New concepts in the therapy of diabetic cardiopathies

Most reasonable cause of diabetic cardiopathy might be the impaired energy fuel supply and metabolism producing inevitably a hypotic condition and needing myocardial cytoprotection. Under diabetic conditions glucose disposal of the heart muscle-decreases, but working myocardial cell remains penetrable for glucose even in the absence of insulin. Therefore, it is worth to stimulate aerobic glycolysis to protect diabetic heart from frequent ischaemic events induced by diabetic late complications, since fatty acids oxidation wastes more oxygen than glycolysis for ATP production. Trimetazidine has an original cytoprotective mode of action reducing oxygen demand without altering heart activity. Consequently, trimetazidine protects structure and functions of the ischemic myocardial cell. On the other hand, glycation and altered turnover of proteins play also an important role in the development of diabetic cardiopathy. Consequently, not only trimetazidine but aminoguanidine could also reduce the development of alterations in diabetic cardiopathy inhibiting the glycation of proteins. Finally, calcium antagonists are also very usefull in myocardial cytoprotection of the diabetic heart, according to the altered cellular calcium regulation and a calcium overload which play the main role in the development of diabetic cardiopathy.