Circulation, Vol 84, 153-159, Copyright © 1991 by American Heart Association
C Fievet, MC Nuttens, P Ducimetiere, JC Fruchart, M Bertrand and JL Salomez
BACKGROUND. This study was designed to investigate the relation of a
molecular analysis of apolipoprotein B (apoB)-containing atherogenic
lipoprotein particles to coronary artery disease (CAD) in middle-aged men.
METHODS AND RESULTS. Two groups of men were studied. The first consisted of
97 patients with angiographically documented CAD (greater than 50% stenosis
of at least one coronary artery). The second group consisted of 145
subjects without symptomatic CAD, who served as controls. In both groups,
measurements were obtained for total cholesterol level, triglyceride level,
cholesterol contents in apoB- and nonapoB-containing particles (LpB,
LpnonB), total apoB and apolipoprotein AI (apoAI levels), lipoprotein
particles recognized by monoclonal antibodies anti-apoB (LpBL3, LpBL5,
LpBL7) and anti-apoAI (LpAI-2GII). Taking into account age, body mass
index, hypertension, diabetes, smoking habits, and drug consumption, the
analysis showed that the mean levels of cholesterol were identical in both
groups but differed when cholesterol content in LpB and LpnonB subfractions
were assessed, thus reflecting an increase in the low density fraction and
a decrease in the high density fraction, respectively. This was confirmed
by an increase in total apoB and a decrease in total apoAI. Measurements of
LpBL3, LpBL5, LpBL7, and LpAI-2GII particles also discriminated between the
two groups. After adjustment for cholesterol content in LpnonB particles, a
difference in total apoB was no longer significant between groups, whereas
LpBL3, LpBL5, and LpBL7 levels remained significantly higher in CAD
patients. CONCLUSIONS. The measurement of separate concentrations of apoB
in different particles may permit a more-accurate assessment of CAD risk
than measurements of total apoB levels.
ARTICLES
Relation of arteriographically defined coronary artery disease to serum lipoprotein particles mapped with monoclonal antibodies
Unite INSERM 325, Institute Pasteur, Monica Lille.
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