The prevalence of the metabolic syndrome of cardiovascular risk factors is increasing in many parts of the world

Atheromatous changes lead to impaired arterial relaxation due to reduced production of nitric oxide, a potent vasodilator; insulin resistance per se may be associated with endothelial dysfunction. Diabetes mellitus is also associated with hypercoagulability, the procoagulant changes on the endothelial surface favouring thrombosis. Platelet-rich thrombus in the coronary arteries is unstable and likely to rupture, causing acute coronary occlusion. Plaque in patients with diabetes may be particularly vulnerable to rupture due to a high inflammatory cell content and other adverse components.

The explanation for the continuing poor prognosis in the diabetic patient may lie, in part, in the secretion of counter-regulatory hormones that ensue after acute myocardial infarction; these result in adverse changes in cellular metabolism that are exacerbated by diabetes (see Chapter 1). Hyperglycaemia - secondary to acutely exacerbated insulin resistance and insulin deficiency - is accompanied by acceleration of adipocyte lipolysis, the latter resulting in release of non-esterified fatty acids (NEFAs). Myocardial glucose uptake and metabolism are reduced by insulin deficiency. Under these circumstances, the oxygen consumption of the ischaemic myocardium is increased by reliance on NEFA oxidation; this results in myocardial dysfunction that can be reduced if cellular glucose uptake and metabolism can be improved (see below). A

chronic diabetic cardiomyopathy has also been described, which may contribute to the excess risk of heart failure after myocardial infarction in diabetic patients; the literature suggests that the size of infarcts is no greater among patients with diabetes.

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