Financiado en parte por Amgen, Pfizer, Novartis Foundation, Regeneron Pharmaceuticals, InfraRedx, Biotronik, Innovative Medicines Initiative, General Insurance Association of Japan, OrbusNeich Medical
Lp(a) Has Specific Effects on Coronary Artery Disease Independent of LDL-C: A Mendelian Randomization Study
Lee MP, Koenigsberg SH, Anwar MY, Raffield LM, Lin Z, Ballou AF, Booth JN, Davy-Mendez T, Kassahun H, Kent ST, López JAG, Monda KL, North KE, Yarosh R, Ballantyne CM, Graff M, Avery CL
JACC. Advances · 0 citas
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Según 73 financiadores declarados y la declaración de financiación del texto completo.
Publicación
- Publicado
- 2026-03-25 · JACC Adv · vol. 5 · número 5 · pág. 102697
- Editorial
- Elsevier BV
- Citado
- 0 citas · más que el 19% de estudios similares · 0.0× el promedio de su campo
- Referencias
- 57 trabajos
- Acceso
- Acceso abierto (revista) · CC-BY
- Áreas de investigación
- Lipoproteins and Cardiovascular Health · Genetic Associations and Epidemiology · Atherosclerosis and Cardiovascular Diseases
- Palabras clave
- lipoprotein(a), coronary artery disease, type 2 diabetes, LDL cholesterol, HbA1c, myocardial infarction risk, cardiovascular risk stratification, polygenic risk score, UK Biobank
17 autores
- Moa P. Lee🇺🇸University of North Carolina at Chapel Hill
- Sarah H. Koenigsberg🇺🇸University of North Carolina at Chapel Hill
- Mohammad Yaser Anwar🇺🇸University of North Carolina at Chapel Hill
- Laura M. Raffield🇺🇸University of North Carolina at Chapel Hill
- Zhaotong Lin🇺🇸Florida State University
- Anna F Ballou🇺🇸University of North Carolina at Chapel Hill
- John N. Booth🇺🇸Amgen (United States)
- Thibaut Davy-Méndez🇺🇸University of North Carolina at Chapel Hill
- Helina Kassahun🇺🇸Amgen (United States)
- Shia T. Kent🇺🇸Amgen (United States)
- J. Antonio G. López🇺🇸Amgen (United States)
- Keri L. Monda🇺🇸Amgen (United States)
- Kari E. North🇺🇸University of North Carolina at Chapel Hill
- Rina Yarosh🇺🇸University of North Carolina at Chapel Hill
- Christie Mitchell Ballantyne🇺🇸Baylor College of Medicine
- Mariaelisa Graff🇺🇸 · autor de correspondenciaUniversity of North Carolina at Chapel Hill
- Christy L. Avery🇺🇸 · autor de correspondenciaUniversity of North Carolina at Chapel Hill
Resumen
El texto original del estudio, en el idioma en que se publicó.
Background
Mendelian randomization studies suggest a causal effect of lipoprotein(a) (Lp(a)) on atherosclerotic cardiovascular disease. Noncardiovascular effects (eg, diabetes risk) are inadequately investigated.
Objectives
In this noninterventional phenome-wide association study designed to better understand the potential causal role of Lp(a), direct causal phenotypic effects of exposure to Lp(a) were estimated. Also, the association between LPA null allele rs41272114 with type 2 diabetes was assessed, and ancestry-specific Lp(a) thresholds were determined.
Methods
In the UK Biobank (n = 425,677 adults, 55% female), we studied 1,456 phenotypes spanning 18 classes using 4 ancestry-specific polygenic risk scores and false discovery rate multiple testing correction. Network deconvolution Mendelian randomization was leveraged to separate direct from indirect (ie, associations via mediating variables) causal phenotypic effects and account for confounding, reverse causation, and bidirectionality.
Results
Lp(a) was significantly associated with 80 phenotypes across 7 classes. Higher Lp(a) exposure had significant direct causal effects, independent of low-density lipoprotein cholesterol, on coronary artery disease (OR: 1.36; 95% CI: 1.21-1.54) and glycated hemoglobin (HbA1c; β = 0.099; 95% CI: 0.051-0.15) only. Very low Lp(a) exposure was not associated with type 2 diabetes (OR: 0.92; 95% CI: 0.64-1.31) or HbA1c (β = -0.016; 95% CI: -0.062 to 0.030). Among European and African ancestries, 86 (77th percentile) and 93 (59th percentile) nmol/L optimally discriminated myocardial infarction risk, respectively.
Conclusions
Increasing Lp(a) exposure had direct, independent causal effects on coronary artery disease and HbA1c only; very low Lp(a) exposure is suggested to not be causally associated with type 2 diabetes. The optimal European and African ancestry threshold to stratify cardiovascular risk is comparable, and below 125/105 nmol/L in current U.S./European medical professional society guidelines.
Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial (CC BY).
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