Relationships between lipoprotein components and risk of myocardial infarction: age, gender and short versus longer follow-up periods in the Apolipoprotein MOrtality RISk study (AMORIS)
机构:
Karolinska Inst, Dept Med, Clin Epidemiol Unit, Stockholm, Sweden
CALAB Res, Stockholm, SwedenUllevaal Univ Hosp, Ctr Prevent Med, Dept Prevent Cardiol, N-0407 Oslo, Norway
Jungner, I.
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Walldius, G.
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机构:
Karolinska Inst, King Gustaf V Res Inst, Stockholm, Sweden
AstraZeneca Sverige AB, Sodertalje, SwedenUllevaal Univ Hosp, Ctr Prevent Med, Dept Prevent Cardiol, N-0407 Oslo, Norway
Objectives. Examine and compare lipoprotein components associated with fatal and nonfatal acute myocardial infarction (AMI) by time period in the Apolipoprotein MOrtality RISk (AMORIS) Study. Design. Prospective follow-up study of nonfatal and fatal myocardial infarction through linkage with Swedish hospital discharge and Swedish mortality registers. Setting. Measurements of lipoprotein components from health check-ups in the larger Stockholm area. Subjects. The AMORIS subjects (n = 149 121) free of AMI at blood sampling were followed from 1985 to 2002 with respect to n = 6794 first cases of AMI. Results. Hazard ratios of nonfatal and fatal AMI by lipoprotein parameters were highly significant and about equally strong in both genders. Apolipoprotein B (apoB), nonhigh density cholesterol and low density cholesterol predicted nonfatal AMI (NFAMI) better than fatal AMI, but high density cholesterol or apolipoprotein A-1 did not. Atherogenic components were weaker predictors after 1997 than before. In multivariate analyses apoB/apoA-1 was a better predictor than TC/HDL-C. ApoB/apoA-1 added clinically significant information to TC/HDL-C in men as reflected by a net reclassification improvement (NRI) of 9.4% (P < 0.0001). Conclusion. ApoB, apoB/apoA-1 and non-HDL-C were found about equally predictive with LDL-C being slightly less, but multivariate analyses showed apoB/apoA-1 to be the strongest predictor. Attenuation of prediction ability between nonfatal and fatal AMI may be due to modern treatment of CHD after a NFAMI and attenuation of hazard ratios after 1997 may be due to selection of lower risk subjects surviving to 1997.