Advanced glycation end-products in myocardium-supported vessels: effects of heart failure and diabetes mellitus.

Background: Disturbed glucose metabolism, particularly in diabetes, is an important but not the sole factor leading to advanced glycation end-product (AGE) formation. The AGE amount and its distribution in cardiopathic myocardial tissues in the presence or absence of diabetes are not well documented. The aim of this study was to assess AGE deposition in unaffected myocardial vessels in heart failure patients with and without diabetes mellitus type 2 (DM2) undergoing transplantation.

Methods: The following groups were established: 14 hearts harvested from subjects with ischemic cardiopathy and DM2; 8 hearts from subjects with dilated cardiopathy with DM2; 67 hearts from subjects with ischemic cardiopathy; 47 hearts from subjects with dilated cardiopathy; and 14 hearts from autopsy cases with diagnosed DM2. A control group consisted of 20 heart donors. AGE localization was determined immunohistochemically in tissue sections. A semi-quantitative scale was used to assess reaction intensity in arteries, arterioles, capillaries, venules and veins.

Results: Both types of cardiomyopathy increased AGE accumulation in intramyocardial veins more than in arteries. The presence of DM2 significantly increased AGE in arterioles and capillaries, especially when coexisting with cardiomyopathy. The type of cardiopathy did not influence the pattern of AGE accumulation in myocardial vessels.

Conclusion: Both chronic heart failure and DM2 intensified AGE pathology and changed the susceptibility of myocardial vasculature to glycation. However, chronic heart failure increases AGE deposition mostly in veins, whereas DM2 predisposes arterioles to AGE accumulation.