any coronary or carotid revascularization, a participant-level meta-analysis of 27,658 patients included in six placebo-controlled statin trials was conducted. Generalized additive models were used to continuously model the multivariable-adjusted relationship between baseline Lp(a) level and ASCVD risk, and Cox proportional hazards models with random effects were used to model the relationship between baseline LDL-C level and ASCVD risk by baseline Lp(a) level. Cox proportional hazards models were used to assess the combined relationship between ASCVD risk and Lp(a) level and statin-achieved LDL-C level.