Summary: Some characteristics of 70 men who had experienced myocardial infarction or angina pectoris between 28 and 40 years of age have been compared with those of a normal Australian population at Busselton.
The coronary men were on average slightly shorter. Their weight at maturity had been the same and when first seen after infarction, at a mean age of 36.9 years, their weight was also the same as Busselton men of the same age. At infarction they were slightly heavier than Busselton men. In 30 percent of coronary men relative body weight at infarction was greater than 120 according to the Davenport standards. At Busselton where slightly different standards were used 20 per cent of healthy men aged 30–39 had relative body weight of 120 or more.
The coronary men had hypercholesterolaemia and hyperuricaemia and their dissimilarity from Busselton men was highly significant. The coronary men also had hypertriglyceridaemia and half of them smoked excessively.
The incidence of hypertension was no greater in coronary men than in Busselton men. Oral glucose tolerance tests revealed a possibly higher incidence of frank diabetes mellitus than could have occurred by chance. It was possible that a minor degree of carbohydrate intolerance was present in many of the non‐diabetic subjects.
There was evidence of family aggregation for in half the men there was a family history of coronary heart disease, often fatal, usually in the father or less frequently in the mother before the age of 65.
Serum cholesterol correlated significantly with serum triglycerides and the latter correlated with serum uric acid and body build. The predominant lipoprotein phenotypes were types 2a and 2b which were three times as common as type 4. The findings demonstrate the very strong association between hypercholesterolaemia and coronary heart disease in young people. Collateral evidence indicates that it is the prime determinant of accelerated atherogenesis in the first half of life. The higher the serum cholesterol the sooner the disease is likely to appear. Hypercholesterolaemia may be due in part to genetic predisposition but a high intake of saturated fat and cholesterol is the most important cause.
The high prevalence of gout and hyperuricaemia and their lack of correlation with hypercholesterolaemia raises once again the question whether they are independent risk factors in coronary heart disease.
The evidence from young coronaries supports the case for population screening for serum cholesterol. Evidence from other studies indicates that this should begin early in life. The Inter‐Society Commission in the United States has concluded that there is a strong case for reform of the national diet for all age groups. We suggest that the least that should be done is to identify those at greatest risk at the earliest possible age and to offer them corrective dietary education.
