Although each LDL partide carries one
apalipoprotein B molecule, the amount of
cholesterol carried, can vary widely. Therefore the
concentration of apalipoprotein B is a guide to the
number of LDL particles, but does not accurately
indicate the amount assimilated by the arterial wall
through these lipoproteins.
Sniderman and Durrington and their respective
colleagues suggested that apalipoprotein B is a
significant risk factor that is stronger than total
serum cholesterol.
[l,
4]. However, as the authors
pointed out, these investigationswere retrospective
case control studies and needed prospective studies
forverification. Our resulls are also consistent with
the recent resulls of the Physicians Health Study
[12].
However, Brown et al [13] showed in atherapeutic
trial that coronary artery disease regression was
associated with a reduction in apo-B levels, which
fell concomitantly with LDL-cholesterol concent–
ration. But similarlythe strong earrelation between
apo-B and LDL-cholesterol wouldseem to preclude
its ability to identify coronary candirlates better
than a LDL-cholesterol concentration.
However, measuring apalipoprotein B may be
easier than measuring LDL-cholesterol by
precipitation or ultracentrifugation. [11].
Our results indicate therefore that the concent–
ration of apo-B does not have greater predictive
power than measuring total serum cholesterol con–
centration, in men at least. Kwiterovich et al [14]
concluded from a retrospective study that apo-B
concentration might be of more importance in
women but that needs to be verified in a prospective
study.
The main reason for assaying apo-8 in clinical
practice may however be in the determination of
CHD risk ·in type IV hyperlipoproteinemia. [15].
There seems to be a little doubt that there are some
patients with hypertriglyceridemia who have
relative!ynormal serum cholesterollevels andLDL–
cholesterollevels, but whose LDL-level proves to
be raised when serum apo-8 is measured. [16].
Even in the most severe type IV hyperlipo–
proteinemia, more than 90% of apo B is in the LDL.
[10]. Apo-8 immunoassay may therefore be of
helpin determining how vigorously to treat apa–
tient with hypertriglyceridemia with only border–
line elevation of serum cholesterol.
Our study showed a strong negative association
Klinisk Umi
i
Norden
2,
1994
between coronary artery disease and apo-A-1 ron–
centration, similar to what has been shown in
smaller prospective studies. [17]. One percent
reduction in apo-A-I levels seems to increase the
risk of a coronary artery disease, by 2%, which is
similar finding as other studies have revealed using
HDL-cholesterol measurements, whereas the 2%
increase in total serum cholesterol increases the
risk similarly by 2%. [18].
Apo-A-I is about 75% of the protein portion of
high density lipoprotein, and activates the enzyme
lecithin cholesteryl acyl transferase LCAT, which
catal yses the estrification of cholesterol to
cholesterylester. ApalipoproteinA-I interacts with
a putative HDL receptor at the cell surface,
facililating the removal and transport of cholesterol
from peripheral cells back to the liver-the reverse
cholesterol transport. [19].
We, and others have found a close earrelation
between apalipoprotein A-I and HDL-cholesterol
concentrations (0.7-0.85) [11], although the latter
was not measured in this prospective survey.
However, since apo-A-I and HDL-cholesterol
correlate so closely and have similar protective
power, they are Iikely to have equal predictive
power for assessing the risk of coronary artery
disease. The measurement of choice therefore
depends rather on methodological feasibility.
We have calculated that if the concentration of
apo-A-I could be raised from the present mean
values in leelandie men to a leve! at the 80th
percentile of the distribution the risk would be
reduced by about 30 percent This level of apo-A-
1 is similar to what is found in women and would
suggest that the sex difference in terms of coronory
artery disease incidence could be explained
substantially by different levels in apo-A-I and
presurnably HDL-cholesterol concentration.
In case control studies serum lipoprotein (a) has
been closely associated with CHD risk. [20, 21].
However, only one prospective case control study
of limited size had been published [22] where apo
(a) was found to be significant risk factor in
univariate analysis. Our investigatibn has
prospective!y validated the findingthat apo (a) and
presurnably lipoprotein (a) is a significant indepen–
dent risk factor for coronary artery disease in men.
The power of this relationship appears however, to
be similar to that for systolic blood pressure and
serum triglycerides levels and significantly less
51
