Like father like son? Sons of patients of European or Indian origin with coronary artery disease reflect their parents' risk factor patterns.

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Abstract
OBJECTIVE--To investigate the extent to which risk factor patterns associated with coronary artery disease (CAD) in patients of Indian origin and in those of North European origin undergoing coronary angiography for suspected angina were reflected in their apparently healthy sons aged 15-30 years. DESIGN--Prospective study in which risk markers were measured in patients of Indian origin and in matched European patients undergoing angiography and in their sons. SETTING--Patients attending a regional cardiac centre and their families. PATIENTS--102 consecutive male patients of Indian origin undergoing diagnostic coronary angiography for suspected angina and 89 of their sons aged between 15 and 30 years; 102 age matched male European patients and 82 sons. MAIN OUTCOME MEASURES--Father son correlations for risk markers predicting the severity of parental CAD; differences in mean levels of these markers between young males of Indian origin and those of North European origin. RESULTS--Lp(a) lipoprotein, total cholesterol, and serum insulin were independent predictors of the severity of CAD in patients of Indian origin and in those of North European origin. In both groups, there was strong correlation between paternal and filial serum insulin (r = 0.41 Indian origin, r = 0.49 North European, P < 0.001), Lp(a) lipoprotein (r = 0.44 Indian origin, r = 0.48 North European, P < 0.001), and total cholesterol (r = 0.39 Indian origin, r = 0.45 North European, P < 0.001) concentrations, and the risk factor profiles of the sons were predictive of CAD severity in their fathers. Sons of patients of Indian origin had significantly higher serum insulin (Indian origin 14.3 mU/l v North European 8.4 mU/l, P = 0.002) and Lp(a) lipoprotein (Indian origin 19.1 mmol/l v North European 10.5 mmol/l, P = 0.001) concentrations than sons of patients of North European origin. CONCLUSIONS--Apparently healthy young men aged 15-30 years from either ethnic community already reflect risk marker patterns associated with coronary artery disease in their parents, both for genetically determined factors such as Lp(a) lipoprotein and environmentally influenced factors such as insulin and cholesterol. Health promotion measures aimed at reducing the prevalence of CAD should include the adolescent and young adult populations, particularly those with a family history of CAD, or who are from ethnic communities in which this diagnosis is prevalent.