Lipoprotein(a) and apolipoproteins B and A-1 in children and coronary vascular events in their grandparents.
Because premature coronary vascular disease in a first-degree relative increases risk of the disease and the mechanisms may include genetically determined abnormal levels of circulating apolipoproteins, we explored the relationships between schoolchildren's apolipoprotein levels and coronary events in their parents and grandparents. We measured capillary blood concentrations of lipoprotein(a) (Lp(a) and apolipoproteins (apo B and apo A-1) in dried blood spot samples obtained by finger prick from 2010 schoolchildren aged 8 to 12 years, and questioned parents about coronary vascular events in the children's parents and grandparents. Of the 2010 questionnaires sent, 1030 (51%) were returned fully completed. Twenty-three fathers, one mother, and 645 grandparents had had coronary vascular events. There were significant associations between increased Lp(a) levels in children and the numbers of grandparents with coronary vascular events and with increasing grandparent coronary history scores (p < 0.01). There were also positive associations for apo B (p < 0.01) but none for apo A-1. Discriminate analysis showed that the log-transformed Lp(a) level was the variable most predictive of event numbers and of history scores in grandparents (Wilks lambda value = 0.984; p = 0.026); the apo B level was also predictive (Wilks lambda value = 0.988; p = 0.041), but neither the apo A-1 level nor the apo B/A-1 ratio was. We conclude that high Lp(a) and apo B levels in children aged 8 to 12 years are associated with increased risk of coronary vascular disease in older family members, even with a generation gap. These apolipoproteins may largely account for the independent contribution of family history to disease risk. Measurements of Lp(a) and apo B in schoolchildren may help to identify children and their families at increased risk and may facilitate targeting of prevention.
Wilcken
D E
DE
Department of Cardiovascular Medicine, University of New South Wales, Sydney, Australia.
Wang
X L
XL
Greenwood
J
J
Lynch
J
J
D000328:Adult; D000368:Aged; D016632:Apolipoprotein A-I / Q000032:analysis*; D001055:Apolipoproteins B / Q000032:analysis*; D002648:Child; D003327:Coronary Disease / Q000453:epidemiology / Q000235:genetics*; D005260:Female; D006801:Humans; D017270:Lipoprotein(a) / Q000097:blood*; D008297:Male; D008487:Medical History Taking; D008875:Middle Aged; D015999:Multivariate Analysis; D010865:Pilot Projects; D012307:Risk Factors; D011795:Surveys and Questionnaires
D016632:Apolipoprotein A-I; D001055:Apolipoproteins B; D017270:Lipoprotein(a)