Type 2 diabetes is by far the most common form of diabetes mellitus, and is estimated to reach epidemic proportions within the next 20 years. Diabetes is now considered an inflammatory, atherothrombotic, insulin resistance syndrome. Genetic predisposition may be important but the dominant factors seem to be the environmental triggers: diet, lifestyle, and ageing.

Atherosclerosis is the most persistent threat to the diabetic patient. Cardiovascular risk is particularly high, with ischaemic heart disease and stroke claiming the lives of 2–4 times as many people as in the non-diabetic population; also, more symptomatic forms of peripheral arterial disease are present in people with diabetes.

The optimal approach for diabetes management should be multifactorial and aggressive. It is just as important to achieve tight glycaemic control in order to limit microvascular disease, as it is to intervene against concomitant risk factors (hypertension, dyslipidaemia, obesity, smoking, etc) to stop atherosclerotic disease progression. Promotion of better patient lifestyle (exercise and diet) is also important.

Symptomatic and high risk cardiac patients may need revascularisation procedures, aimed at reducing ischaemic complications and improving quality of life, with an expected favourable impact on prognosis.

ATHEROSCLEROTIC BURDEN IN DIABETICS

Physicians facing the problem of selecting the revascularisation option in diabetics need to consider the global atherosclerotic burden, which may play the most important role in prognosis.

Activation of hyperglycaemia, excess free fatty acid release, and insulin resistance impair endothelial function in diabetes. By decreasing nitric oxide and increasing endothelin-1 and angiotensin II concentrations, both vascular tone and vascular smooth muscle cell growth and migration are increased. The activation of transcription factors induces inflammatory gene expression and increased production of inflammatory cytokines. Moreover, the increased production of tissue factor and plasminogen activator inhibitor-1 creates a prothrombotic milieu, while decreased endothelium derived nitric oxide and prostacyclin favours platelet activation. All these mechanisms lead to …