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  • br Conclusions Based on our findings

    2019-06-17


    Conclusions Based on our findings using a chronic animal model in vivo that repeated VF and defibrillation, not shocks, are associated with striking CaMKII activation, together with accumulating evidence that CaMKII is crucially involved in cellular processes for HF, it is conceivable that CaMKII activation contributes to HF progression and associated mortality in patients with shocked VTAs. Development of cardiospecific CaMKII inhibitory molecules with safe drug-like properties is desirable and necessary for confirming the efficacy on the HF phenotype, as well as clarifying this notion in diseased human hearts in further studies.
    Conflict of interest
    Acknowledgments Daiichi-Sankyo Co. Ltd. (Tokyo, Japan), APEX Co., Ltd. (Nagoya, Japan), Suzuken Memorial Foundation, and Japan Society for the Promotion of Science (Grant no. 26461074) supported this work.
    Introduction The term “electrical storm” describes a state of electrical instability of the PD-1/PD-L1 Inhibitor 3 characterized by clustering of recurrent episodes of ventricular tachycardia (VT) or ventricular fibrillation (VF) in a short period of time. In recent years, implantable cardioverter defibrillators (ICDs) have significantly improved the survival of patients with VT/VF. However, electrical storms remain associated with high mortality and morbidity, and have a negative impact on long-term outcomes [1]. Although there is no consensus regarding the definition of an electrical storm, the generally accepted definition in clinical practice and recent literature is the occurrence of ≥2 separate VT/VF episodes or ≥3 appropriate ICD therapies for VT/VF in a 24-h period [2]. In more than half of the patients with an electrical storm, the intervals between the VT/VF episodes are <1h, with the shortest interval of <1min [3]. A sustained VT/VF that resumes immediately after (≥1 sinus cycle) successful defibrillation/cardioversion is regarded as a severe form of electrical storm. This may masquerade as shock-refractory VT/VF, since a brief sinus period followed by immediate VT/VF recurrence can be concealed by post-shock electrocardiographic (ECG) saturation [4]. Therefore, a severe form of electrical storm might also be responsible for the events that occur in some patients with shock-refractory VT/VF, which are commonly seen during cardiopulmonary resuscitation. It is imperative to improve the treatment strategy for electrical storms, because the incidence of electrical storms is not low (10–28% in patients with an ICD implanted for secondary prevention and 4% for primary prevention) [1].
    Principles of management Patients who present with an electrical storm often have structural heart disease; however, functional electrical abnormalities also provoke electrical storms in patients with structurally normal hearts. The underlying conditions that cause electrical storms are listed in Table 1. Since an electrical storm is a medical emergency, it is generally managed in line with a treatment algorithm, typically the Advanced Cardiovascular Life Support (ACLS) protocol [5], regardless of the etiology of the electrical storm. Such a pre-specified algorithmic approach is highly effective in critical patient care, which requires a prompt response to life-threatening conditions. Nevertheless, I propose that treatment should be as specific to the underlying mechanism as possible, because electrical storms of some etiologies actually require a completely opposite treatment. Specifically, sympathetic blockade is effective in controlling electrical storms in patients with the majority of structural heart diseases [6–8], congenital long QT syndrome (LQTS) [9], and catecholaminergic polymorphic VT (CPVT) [10], whereas sympathetic stimulation with isoproterenol is useful for inhibiting electrical storms caused by Brugada syndrome [11], early repolarization syndrome [12], and short QT syndrome (SQTS) [13]. Alternatively, antiarrhythmic drugs commonly used for the treatment of electrical storms [5] can aggravate the situation in LQTS by further lengthening the QT interval [14]. Therefore, an empirical approach to treat recurrent VT/VF is potentially harmful in certain cases, and a mechanism-directed therapy would be preferable. Although it is difficult to perform a complete diagnostic evaluation during an electrical storm, standard workups such as transthoracic echocardiography and 12-lead ECG can help one understand whether patients have structural heart disease, and/or some specific ECG findings including ischemic ST-T changes, abnormal QT interval, Brugada-type ECG, and others. Myocardial ischemia, worsening heart failure, and electrolyte disturbances are a common trigger of electrical storms [15]. If such an inciting factor is found, emergent revascularization, correcting the electrolyte abnormality or treatment for heart failure must be performed.