Financiado en parte por Eli Lilly and Company, Pfizer, Sanofi, InfraRedx
Non-HDL Cholesterol and Triglycerides: Implications for Coronary Atheroma Progression and Clinical Events
Puri R, Nissen SE, Shao M, Elshazly MB, Kataoka Y, Kapadia SR, Tuzcu EM, Nicholls SJ
Arteriosclerosis, thrombosis, and vascular biology · 114 citas
Etiquetas de revisión
Financiado por la industriaDatos 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 (clasificado por nuestro filtro de IA)
- Estudiado en
- Personas
- Resultado principal
- Eventos clínicos como enfermedad o muerte
Quién lo pagó
- Financiación
- Financiado por la industria
- Empresa
- Eli Lilly and Company
- Empresa
- Pfizer
- Empresa
- Sanofi
- Universidad u hospital
- Cleveland Clinic
- Empresa
- InfraRedx
Según 5 financiadores declarados.
Publicación
- Publicado
- 2016-08-12 · Arterioscler Thromb Vasc Biol · vol. 36 · número 11 · págs. 2220–2228
- Editorial
- Lippincott Williams & Wilkins
- Citado
- 142 citas · más que el 100% de estudios similares · 20.2× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 46 trabajos
- Acceso
- Lectura gratuita
- Áreas de investigación
- Lipoproteins and Cardiovascular Health · Diabetes, Cardiovascular Risks, and Lipoproteins · Coronary Interventions and Diagnostics
- Palabras clave
- non-HDL cholesterol, triglycerides, atherosclerosis progression, LDL cholesterol, triglyceride-rich lipoproteins, residual cardiovascular risk, major adverse cardiovascular events, intravascular ultrasound, coronary artery disease, diabetes mellitus, C-reactive protein
- MeSH
- coronary vessels, humans, disease progression, cholesterol, triglycerides, ultrasonography, interventional, treatment outcome, multivariate analysis, linear models, risk factors, predictive value of tests, time factors, aged, middle aged, female, male, clinical trials as topic, coronary artery disease, hypolipidemic agents, kaplan-meier estimate, plaque, atherosclerotic, biomarkers
8 autores
- Rishi Puri🇺🇸🇦🇺Cleveland Clinic; South Australian Health and Medical Research Institute; The University of Adelaide
- Steven E. Nissen🇺🇸🇦🇺Cleveland Clinic; South Australian Health and Medical Research Institute; The University of Adelaide
- Mingyuan Shao🇺🇸🇦🇺Cleveland Clinic; South Australian Health and Medical Research Institute; The University of Adelaide
- Mohamed Badreldin Elshazly🇺🇸🇦🇺Cleveland Clinic; South Australian Health and Medical Research Institute; The University of Adelaide
- Yu Kataoka🇺🇸🇦🇺Cleveland Clinic; South Australian Health and Medical Research Institute; The University of Adelaide
- Samir Ramesh Kapadia🇺🇸🇦🇺Cleveland Clinic; South Australian Health and Medical Research Institute; The University of Adelaide
- Emin Murat Tuzcu🇺🇸🇦🇺Cleveland Clinic; South Australian Health and Medical Research Institute; The University of Adelaide
- Stephen James Nicholls🇺🇸🇦🇺Cleveland Clinic; South Australian Health and Medical Research Institute; The University of Adelaide
Resumen
El texto original del estudio, en el idioma en que se publicó.
Objectives
Non-high-density lipoprotein cholesterol (non-HDLC) levels reflect the full burden of cholesterol transported in atherogenic lipoproteins. Genetic studies suggest a causal association between elevated triglycerides (TGs)-rich lipoproteins and atherosclerosis. We evaluated associations between achieved non-HDLC and TG levels on changes in coronary atheroma volume.
Approach and results
Data were analyzed from 9 clinical trials involving 4957 patients with coronary disease undergoing serial intravascular ultrasonography to assess changes in percent atheroma volume (ΔPAV) and were evaluated against on-treatment non-HDLC and TG levels. The effects of lower (0) was associated with achieved TG levels >200 mg/dL, respectively. Lower on-treatment non-HDLC and TG levels associated with significant PAV regression compared with higher non-HDLC and TG levels across all levels of LDLC and C-reactive protein and irrespective of diabetic status (P<0.001 across all comparisons). ΔPAV were more strongly influenced by changes in non-HDLC (β=0.62; P<0.001) compared with changes in LDLC (β=0.51; P<0.001). Kaplan-Meier sensitivity analyses demonstrated significantly greater major adverse cardiovascular event rates in those with higher versus lower non-HDLC and TG levels, with an earlier separation of the non-HDLC compared with the LDLC curve.
Conclusions
Achieved non-HDLC levels seem more closely associated with coronary atheroma progression than LDLC. Plaque progression associates with achieved TGs, but only above levels of 200 mg/dL. These observations support a more prominent role for non-HDLC (and possibly TG) lowering in combating residual cardiovascular risk.
Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial.
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