Source identification of QT interval changes in diabetic patients

Abstract

We acquired experimental 12‐lead ECG and developed a hearttorso computer model to simulate 12‐lead ECG to 1) reproduce QT interval prolongation seen in diabetic patients, and 2) describe a possible mechanism of QT interval prolongation by linking QT interval to regional cardiac sympathetic denervation at the cellular level in the model. Twelve‐lead ECG were acquired in 11 able‐bodied subjects (AB), 7 diabetics without (D0), 7 diabetics with mild (D1) and 8 diabetics with severe (D2) neuropathy. Heart rate‐corrected QT interval (QTc) was computed. Action potentials were modeled phenomena logically. Twelve‐lead ECG were produced as forward solutions from equivalent cardiac source. Different patterns of regional denervation taken from previous studies of cardiac images of diabetic patients, guided the simulation of pathological changes, generating 12‐lead ECG from every trial. The minimum QTc interval from the lateral leads was longer in D2 than in AB. Prolonging action potential duration (APD) in the basal septal region in the model produced ECG and QT interval similar to that of D2 subjects. We conclude that minimum QTc interval of lateral leads was more diagnostic than that from other leads. The simulation suggested that QT interval prolongation in our diabetic patients with neuropathy may have been due to APD prolongation in basal septal region, secondary to sympathetic denervation in this region. This study was supported by NIH RO1 NS39774, Kentucky NASA EPSCOR WKU 52611, UK GCRC USPHS grant M01RR02602, and the University of Kentucky Center for Clinical and Translational Sciences.