[Metabolic considerations in the treatment of coronary disease in diabetic patients].
Coronary heart disease represents the first cause of death in diabetic patients. The poor outcome of this ischemic disease is multifactorial. The abnormalities in myocardial energy metabolism encountered by the diabetic heart explain both the ischemic severity and the worsening of reperfusion lesions. The metabolic abnormalities in diabetic heart consist in both an impairment of glucose metabolism (diminished glucose uptake, reduced glycolysis, decreased glucose oxidation...) and an increase in fatty acid oxidation. During ischemia, glucose oxidation is reduced and anaerobic glycolysis becomes the main ATP substrate. Lactate accumulate in myocardial cells, inducing both a metabolic acidosis and an intracellular calcium overload. During reperfusion, intracellular homeostasis is restored very slowly in diabetic heart. Several therapeutic approaches are used to correct these metabolic disturbances. Glucose--insulin--potassium infusion in acute myocardial infarction leads to a significant reduction in the mortality relative risk in diabetic patients (ECLA and DIGAMI studies). The benefit is greater in diabetic patients who where non-insulin-treated prior to ischemia followed by myocardial reperfusion therapy. Others more direct pharmacological approaches improve glucose oxidation during myocardial ischaemia and myocardial reperfusion. The reference drug remains trimetazidine for which one of the fundamental mechanism of action was discovered recently. This specific metabolic, non haemodynamic approach, complete the gold-standard treatment of coronary heart disease in diabetic patients (e.g. aspirin, beta-blockers, ACE inhibitors and statins).
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Service de Cardiologie B, Hôpital A. de Villeneuve, CHU de Montpellier, 371, avenue du Doyen G. Giraud, 34295 Montpellier. c-piot@chu-montpellier.fr
D003327:Coronary Disease / Q000378:metabolism* / Q000401:mortality / Q000628:therapy*; D003925:Diabetic Angiopathies / Q000378:metabolism* / Q000628:therapy*; D004734:Energy Metabolism; D006801:Humans; D017202:Myocardial Ischemia / Q000209:etiology; D015425:Myocardial Reperfusion