NLA Releases an Update on Lp(a)

Two key takeways:

1. Lp(a) is considered a continuous independent risk factor, not dichotomous.
2. Recognition of 3 levels of risk and recommendation to re-measure in patients with intermediate-risk levels.

The summary below was generated with the Adobe AI Assistant and edited by me.

This document is a focused update to the 2019 National Lipid Association (NLA) scientific statement on the use of lipoprotein(a) in clinical practice, providing new recommendations based on emerging evidence regarding lipoprotein(a) as a cardiovascular risk factor.

The risk classifications based on Lp(a) levels are as follows: ​

• Low risk: Lp(a) levels below 75 nmol/L (30 mg/dL). ​​
• Intermediate risk: Lp(a) levels between 75 and 125 nmol/L (30-50 mg/dL). ​​
• High risk: Lp(a) levels equal to or above 125 nmol/L (50 mg/dL). ​ These risk classifications are used to assess the risk of atherosclerotic cardiovascular disease (ASCVD) events and guide treatment decisions. ​ It is important to note that these risk classifications are specific to Lp(a) levels and should be interpreted in the context of a patient’s overall cardiovascular risk profile. ​ The intermediate risk category is sometimes referred to as the “gray zone” and may warrant repeat measurement. ​ These risk categories apply across races and ethnicities. ​

The relationship between baseline lipoprotein(a) (Lp(a)) level and atherosclerotic cardiovascular disease (ASCVD) events is continuous and log-linear. ​​ This means that there is a direct and proportional relationship between higher baseline Lp(a) levels and increased risk of ASCVD events. ​ Even at lower levels of Lp(a) that were previously considered “low-risk,” there is still a small but significant increase in the risk of ASCVD events. ​ The old concept of a dichotomous threshold for Lp(a) levels should be retired, and clinical decision-making should be influenced by the degree of Lp(a) elevation and the patient’s other risk factors. ​ The risk of ASCVD events increases with higher Lp(a) levels, and the level of risk is influenced by the degree of Lp(a) elevation and other individual risk factors. ​ Elevated Lp(a) levels are independently associated with an increased risk of incident ASCVD events, and individuals in the highest quintile of Lp(a) levels had a 29% increased risk of incident ASCVD compared to those in lower quintiles. ​ Elevated Lp(a) is associated with increased ASCVD risk through mechanisms such as promoting atherosclerosis, prothrombotic effects, and proinflammatory effects. ​

Statins have a variable effect on Lp(a) levels, with some individuals experiencing a modest increase, while others may see no significant effect or even a decrease. ​ The exact mechanism behind this variability is not fully understood. However, it is important to note that the increase in Lp(a) levels should not discourage or discontinue statin treatment, as statins have been proven to be highly effective in reducing cardiovascular events and mortality. ​ For individuals with high-risk profiles, including those with elevated Lp(a) levels, additional LDL cholesterol lowering may be necessary, and the use of PCSK9 inhibitors may be considered. ​ It is important to consult with a healthcare professional to determine the most appropriate treatment strategy.

The document mentions that extended-release niacin has been shown to have a significant 23% reduction in plasma lipoprotein(a) (Lp(a)) levels. ​ However, recent studies combining niacin with statin therapy did not show clinical benefit in terms of reducing atherosclerotic cardiovascular disease (ASCVD) events. ​ Therefore, niacin is not recommended specifically for lowering Lp(a) levels. ​

The document does not provide specific recommendations for using aspirin in patients with elevated lipoprotein(a) (Lp(a)). However, it does mention that aspirin therapy may have potential benefits in certain individuals with elevated Lp(a) levels. ​ Here is a general approach that can be considered: