کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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5972788 | 1576187 | 2014 | 6 صفحه PDF | دانلود رایگان |
BackgroundSinoatrial node (SAN) dysfunction increases the occurrences of atrial fibrillation (AF). The pulmonary veins (PVs) play a critical role in the pathophysiology of AF. The purpose of this study was to evaluate whether SAN electrical activity can modulate PV arrhythmogenesis.MethodsConventional microelectrodes and multi-electrode array system were used to simultaneously record the electrical activity and conduction properties of rabbit SAN and PV tissue preparations with and without SAN-PV interruptions before and after perfusion with Anemonia sulcata toxin (ATX)-II (100 nM) or isoproterenol (1 μM).ResultsATX-II significantly increased PV beating rates, which overdrove SAN electrical activity with the occurrences of PV burst firings in 5 (56%) of 9 tissue preparations, and induced SAN-PV conduction block in 6 (67%) of 9 preparations. After SAN-PV disconnection, ATX-II induced burst firing and early afterdepolarizations in 8 (89%) of 9 PVs. Moreover, the multi-electrode array found that ATX-II reversed the electrical conduction between the SAN and PV with an increase in electrical activity from 1.8 ± 0.6 to 2.9 ± 0.6 Hz (P < 0.05) in SAN-PV preparations (n = 7). In contrast, isoproterenol did not reverse electrical conduction between the SAN and PV with an increase in electrical activity from 1.8 ± 0.2 to 3.0 ± 0.3 Hz (P < 0.005) in SAN-PV preparations (n = 7).ConclusionsSAN electrical activity modulates PV arrhythmogenesis. SAN-PV conduction blocks can increase PV arrhythmogenesis.
Journal: International Journal of Cardiology - Volume 173, Issue 3, 15 May 2014, Pages 447-452