ELN and diabetic cardiomyopathy: This finding is in accordance with the hypotheses of increased myocardial stiffness, increased resting myocyte tension and deposition of advanced glycated end products associated with diabetic cardiomyopathy; In fact, intracellular hyperglycemia is at basis of formation of advanced-glycated end products (AGEs) as collagen, elastin and other connective tissue proteins [31] which produce myocardial fibrosis resulting in diastolic dysfunction.