AIM: Schoolchildren aged 10-11 with a family history of premature coronary artery disease (CAD), were examined in order to identify children with genetically determined dyslipidemias and a combination of risk factors. METHODS: A total of 4000 questionnaires were distributed by the school; 55% of the families answered and returned the questionnaire. Blood lipids, apolipoprotein B, and Lp(a) lipoprotein were analysed in high risk children and their parents. RESULTS: A family history of premature CAD in parents or grandparents was identified in 208 families; 175 agreed to take part in a clinical examination and laboratory tests. Normal blood lipid tests were found in 89 children. Another 48 had an isolated increase of Lp(a) lipoprotein of minor clinical importance. Of the remaining 38 children, 23 had non-hereditary abnormalities of low (LDL) or high density lipoprotein (HDL) cholesterol or apolipoprotein B. Fifteen children were suspected to have genetically determined dyslipidemias or a combination of risk factors: in four, possible familial hypercholesterolaemia (FH); in five, possible familial combined hyperlipidaemia; in three, hereditary low HDL cholesterol; and in three a combination of high LDL cholesterol and Lp(a) lipoprotein concentrations. In addition, possible FH was detected in eight of the parents. CONCLUSION: It is worthwhile asking parents about the occurrence of premature CAD among their child's closest relatives.
AIM: Schoolchildren aged 10-11 with a family history of premature coronary artery disease (CAD), were examined in order to identify children with genetically determined dyslipidemias and a combination of risk factors. METHODS: A total of 4000 questionnaires were distributed by the school; 55% of the families answered and returned the questionnaire. Blood lipids, apolipoprotein B, and Lp(a) lipoprotein were analysed in high risk children and their parents. RESULTS: A family history of premature CAD in parents or grandparents was identified in 208 families; 175 agreed to take part in a clinical examination and laboratory tests. Normal blood lipid tests were found in 89 children. Another 48 had an isolated increase of Lp(a) lipoprotein of minor clinical importance. Of the remaining 38 children, 23 had non-hereditary abnormalities of low (LDL) or high density lipoprotein (HDL) cholesterol or apolipoprotein B. Fifteen children were suspected to have genetically determined dyslipidemias or a combination of risk factors: in four, possible familial hypercholesterolaemia (FH); in five, possible familial combined hyperlipidaemia; in three, hereditary low HDL cholesterol; and in three a combination of high LDL cholesterol and Lp(a) lipoprotein concentrations. In addition, possible FH was detected in eight of the parents. CONCLUSION: It is worthwhile asking parents about the occurrence of premature CAD among their child's closest relatives.
Authors: J J Genest; S S Martin-Munley; J R McNamara; J M Ordovas; J Jenner; R H Myers; S R Silberman; P W Wilson; D N Salem; E J Schaefer Journal: Circulation Date: 1992-06 Impact factor: 29.690