In 98 children from 98 kindreds, 49 with and 49 without parental premature myocardial infarction (age ≤45 y), our specific aim was to determine whether, and to what degree, lipoprotein(a) [Lp(a)] and other atherogenic lipids and lipoproteins might be overexpressed in children from premature infarction kindreds. Median Lp(a) (270 mg/L) in case boys was nearly twice that in control boys (140 mg/L) (p ≤ 0.001). In a logistic regression model including age, Quctelet index (relative ponderosity), Lp(a), apo Al, apo B, triglyceride, and pubcrtal status, the 24 case boys had higher Lp(a) (p = 0.03), higher triglyceride (p = 0.036), and marginally lower apo Al (p = 0.06) than the 26 control boys. Median Lp(a) in case girls (200 mg/L) was much higher than in control girls (150 mg/L) (p ≤ 0.01). In a logistic regression model including age, Quetelet index, Lp(a), apo Al, apo B, triglyceride, and menarchal status, Lp(a) was higher (p = 0.02), apo B was marginally higher (p = 0.07), and apo Al was lower (p = 0.008) in 25 case girls than in 23 control girls. Reflecting familial clustering of major lipid-lipoprotein risk factors for coronary heart disease, children from kindreds with premature parental myocardial infarction were distinguished from children from control kindreds by high Lp(a) and also had higher apo B and triglyceride and lower apo Al levels.