Diabetic cardiomyopathy is a disease process which affects the myocardium (heart muscle) in diabetic patients, causing a wide range of structural abnormalities and eventually leading to left ventricular hypertrophy and diastolic and systolic dysfunction, which is an impairment in the ability of the heart to eject blood. In diabetic cardiomyopathy, diabetes leads to changes at the cellular level and structural abnormalities. In patients with diabetes, hyperglycaemia, hyperlipidaemia, and increased reactive oxygen species induce alteration in downstream transcription factors, which results in changes in gene expression, myocyte growth, myocardial substrate utilization, endothelial function and myocardial compliance. In diabetic cardiomyopathy, hyperglycaemia causes excess formation of mitochondrial reactive oxygen species, which affects transcription, leading to contractile dysfunction.
After the development of systolic dysfunction, left ventricular dilation and symptomatic heart failure, the jugular venous pressure may become elevated, the apical impulse would be displaced downward and to the left. Systolic mitral murmur is not uncommon in these cases. These changes are accompanied by a variety of electrocardiographic changes that may be associated with diabetic cardiomyopathy in 60% of patients without structural heart disease, although usually not in the early asymptomatic phase. Later in the progression, a prolonged QT interval may be indicative of fibrosis. About 50% of diabetics with DCM show pathologic evidence for microangiopathy such as sub-endothelial and endothelial fibrosis, compared to only 21% of non-diabetic heart failure patients. Over the years, several hypotheses were postulated to explain the endothelial dysfunction observed in diabetes. It was hypothesized that the extracellular hyperglycemia leads to an intracellular hyperglycemia in cells unable to regulate their glucose uptake, most predominantly, endothelial cells. Indeed, while hepatocytes and myocytes have mechanisms allowing them to internalize their glucose transporter, endothelial cells do not possess this ability.
At present, there is not a single clinically effective treatment for diabetic cardiomyopathy. Treatment centers around intense glycemic control through diet, oral hypoglycemics and frequently insulin and management of heart failure symptoms. There is a clear correlation between increased glycemia and risk of developing diabetic cardiomyopathy, therefore, keeping glucose concentrations as controlled as possible is paramount. Thiazolidinediones are not recommended in patients with NYHA Class III or IV heart failure secondary to fluid retention.