[Optimising the equilibrium of diabetes and atheromatous progression: myth or reality?]

Is chronic hyperglycaemia, which defines diabetes of whatever type, a simple marker of cardiovascular risk, with no effect on atheroma independent of the other factors with which it is associated such as dyslipidaelia or hypertension? Whatever the case, its treatment, although fundamental for preventing the progression of microangiopathy and neuropathy, has another significance regarding the progression of atheromatous disease. Chronic hyperglycaemia acts as an independent factor for the genesis and progression of atheromatous disease and the beneficial effect of treating it aggressively could add to that obtained by treatment of the classic atherogenic factors such as hypercholesterolaemia or hypertension. This controversy, renewed by the interpretation of the UKPDS results, still remains. There is also a 2nd question: how does chronic hyperglycaemia, which is generally well evaluated in the medium term by HbA1c, overlap with other physiological situations? In particular, does post-prandial hyperglycaemia have greater atherogenic effects than the same level of fasting hyperglycaemia? Whatever the case, greater attention must be paid to post-prandial glycaemic control, which has been rather neglected up to now in favour of fasting glycaemic control, taken to mean overall glycaemic control.