b-Adrenergic stimulation and rapid pacing mutually promote heterogeneous electrical failure and XXXX in the globally ischemic heart.

@entity1164 @entity308 @entity1165 @entity5733 @entity63 @entity95 @entity15480 @entity2224 @entity1167 @entity3044 @entity2661
Global @entity63 , @entity5733 surge, and rapid heart rhythm (RHR) due to @entity1165 or @entity2224 ( @entity2224 ) are the three major factors of @entity1164 ( @entity1164 ). Loss of excitability culminating in global electrical failure ( @entity1167 ) is the major adverse outcome of @entity1164 with increasing prevalence worldwide. The roles of @entity2661 and RHR in the electrical failure during @entity1164 remain unclear. We hypothesized that both b-adrenergic stimulation (bAS) and RHR accelerate electrical failure in the globally ischemic heart. We performed optical mapping of the action potential (OAP) in the right ventricular (RV) and left (LV) ventricular epicardium of isolated @entity95 hearts subjected to 30-min global @entity63 . Hearts were paced at a cycle length of either 300 or 200 ms, and either in the presence or in the absence of b-agonist @entity3044 (30 nM). @entity15480 (20 mM) was used to reduce motion artifact. We found that RHR and bAS synergistically accelerated the decline of the OAP upstroke velocity and the progressive expansion of inexcitable regions. Under all conditions, inexcitability developed faster in the LV than in the RV. At the same time, both RHR and bAS shortened the time to @entity2224 (TVF) during @entity63 . Moreover, the time at which 10% of the mapped LV area became inexcitable strongly correlated with TVF (R(2) = 0 .72, P < 0.0001). We conclude that both bAS and RHR are major factors of electrical @entity308 and failure in the globally ischemic heart and may contribute to adverse outcomes of @entity1164 such as @entity1167 and recurrent/persistent @entity2224 .
