Thoughts:

1) Is low LDL a Risk factor for MCACE in diabetic patients? Implying that more of the LDL is deposited at vascular beds (see #4 below) 

2) Does high LDL (or something else in those with high LDL) interacts somehow with the drug, reducing its bioavailability /effectiveness -

3) In case of #2, would higher drug does perform better?

4) Is the higher efficacy at low LDL in circulation indicative of higher levels of oxidized LDL at vascular bed (oxidized LDL is known to adhere to vascular bed), providing a seed for atherosclerotic plagues, which is know to be associated with enhanced immune response/ inflammation that the drug is reportedly corrects? 

5) in case of #4, efficacy might be more to do with reducing inflammation at the vascular beds & not to the circulating LDL levels!!!