Atherogenic Lipoprotein Subfractions Determined by Ion Mobility and First Cardiovascular Events After Random Allocation to High-Intensity Statin or Placebo
Autor: | Samia Mora, Paul M. Ridker, Jay Wohlgemuth, Robert J. Glynn, Charles M. Rowland, Zhihong Chen, H.Robert Superko, Michael P. Caulfield, Ronald M. Krauss |
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Rok vydání: | 2015 |
Předmět: |
medicine.medical_specialty
Statin Apolipoprotein B medicine.drug_class Population chemistry.chemical_compound Physiology (medical) Internal medicine JUPITER trial Medicine Rosuvastatin education education.field_of_study biology business.industry Cholesterol Rosuvastatin Calcium Endocrinology chemistry biology.protein Cardiology lipids (amino acids peptides and proteins) Cardiology and Cardiovascular Medicine business medicine.drug Lipoprotein |
Zdroj: | Circulation. 132:2220-2229 |
ISSN: | 1524-4539 0009-7322 |
DOI: | 10.1161/circulationaha.115.016857 |
Popis: | Background— Cardiovascular disease (CVD) can occur in individuals with low low-density lipoprotein (LDL) cholesterol (LDL-C). We investigated whether detailed measures of LDL subfractions and other lipoproteins can be used to assess CVD risk in a population with both low LDL-C and high C-reactive protein who were randomized to high-intensity statin or placebo. Methods and Results— In 11 186 Justification for the Use of Statins in Prevention: An Intervention Trial Evaluating Rosuvastatin (JUPITER) participants, we tested whether lipids, apolipoproteins, and ion mobility–measured particle concentrations at baseline and after random allocation to rosuvastatin 20 mg/d or placebo were associated with first CVD events (n=307) or CVD/all-cause death (n=522). In placebo-allocated participants, baseline LDL-C was not associated with CVD (adjusted hazard ratio [HR] per SD, 1.03; 95% confidence interval [CI], 0.88–1.21). In contrast, associations with CVD events were observed for baseline non–high-density lipoprotein (HDL) cholesterol (HR, 1.18; 95% CI, 1.01–1.38), apolipoprotein B (HR, 1.28; 95% CI, 1.11–1.48), and ion mobility–measured non-HDL particles (HR, 1.19; 95% CI, 1.05–1.35) and LDL particles (HR, 1.21; 95% CI, 1.07–1.37). Association with CVD events was also observed for several LDL and very-low-density lipoprotein subfractions but not for ion mobility–measured HDL subfractions. In statin-allocated participants, CVD events were associated with on-treatment LDL-C, non-HDL cholesterol, and apolipoprotein B; these were also associated with CVD/all-cause death, as were several LDL and very-low-density lipoprotein subfractions, albeit with a pattern of association that differed from the baseline risk. Conclusions— In JUPITER, baseline LDL-C was not associated with CVD events, in contrast with significant associations for non-HDL cholesterol and atherogenic particles: apolipoprotein B and ion mobility–measured non-HDL particles, LDL particles, and select subfractions of very-low-density lipoprotein particles and LDL particles. During high-intensity statin therapy, on-treatment levels of LDL-C and atherogenic particles were associated with residual risk of CVD/all-cause death. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT00239681. |
Databáze: | OpenAIRE |
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