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03-10-2011 | Diabetes | Article

Poor diastolic function in diabetes not dependent on previously described mechanisms

Abstract

Free abstract

MedWire News: The altered myocardial and microvasculature structure previously described in diabetic heart disease is a consequence rather than a cause of cardiac dysfunction, research suggests.

The impaired diastolic function of Type 2 diabetes is not dependent on increased myocardial fibrosis, carboxymethylysine (CML) expression, cardiomyocyte hypertrophy, or altered microvascular structure, report Duncan Campbell and team (St Vincent's Institute of Medical Research, Fitzroy, Australia) in the journal Cardiovascular Diabetology.

The researchers performed a histologic analysis of left ventricular biopsies from 46 men undergoing coronary artery bypass graft surgery. Ten of the men had diabetes, 23 had the metabolic syndrome (MetS), and 13 had neither condition (control group).

The men did not have heart failure or atrial fibrillation, had not received loop diuretic therapy, and did not have evidence of previous myocardial infarction.

The authors found that patients with diabetes and MetS patients had higher pulmonary pressures than the control participants and patients with diabetes had reduced mitral diastolic peak velocity of the septal mitral annulus, confirming the impaired diastolic function of Type 2 diabetes and MetS patients.

The authors also found that total and interstitial fibrosis were similar for the three groups and that perivascular fibrosis of MetS and patients with diabetes was less than in control patients.

Total collagen I was lower in patients with diabetes than for MetS patients, but collagen III and the collagen I/collagen III ratio were similar in the three groups.

Cardiomyocyte width, capillary length density, diffusion radius, and arteriolar wall area/circumference ratio also did not differ among the three groups.

Immunostaining revealed no differences in the expression of either CML or advanced glycation end-products (AGE) receptors.

Campbell and co-authors found that, although the duration of diabetes ranged from 0 to 30 years, myocardial structure, microvasculature, and AGE/AGE receptor expression were not correlated with diabetes duration.

In addition, fasting plasma glucose, fasting plasma insulin concentrations, and insulin resistance, as measured by the homeostasis model assessment, were not correlated with these parameters.

The authors say their study highlights possible differences between diabetes in humans and animal models.

"In addition to the lack of increased myocardial fibrosis, we found no evidence for the cardiomyocyte and arteriolar hypertrophy and reduced myocardial capillary density reported in animal models of diabetes, which may be related to poorer diabetic control in animal models," explains the team.

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By Sally Robertson