Autonomic Nervous System Activity Measured Directly and QT Interval Variability in Normal and Pacing-Induced Tachycardia Heart Failure Dogs

Abstract

Objectives This study sought to find out more about the relationship between sympathetic and vagal nerve activity and the cardiac repolarization in a canine model of pacing-induced tachycardia congestive heart failure (CHF). Background The QT variability index (QTVI), a noninvasive marker of temporal cardiac repolarization dispersion, is among the risk factors for sudden death during CHF. Among factors influencing this variable are the myocardial damage and the autonomic nervous system activity typical of dilated cardiomyopathy. Methods We assessed autonomic nervous system activity recorded from an implanted data transmitter that monitored integrated left stellate-ganglion nervous activity, integrated vagus nerve activity, and electrocardiogram. We collected 36 segments recorded at baseline and 36 after induced CHF. We then arbitrarily identified recording segments as containing low or high sympathetic activity values, and we compared corrected QT intervals and the QTVI under a given sympathetic activity condition at baseline and after inducing CHF. Results In the high sympathetic activity subgroup, both QT variables increased from baseline to CHF (corrected QT intervals, p < 0.01; QTVI, p < 0.05) whereas in the low sympathetic activity subgroup they remained unchanged. The baseline QTVI correlated inversely with integrated vagus nerve activity (r2 = 0.16; β = −0.47; p < 0.05) whereas, during CHF, the QTVI correlated directly with integrated left stellate-ganglion nervous activity (r2 = 0.32; β = 0.27, p < 0.01). Conclusions During 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, no relationship exists between sympathetic activation and the QT variables.

The QT Variability Index and Cardiac Autonomic Modulation: Perspectives from Apparently Healthy Men with Spinal Cord Injury

“…The QT interval characterizes ventricular repolarization, and the RR interval measures SA nodal automaticity, which are affected on a beat-to-beat basis by alterations to autonomic activity [6,18]. Increased QTVI, or a value closer to zero, reflects an unfavorable electrophysiological state that is associated with the development of malignant ventricular arrhythmias and predicts sudden cardiac death in asymptomatic patients with mild or moderate left ventricular systolic dysfunction [12,15,18,19,20,21]. Under these constructs, a given QTVI has been posited to reflect the progression or stage of coronary artery disease [15,16,17,21].…”

Relation between QT interval variability and cardiac sympathetic activity in hypertension

“…Previous studies addressing this issue have provided conflicting results. A recent study in dogs showed that QT variability was related to left stellate-ganglion activity, but only after the dogs had developed heart failure (28). In healthy humans, pharmacological activation or blockade of ␤-adrenoreceptors augmented and reduced QT variability, respectively (23,35).…”

RT variability unrelated to heart period and respiration progressively increases during graded head-up tilt

“…We propose the utilization of the amount of RR-R-unrelated RT variability instead of overall RT variability as an indirect measure of autonomic regulation directed to ventricles. QT measurement; QT variability; QT-RR relationship; modelling; autonomic nervous system THERE IS INCREASING INTEREST in quantifying the amount of the beat-to-beat changes of ventricular repolarization duration (VRD), i.e., VRD variability (2,4,6,12,15,20,27,40). This interest is based on the original suggestion that VRD variability provides an indirect measure of the autonomic regulation directed to ventricles (7).…”

“…THERE IS INCREASING INTEREST in quantifying the amount of the beat-to-beat changes of ventricular repolarization duration (VRD), i.e., VRD variability (2,4,6,12,15,20,27,40). This interest is based on the original suggestion that VRD variability provides an indirect measure of the autonomic regulation directed to ventricles (7).…”