Abstract

Patients with end-stage renal disease (ESRD) have an elevated cardiovascular mortality. Although much interest has been focused on the understanding of the accelerated nature of their coronary artery disease, sudden cardiac death (SCD) has emerged as the single largest cause of cardiac death in our patient population. Multiple traditional and novel cardiovascular risk factors contribute to the particular vulnerability of dialysis patients towards SCD, including myocardial ischaemia, left ventricular hypertrophy/dilatation, electrolytes abnormalities, volume overload, sleep apnoea and sympathetic overactivity [1]. Despite our best efforts with revascularization and medical therapy, the risk of arrhythmically mediated death remains elevated and uncorrected in ESRD [2]. Careful examination of the impairments in heart rate variability (HRV) may allow for better insights into the ‘non-ischemic’ contributors of SCD and may have the potential to serve as both a monitoring and a prognostic tool in the ESRD population. There are multiple validated methods in quantifying HRV, which have been reviewed previously [3–5]. Commonly used techniques include time domain and spectral or frequency domain analysis of HRV. Basic pharmacological studies using animals and humans have formed the rationale for identifying high frequency (HF) power [>0.15 Hz] as an indicator of parasympathetic modulation of heart rate given that the administration of atropine or other blockers of the parasympathetic nervous system was able to abolish the HF component of HRV. Similarly, classical manoeuvres in augmenting central sympathetic outflow (e.g. tilt, lower body negative pressure) have resulted in increases in low frequency (LF) [0.05–0.15 Hz] power of HRV [6]. Further refinements of normalized ratios such as LF/HF have been used to estimate the sympathetic/vagal influence of HRV. It is important to note that most of the validation studies

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