The slightly lower MACE rate in the low LDL group might have been due to differences between the low and high LDL groups in other CVD risk factors - HDL, blood pressure, cigarettes, severity of diabetes, etc. Perhaps I overlooked it, but I don’t recall seeing those data anywhere. It could akso have been due to chance. A third theoretical possibility would be that ABL binds to LDL particles in blood. If that happens, a low LDL would probably result in more ABL being unbound (free in solution) which for most drugs is the only active fraction. I have written to Don to ask him if ABL binds to LDL (some drugs do) but have not received a reply. 

Sorry if this is all a bit technical!