5 Lp(a) at a Glance 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.4 z Lp(a) is approximately 6 times more atherogenic than LDL on a per particle basis.5 z Up to 90% of Lp(a) plasma concentration is determined by genetics.4,6 z Other factors that influence Lp(a) levels include age, sex, ethnicity7 and comorbid conditions, such as Familial Hypercholesterolemia8 and liver or kidney disease.7 z Lp(a) levels are approximately 10-15% higher in women than men.9 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. However, commitment to both will improve overall cardiovascular health.7 z Statins are ineffective in lowering Lp(a). To the contrary, research shows statins can modestly increase Lp(a) levels by, on average, approximately 10-15%.11 The mechanism is not understood. z PCSK9 inhibitors can modestly lower Lp(a) levels.12 Up to 90% of Lp(a) plasma concentration is determined by genetics4,8 Other factors that influence Lp(a) levels include age, sex, ethnicity7 and comorbid conditions, such as Familial Hypercholesterolemia8 and liver or kidney disease.7 Lp(a): A Toolkit for Health Care Professionals Scan to view a video on Lp(a) at a glance.
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