Molecular mechanisms of heart failure progression associated with implantable cardioverter-defibrillator shocks for ventricular tachyarrhythmias.
Molecular mechanisms of heart failure progression associated with implantable cardioverter-defibrillator shocks for ventricular tachyarrhythmias.
复制标题
室性快速心律失常与植入式心脏复律除颤器电击相关的心力衰竭进展的分子机制。
DOI:
10.1016/j.joa.2014.04.003
复制
发表时间:
2014
期刊:
影响因子:
--
通讯作者:
Makita N.
中科院分区:
文献类型:
--
作者:
Tsuji Y;Ishikawa T;Makita N.
Implantable cardioverter-defibrillators (ICDs) are highly effective in reducing mortality related to ventricular tachyarrhythmias (VTAs). Despite this benefit, the occurrence of ICD shocks for VTAs in patients with heart failure (HF) and depressed left ventricular function has been associated with adverse outcomes. Patients with shocked VTAs are at an elevated risk of HF and death. While VTAs may be markers for high-risk patients, it is possible that the harmful effects of electrical shocks and VTAs are involved in HF progression and associated mortality. Some investigators have speculated that shocked VTAs may activate signaling pathways in the molecular cascade of HF. We recently reported in an experimental model of ventricular fibrillation storm that multiple ICD shocks for recurrent ventricular fibrillation caused striking activation of Ca2+/calmodulin-dependent protein kinase II, a validated signaling molecule for HF. This review article describes the harmful effects of shocks and VTAs and proposes that Ca2+/calmodulin-dependent protein kinase II could connect shocked VTAs to adverse outcomes.