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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.