Fig 1

Atherosclerosis progression by different LPL markers. a, Location of markers. Location of polymorphisms in the LPL gene was assembled from Genbank accession nos. G187209, G34390, M76722, and M76723. Vertical bars represent exons. “Recombinational hotspot” spans the 3′-half of exon 6 and the 5′-half of intron 6, ending approximately at the position of LPL-(TTTA)_n.²⁴ b, Percent subjects with progression of atherosclerosis. Each pair of vertical bars represents two genotype groups for each marker as shown, with the size of each group (N). LPL-D9N and N291S were binned as shown because the low frequency of the rare allele did not permit testing for association. PvuII and HindIII were binned as shown because of previous reports that the effect of these polymorphisms on atherosclerosis is greatest for the 2/2 homozygote.^16,18 There was no association observed when the LPL-PvuII polymorphism was tested using other models and hence alternative binning schemes. LPL-(TTTA)_n was binned as shown because the 4/4 haplotype showed the greatest association with the progression of atherosclerosis in grafts. Complete progression and genotyping data for each marker were available as listed. Genotypes were determined using published methods modified for semiautomated gel electrophoresis (ABI 373, Genescan & Genotyper software, Applied Biosystems, Foster City, CA): D9N,⁴ N291S,⁹ PvuII (“1” = site present, “2” = site absent),³¹ (TTTA)_n (allele 1 is 119bp, 2 = 123bp, 3 = 127bp, 4 = 131bp, 5 = 135bp),³² HindIII (intron 8; “1” = site present, “2” = site absent).³³ “X” denotes “other” genotypes. Allele frequencies were in Hardy-Weinberg equilibrium for each marker. Percent of subjects with atherosclerosis progression is defined in Methods. c, Odds Ratios for Progression. ORs for progression of atherosclerosis in grafts post-CABG with 95%CI are given for each polymorphism.