Autonomic nervous system Activity Measured Directly and QT-Interval Variability in Normal and Pacing-Induced Tachycardia Heart Failure Dogs.

BACKGROUND- The QT variability index (QTVI), a noninvasive marker of temporal cardiac repolarization dispersion, is among the risk factors for sudden death during congestive heart failure (CHF). Among factors influencing the duration and temporal dispersion of cardiac repolarization are the myocardial damage and the autonomic nervous system activity typical of dilated cardiomyopathy. In this study, to find out more about relationship between sympathetic and vagal nerve activity and the cardiac repolarization, we measured QTVI in a canine model of pacing-induced tachycardia CHF. METHODS and RESULTS- Using the data previous recorded in 6 ambulatory dogs before and after pacing-induced tachycardia CHF, we assessed autonomic nervous system activity recorded from an implanted data transmitter that monitored integrated left stellate-ganglion nervous activity (iSGNA), integrate vagus nerve activity (iVNA), and electrocardiogram (ECG). We selected for analysis 36 segments recorded at baseline and 36 after induced CHF. We then arbitrarily identified recording segments as containing low or high sympathetic activity values according to whether they contained more than or less than or equal to the 50th percentile of sympathetic activity, and we compared corrected QT intervals and the QTVI under a given sympathetic activity condition at baseline and after inducing CHF. In the high sympathetic activity subgroup, both QT variables increased significantly from baseline to CHF (corrected QTs, p<0.01; QTVI, p<0.05) whereas in the low sympathetic activity group they remained unchanged. The baseline QTVI correlated inversely with iVNA (r2: 0.16; b: -0.47; p<0.05) whereas, during CHF, the QTVI correlated directly with iSGNA (r2: 0.32; b: 0.27, p<0.01). CONCLUSIONS- In a canine model of pacing-induced tachycardia CHF, sympathetic activation is associated with an increase in the QT interval and QTVI. Because these changes vary over time, they could result from myocardial structural damage and sympathetic activation combined. Conversely, under normal conditions, when myocardial damage is missing, no relationship exists between sympathetic activation and the QT interval or QTVI.