Nj. Samani et al., APOLIPOPROTEIN-E POLYMORPHISM DOES NOT PREDICT RISK OF RESTENOSIS AFTER CORONARY ANGIOPLASTY, Atherosclerosis, 125(2), 1996, pp. 209-216
A recent report has suggested that the E4 allele of apolipoprotein (ap
o) E increases the risk of restenosis after percutaneous transluminal
coronary angioplasty (PTCA) and also that it interacts synergistically
with the deletion (D) allele of the angiotensin-converting enzyme (AC
E) to increase the risk sixteen-fold. To investigate this further, we
genotyped 231 subjects with successful PTCA who underwent planned repe
at angiography at 4 months to assess the degree of restenosis. Subject
s carrying the apo E4 allele (n = 71) were well matched with non-carri
ers (n = 160) for clinical and pre- and post-PTCA angiographic feature
s. We found no increase in either apo E4 allele frequency (18.4% versu
s 15.6%,; P = 0.42) or apo E4 homozygosity (2/106 versus 5/125, P = 0.
30) in those with restenosis compared with those without. The relative
risk of restenosis for apo E4 carriers was 1.11 (95% CI = 0.87-1.42).
In apo E4 carriers, restenosis frequency was similar in those also ca
rrying the ACE D allele and those without (28/55 (50.9%) versus 9/16 (
56.2%), P = 0.71) and there was no significant increase in restenosis
risk in carriers of both the apo E4 and ACE D alleles compared to the
rest (odds ratio 1.30, 95% CI 0.68-2.50, P = 0.39). We conclude that i
n our cohort, the apo E4 allele does not either independently or actin
g synergistically with the ACE D allele increase the risk of restenosi
s after PTCA, and that apo E genotyping will not be a useful predictor
of risk before the procedure.