Independence of Lipoprotein(a) and Low-Density Lipoprotein Cholesterol-Mediated Cardiovascular Risk: A Participant-Level Meta-Analysis
Bhatia HS, Wandel S, Willeit P, Lesogor A, Bailey K, Ridker PM, Nestel P, Simes J, Tonkin A, Schwartz GG, Colhoun H, Wanner C, Tsimikas S
Circulation · 98 citas
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Cómo se estudió
- Diseño
- Metaanálisis (indexado por PubMed)
- Estudiado en
- Personas
- Resultado principal
- Eventos clínicos como enfermedad o muerte
Quién lo pagó
- Financiación
- Financiado por la industria
- Gobierno
- National Institutes of Health
- Gobierno
- National Heart, Lung, and Blood Institute
- Gobierno
- NHLBI NIH HHS
- Autores
- Al menos un autor declara un vínculo económico con la industria
- Subvenciones
- National Institutes of Health (KL2TR001444); National Heart, Lung, and Blood Institute (K08HL166962); National Heart, Lung, and Blood Institute (R01HL159156)
Según 3 financiadores declarados y la declaración de financiación del texto completo.
Publicación
- Publicado
- 2024-11-04 · Circulation · vol. 151 · número 4 · págs. 312–321
- Editorial
- Lippincott Williams & Wilkins
- Citado
- 113 citas · más que el 100% de estudios similares · 43.2× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 44 trabajos
- Acceso
- Acceso abierto (revista híbrida) · CC-BY
- Áreas de investigación
- Lipoproteins and Cardiovascular Health · Diabetes, Cardiovascular Risks, and Lipoproteins · Cholesterol and Lipid Metabolism
- Palabras clave
- lipoprotein(a), LDL cholesterol, atherosclerotic cardiovascular disease, cardiovascular risk, statin therapy, LDL cholesterol lowering, coronary artery disease, stroke, carotid revascularization, additive risk, LDL-C thresholds
- MeSH
- humans, cardiovascular diseases, lipoprotein(a), hydroxymethylglutaryl-coa reductase inhibitors, risk factors, aged, middle aged, female, male, cholesterol, ldl, randomized controlled trials as topic
13 autores
- Harpreet Singh Bhatia🇺🇸University of California San Diego
- Simon Wandel🇨🇭Novartis (Switzerland)
- Peter Willeit🇦🇹Innsbruck Medical University; Universität Innsbruck
- Anastasia Lesogor🇨🇭Novartis (Switzerland)
- Keith Bailey🇨🇭Novartis (Switzerland)
- Paul M. Ridker🇺🇸Brigham and Women's Hospital; Harvard University
- Paul John Nestel🇦🇺Baker Heart and Diabetes Institute
- Robert John Simes🇦🇺The University of Sydney; National Health and Medical Research Council
- Andrew Maxwell Tonkin🇦🇺Monash University
- Gregory G. Schwartz🇺🇸University of Colorado Anschutz
- Helen Martina Colhoun🇬🇧Institute of Genetics and Cancer; MRC Human Genetics Unit
- Christoph Wanner🇩🇪University of Würzburg; Universitätsklinikum Würzburg
- Sotirios Tsimikas🇺🇸University of California San Diego
Resumen
El texto original del estudio, en el idioma en que se publicó.
Background
Low-density lipoprotein cholesterol (LDL-C) and lipoprotein(a) (Lp[a]) levels are independently associated with atherosclerotic cardiovascular disease (ASCVD). However, the relationship between Lp(a) level, LDL-C level, and ASCVD risk at different thresholds is not well defined.
Methods
A participant-level meta-analysis of 27 658 participants enrolled in 6 placebo-controlled statin trials was performed to assess the association of LDL-C and Lp(a) levels with risk of fatal or nonfatal coronary heart disease events, stroke, or any coronary or carotid revascularization (ASCVD). The multivariable-adjusted association between baseline Lp(a) level and ASCVD risk was modeled continuously using generalized additive models, and the association between baseline LDL-C level and ASCVD risk by baseline Lp(a) level by Cox proportional hazards models with random effects. The joint association between Lp(a) level and statin-achieved LDL-C level with ASCVD risk was evaluated using Cox proportional hazards models.
Results
Compared with an Lp(a) level of 5 mg/dL, increasing levels of Lp(a) were log-linearly associated with ASCVD risk in statin- and placebo-treated patients. Among statin-treated individuals, those with Lp(a) level >50 mg/dL (≈125 nmol/L) had increased risk across all quartiles of achieved LDL-C level and absolute change in LDL-C level. Even among those with the lowest quartile of achieved LDL-C level (3.1-77.0 mg/dL), those with Lp(a) level >50 mg/dL had greater ASCVD risk (hazard ratio, 1.38 [95% CI, 1.06-1.79]) than those with Lp(a) level ≤50 mg/dL. The greatest risk was observed with both Lp(a) level >50 mg/dL and LDL-C level in the fourth quartile (hazard ratio, 1.90 [95% CI, 1.46-2.48]).
Conclusions
These findings demonstrate the independent and additive nature of Lp(a) and LDL-C levels for ASCVD risk, and that LDL-C lowering does not fully offset Lp(a)-mediated risk.
Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial (CC BY).
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