Advanced nuclear imaging reveals that cardiac sympathetic dysfunction in diabetes correlates with reduced endothelial-dependent vasodilatation, potentially driving the progression of diabetic cardiomyopathy.
Cardiac sympathetic dysfunction may underlie endothelial impairment in diabetes; leaves open whether targeted interventions alter cardiomyopathy progression.
A key problem in ischemia-induced impairment of the vascular performance of the diabetic heart is the often-unrecognized cardiac sympathetic dysfunction. Advanced single-photon emission computed tomography (SPECT) and positron emission tomography (PET) using the radiopharmaceuticals, (123)I-metaiodobenzylguanidine ((123)I-MIBG) and (11)C-hydroxyephedrine ((11)C-HED), have shown that dysfunction of cardiac sympathetic nerves is present to a large extent in both type 1 and type 2 diabetes. The pattern of sympathetic disturbances is heterogeneous with a predominant effect in the posterior myocardial region. Furthermore, myocardial blood flow assessment with PET has shown that endothelial-dependent vasodilatation is reduced in proportion to the magnitude of cardiac sympathetic dysfunction. These mechanisms are currently proposed to lead from early changes to advanced impairment of cardiac function in diabetes.
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Oliver Schnell (2001) studied this question.
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