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Diabetes mellitus is one of the most important cardiovascular risk factors. An increased prevalence of silent or paucisymptomatic myocardial ischaemia has been described in diabetic patients. The authors examined the relationship between glucose metabolism balance and acute ischemic heart disease symptoms in 174 patients: 46 diabetics and 128 non diabetics. Diagnosis of diabetes mellitus was made during admission to hospital in four patients. No differences of strength, length, type, site and radiation of pain between 46 diabetic patients and 128 non diabetics were found. As regards the other symptoms, the authors found that only dyspnoea and palpitations were prevalent in diabetic patients with ten-year or more-disease length. On the other hand, the prevalence of these two symptoms was not different between non diabetics and diabetics with less than ten-year-disease length.

Accelerated atherosclerosis occurs in patients with type III hyperlipoproteinemia and familial hypercholesterolemia. The accumulation of chylomicron remnants of intestinal origin and of VLDL remnants or IDL of hepatic origin observed in type III hyperlipoproteinemia appears to correlate with coronary disease. The presence of defective forms of Apo E prevents normal receptor-mediated catabolism of these lipoproteins. Patients with familial hypercholesterolemia have an elevation of plasma IDL secondary to defective LDL receptors that impair normal catabolism. Familial defective Apo B100 is secondary to an abnormality of Apo B100 that prevents the normal interaction of LDL with the LDL receptor and increases plasma LDL. Macrophages (which are derived from circulating monocytes) have emerged as a key component in atherogenesis because they appear to be progenitors of foam cells in arterial lesions. Macrophages express receptors that recognize chylomicron remnants and VLDL remnants and chemically modified LDL. Thus, in the presence of these specific lipoproteins, macrophages are converted to cells that resemble foam cells.

In this review we have concentrated on the ways in which modification of LDL structure may account for foam cell formation. We have presented in vivo evidence as well as in vitro evidence supporting the proposition that modification of native LDL is a prerequisite for foam cell formation and atherogenesis. If further research supports the importance of LDL modification in atherogenesis, a whole new array of possibilities opens itself to us for intervention. At the moment, the only intervention that appears to be feasible is prevention of LDL oxidation; conceivably we might be able to interfere with the aggregation of LDL with itself or with other complexes in the artery wall that appear also to favor initiation of the atherogenic process.