Diabetic Cardiomyopathy

It has been over 30 years since Rubler et al. (1) described four diabetic patients with congestive heart failure (CHF), normal coronary arteries, and no other etiologies for CHF and proposed that it was due to diabetic cardiomyopathy. Eight years ago, I reviewed the evidence for diabetic cardiomyopathy as a unique entity unassociated with coronary artery disease and concluded that diabetic cardiomyopathy was a distinct entity characterized by diastolic dysfunction, which was rarely clinically apparent unless associated with hypertension (when it was likely to become clinically apparent) and/or with myocardial ischemia (when it was likely to present with severe clinical manifestations) (2). At that time the evidence also suggested that diastolic dysfunction was due to myocellular hypertrophy and myocardial fibrosis, and at the cellular level there were defects in calcium transportation, myocardial contractile protein collagen formation, and fatty acid metabolism (2). Since then we have learned that diabetic cardiomyopathy is not a rare condition but instead a very common one, and that its etiology is largely due to hyperglycemia with contributions from the insulin resistance syndrome that cause left ventricular hypertrophy.

Left ventricular diastolic dysfunction is characterized by impairment in early diastolic filling, prolongation of isovolumetric relaxation, and increased atrial filling, and these characteristics have even been documented in young type 1 diabetic patients (3). Older studies (4–6) of well-controlled type 2 diabetic subjects showed that 30% had diastolic dysfunction. However, this prevalence was based on standard echocardiography testing, in which mild and early diastolic dysfunction is not …