Does the kidney play an important role in the generation of ventricular arrhythmias and sudden cardiac death?

Abstract

Recently, Scholz et al. [1] presented an interesting case of ventricular electrical storm in a patient with dilated cardiomyopathy. After high-dose amiodarone therapy (200 mg QD), endocardial ventricular tachycardia (VT)ablation, epicardial VT-ablation, and followed maximal antiarrhythmic drug therapy, the patient still showed recurrent VT episodes. Subsequently, renal sympathetic denervation (RDN) was successfully performed without affecting blood pressure and renal function. Only one more VT episode that required implantable cardioverter defibrillator therapy recurred during a 5-month follow-up. Before that, similar attempts were made by Ukena et al. [2], Hoffmann et al. [3], and Remo et al. [4], who showed that RDN was an effective and safe approach to the treatment of ischemic or nonischemic electrical storm. However, the underlying mechanisms and the potential role of kidney in the generation of ventricular arrhythmias (VAs) and sudden cardiac death (SCD) remain unclear. VAs and SCD remain major causes of mortality in patients with cardiac disease. Increased sympathetic tone has been shown to contribute to the genesis and maintenance of VAs [5]. The kidney communicates the systemic sympathetic nervous system through the renal sympathetic nerve, which comprises efferent and afferent pathways [6]. It has been shown that renal sympathetic efferent and afferent nerves play an important role in regulating systemic sympathetic activity [6]. Therefore, the kidney may be involved in the pathogenesis of VAs and SCD. The 2013 annual data report of The United States Renal Data System showed that up to 26.9 % of all deaths in dialysis patients was due to arrhythmia/cardiac arrest [7]. Recently, Dalal et al. [8] found that mild-to-moderate kidney dysfunction was associated with a significant increase in the risk of ventricular fibrillation in the setting of acute myocardial infarction. The mechanisms underlying the increased risk of SCD in patients with chronic kidney disease are unknown, but appear to arise from the complex interactions between renal and central sympathetic nervous system. We have shown recently that renal sympathetic activation by applying 3 h of electrical stimulation to left renal nerves significantly increased blood pressure, sympathetic indices of heart rate variability, serum norepinephrine level, nerve activity of left stellate ganglion, as well as the incidence of acute ischemia-induced VAs [9]. These results indicate that renal sympathetic activation is able to increase both systemic and cardiac sympathetic tone, which are potential triggers for the development of VAs and SCD. These findings demonstrated that the kidney may play an important role in the generation of VAs and SCD, and renal sympathetic nerve may be a promising target for therapeutic intervention in VAs. However, large scalerandomized clinical trials are warranted to evaluate the effectiveness and safety of RDN for the treatment of VAs.