lp-a.org

Testing

Taiwan Society of Lipid and Atherosclerosis issues 2026 Lp(a) consensus on diagnosis and risk management (J Formos Med Assoc 2026)

Original title: 2026 Consensus and review of Lipoprotein(a) from Taiwan Society of Lipid and Atherosclerosis: Molecular pathogenesis, epidemiology, clinical implications, and advances in diagnostic strategies

J Formos Med Assoc · · 8

Cheng CY, Wu YJ, Yeh CF, Huang PH, Hsu CY, Lin TH, Wang YC, Wang CY, Wang CY, Huang YC, Shyu KG, Hsieh IC et al.

2026 consensus and review from the Taiwan Society of Lipid and Atherosclerosis on lipoprotein(a), covering its molecular pathogenesis, epidemiology, clinical implications and diagnostic strategies. Lp(a)'s atherogenic, thrombogenic and inflammatory properties stem largely from carrying oxidised phospholipids, and plasma concentration is predominantly set by kringle IV type 2 (KIV-2) repeat number in the LPA gene, with minimal lifestyle influence. Despite strong evidence linking elevated Lp(a) to cardiovascular risk, clinical testing remains underused, especially in East Asian countries; although Taiwanese population Lp(a) concentrations are comparatively low, a meaningful subset exceeds risk thresholds, and local studies confirm its prognostic value in coronary artery disease and ischaemic stroke. The consensus attributes under-recognition to limited physician awareness, implementation barriers and therapeutic nihilism, and sets out priorities for improving Lp(a) diagnosis and cardiovascular risk management in Taiwan.

Read the paper (DOI)PubMed

Original abstract

Lipoprotein(a) [Lp(a)] is a genetically determined lipoprotein that has been established as an independent and causal risk factor for atherosclerotic cardiovascular disease (ASCVD) and calcific aortic valve disease (CAVD). Structurally composed of a low-density lipoprotein (LDL)-like particle covalently linked to apolipoprotein(a) [apo(a)], Lp(a) exhibits unique atherogenic, thrombogenic, and inflammatory properties, largely due to its role as a carrier of oxidized phospholipids (OxPL). Plasma Lp(a) concentrations are predominantly determined by the number of kringle IV type 2 (KIV-2) repeats in the LPA gene, with minimal influence from lifestyle or environmental factors. Despite substantial evidence linking elevated Lp(a) to cardiovascular risk, clinical testing remains underutilized, especially in East Asian countries. In Taiwan, although population-level Lp(a) concentrations are comparatively low, a significant subset exceeds risk thresholds, with local studies confirming its prognostic value in coronary artery disease and ischemic stroke. Barriers, including limited physician awareness, implementation barriers, and therapeutic nihilism, contribute to its under-recognition. This review highlights the molecular features of Lp(a), its pathogenesis of cardiovascular disorders, epidemiology, and current barriers and future advances in diagnostic testing, with a particular focus on implications for cardiovascular risk management in Taiwan.

ancestryguidelinestesting

Summary written by lp-a.org from the published abstract; figures as published. Page updated 17 August 2026. Methods.