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• W2023748096 abstract "BACKGROUND In congestive heart failure (CHF), autonomic nervous system (ANS) activity is known to modulate arrhythmic risk through its effects on myocardial repolarization. An increased interval between the peak and the end of the T wave (Tpeak-Tend) has been reported to increase the incidence of sudden cardiac death. However, the ANS influence on the Tpeak-Tend interval remains unclear. OBJECTIVE We directly measured ANS nerve activity in ambulatory dogs with pacing-induced CHF to test the hypothesis that ANS activity modulates the Tpeak-Tend variability index (Tpeak-TendVI), the short-term variability of the Tpeak-Tend interval obtained on 30 beats (Tpeak-TendSTV30), and the short-term variability of the Tpeak-Tend interval obtained on 5-minute ECG recording (Tpeak-TendSTVT). METHODS By using data previously recorded in 6 ambulatory dogs before and after pacing-induced CHF, we assessed ANS activity recorded with an implanted radiotransmitter that monitored integrated left stellate ganglion nervous activity (iSGNA), integrated vagus nerve activity (iVNA), and electrocardiogram (ECG). We selected for analysis 36 segments recorded at baseline and 36 after pacing-induced CHF with similar iSGNA. RESULTS During CHF, Tpeak-TendSTV30 (P<.001) and Tpeak-TendSTVT (P<.05) were significantly higher than those at baseline. The multiple linear mixed regression analysis disclosed a significant positive correlation between iSGNA and Tpeak-TendSTVT (baseline: β 2.92, P<.001; CHF: β 1.13, P<.001) and a significant negative correlation between iVNA and Tpeak-TendSTVT (baseline: β−6.74, P<.001; CHF: β−1.42, P< .001). CONCLUSIONS In a canine model of pacing-induced CHF, iSGNA correlates positively while iVNA correlates negatively with Tpeak-TendSTVT. These findings suggest that SGNA increases while VNA decreases the dispersion of ventricular repolarization in ambulatory dogs with CHF. In congestive heart failure (CHF), autonomic nervous system (ANS) activity is known to modulate arrhythmic risk through its effects on myocardial repolarization. An increased interval between the peak and the end of the T wave (Tpeak-Tend) has been reported to increase the incidence of sudden cardiac death. However, the ANS influence on the Tpeak-Tend interval remains unclear. We directly measured ANS nerve activity in ambulatory dogs with pacing-induced CHF to test the hypothesis that ANS activity modulates the Tpeak-Tend variability index (Tpeak-TendVI), the short-term variability of the Tpeak-Tend interval obtained on 30 beats (Tpeak-TendSTV30), and the short-term variability of the Tpeak-Tend interval obtained on 5-minute ECG recording (Tpeak-TendSTVT). By using data previously recorded in 6 ambulatory dogs before and after pacing-induced CHF, we assessed ANS activity recorded with an implanted radiotransmitter that monitored integrated left stellate ganglion nervous activity (iSGNA), integrated vagus nerve activity (iVNA), and electrocardiogram (ECG). We selected for analysis 36 segments recorded at baseline and 36 after pacing-induced CHF with similar iSGNA. During CHF, Tpeak-TendSTV30 (P<.001) and Tpeak-TendSTVT (P<.05) were significantly higher than those at baseline. The multiple linear mixed regression analysis disclosed a significant positive correlation between iSGNA and Tpeak-TendSTVT (baseline: β 2.92, P<.001; CHF: β 1.13, P<.001) and a significant negative correlation between iVNA and Tpeak-TendSTVT (baseline: β−6.74, P<.001; CHF: β−1.42, P< .001). In a canine model of pacing-induced CHF, iSGNA correlates positively while iVNA correlates negatively with Tpeak-TendSTVT. These findings suggest that SGNA increases while VNA decreases the dispersion of ventricular repolarization in ambulatory dogs with CHF." @default.
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• W2023748096 date "2012-12-01" @default.
• W2023748096 modified "2023-10-17" @default.
• W2023748096 title "Autonomic nerve activity and the short-term variability of the Tpeak-Tend interval in dogs with pacing-induced heart failure" @default.
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• W2023748096 doi "https://doi.org/10.1016/j.hrthm.2012.08.030" @default.
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