Markers of risk in young offspring with paternal history of myocardial infarction.

Coronary heart disease clusters within families, but there may be several reasons for this phenomenon to occur. A possible way to elucidate this is to study biological relatives of affected individuals. The aim of our study was thus to compare a number of clinical, metabolic, clotting and immunologic factors between offspring with paternal history of premature myocardial infarction and controls and to propose a model which could safely allow to identify the high risk subgroup among them. Sixty-nine offspring of both sexes mean age 18.1 years old (cases) and thirty-two frequency matched relative to age and gender controls were studied. Cases compared to controls had significantly increased diastolic blood pressure levels (74.0+/-9.9 vs. 67.4+/-8.3 mmHg, P=0.002), leptin plasma levels (11.8+/-10.8 vs. 6.8+/-3 ng/ml, P=0.046) and fibrinogen, plasminogen, fibrin degradation products and plasminogen activator inhibitor-1 plasma levels (306.6+/-52.5 vs. 280.6+/-28.9 mg%, P=0.03, 97.4+/-23.5 vs. 83.6+/-15 mg%, P=0.0007, 292.0+/-148.5 vs. 219.2+/-69.4 ng/ml, P=0.036, 14.7+/-5.3 vs. 8.7+/-3.1 I.U./ml, P=0.0001, respectively), while cases had significantly decreased HDL-cholesterol serum levels (45.9+/-12.5 vs. 50.5+/-8.8 mg%, P=0.03) and protein S plasma levels (89.9+/-17.5 vs. 101.3+/-13.7%, P=0.001). Our findings suggest that offspring of affected individuals may be considered as a high risk group for cardiovascular disease.