| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 5961628 | Heart Rhythm | 2010 | 9 Pages |
Abstract
The study data suggest that arrhythmias during DI-ATS1 may be a result of triggered activity secondary to prolonged APD and altered [Ca2+]i cycling and less likely dependent on large epicardial APD gradients forming the substrate for reentry. Therefore, therapies aimed at reducing [Ca2+]i rather than APD gradients may prove effective in treatment of ATS1.
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Authors
PrzemysÅaw B. PharmD, Rengasayee Veeraraghavan, Steven PhD,