Electrophysiology Models for End-Stage Renal Disease Maladaptations That Promote Asystole.

Abstract

Many patients with chronic renal impairment experience cardiac comorbidities throughout their lives, and the incidence of electrophysiological demise for patients with terminal renal impairment requiring renal replacement therapy is higher than in patients with normal renal function. Thus, this relationship warrants continued examination, such that the risk of subsequent cardiac complications might eventually be mitigated. This review aims to outline the electrophysiology concepts, both basic and clinical, underlying the pathophysiology mediated by end-stage renal disease (ESRD). An evaluation of how chronic kidney disease may accelerate adverse cardiac remodeling, as well as the mechanisms through which hemodialysis may precipitate electrophysiological aberrations that impair the ability of the conduction system to maintain normal sinus rhythm, are provided. Furthermore, relevant animal models for this pathophysiology, with respect to their innate ability to recapitulate human renal and cardiac electrophysiology, are outlined. Specifically, the concepts of hyperkalemia, pericarditis, and arrhythmia are discussed in relation to ESRD. Furthermore, murine, porcine, and human species are compared and contrasted on all structural levels, from subcellular to clinical, illustrating which models best recapitulate this propensity to asystole.