TY - JOUR
T1 - Major lipids, apolipoproteins, and risk of vascular disease
AU - The Emerging Risk Factors Collaboration
AU - Di Angelantonio, Emanuele
AU - Sarwar, Nadeem
AU - Perry, Philip
AU - Kaptoge, Stephen
AU - Ray, Kausik K.
AU - Thompson, Alexander
AU - Wood, Angela M.
AU - Lewington, Sarah
AU - Sattar, Naveed
AU - Packard, Chris J.
AU - Collins, Rory
AU - Thompson, Simon G.
AU - Danesh, John
AU - Tipping, R. W.
AU - Ford, C. E.
AU - Pressel, S. L.
AU - Walldius, G.
AU - Jungner, I.
AU - Folsom, A. R.
AU - Chambless, L. E.
AU - Panagiotakos, D. B.
AU - Pitsavos, C.
AU - Chrysohoou, C.
AU - Stefanadis, C.
AU - Knuiman, M.
AU - Goldbourt, U.
AU - Benderly, M.
AU - Tanne, D.
AU - Whincup, P. H.
AU - Wannamethee, S. G.
AU - Morris, R. W.
AU - Kiechl, S.
AU - Willeit, J.
AU - Santer, P.
AU - Mayr, A.
AU - Wald, N.
AU - Ebrahim, S.
AU - Lawlor, D. A.
AU - Yarnell, J. W.G.
AU - Gallacher, J.
AU - Casiglia, E.
AU - Tikhonoff, V.
AU - Nietert, P. J.
AU - Sutherland, S. E.
AU - Bachman, D. L.
AU - Keil, J. E.
AU - Cushman, M.
AU - Psaty, B. M.
AU - Tracy, R. P.
AU - Grandits, G.
N1 - Publisher Copyright:
© 2009 American Medical Association. All rights reserved.
PY - 2009/1/1
Y1 - 2009/1/1
N2 - Context: Associations of major lipids and apolipoproteins with the risk of vascular disease have not been reliably quantified. Objective: To assess major lipids and apolipoproteins in vascular risk. Design, Setting, and Participants: Individual records were supplied on 302 430 people without initial vascular disease from 68 long-term prospective studies, mostly in Europe and North America. During 2.79 million person-years of follow-up, there were 8857 nonfatal myocardial infarctions, 3928 coronary heart disease [CHD] deaths, 2534 ischemic strokes, 513 hemorrhagic strokes, and 2536 unclassified strokes. Main Outcome Measures: Hazard ratios (HRs), adjusted for several conventional factors, were calculated for 1-SD higher values: 0.52 loge triglyceride, 15 mg/dL high-density lipoprotein cholesterol (HDL-C), 43 mg/dL non-HDL-C, 29 mg/dL apolipoprotein AI, 29 mg/dL apolipoprotein B, and 33 mg/dL directly measured low-density lipoprotein cholesterol (LDL-C). Within-study regression analyses were adjusted for within-person variation and combined using meta-analysis. Results: The rates of CHD per 1000 person-years in the bottom and top thirds of baseline lipid distributions, respectively, were 2.6 and 6.2 with triglyceride, 6.4 and 2.4 with HDL-C, and 2.3 and 6.7 with non-HDL-C. Adjusted HRs for CHD were 0.99 (95% CI, 0.94-1.05) with triglyceride, 0.78 (95% CI, 0.74-0.82) with HDL-C, and 1.50 (95% CI, 1.39-1.61) with non-HDL-C. Hazard ratios were at least as strong in participants who did not fast as in those who did. The HR for CHD was 0.35 (95% CI, 0.30-0.42) with a combination of 80 mg/dL lower non-HDL-C and 15 mg/dL higher HDL-C. For the subset with apolipoproteins or directly measured LDL-C, HRs were 1.50 (95% CI, 1.38-1.62) with the ratio non-HDL-C/HDL-C, 1.49 (95% CI, 1.39-1.60) with the ratio apo B/apo AI, 1.42 (95% CI, 1.06-1.91) with non-HDL-C, and 1.38 (95% CI, 1.09-1.73) with directly measured LDL-C. Hazard ratios for ischemic stroke were 1.02 (95% CI, 0.94-1.11) with triglyceride, 0.93 (95% CI, 0.84-1.02) with HDL-C, and 1.12 (95% CI, 1.04-1.20) with non-HDL-C. Conclusion: Lipid assessment in vascular disease can be simplified by measurement of either total and HDL cholesterol levels or apolipoproteins without the need to fast and without regard to triglyceride.
AB - Context: Associations of major lipids and apolipoproteins with the risk of vascular disease have not been reliably quantified. Objective: To assess major lipids and apolipoproteins in vascular risk. Design, Setting, and Participants: Individual records were supplied on 302 430 people without initial vascular disease from 68 long-term prospective studies, mostly in Europe and North America. During 2.79 million person-years of follow-up, there were 8857 nonfatal myocardial infarctions, 3928 coronary heart disease [CHD] deaths, 2534 ischemic strokes, 513 hemorrhagic strokes, and 2536 unclassified strokes. Main Outcome Measures: Hazard ratios (HRs), adjusted for several conventional factors, were calculated for 1-SD higher values: 0.52 loge triglyceride, 15 mg/dL high-density lipoprotein cholesterol (HDL-C), 43 mg/dL non-HDL-C, 29 mg/dL apolipoprotein AI, 29 mg/dL apolipoprotein B, and 33 mg/dL directly measured low-density lipoprotein cholesterol (LDL-C). Within-study regression analyses were adjusted for within-person variation and combined using meta-analysis. Results: The rates of CHD per 1000 person-years in the bottom and top thirds of baseline lipid distributions, respectively, were 2.6 and 6.2 with triglyceride, 6.4 and 2.4 with HDL-C, and 2.3 and 6.7 with non-HDL-C. Adjusted HRs for CHD were 0.99 (95% CI, 0.94-1.05) with triglyceride, 0.78 (95% CI, 0.74-0.82) with HDL-C, and 1.50 (95% CI, 1.39-1.61) with non-HDL-C. Hazard ratios were at least as strong in participants who did not fast as in those who did. The HR for CHD was 0.35 (95% CI, 0.30-0.42) with a combination of 80 mg/dL lower non-HDL-C and 15 mg/dL higher HDL-C. For the subset with apolipoproteins or directly measured LDL-C, HRs were 1.50 (95% CI, 1.38-1.62) with the ratio non-HDL-C/HDL-C, 1.49 (95% CI, 1.39-1.60) with the ratio apo B/apo AI, 1.42 (95% CI, 1.06-1.91) with non-HDL-C, and 1.38 (95% CI, 1.09-1.73) with directly measured LDL-C. Hazard ratios for ischemic stroke were 1.02 (95% CI, 0.94-1.11) with triglyceride, 0.93 (95% CI, 0.84-1.02) with HDL-C, and 1.12 (95% CI, 1.04-1.20) with non-HDL-C. Conclusion: Lipid assessment in vascular disease can be simplified by measurement of either total and HDL cholesterol levels or apolipoproteins without the need to fast and without regard to triglyceride.
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U2 - 10.1001/jama.2009.1619
DO - 10.1001/jama.2009.1619
M3 - Article
C2 - 19903920
AN - SCOPUS:70450081001
SN - 0098-7484
VL - 302
SP - 1993
EP - 2000
JO - JAMA
JF - JAMA
IS - 18
ER -