The benefit of the highest possible ECD in the first year after PKP is obvious. The extra endothelial cell reserve, especially in this population, allows patients to cope better with events liable to affect the endothelium, in particular elevated IOP and endothelial rejection. Both occur most often in the first year after grafting.23- 28 As Bourne et al7 emphasize, the number of endothelial cells surviving on corneal transplants is important for long-term graft survival because grafts with more cells probably have a greater capacity to withstand the effects of aging, inflammation, and rejection episodes. Although our as yet limited perspective prevents a formal conclusion, this extra cell reserve is likely to prolong graft survival into the very long term by reducing late endothelial failure. In this young population with a low rejection risk, late endothelial failure is one of the main causes of late graft failure.3,20,21 Several studies of all-comer recipients, comprising high and low preoperative ECD and variable rejection risks, have shown that an early deficit of 500 cells/mm2 is associated with a significant rise in late endothelial failure risk.3,20,21 Of a selected population of recipients such as ours, a smaller difference of about 250 cells/mm2 probably would have similar effects. To predict late endothelial failure, Redmond et al9 fitted a monoexponential decay curve to the postoperative loss of endothelial cells from grafts for 4 years in all-comer recipients. This model, however, greatly overestimates cell loss in the longer term. Adapting a more complex model based on the sum of 2 exponentials(e), ECDt = ae−pt+ be−qt(W.J.A., unpublished data; ECDt is cell density at time t [postoperative time in months], p is equal to 0.693/half-life of the first curve component, q is equal to 0.693/half-life of the second curve componenet, a and b are constants whose sum is equal to the initial ECD), to our data allows the percentage of the loss of cells with increasing postoperative time to be estimated. The model was fitted separately to the short- and long-term storage groups (Figure 2). The rate of decline in ECD during the 12-month follow-up was very similar in both groups. Given that these equations were derived from such a limited follow-up period, it would not be justified to extrapolate them into the long term. An equation that had been derived from a data set of long-term measurements of ECD was therefore used to determine the percentage of fall in ECD with time (Figure 3).This allowed the change in ECD with time to be calculated for initial donor ECDs of 2551 (group 1) and 2278 cells/mm2 (group 2). These curves allowed estimation of the long-term survival times, assuming different endothelial decompensation thresholds. The ECD threshold below which the endothelium can no longer ensure corneal deturgescence is difficult to define because it varies according to the circumstances of endothelial loss.29 Different authors have reported decompensation thresholds of 250, 30 300, 31 400, 32,33 or 50034 cells/mm2. Figure 3 shows the predicted decline in ECD in the 2 groups and the time taken to reach ECD thresholds of 500 and 250 cells/mm2.If decompensation is expected to occur at an ECD of 500 cells/mm2, graft survival in groups 1 and 2 would be 28 and 25 years, respectively. A lower decompensation threshold of 250 cells/mm2 is probably more realistic, based on personal observation by means of specular microscopy of numerous keratoconi grafted more than 30 years ago with a still-transparent cornea (J.M., unpublished data, 2000). If decompensation did not occur until an ECD of 250 cells/mm2 had been reached, graft survival would be 50 and 46 years in groups 1 and 2, respectively. Whether these differences would be considered clinically significant in grafts that may be predicted to last for more than 25 years is a difficult question, but one that needs to be addressed.