5 z Lp(a) is independently associated with CVD risk. z Lp(a) levels are established in early childhood and remain relatively consistent over an individual’s lifetime. z Lp(a) is composed of apolipoprotein(a) [apo(a)] covalently bound to an apolipoprotein B (apoB)-100-containing lipoprotein particle and is the preferential carrier of proinflammatory oxidized phospholipids in plasma. z Although definitive data are lacking, Lp(a) likely increases cardiovascular risk through multiple mechanisms, including those attributed both to its LDL-like moiety, as well as its unique apo(a) protein. The latter may confer prothrombotic and/or additional proinflammatory effects that can cause vascular cell dysfunction.5 z Lp(a) is approximately 6 times more atherogenic than LDL-C on a per particle basis.6 z Up to 90% of Lp(a) plasma concentration is determined by genetics.5,7 z Other factors that influence Lp(a) levels include age, sex, (pregnancy and post-menopausal status), ancestry and comorbid conditions, such as Familial Hypercholesterolemia and liver, thyroid, or kidney disease.8,9 z Distribution of Lp(a) levels may also vary by population-specific percentiles, due to differences in the distribution of Lp(a) levels among ancestry groups.10 z There is limited evidence that heart-healthy eating and regular physical activity reduce Lp(a) levels.8 However, commitment to both will improve overall cardiovascular health. z Although statins are a cornerstone therapy in the treatment of CVD, they are ineffective in lowering Lp(a). While some studies report that statins raise Lp(a), the increase is minimal and does not outweigh the benefit of statins in high-Lp(a) patients.11 z PCSK9 inhibitors can modestly lower Lp(a) levels, and patients with elevated Lp(a) may get greater cardiovascular benefit from these drugs.12 Lp(a) at a Glance Lp(a): A Toolkit for Healthcare Professionals Up to 90% of Lp(a) plasma concentration is determined by genetics5,7 Other factors that influence Lp(a) levels include age, sex, (pregnancy and post-menopausal status), ancestry and comorbid conditions, such as Familial Hypercholesterolemia and liver, thyroid, or kidney disease.8,9
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