Structural changes in the myocardium during diabetes-induced cardiomyopathy

Diabetes mellitus (DM) is a major metabolic disorder currently affecting over 250 million people globally. It costs the worldwide health services almost £800 billion annually to diagnose, treat and care for patients with diabetes. DM is predicted to rise to 350 million by 2030. If left unmanaged, DM can lead to numerous long-term complications including micro- and macro-angiopathy and heart failure (HF). Most diabetics usually die as a result of HF resulting from diabetes-induced coronary artery disease and cardiomyopathy. Coronary artery disease and cardiomyopathy are normally preceded by hyperglycaemia (HG). This review examines the structural changes, which occur within the myocardium and cardiomyocytes during exposure of the heart to diabetes-induced HG and HG-induced oxidative stress. HG and the resulting oxidative stress are associated with marked myocardial hypertrophy and fibrosis compared to control heart. At the ultrastructural level, cardiomyocytes subjected to chronic HG and subsequent oxidative stress display swollen mitochondria, reduced mitochondrial number and defective myofibrils and intercalated discs. Evidence from many studies shows that both type 1 and type 2 diabetes-induced HG can cause myocardial fibrosis, mitochondriopathy, myocyte hypertrophy and deranged myofibrils. All of these structural changes may eventually result in HF if left untreated.