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Diabetes Slows Nerve Recovery After Heart Transplant

Understanding Nerve Abnormalities May Guide Treatment Aimed at Reducing Cardiac Risk With Diabetes Mellitus Patients

Diabetes has a detrimental effect on a person’s ability to recover from a heart transplant, notes a study in the September Journal of Nuclear Medicine.

“Using positron emission tomography (PET) and the transplanted heart as a very specific model to study the regenerative capacity of the heart’s sympathetic nervous system, we determined that reinnervation—or the heart’s ability to develop new nerves to replace damaged ones—is slower in diabetic patients,” said Frank M. Bengel, a visiting associate professor of radiology and the director of cardiovascular nuclear medicine at Johns Hopkins Medicine’s Russell H. Morgan Department of Radiology and Radiological Science in Baltimore, Md. “Our results confirm a detrimental effect of diabetes on the potential for recovery of sympathetic nerve fibers of the heart,” added the co-author of “Effect of Diabetes Mellitus on Sympathetic Neuronal Regeneration Studied in the Model of Transplant Reinnervation.”

“A better understanding of the importance of nervous system abnormalities and an imaging technique to precisely characterize nerve damage may be of value to guide future therapeutic efforts aimed at reducing cardiac risk with diabetes mellitus patients,” explained Bengel, who was an associate professor at the Technical University of Munich, where the study was performed, prior to his move to Johns Hopkins. “Even if a transplant recipient is suffering from diabetes, there is still a chance for reinnervation—just at a slower speed,” he added. “Unfortunately, there are no techniques developed yet that speed the nerve regeneration process,” he said.

Currently, nuclear medicine techniques (such as PET) are the only imaging techniques that can measure the presence and function of the sympathetic nervous system of the heart, said Bengel. “There are invasive methods that allow for the measurement of neurotransmitters released to the blood, offering indirect conclusions about the presence, storage and release of neurotransmitters from neurons. These methods require complicated and laborious sampling of blood from coronary arteries and veins,” he added.

Diabetes mellitus is a chronic disease that occurs when the pancreas does not produce enough insulin or when the body cannot effectively use the insulin it produces. Such a deficiency results in increased concentrations of glucose (sugar) in the blood, which can damage many of the body’s systems. Diabetes mellitus is a known major risk factor of heart disease, negatively affecting the heart’s contraction and rhythm, said Bengel.

Future research will need to focus on how regeneration of sympathetic nerves can be facilitated and how changes of the sympathetic nerve integrity in the heart are interrelated with changes of prognosis and outcome of diseases like diabetes mellitus, said Bengel.

“Effect of Diabetes Mellitus on Sympathetic Neuronal Regeneration Studied in the Model of Transplant Reinnervation” appears in the September issue of the Journal of Nuclear Medicine, which is published by SNM. Other co-authors include Peter Ueberfuhr and Bruno Reichart, Ludwig-Maximilians University in Munich, Germany; and Dominik Schäfer, Stephan G. Nekolla and Markus Schwaiger, all with the Technical University of Munich, Germany.

Maryann Verrillo | EurekAlert!
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