Lp(a) and apoE polymorphisms in young South African Indians with myocardial infarction : cardiovascular topics
2004
Summary
The lipoprotein(a) [Lp(a)] and apolipoprotein E (apoE)
polymorphisms have been shown to be important genetic
determinants of cardiovascular risk. Their effect on
coronary heart disease (CHD) is less clear, particularly
in Asian Indians who are at high risk for this disease. The aim of this study was to examine the association
of the Lp(a) promoter pentanucleotide repeat polymorphism
and the apoE codon 112 and 158 genotypes in 195
young South African Indian patients (lugll/ug 45 years) with
myocardial infarction (MI). Results were compared with
300 healthy age-matched control subjects drawn from
the same community and 107 unaffected siblings (18-45
years). In addition, fasting lipograms were performed
on all patients and a detailed history of conventional
risk factors and family background was obtained. Of the six different Lp(a) alleles detected, the 8-repeat
sequence was most frequently seen. However, no difference
in frequencies existed between patient and control
groups. The most frequently occurring apoE genotype
in the three study groups was E3/E3 (patients 71%;
siblings 70%; controls 70%). A significant difference
in the E3/E4 genotype was seen between patients and
controls (23% vs 14%; lIgpl/Ig = 0.018) and between siblings
and controls (24% vs 14%; lIgpl/Ig = 0.027). These patients
were also more likely to have significantly higher lowdensity
lipoprotein (LDL) and lower high-density lipoprotein
(HDL) levels (lIgpl/Ig = 0.005 and 0.045, respectively).
No association was observed between any of the Lp(a)
or apoE genotypes and conventional risk factors such
as smoking, diabetes, hypertension, obesity or a family
history of CHD. In conclusion, the apoE3/E4 genotype is strongly
associated with the incidence of myocardial infarction
in young South African Indians. This genotype also
adversely affects LDL and HDL cholesterol levels,
both of which contribute to premature atherosclerosis.
In contrast, the Lp(a) pentanucleotide repeat polymorphism
does not appear to have any aetiological role in
MI in this population.
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