Abstract
Perlecan is one of the three major classes of heparan sulfate proteoglycans (HSPGs) within the cardiovascular system; it interacts with lipid metabolism by binding to lipoprotein lipase (LpL) and apolipoprotein B (apo B) and may be related to vascular disease. We explored interactions between an HSPG2 polymorphism (BamHI marker), and apo B and coronary artery disease (CAD) in patients undergoing coronary angiography. The frequencies of the HSPG2 BamHI +/+, +/−, and −/− genotypes were 4.7, 31.7 and 63.6%, respectively, with a ‘+’ allele frequency of 20.6%. The genotype distribution was in Hardy–Weinberg equilibrium ( χ 2=0.669, P>0.05). The +/+homozygotes had the lowest apo B levels (0.74±0.06 g/l, n=36) compared to +/− (0.89±0.03 g/l, n=241) and −/− (0.93±0.02 g/l, n=480) genotypes. Although plasma apo B concentration was the strongest lipid risk factor for significant CAD, the HSPG2 genotypes were not independently associated with the presence of CAD ( P=0.640 in males; P=0.224 in females), with significant CAD ( P=0.764; P=0.110) or with the number of significantly stenosed coronary arteries ( P=0.945; P=0.335). In Australian Caucasians undergoing coronary angiography the HSPG2 BamHI polymorphism is associated with lower circulating apo B but not with the occurrence or severity of CAD. This may be due to HSPG2-mediated alterations in the HSPG2-apo B-LpL system and requires further exploration.
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