Calcium-Handling Protein Phosphorylation Abnormalities in a Rabbit Model with Recurrent Ventricular Fibrillation Storm

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概要

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• Electrical storm (ES), characterized by recurrent ventricular tachycardia/fibrillation (VT/VF), is an increasing problem among implantable cardioverter-defibrillators (ICDs) patients. While acute cessation of ES is generally achievable with medical therapy, ES is associated with a high risk of mortality in a few months after its occurrence, mostly due to non-sudden cardiac causes. The underlying mechanisms are unknown. Here, we investigated ES effects on Ca<SUP>2+</SUP>-handling protein expression/phosphorylation in an experimental ES model. Thirty-seven rabbits with chronic complete atrioventricular block, equipped with ICDs, were studied. All had QT-prolongation and ICD-detected VT/VF-episodes. Twenty-two rabbits (59%) developed ES (defined as ≥3 VF-episodes/24-hr period; 108±29 VF-episodes/rabbit). ES-rabbits showed left-ventricular function deterioration, along with striking activation of Ca<SUP>2+</SUP>/calmodulin-dependent protein-kinase II (CaMKII) and enhanced protein-phosphatase expression. These alterations produced changes in phosphorylation-pattern, markedly hyperphosphorylation of L-type Ca<SUP>2+</SUP>-channel and sarcoplasmic reticulum (SR) Ca<SUP>2+</SUP>-release channel ryanodine receptor and dephosphorylation of SR Ca<SUP>2+</SUP>-uptake regulator phospholamban (PLB). Repeated VF induction/defibrillation with ICD-shocks in control rabbits reproduced ES-related changes in CaMKII and PLB phosphorylation. Continuous infusion of calmodulin-antagonist W-7 to ES-rabbits reduced CaMKII-activation, suppressed VT/VF-episodes and rescued LV-dysfunction without significantly altering hypertrophic or apoptotic markers. In conclusions, ES causes marked CaMKII-activation and Ca<SUP>2+</SUP>-handling protein phosphorylation abnormalities, which may be responsible for adverse outcomes in ES-patients.

著者

• Inden Yasuya

  Department Of Cardiology Nagoya University Graduate School Of Medicine

• Tsuji Yukiomi

  Department Of Cardiology Nagoya University Graduate School Of Medicine

• Kamiya Kaichiro

  Department Of Cardiovascular Research Research Institute Of Environmental Medicine Nagoya University

• Kodama Itsuo

  Department Of Cardiovascular Research R.i.e.m. Nagoya University

• Niwa Ryoko

  Department Of Cardiovascular Research Research Institute Of Enviromental Medicine Nagoya University

• Murohara Toyoaki

  Department Of Cardiology Nagoya Graduate School Of Medicine

• Kodama Itsuo

  Department of Cardiovascular Research, Research Institute of Environmental Medicine, Nagoya University

• Tsuji Yukiomi

  Department of Cardiovascular Research, Research Institute of Environmental Medicine, Nagoya University

• Niwa Ryoko

  Department of Cardiovascular Research, Research Institute of Environmental Medicine, Nagoya University

• Inden Yasuya

  Department of Cardiology, Nagoya Graduate School of Medicine

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