LpA-I, LpA-I:A-II HDL and CHD-risk: The Framingham Offspring Study and the Veterans Affairs HDL Intervention Trial

Bela F. Asztalos; Serkalem Demissie; L. Adrienne Cupples; Dorothea Collins; Caitlin E. Cox; Katalin V. Horvath; Hanna E. Bloomfield; Sander J. Robins; Ernst J. Schaefer

doi:10.1016/j.atherosclerosis.2005.10.018

LpA-I, LpA-I:A-II HDL and CHD-risk: The Framingham Offspring Study and the Veterans Affairs HDL Intervention Trial

Bela F. Asztalos, Serkalem Demissie, L. Adrienne Cupples, Dorothea Collins, Caitlin E. Cox, Katalin V. Horvath, Hanna E. Bloomfield, Sander J. Robins, Ernst J. Schaefer

Medicine - Veteran's Administration Medical Center

Research output: Contribution to journal › Article › peer-review

37 Scopus citations

Abstract

Objective: We tested the hypothesis that concentrations of LpA-I and/or LpA-I:A-II HDL subclasses are significantly associated with CHD prevalence and recurrent cardiovascular events. Methods: LpA-I levels were determined by differential electroimmunoassay in male participants with (n = 169) and without CHD (n = 850) from the Framingham Offspring Study (FOS) and in male participants with CHD from the placebo arm of the Veterans Affairs HDL Intervention Trial (VA-HIT) (n = 741). Data were analyzed cross-sectionally (FOS) and prospectively (VA-HIT) and were adjusted for established lipid and non-lipid CHD risk factors. Results: We observed slightly but significantly higher LpA-I levels in CHD cases compared to all or to HDL-C-matched controls and slightly but significantly higher LpA-I:A-II levels in CHD cases compared to HDL-C-matched controls it the FOS. Neither LpA-I nor LpA-I:A-II levels were significantly different between groups with and without recurrent cardiovascular events in the VA-HIT. No significant differences were observed in LpA-I and LpA-I:A-II levels in low HDL-C (≤40mg/dl) subjects with CHD (VA-HIT, n = 711) and without CHD (FOS, n = 373). Plasma LpA-I concentration had a positive correlation with the large LpA-I HDL particle (α-1) but no correlation with the small LpA-I HDL particle (preβ-1). LpA-I:A-II concentration had a positive correlation with the large (α-2) and an inverse correlation with the small (α-3) LpA-I:A-II HDL particles. Conclusion: Our data do not support the hypothesis that CHD prevalence (FOS) or recurrence of cardiovascular events (VA-HIT) are associated with significant reductions in the concentrations of LpA-I and/or LpA-I:A-II HDL subclasses.

Original language	English (US)
Pages (from-to)	59-67
Number of pages	9
Journal	Atherosclerosis
Volume	188
Issue number	1
DOIs	https://doi.org/10.1016/j.atherosclerosis.2005.10.018
State	Published - Sep 2006

Bibliographical note

Funding Information:
We would like to thank the participants of the Framingham and VA-HIT studies. This study was supported by the NIH/NHLBI (HL-64738 to Bela Asztalos) and by the NHLBI's Framingham Heart Study in collaboration with Boston University (Contract N01-HC-38038 and HL-54776). VA-HIT cohort was supported by the VA Cooperative Studies Program of the Department of Veterans Affairs Office of Research and Development, Washington, DC.

Keywords

ApoA-I
CHD-risk
HDL subpopulations
HDL-C
LpA-I

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10.1016/j.atherosclerosis.2005.10.018

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@article{892e73f2f0db44179137c186067f7728,

title = "LpA-I, LpA-I:A-II HDL and CHD-risk: The Framingham Offspring Study and the Veterans Affairs HDL Intervention Trial",

abstract = "Objective: We tested the hypothesis that concentrations of LpA-I and/or LpA-I:A-II HDL subclasses are significantly associated with CHD prevalence and recurrent cardiovascular events. Methods: LpA-I levels were determined by differential electroimmunoassay in male participants with (n = 169) and without CHD (n = 850) from the Framingham Offspring Study (FOS) and in male participants with CHD from the placebo arm of the Veterans Affairs HDL Intervention Trial (VA-HIT) (n = 741). Data were analyzed cross-sectionally (FOS) and prospectively (VA-HIT) and were adjusted for established lipid and non-lipid CHD risk factors. Results: We observed slightly but significantly higher LpA-I levels in CHD cases compared to all or to HDL-C-matched controls and slightly but significantly higher LpA-I:A-II levels in CHD cases compared to HDL-C-matched controls it the FOS. Neither LpA-I nor LpA-I:A-II levels were significantly different between groups with and without recurrent cardiovascular events in the VA-HIT. No significant differences were observed in LpA-I and LpA-I:A-II levels in low HDL-C (≤40mg/dl) subjects with CHD (VA-HIT, n = 711) and without CHD (FOS, n = 373). Plasma LpA-I concentration had a positive correlation with the large LpA-I HDL particle (α-1) but no correlation with the small LpA-I HDL particle (preβ-1). LpA-I:A-II concentration had a positive correlation with the large (α-2) and an inverse correlation with the small (α-3) LpA-I:A-II HDL particles. Conclusion: Our data do not support the hypothesis that CHD prevalence (FOS) or recurrence of cardiovascular events (VA-HIT) are associated with significant reductions in the concentrations of LpA-I and/or LpA-I:A-II HDL subclasses.",

keywords = "ApoA-I, CHD-risk, HDL subpopulations, HDL-C, LpA-I",

author = "Asztalos, {Bela F.} and Serkalem Demissie and Cupples, {L. Adrienne} and Dorothea Collins and Cox, {Caitlin E.} and Horvath, {Katalin V.} and Bloomfield, {Hanna E.} and Robins, {Sander J.} and Schaefer, {Ernst J.}",

note = "Funding Information: We would like to thank the participants of the Framingham and VA-HIT studies. This study was supported by the NIH/NHLBI (HL-64738 to Bela Asztalos) and by the NHLBI's Framingham Heart Study in collaboration with Boston University (Contract N01-HC-38038 and HL-54776). VA-HIT cohort was supported by the VA Cooperative Studies Program of the Department of Veterans Affairs Office of Research and Development, Washington, DC.",

year = "2006",

month = sep,

doi = "10.1016/j.atherosclerosis.2005.10.018",

language = "English (US)",

volume = "188",

pages = "59--67",

journal = "Atherosclerosis",

issn = "0021-9150",

publisher = "Elsevier Ireland Ltd",

number = "1",

}

TY - JOUR

T1 - LpA-I, LpA-I:A-II HDL and CHD-risk

T2 - The Framingham Offspring Study and the Veterans Affairs HDL Intervention Trial

AU - Asztalos, Bela F.

AU - Demissie, Serkalem

AU - Cupples, L. Adrienne

AU - Collins, Dorothea

AU - Cox, Caitlin E.

AU - Horvath, Katalin V.

AU - Bloomfield, Hanna E.

AU - Robins, Sander J.

AU - Schaefer, Ernst J.

N1 - Funding Information: We would like to thank the participants of the Framingham and VA-HIT studies. This study was supported by the NIH/NHLBI (HL-64738 to Bela Asztalos) and by the NHLBI's Framingham Heart Study in collaboration with Boston University (Contract N01-HC-38038 and HL-54776). VA-HIT cohort was supported by the VA Cooperative Studies Program of the Department of Veterans Affairs Office of Research and Development, Washington, DC.

PY - 2006/9

Y1 - 2006/9

N2 - Objective: We tested the hypothesis that concentrations of LpA-I and/or LpA-I:A-II HDL subclasses are significantly associated with CHD prevalence and recurrent cardiovascular events. Methods: LpA-I levels were determined by differential electroimmunoassay in male participants with (n = 169) and without CHD (n = 850) from the Framingham Offspring Study (FOS) and in male participants with CHD from the placebo arm of the Veterans Affairs HDL Intervention Trial (VA-HIT) (n = 741). Data were analyzed cross-sectionally (FOS) and prospectively (VA-HIT) and were adjusted for established lipid and non-lipid CHD risk factors. Results: We observed slightly but significantly higher LpA-I levels in CHD cases compared to all or to HDL-C-matched controls and slightly but significantly higher LpA-I:A-II levels in CHD cases compared to HDL-C-matched controls it the FOS. Neither LpA-I nor LpA-I:A-II levels were significantly different between groups with and without recurrent cardiovascular events in the VA-HIT. No significant differences were observed in LpA-I and LpA-I:A-II levels in low HDL-C (≤40mg/dl) subjects with CHD (VA-HIT, n = 711) and without CHD (FOS, n = 373). Plasma LpA-I concentration had a positive correlation with the large LpA-I HDL particle (α-1) but no correlation with the small LpA-I HDL particle (preβ-1). LpA-I:A-II concentration had a positive correlation with the large (α-2) and an inverse correlation with the small (α-3) LpA-I:A-II HDL particles. Conclusion: Our data do not support the hypothesis that CHD prevalence (FOS) or recurrence of cardiovascular events (VA-HIT) are associated with significant reductions in the concentrations of LpA-I and/or LpA-I:A-II HDL subclasses.

AB - Objective: We tested the hypothesis that concentrations of LpA-I and/or LpA-I:A-II HDL subclasses are significantly associated with CHD prevalence and recurrent cardiovascular events. Methods: LpA-I levels were determined by differential electroimmunoassay in male participants with (n = 169) and without CHD (n = 850) from the Framingham Offspring Study (FOS) and in male participants with CHD from the placebo arm of the Veterans Affairs HDL Intervention Trial (VA-HIT) (n = 741). Data were analyzed cross-sectionally (FOS) and prospectively (VA-HIT) and were adjusted for established lipid and non-lipid CHD risk factors. Results: We observed slightly but significantly higher LpA-I levels in CHD cases compared to all or to HDL-C-matched controls and slightly but significantly higher LpA-I:A-II levels in CHD cases compared to HDL-C-matched controls it the FOS. Neither LpA-I nor LpA-I:A-II levels were significantly different between groups with and without recurrent cardiovascular events in the VA-HIT. No significant differences were observed in LpA-I and LpA-I:A-II levels in low HDL-C (≤40mg/dl) subjects with CHD (VA-HIT, n = 711) and without CHD (FOS, n = 373). Plasma LpA-I concentration had a positive correlation with the large LpA-I HDL particle (α-1) but no correlation with the small LpA-I HDL particle (preβ-1). LpA-I:A-II concentration had a positive correlation with the large (α-2) and an inverse correlation with the small (α-3) LpA-I:A-II HDL particles. Conclusion: Our data do not support the hypothesis that CHD prevalence (FOS) or recurrence of cardiovascular events (VA-HIT) are associated with significant reductions in the concentrations of LpA-I and/or LpA-I:A-II HDL subclasses.

KW - ApoA-I

KW - CHD-risk

KW - HDL subpopulations

KW - HDL-C

KW - LpA-I

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UR - http://www.scopus.com/inward/citedby.url?scp=33746527110&partnerID=8YFLogxK

U2 - 10.1016/j.atherosclerosis.2005.10.018

DO - 10.1016/j.atherosclerosis.2005.10.018

M3 - Article

C2 - 16298372

AN - SCOPUS:33746527110

SN - 0021-9150

VL - 188

SP - 59

EP - 67

JO - Atherosclerosis

JF - Atherosclerosis

IS - 1

ER -

LpA-I, LpA-I:A-II HDL and CHD-risk: The Framingham Offspring Study and the Veterans Affairs HDL Intervention Trial

Abstract

Bibliographical note

Keywords

Publisher link

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