Eduard Tiozzo1, Hannah Gardener2, Barry I Hudson3, Chuanhui Dong4, David Della-Morte5, Milita Crisby6, Ronald B Goldberg7, Mitchell S V Elkind8, Ying Kuen Cheung9, Clinton B Wright10, Ralph L Sacco11, Tatjana Rundek12. 1. Department of Psychiatry and Behavioral Sciences, Miller School of Medicine, University of Miami, Miami, FL, USA. Electronic address: etiozzo@med.miami.edu. 2. Department of Neurology, Miller School of Medicine, University of Miami, Miami, FL, USA. Electronic address: hgardener@med.miami.edu. 3. Division of Endocrinology, Diabetes and Metabolism, University of Miami, Miami, FL, USA. Electronic address: bhudson@med.miami.edu. 4. Department of Neurology, Miller School of Medicine, University of Miami, Miami, FL, USA. Electronic address: cdong@med.miami.edu. 5. Department of Neurology, Miller School of Medicine, University of Miami, Miami, FL, USA; Department of System Medicine, University of Rome Tor Vergata, Rome, Italy; IRCCS San Raffaele Pisana, Rome, Italy. Electronic address: ddellamorte@stroke.med.miami.edu. 6. Karolinska Institute, Department of Neurobiology, Care Sciences and Society, Stockholm, Sweden. Electronic address: milita.crisby@ki.se. 7. Diabetes Research Institute and Lipid Disorder Clinic, University of Miami, Miami, FL, USA. 8. Department of Neurology, Columbia University College of Physicians and Surgeons, New York, NY, USA. Electronic address: mse13@cumc.columbia.edu. 9. Department of Biostatistics, Mailman School of Public Health, Columbia University, New York, NY, USA. Electronic address: yc632@columbia.edu. 10. Department of Neurology, Miller School of Medicine, University of Miami, Miami, FL, USA. Electronic address: cwright@med.miami.edu. 11. Department of Neurology, Miller School of Medicine, University of Miami, Miami, FL, USA. Electronic address: rsacco@med.miami.edu. 12. Department of Neurology, Miller School of Medicine, University of Miami, Miami, FL, USA. Electronic address: trundek@med.miami.edu.
Abstract
OBJECTIVE: The objective of this cross-sectional analysis was to investigate the relation between two major high-density lipoprotein cholesterol (HDL-C) subfractions (HDL2-C and HDL3-C) and carotid plaque in a population based cohort. METHODS: We evaluated 988 stroke-free participants (mean age 66 ± 8 years; 40% men; 66% Hispanic and 34% Non-Hispanic) with available data on HDL subfractions using precipitation method and carotid plaque area and thickness assessed by a high-resolution 2D ultrasound. The associations between HDL-C subfractions and plaque measurements were analyzed by quantile regression. RESULTS: Plaque was present in 56% of the study population. Among those with plaque, the mean ± SD plaque area was 19.40 ± 20.46 mm² and thickness 2.30 ± 4.45 mm. The mean ± SD total HDL-C was 46 ± 14 mg/dl, HDL2-C 14 ± 8 mg/dl, and HDL3-C 32 ± 8 mg/dl. After adjusting for demographics and vascular risk factors, there was an inverse association between HDL3-C and plaque area (per mg/dl: beta = -0.26 at the 75th percentile, p = 0.001 and beta = -0.32 at the 90th percentile, p = 0.02). A positive association was observed between HDL2-C and plaque thickness (per mg/dl; beta = 0.02 at the 90% percentile, p = 0.003). HDL-C was associated with plaque area (per mg/dl: beta = -0.18 at the 90th percentile, p = 0.01), but only among Hispanics. CONCLUSION: In our cohort we observed an inverse association between HDL3-C and plaque area and a positive association between HDL2-C and plaque thickness. HDL-C subfractions may have different contributions to the risk of vascular disease. More studies are needed to fully elucidate HDL-C anti-atherosclerotic functions in order to improve HDL-based treatments in prevention of vascular disease and stroke.
OBJECTIVE: The objective of this cross-sectional analysis was to investigate the relation between two major high-density lipoprotein cholesterol (HDL-C) subfractions (HDL2-C and HDL3-C) and carotid plaque in a population based cohort. METHODS: We evaluated 988 stroke-freeparticipants (mean age 66 ± 8 years; 40% men; 66% Hispanic and 34% Non-Hispanic) with available data on HDL subfractions using precipitation method and carotid plaque area and thickness assessed by a high-resolution 2D ultrasound. The associations between HDL-C subfractions and plaque measurements were analyzed by quantile regression. RESULTS: Plaque was present in 56% of the study population. Among those with plaque, the mean ± SD plaque area was 19.40 ± 20.46 mm² and thickness 2.30 ± 4.45 mm. The mean ± SD total HDL-C was 46 ± 14 mg/dl, HDL2-C 14 ± 8 mg/dl, and HDL3-C 32 ± 8 mg/dl. After adjusting for demographics and vascular risk factors, there was an inverse association between HDL3-C and plaque area (per mg/dl: beta = -0.26 at the 75th percentile, p = 0.001 and beta = -0.32 at the 90th percentile, p = 0.02). A positive association was observed between HDL2-C and plaque thickness (per mg/dl; beta = 0.02 at the 90% percentile, p = 0.003). HDL-C was associated with plaque area (per mg/dl: beta = -0.18 at the 90th percentile, p = 0.01), but only among Hispanics. CONCLUSION: In our cohort we observed an inverse association between HDL3-C and plaque area and a positive association between HDL2-C and plaque thickness. HDL-C subfractions may have different contributions to the risk of vascular disease. More studies are needed to fully elucidate HDL-C anti-atherosclerotic functions in order to improve HDL-based treatments in prevention of vascular disease and stroke.
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