The research isn't specific to this point yet -- in other words, no one knows for certain -- but chronic hypertension is an immune characteristic as well, an activation of the innate immune response. Implantation could by dysregulated in chronic hypertensives because of their genetic tendency to hypertension. If that's true, my guess is that implantation can't proceed normally in chronics because other chemical responses unique to chronics are operating at the same time and interfere with a clean line of communication between the maternal and paternal cells -- like noisy crosstalk on a radio.
This is very difficult to study, but it's an ongoing, very intriguing, area of research. One thing that I find fascinating about it is that some chronics have babies who are *big* for gestational age, which might suggest that even though the placenta is shallowly implanted it's developing a decent blood supply anyway, or might suggest that implantation is deep enough to grow a big baby but at the same time the maternal immune response to it is creating hypoxia and triggering the same downstream effects that a shallow implantation would cause. There are multiple pathways operating here, multiple placental strategies for maximising bloodflow, so you could simultaneously have shallow implantation and then other strategies that compensated somewhat for that shallow implantation, like upregulation of maternal respiration rate and heart rate and appetite (so the little blood that does make it 'round to perfuse the placenta is still packed with supplies. (I think this is a useful way to explain tachycardia and breathlessness in some PE patients.)
The chemicals that are upregulated in PE, sFlt-1 and sEng, are upregulated in patients regardless of their predisposing underlying conditions, so hypoxia has to be a player in chronics, which suggests that chronics have shallow placentation going on, in some fashion.