Epidemiology
Review reports elevated Lp(a) affects 25% of Indians versus 1 in 5 worldwide, and correlated with severe disease in 1,021 Indian CAD patients (Indian Heart J 2024)
Original title: Lipoprotein a - Lp(a)
This review summarises Lp(a) as a genetically determined, independent, causal ASCVD risk factor, noting that while roughly 1 in 5 people worldwide have elevated Lp(a) (above 50 mg/dL or 125 nmol/L), the prevalence reaches 25% in Indians. Lp(a) reaches its peak level by age 5 and remains stable thereafter, minimally influenced by diet or environment though it can shift with thyroid disease, chronic kidney disease, inflammation or sepsis, and the author recommends measuring it at least once in a lifetime with cascade testing in familial hypercholesterolaemia, family history of very high Lp(a), or personal or family ASCVD history. Currently available agents offer only modest reduction, PCSK9 inhibitors and inclisiran by 25% and pelacarsen (an antisense oligonucleotide) by 80%. In a recent Indian study of 1,021 coronary artery disease patients, elevated Lp(a) (above 50 mg/dL) correlated with more severe angiographic disease, was present in 37% of acute coronary syndrome patients, and reached 43% among young CAD patients with familial hypercholesterolaemia.
Original abstract
Lp(a) is a genetically determined, heritable, independent and causal risk factor for ASCVD. About 1 in 5 people worldwide have elevated Lp(a) (>50 mg/dL or >125 nmol/L) whereas in Indians it is 25 %. Epidemiological, genome-wide association and mendelian randomization studies have demonstrated an association between elevated Lp(a) levels and increased incidence of myocardial infarction, aortic valve stenosis, ischemic stroke, heart failure, CV and all-cause mortality. The increased Lp(a)-mediated CV risk is mediated by pro-inflammatory, pro-thrombotic and pro-atherogenic processes, leading to progression of atherosclerosis and increased risk of thrombosis. Lp(a) level reaches peak by 5 years of age and remains stable over time. Levels are not much influenced by dietary and environmental factors but it can vary in certain clinical situations like thyroid diseases, chronic kidney disease, inflammation and sepsis. It should be measured at least once in life time. Cascade testing for high Lp(a) is recommended in the settings of FH, family history of (very) high Lp(a), and personal or family history of ASCVD. In the absence of specific Lp(a)-lowering therapies, comprehensive risk factor management is recommended as per guidelines for individuals with elevated Lp(a). PCSK9 inhibitors and Inclisiran reduce Lp(a) by 25%. Pelacarsen is an antisense oligonucleotide and is found to reduce Lp(a) by 80%. In a recent Indian study of 1,021 CAD patients, presence of elevated Lp(a) (>50 mg/dL) correlated with severe angiographic disease. 37% of ACS patients exhibited elevated Lp(a) and it was higher in young CAD patients with FH (43%).
Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.