Stephen L Wasmund1, Christina F Pacchia2, Richard L Page3, Mohamed H Hamdan4. 1. Department of Cardiovascular Medicine, University of Wisconsin, H4/534 Clinical Science Center, 600 Highland Avenue, Madison, WI, 53792-3248, USA. swasmund@medicine.wisc.edu. 2. Department of Internal Medicine, University of Utah Health Sciences Center and Nora Eccles Harrison Cardiovascular Research and Training Institute, Salt Lake City, UT, 84112, USA. 3. Department of Cardiovascular Medicine, University of Wisconsin, H4/534 Clinical Science Center, 600 Highland Avenue, Madison, WI, 53792-3248, USA. 4. Department of Cardiovascular Medicine, University of Wisconsin, H4/534 Clinical Science Center, 600 Highland Avenue, Madison, WI, 53792-3248, USA. mhamdan@medicine.wisc.edu.
Abstract
OBJECTIVE: We have previously shown that up to one-third of patients develop no change or an increase in sinus node cycle length (SNCL) during ventricular fibrillation (VF). The purpose of the present study was to investigate the mechanism of SNCL changes during VF in a swine model. We hypothesized that changes in SNCL during VF are vagally-mediated. METHODS: In 33 anesthetized pigs DC current was used to induce VF for 10 s followed by defibrillation. SNCL changes were assessed during VF and compared to baseline. Animals that had ventriculo-atrial conduction during VF were excluded. Post-defibrillation, the pigs were randomized to receive atropine, propranolol, atropine + propranolol or placebo followed by repeat VF induction and measurement of SNCL changes. RESULTS: Ventriculo-atrial conduction was present in 14 pigs prohibiting SNCL measurements. In the remaining 19 animals, 10 demonstrated SNCL shortening (S-Group) and 9 demonstrated non-shortening (NS-Group). Atropine decreased the absolute change in SNCL from 51.2 to 26.6 ms (n = 6; p = 0.03). It attenuated the SNCL shortening previously observed in the S-Group (-99.2 ms versus -47.9 ms, p = 0.04) and reversed the SNCL prolongation initially observed in the NS-Group (27.1 ms versus -6.5 ms, p = 0.13). Similarly, atropine + propranolol decreased the absolute change in SNCL from 33.3 to 12.2 ms (n = 4; p = 0.05). No significant changes were noted with propranolol or placebo. INTERPRETATION: The SNCL changes during VF appear to be vagally-mediated. The clinical implications vis-à-vis defibrillation threshold and future device programming await future studies.
OBJECTIVE: We have previously shown that up to one-third of patients develop no change or an increase in sinus node cycle length (SNCL) during ventricular fibrillation (VF). The purpose of the present study was to investigate the mechanism of SNCL changes during VF in a swine model. We hypothesized that changes in SNCL during VF are vagally-mediated. METHODS: In 33 anesthetized pigs DC current was used to induce VF for 10 s followed by defibrillation. SNCL changes were assessed during VF and compared to baseline. Animals that had ventriculo-atrial conduction during VF were excluded. Post-defibrillation, the pigs were randomized to receive atropine, propranolol, atropine + propranolol or placebo followed by repeat VF induction and measurement of SNCL changes. RESULTS: Ventriculo-atrial conduction was present in 14 pigs prohibiting SNCL measurements. In the remaining 19 animals, 10 demonstrated SNCL shortening (S-Group) and 9 demonstrated non-shortening (NS-Group). Atropine decreased the absolute change in SNCL from 51.2 to 26.6 ms (n = 6; p = 0.03). It attenuated the SNCL shortening previously observed in the S-Group (-99.2 ms versus -47.9 ms, p = 0.04) and reversed the SNCL prolongation initially observed in the NS-Group (27.1 ms versus -6.5 ms, p = 0.13). Similarly, atropine + propranolol decreased the absolute change in SNCL from 33.3 to 12.2 ms (n = 4; p = 0.05). No significant changes were noted with propranolol or placebo. INTERPRETATION: The SNCL changes during VF appear to be vagally-mediated. The clinical implications vis-à-vis defibrillation threshold and future device programming await future studies.
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