EVALUATION OF QT INTERVAL LENGTH, QT DISPERSION AND MYOCARDIAL M-IODOBENZYLGUANIDINE UPTAKE IN INSULIN-DEPENDENT DIABETIC-PATIENTS WITH ANDWITHOUT AUTONOMIC NEUROPATHY

1. An association has been reported between QT interval abnormalities and cardiovascular autonomic neuropathy in diabetic patients. The QT i nterval abnormalities reflect local inhomogeneities of ventricular rec overy time and may be related to an imbalance in cardiac sympathetic i nnervation. Sympathetic innervation of the heart can be visualized and quantified by single-photon emission-computed tomography,vith m-[I-12 3] iodobenzylguanidine. In this study we evaluated cardiac sympathetic integrity by m-[I-123] iodobenzylguanidine imaging and the relationsh ip between both QT interval prolongation and QT dispersion from standa rd 12-lead ECG variables and m-[I-123] iodobenzylguanidine uptake in i nsulin-dependent diabetic patients. 2. Three patient groups were studi ed, comprising six healthy control subjects, nine diabetic patients wi thout cardiovascular autonomic neuropathy (CAN -) and 12 diabetic pati ents with cardiovascular neuropathy (CAN+). Resting 12-lead ECG was re corded for measurement of maximal QT interval and QT dispersion. The Q T interval was heart rate corrected using Bazett's formula (QTc) and t he Karjalainen approach (QTk). Quantitative measurement (in counts/min per g) and visual defect pattern of m-[I-123] iodobenzylguanidine upt ake were performed using m-[I-123] iodobenzylguanidine single-photo em ission-computed tomography. 3. Global myocardial m-[I-123] iodobenzylg uanidine uptake was significantly reduced in both diabetic patient gro ups compared with control subjects. The visual defect score of m-[I-12 3] iodobenzylguanidine uptake was significantly higher in CAN+ diabeti c patients than in control subjects and in CAN- patients. This score w as not significantly different between control subjects and CAN- patie nts. QTc interval and QT dispersion were significantly increased in CA N+ diabetic patients as compared with control subjects (QTc: 432 +/- 1 5 ms versus 404 +/- 19 ms, P<0.05; QT dispersion: 42 +/- 10 versus 28 +/- 8 ms, P<0.05). QT dispersion was also significantly longer in CAN- diabetic patients than in control subjects (41 +/- 9 ms versus 28 +/- 8 ms, P<0.05). QTc interval was significantly related to global myocar dial m-[I-123] iodobenzylguanidine uptake and defect score in diabetic (r = -0.648, P<0.01, and r = 0.527, P<0.05, respectively). There was no correlation between QT dispersion and both m-[I-123] iodobenzylguan idine uptake measures. 4. In conclusion, these findings suggest that m -[I-123] iodobenzylguanidine imaging is a valuable tool for the detect ion of early alterations in myocardial sympathetic innervation in long -term diabetic patients without cardiovascular autonomic neuropathy. I nsulin-dependent diabetic patients with cardiovascular autonomic neuro pathy have a delayed cardiac repolarization and increased variability of ventricular refractoriness. The cardiac sympathetic nervous system seems to be one of the determinants of QT interval lengthening, but do es not appear to be involved in dispersion of ventricular recovery tim e. It is assumed that QT dispersion is based on more complex electroph ysiological mechanisms which remain to be elucidated.