Prostacyclin and thromboxane A2 levels in children and adolescents with an inherited predisposition to coronary heart disease: a family study.

The aim of this study was to trace the possible mechanisms of premature atherosclerosis in its early stages and to expand our knowledge of the genetic structure of an inherited predisposition to coronary heart disease (CHD) by monitoring of TXA2 and PGI2 levels in the children of fathers who have suffered a premature myocardial infarction. Prostacyclin (PGI2) and thromboxane A2 (TXA2) levels were estimated by radioimmunoassay in 90 children (aged 7-18 years) of fathers who had suffered premature infarction and in both their parents (the 'main' group, n = 191), and in 59 of their healthy contemporaries with no family history of ischaemic events, hypertension, or diabetes, and both their parents (the 'control' group, n = 110). Sons of early infarction patients presented an average TXA2 level of 158.94 +/- 16.60 pg/ml (versus 86.88 +/- 12.71 pg/ml in the control group, P < 0.001), and daughters presented an average TXA2 level of 230.13 +/- 33.68 pg/ml (versus 69.67 +/- 14.99 pg/ml in the control group, P < 0.001). This hyperproduction was independent of the children's sex and could not be attributed to health problems. A significant increase (two-fold) of PGI2 in the boys but not in the girls of the main group was noted. Daughters of infarction patients had significantly higher levels of TXA2 than PGI2. The wives of early infarction patients presented a significantly higher level of both TXA2 and PGI2 (two and three times the level in the control group, P < 0.02 and P < 0.05, respectively). Spontaneous TXA2 hyperproduction is intrinsic among children with an inherited propensity for CHD and is strongly determined by genetic factors, which is evident from the structure of in-family phenotypic correlations of PGI2 and TXA2 levels.