Lipoprotein(a) and atrial fibrillation: Meta-analysis of observational and mendelian randomization studies shows no clinically meaningful association
Fahim M, Eldawud D, Wang R, Gorantla A, Khouri P, Mitre CA, Budzikowski AS
Journal of clinical lipidology · 0 citas
Etiquetas de revisión
Financiación no declaradaDatos neutrales que nuestra revisión registró sobre cómo se hizo este estudio. Describen el método, nunca si nos gusta el resultado.
Cómo se estudió
- Diseño
- Metaanálisis (indexado por PubMed)
- Estudiado en
- Personas
- Resultado principal
- Eventos clínicos como enfermedad o muerte
Quién lo pagó
- Financiación
- Financiación no declarada
Publicación
- Publicado
- 2026-07-10 · J Clin Lipidol · vol. 20 · número 9 · págs. 1965–1977
- Editorial
- Elsevier BV
- Citado
- 0 citas · más que el 47% de estudios similares · 0.0× el promedio de su campo
- Referencias
- 51 trabajos
- Acceso
- De pago
- Áreas de investigación
- Atrial Fibrillation Management and Outcomes · Lipoproteins and Cardiovascular Health · Genetic Associations and Epidemiology
- Palabras clave
- lipoprotein(a), atrial fibrillation, Mendelian randomization, causal effects, genetic instruments, cardiovascular risk factors, atherosclerotic cardiovascular disease
- MeSH
- humans, atrial fibrillation, lipoprotein(a), mendelian randomization analysis, observational studies as topic
7 autores
- Md Fahim🇺🇸 · autor de correspondenciaSUNY Downstate Health Sciences University
- Daoud Eldawud🇺🇸SUNY Downstate Health Sciences University
- Roy Wang🇺🇸SUNY Downstate Health Sciences University
- Asher Gorantla🇺🇸SUNY Downstate Health Sciences University
- Peter Khouri🇺🇸SUNY Downstate Health Sciences University
- Cristina A. Mitre🇺🇸VA NY Harbor Healthcare System
- Adam Budzikowski🇺🇸SUNY Downstate Health Sciences University
Resumen
El texto original del estudio, en el idioma en que se publicó.
Background
Elevated lipoprotein(a) [Lp(a)] is an established risk factor for atherosclerotic cardiovascular disease, but its relationship with atrial fibrillation (AF) remains uncertain. We conducted a meta-analysis of observational studies and Mendelian randomization (MR) analyses to clarify whether Lp(a) is associated with AF.
Objective
To clarify the relationship between Lp(a) and AF.
Methods
We systematically pooled 16 observational studies analyzing odds ratios (ORs) and hazard ratios (HRs) for AF across higher vs lower Lp(a) exposure, as defined within each study, in 2 separate random-effects models. In parallel, we pooled 7 MR studies that used genetic instruments for Lp(a) to estimate the causal effect on AF. Subgroup analyses were performed by ancestry (European and East Asian).
Results
Observational studies showed no association between Lp(a) and AF (OR 0.980 [0.901, 1.070], P = 0.581; HR 1.058 [0.998, 1.110], P = 0.057). Stratification by ancestry showed no association either (European, OR 1.079 [0.759, 1.533], P = 0.673; East Asian, OR 0.978 [0.896, 1.068], P = 0.621). In MR studies accounting for sample overlap, we observed no association between Lp(a) and AF (OR 0.976 [0.940, 1.013], P = 0.208). All MR studies pooled with substantial sample overlap showed statistically significant but very small positive effects (OR 1.023 [1.002, 1.044], P < 0.001).
Conclusion
Lp(a) is not associated with AF in observational or MR meta-analysis. MR analyses do not demonstrate a significant association when restricted to independent datasets, indicating that any true causal relationship is unlikely to be clinically meaningful.
Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial.
Confianza de la comunidad
Cargando…
¿Cuánto confías en los hallazgos de este estudio?
Comentarios
¿Algo está mal aquí?
Señala este estudio si su información, etiquetas o financiación parecen incorrectas. Un editor revisa cada señalamiento.
Información educativa sobre investigación publicada. No es consejo médico ni una recomendación para empezar o dejar nada.