PMC:6019327 / 49128-49732 JSONTXT

{"project":"2_test","denotations":[{"id":"28506916-24463369-29307263","span":{"begin":193,"end":196},"obj":"24463369"},{"id":"28506916-24463369-29307263","span":{"begin":193,"end":196},"obj":"24463369"},{"id":"T53916","span":{"begin":193,"end":196},"obj":"24463369"},{"id":"T53612","span":{"begin":193,"end":196},"obj":"24463369"},{"id":"T20842","span":{"begin":193,"end":196},"obj":"24463369"},{"id":"T44469","span":{"begin":193,"end":196},"obj":"24463369"}],"text":"The above results in patients are consistent with data derived from western blot analyses in sheep, designed to test whether remodeling was related to altered intracellular calcium dysfunction.158 Although the Na+-Ca2+ exchange was increased in the LAA of animals with persistent AF, both total RyR2 and phosphorylated RyR2 proteins were decreased, and the ratio of phosphorylated RyR2 to total RyR2 phosphorylation was unaffected. Thus, the transition from paroxysmal to persistent AF in the sheep model of atrial tachypacing did not appear to depend on Ca2+ leak or delayed afterdepolarizations (DADs)."}