The Uremic Myocardium and Ischemic Tolerance

Uremia is associated with an increased prevalence of ischemic heart disease. Already, at the start of dialysis, the prevalence of coronary artery disease is 38%.1 The frequency of myocardial infarction in renal patients is high and the outcome is poor.2 Despite significant improvement of therapeutic modalities, the unadjusted 2-year mortality for dialysis patients after acute myocardial infarction (MI) has not changed over the past decades, remaining ≈73%.2,3 It is of particular note that the risk of cardiac events is 20-fold higher in young adults starting dialysis in the first 2 decades of life in comparison with an age-matched background population.4Article see p 1256The reasons for the poor outcome are manifold: underdiagnosis due to atypical presentations (eg, fewer transmural infarctions), therapeutic nihilism due to the burden of disease, and the consequences of uremic cardiomyopathy itself.3Experimental uremic cardiomyopathy leads to reduced ischemic tolerance and consecutively larger MI size.5,6 The latter was independent of confounders such as hypertension, anemia, sympathetic overactivity, and hypervolemia.5 These findings are, at least in part, the consequence of morphological changes in uremic myocardial tissue. The number of cardiomyocytes is decreased presumably as a result of apoptosis. Furthermore, the cardiomyocyte diameter and cardiomyocyte area are increased,7 whereas the growth of capillaries does not keep pace, so that oxygen diffusion distance is critically extended. Another explanation for reduced ischemic tolerance is the increased oxygen demand of …