Lp(a) elevation massively increases risk of heart attack and stroke

Lp(a) elevation massively increases risk of heart attack and stroke

Lp(a) concentrations are mostly genetically determined by the LPA gene, and population distributions vary by ancestry (highest levels in individuals of African ancestry). Prospective studies have found robust associations for Lp(a) with ASCVD outcomes and calcific aortic valve disease, and genetic studies support causal associations. ASCVD risk increases in a continuous manner with higher Lp(a) concentrations, regardless of ancestry. An Lp(a) concentration of 125 nmol/L (50 mg/dL) is considered high and is associated with approximately a 40% relative risk increase in ASCVD (Table 4) compared with individuals with low Lp(a) levels.

Lp(a) likely contributes to ASCVD through multiple mechanisms, including proatherogenic and proinflammatory effects that may be in part mediated by the oxidized phospholipids on Lp(a). As Lp(a) concentrations remain similar over time and are minimally modified by lifestyle factors, a single measurement is generally sufficient.

ASCVD risk is particularly high for individuals with elevated Lp(a) and other risk factors, and measuring Lp(a) helps with risk stratification.

From: https://www.ahajournals.org/doi/10.1161/CIR.0000000000001423#sec-7-3