1. ¹Department of Renal Medicine, Derby City Hospital, Derby, UK
2. ²School of Graduate Entry Medicine and Health, University of Nottingham, Nottingham, UK

Correspondence: Christopher W. McIntyre, Department of Renal Medicine, Derby City Hospital, Uttoxeter Road, Derby DE22 3NE, UK. E-mail: chris.mcintyre@nottingham.ac.uk

Received 18 June 2008; Revised 23 February 2009; Accepted 15 April 2009; Published online 10 June 2009.

Abstract

Hemodialysis (HD) patients are subject to an enormous excess of cardiovascular morbidity and mortality. This appears to be largely driven by factors that are different from those at play in the general population. Chronic HD patients are already primed by a large number of structural and functional peripheral vascular and cardiac abnormalities to experience demand myocardial ischemia. Conventional HD is capable of inducing myocardial ischemia. Recurrent ischemic insults lead to myocardial functional and structural changes, eventually resulting in fixed systolic dysfunction and heart failure (conferring a dismal prognosis for patients undergoing dialysis). Modifications of the HD process to improve the hemodynamic tolerability of the treatment have been shown to reduce the perturbation of myocardial blood flow and functional evidence of dialysis-induced ischemia. Although it is uncomfortable to consider that much of the observed disease burden in HD patients may be an artifact of current dialysis treatment regimes, understanding the role that conventional dialysis plays in the pathophysiology of cardiac injury in HD patients has the potential to provide us with additional dialysis, and non-dialysis, based novel therapeutic targets to reduce currently excessive rates of cardiovascular morbidity and mortality.