Chronic haemodialysis (HD) patients are already primed by a large number of structural and functional peripheral vascular and cardiac abnormalities to experience demand myocardial ischaemia. Transient myocardial ischaemia may lead to left ventricular (LV) dysfunction that can persist after the return of normal perfusion. This prolonged dysfunction is known as myocardial stunning. Repetitive episodes of ischaemia can be cumulative and have been shown to lead to prolonged LV dysfunction (in patients with ischaemic heart disease). Conventional HD itself is a sufficient cardiovascular functional stressor to precipitate such recurrent ischaemic insults, leading to myocardial functional and structural changes, eventually resulting in fixed systolic dysfunction and heart failure (conferring a dismal prognosis for patients undergoing dialysis). Furthermore these same haemodynamic insults may also adversely affect other vascular beds in other vulnerable organ systems, driving an even wider range of pathophysiological processes. A variety of therapeutic manoeuvres aimed at improving the haemodynamic tolerability of treatment have been shown to reduce acute dialysis-induced myocardial ischaemia. This article aims to give an appreciation of the possibility that modification of the dialysis treatment to improve tolerability of therapy may have the potential to provide us with additional therapeutic targets, to reduce currently excessive rates of cardiovascular morbidity and mortality.

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