than for total serum cholesterol and apalipoprotein
A-1. This association is maintained from low to
high values and was independent of cholesterol
levels with a earrelation coefficient between serum
cholesterol and apo (a) of only 0.06.
Lipoprotein (a) concentration is high!ygenetically
determined. [23] . Our investigation has validated
previous findings ofhigher mean apo (a) values for
persons with a family history of coronary artery
disease, suggesting that lipoprotein (a) may
contribute significantly to the genetics of coronary
artery disease. [24]. The main clinical utility of
measuring lipoprotein (a) may therefore be in
families with premature coronary artery disease
without other known risk factors. Under these
circumstances it may be justifiable to reduce even
normal LDL-cholesterol values in order to reduce
the additional absolute risk in these families. Most
studies have shown that diet and most cholesterol
lowering drugs do not have a significant effect on
Lp(a) concentration. [21]
The moleeular basis for the association between
lipoprotein (a) and coronary artery disease is yet to
be foundalthoughlipoprotein (a) has beensuggested
as the missing !ink between the atherogenesis and
thrombogenesis because ofthe structural homology
of apalipoprotein (a) and plasminogen. [25]. Two
other prospective studies have not verified that
lipoprotein (a) is an independent risk factor, so
Lp(a) continues to confuse and mistify. [26, 27].
We didnot perform apalipoprotein Ephenotyping
in this survey but retrospective case control studies
have indicated that apo E4 carriesan increased risk
of coronary artery disease compared to apo E3,
whereas apo E2/3 heterozygosity may be protective
against coronary artery disease. [28]. In a subgroup
of 316 healthy leelanders we campared the E
phenotypes to the levels ofknownrisk factors (total
cholesterol, apo-A-
I
and apo (a)), andwe found that
the phenotype E2/3 had roughly half the relative
risk ofdeveloping coronary arterydisease compared
to those of the phenotype E3/4, based on the levels
of these risk factors. [29]. However, this needs to
be verified in a prospective study before it can be
concluded that apo-E phenotyping is of any
additional value to the estimate of risk for coronary
heart disease more so than cholesterol,
triglycerides and HDL-cholesterol. However, such
an apo-E phenotyping is of course of clinical utility
in the detection of dislipidemia, such as type
III,
52
common!y due to E2/2 homozygosity.
The future utility of apalipoprotein measurements
in estimating coronary heart disease risk depends
therefore most!y on the availability of standardized
methods and the feasibility of such measurements
compared to LDL-cholesterol andespecially HDL–
cholesterol. [11]. Such measurements have the
advantage of being obtained directly in analysis
and not calculated indirectly using the Friedewald
formula, as is the case for LDL-cholesterol or de–
pendent on precipitation of apo-B containing
lipoproteins as for HDL-cholesterol concentration.
At present some researchers would, however,
conclude that most routine laboratories would
benefit more from concentrating on improving the
cholesterol and HDL methodology rather than set–
ting up apalipoprotein assays. [15].
References
l.
Durrington PN, Hunt L, Ishola M, Kane
J,
Stephens WP.
Serum apalipoproteins Al and B and lipoproteins in middle
aged men with and without previous myocardial infarction.
Br Heart
J
1986; 56: 206-12.
2. Barbir M, Wile D, Trayner I, Aber VR, Thompson GR.
High prevalence ofhypertriglyceridaemia and apolipoprotein
abnorrnalities in coronary artery disease. Br Heart
J
1988;
60: 397-403.
3. Naito HK. The association of serum lipids, lipoproteins,
and apalipoproteins with coronary artery disease assessed
by coronary arteriography. Ann N Y Acad Sci 1985; 454:
230-8.
4. Sniderman A, Shapiro S, Marpole D, Skinner B, Teng B,
Kwiterovich PO, Jr. Association ofcoronary atherosclerosis
with hyperapobetalipopro-teinemia (increased protein but
normal cholesterollevels in human plasma low density (B)
lipoproteins]. Proc Nall Acad Sci 1980; 77: 604-8.
5. Whayne TF, Alaupovic P, Curry MD, Lee ET, Anderson
PS, Schechter E. Plasma apalipoprotein B and VLDL-,
LDL-, and HDL-cholesterol as risk factors in thedevelopment
of coronary heart disease in male patients examined by
angiography . Atherosclerosis 1981; 39: 411-24.
6. Jauhiainen M, Metso
J,
Ehnholm C. A comparison of RIA
and ELISA methods for Lp(a) quantitation. 55'b Meeting of
the European Atherosclerosis Society (EAS). Control of
blood cholesterol. Brugge, Belgium, May 1990: 42.
7. Wang XL, Dudman NPB, Biades BL, Wilcken DEL.
Changes in the immunoreactivity ofApo A-I duringstorage.
Clin Chim Acta 1989; 179: 285-94.
8. Bachorik PS, Kwiterovich PO,
Jr.
Apalipoprotein
measurements in clinical biochemistry and their utility vis–
a-vis conventional assays. Clin Chim Acta 1988; 178: 1-34.
9. Cox D.R. Regression models and Iife tables . J Stat Soc
1972; 34(series B): 187-220.
10. Durrington PN, Bolton CH, Hartog M. Serum and
lipoprotein apalipoprotein B levels in normal subjects and
patients with hyperlipoproteinaemia. C!in Chem Acta 1978;
82: 151-60.
Klinisk kemi
i
Nordefl
2,
1994
