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.
|Number of pages||11|
|Journal||Journal of the American College of Cardiology|
|Publication status||Published - 2009 Aug 25|
Bibliographical noteFunding Information:
This study was supported in part by National Institutes of Health grants P01 HL78931, R01 HL78932, 71140, International Research Fund for Subsidy of Kyushu University, and International Research Funds for Subsidy of Fukuoka University School of Medicine Alumni (to Dr. Ogawa), by an AHA Established Investigator Award (to Dr. Lin) and by Medtronic-Zipes Endowments (to Dr. Chen).
All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine