Cardiomyopathy is a common, heterogeneous and important cause of cardiac morbidity and mortality in uraemic patients. The risks of ischaemic heart disease, cardiac failure, and death increase progressively from lowest risk in patients with concentric left-ventricular hypertrophy, to medium risk in patients with left-ventricular dilatation but intact systolic function, to highest risk in patients with systolic dysfunction. Anaemia and hypertension are the reversible risk factors most consistently linked with the development of cardiomyopathy in these patients. Longitudinal data show that anaemia predisposes individuals to initial left ventricular dilatation, with compensatory hypertrophy, which may progress to systolic dysfunction. This process typically begins at glomerular filtration rates between 25 and 50 ml/min, and haemoglobin concentrations that are even slightly below normal are associated with progressive cardiac enlargement. Several observational studies have suggested that the correction of anaemia may reduce mortality and hospitalization rates in dialysis patients. The available evidence supports maintaining haemoglobin concentrations to greater than 11 g/dl. Whether a haemoglobin threshold exists above which no further benefit is seen remains controversial, partially because recent randomized controlled trials have intervened relatively late in the anaemia-cardiomyopathy-cardiac failure-death continuum. One large randomized controlled trial showed no benefit from normalizing the haemoglobin concentration in haemodialysis patients with well-established cardiac disease; however, these patients had been exposed to anaemia for long periods of time and were at the extreme end of the cardiorenal disease spectrum. Other researchers have demonstrated a protective effect of normalizing the haemoglobin concentration in patients with asymptomatic, and hence presumably early, cardiomyopathy. The psychological benefits and improvements in exercise tolerance and quality of life resulting from normalization of the haemoglobin concentration are becoming clearer. However, conclusive evidence of the cardiovascular benefits of earlier, more aggressive treatment of renal anaemia as well as of the exact target haemoglobin concentration at which risk begins to develop is still lacking. The results of ongoing trials should help to clarify both of these issues within the next 5 years.
|Original language||English (US)|
|Number of pages||4|
|Journal||Nephrology Dialysis Transplantation|
|Issue number||SUPPL. 3|
|State||Published - 2000|
- Cardiovascular disease
- Chronic renal failure