Association between QT dispersion and autonomic dysfunction in patients with diabetes mellitus

Abstract

We hypothesized that QT dispersion would be increased in patients with diabetes mellitus and autonomic dysfunction and that QT dispersion would be related to abnormal iodine-123 (I-123) metaiodobenzylguanidine (MIBG) uptake. Patients with diabetes mellitus and autonomic dysfunction have an increased incidence of sudden death. This event may be due to a sympathetic imbalance causing disturbances of repolarization. QT dispersion has recently been demonstrated to reflect dispersion of ventricular refractoriness and is a marker of arrhythmogenic potential. Uptake of I-123 MIBG is a reliable measure of whether the tissue examined receives sympathetic neuronal innervation. Fifty-one diabetic patients and 11 normal subjects were studied. All patients had clinical evaluation for autonomic dysfunction (defined as at least two abnormal heart rate and blood pressure responses to five validated tests). Rest 12-lead electrocardiograms were recorded for measurement of QT dispersion, defined as the longest QT interval minus the shortest QT interval, and corrected for heart rate using Bazett's formula. Visual and quantitative measurements of I-123 MIBG uptake were performed using I-123 MIBG, and technetium-99m sestamibi uptake was used to assess perfusion. Thirty-five diabetic patients had autonomic dysfunction. Corrected QT dispersion was significantly greater in the patients than in the normal subjects (p = 0.02). The I-123 MIBG scores were also significantly greater in patients with than without autonomic dysfunction (p = 0.0004) and in normal subjects (p = 0.008). There was no correlation between QT dispersion and I-123 MIBG uptake score (r = 0.006, p = 0.97). Diabetic patients with autonomic dysfunction have increased QT dispersion and larger I-123 MIBG uptake defects. This finding suggests that such patients have a greater inhomogeneity of repolarization. The lack of correlation between QT dispersion and I-123 MIBG uptake suggests that these abnormalities are mediated by different mechanisms.