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  • cycloastragenol br Conclusion br Conflict of interest br Int

    2019-05-07


    Conclusion
    Conflict of interest
    Introduction The implantable cardioverter-defibrillator (ICD) has dramatically reduced the risk of sudden death in patients with malignant ventricular tachyarrhythmias [1,2]. However, 10–30% of patients who have undergone ICD implantation experience “electrical storms,” in which ventricular tachyarrhythmias occur ≥2 times within a 24-h period [3]. Patients with severe electrical storm are known to have a worse prognosis [4]. Some studies have demonstrated that ICD shocks increase the dispersion of ventricular repolarization [5,6]. The spatial dispersion of ventricular repolarization plays a role in the initiation and maintenance of malignant ventricular tachyarrhythmias, including electrical storms. The QT dispersion and recovery time dispersion are assumed to reflect the spatial heterogeneity [7,8]. Few therapeutic options are currently available for controlling electrical storms. Nifekalant hydrochloride (NIF) is a class III antiarrhythmic drug that causes dose-dependent prolongation of the cycloastragenol duration in both atrial and ventricular muscle, mainly by reducing the rapid component of the delayed rectifier K+ current (Ikr) [9,10]. Several clinical studies have demonstrated the effectiveness of intravenous NIF for recurrent ventricular tachyarrhythmias that are resistant to other antiarrhythmic drugs and ICD shock [11], especially electrical storms [12]. However, little is known about the electropharmacological basis of the efficacy of NIF in treating these arrhythmias. Moreover, the effect of NIF on the spatial dispersion of repolarization (SDR) has not been reported yet in any clinical study.
    Methods
    Results
    Discussion The major finding of the present study is that administration of NIF significantly suppressed the deterioration of SDR just after ICD shock. To the best of our knowledge, this is the first study to show that NIF significantly reduces the SDR after ICD shock in patients receiving oral amiodarone and β-blocker agents. A recent study reported that the SDR after ICD shock played an important role in the initiation and maintenance of ventricular tachyarrhythmias [5–7]. We therefore speculate that the reduction in SDR may be one of the mechanisms by which NIF suppresses the recurrence of ventricular tachyarrhythmias just after ICD shock in the presence of oral amiodarone and β-blocker administration.
    Conclusion
    Disclosure
    Conflicts of interest
    Introduction Abnormal repolarization facilitates the advent of ventricular tachyarrhythmias (VT). Bradycardia, ischemia, hypokalemia, and some cardiotoxic drugs increase the cardiac vulnerability to abnormal repolarization-related VT. Vasodilating agents such as carperitide [1] and clonidine [2] inhibit VT in an experimental model of acquired long QT syndrome (LQT). However, most vasodilating agents concomitantly have a certain cardioactive effect to some extent. In an earlier study, physiologically conceivable fluctuation of volume load did not markedly influence the electrophysiological properties or arrhythmogenicity of the canine ventricle [3]. Thus, it still seems disputable if vasodilation can have an appreciable impact on VT associated with acquired LQT.
    Methods
    Results
    Discussion Because of its little cardiac effect, hydralazine is known as a “direct vasodilator.” The main action of hydralazine is to inhibit the IP3-induced release of Ca2+ from the sarcoplasmic reticulum in vascular smooth muscle cells [5]. The present results demonstrated that vasodilation has a therapeutic implication for abnormal repolarization-related VT. Mechanical stretch is one of the modulating factors of myocardial electrophysiologic property, i.e., “mechano-electrical feedback,” and presumably its arrhythmogenicity. Ventricular loading causes the following: (1) reduction of action potential duration and refractoriness, (2) development of EAD, and (3) ectopic beats originating from the afterdepolarization [6,7].