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Myocardial stunning is now suspected to be a major contributor to the increased CV mortality rate in the HD population.
Repetitive and at times prolonged myocardial stunning can lead to a proliferation of fibrous connective tissue, called myocardial fibrosis.
The myocardial stunning that contributes to this process may be a potentially modifiable risk factor in the development of chronic heart failure, arrhythmias, and sudden cardiac death.
It is felt that these changes may also occur during HD when myocardial stunning occurs.
A small study by Selby and McIntyre (2011) assessed 10 patients on peritoneal dialysis (PD) for regional wall motion abnormalities and myocardial stunning.
These findings underscored the contribution of the HD treatment itself to myocardial stunning because children do not have the classical atheromatous coronary artery disease.
A number of both patient and treatment factors have been postulated to contribute to HD-induced myocardial stunning.
Myocardial stunning would be a plausible, if only presumed, contributing etiology.
In a follow-up study to evaluate in more detail the factors involved in HD-induced myocardial stunning, Assa et al.
Avoiding UFRs in excess of 13/mL/kg/hour might help minimize non-physiologic fluid shifts, hemodynamic instability, and hypotension, perhaps decreasing the risk of HD-induced myocardial stunning and CV and all cause mortality.
To our knowledge, no study of myocardial stunning has been undertaken while using UF profiling, but might be an area for future research.
This has been shown to virtually eliminate intradialytic hypotension and greatly reduce episodes of myocardial stunning (Jefferies, Virk, Moran, & McIntyre, 2011).