Premature coronary heart disease: the influence of positive family history on platelet activity in vivo in children and adolescents (family study).

Abstract

Hypercoagulative disturbances are an integral part of atherosclerosis. The estimation of beta-thromboglobulin (BTG) concentrations in the offspring of parents suffering from premature coronary heart disease (CHD) makes it possible to evaluate platelet activity in vivo in this high-risk group. The study included 292 individuals. BTG concentrations in platelet-poor plasma were estimated in 90 offspring (60 boys and 30 girls, aged 7-18 years) of fathers who had experienced a premature infarct (aged 45 years or younger) and in their parents (the main group, n = 185). All the participants were tested under their usual living conditions. Fifty-nine healthy children and adolescents of the same age with no family history of vascular events, diabetes or hypertension, together with their parents, formed the control group (n = 107). The mean BTG level in the main group was significantly elevated (86.04 +/- 8.14 ng/ml in the boys and 75.57 +/- 8.55 ng/ml in the girls), when compared with the values for their respective controls (49.30 +/- 3.54 ng/ml and 52.56 +/- 3.42 ng/ml, P < 0.001 and P < 0.005). High BTG levels (higher than the 95th percentile in the controls) were observed in 33.3 +/- 6.1% of the boys and in 23.3 +/- 7.7% of the girls in the main group. Twelve months later, a follow-up study of 16 offspring from the main group and 12 from the control group demonstrated that the increase in BTG levels in children and adolescents with infarction heredity over those observed in children without such a background was sustained (85.86 +/- 16.88 ng/ml compared with 75.90 +/- 14.02 ng/ml, P > 0.5). Significantly raised levels of BTG were also detected in the wives of men who had experienced premature infarcts, when these women were compared with respective controls (86.13 +/- 9.85 ng/ml and 45.04 +/- 4.82 ng/ml, P < 0.0001). Spontaneous platelet activation in vivo under normal living conditions was observed in a considerable proportion of children and adolescents with a family history of premature CHD. This activation is expected to constitute an endogenous risk-factor and is probably one of the mechanisms by which atherosclerosis advances before it becomes clinically apparent.