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The concept of a “diabetic cardiomyopathy” has been invoked to explain the higher than expected occurrence of congestive heart failure (CHF) in subjects with diabetes (1,2). However, the evidence supporting the existence of such a condition in humans is mostly inferential. Cardiomyopathies are chronic diseases of the myocardium in which the heart is abnormally enlarged, thickened, and/or stiffened. The weakened heart muscle has a reduced ability to pump blood effectively. Diabetic cardiomyopathy is frequently considered to be present when there is any abnormality of myocardial diastolic or systolic function, even when very mild, in a diabetic subject (or animal) without known hypertension or coronary artery disease. Isolated metabolic or biochemical abnormalities in the heart have also been taken as evidence of this entity. It has been referred to as a “specific” cardiomyopathy that may include features such as left ventricular (LV) hypertrophy, myocardial fibrosis, altered myocardial energetics, and variable degrees of myocardial mechanical dysfunction.There is some controversy about the existence and/or nature of a diabetic cardiomyopathy because there are inconsistencies in the definition of the syndrome, there is a high reliance on findings in small animal models, there are problems with referral bias in many clinical studies, and there is a lack of prospective or longitudinal human studies (3,4). It may be argued that the simple criteria frequently used to characterize this condition are not adequate for defining a cardiomyopathy. The structural, mechanical, histological, and biochemical features mentioned above also are not specific to one disease state. Rather they are common features of nearly all myocardial diseases. Inclusion of type 2 diabetic patients in studies of diabetic cardiomyopathy is problematic because it is very difficult to separate the cardiovascular effects of obesity and diabetes. If we draw …

Diabetes and the Heart: Is There Objective Evidence of a Human Diabetic Cardiomyopathy?