Different Role of Advanced Glycation End Products in Pathology of Transplanted Heart in Patients With or Without Diabetes Mellitus Type 2

Acute Heart Transplant Graft Failure in Association with Hyperosmolar Hyperglycemia State

“…Animal experiments showed that hyperglycemia and insulin resistance induce abnormal myocardial contractility and endothelial dysfunction at the cellular level with interstitial fibrosis and myocardial deposition of glycated end‐products and oxidative stress. This may injure the proteins myelin and tubulin, as well as the extracellular matrix proteins‐collagens Type I, II, IV, and VI, laminin and elastin causing LV chamber stiffness and diastolic dysfunction . Long‐term survival for the transplanted patient is also reduced in DM by 33% over 10 years.…”

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

“…21 We assumed that the lack of AGE in CAV-affected arteries might be a result of the high cell turnover-a part of the process of vascular remodeling based on the proliferative thickening of the intimal layer. 22 With this analogy, we can speculate that AGE accumulation in veins of the failing heart may be a marker of the deteriorating ability to replace aging cells with new ones.…”

Risk factors of cardiac allograft vasculopathy

“…Similar observations regarding the lack of the impact of type 2 diabetes on CAV development were made by Zakliczyński et al . [ 31 ]. Due to ambiguous data on the impact of diabetes on the development of vasculopathy, there is a need for further studies that will define the role of diabetes in CAV development.…”

“…Markers of insulin resistance, defined as TG/HDL ratio ≥ 3, and CRP level in excess of 3 mg/l of insulin can also lead to endothelial dysfunction and CAV development [ 1 , 31 ]. The significant correlation between markers of insulin resistance and systemic inflammation suggests a pathophysiological link between immuno-inflammatory activation and insulin resistance.…”