You know, I'm just not sure what to think about chronic hypertension, either - because technically, I was considered an unmasked chronic due to the length of time my postpartum recovery lasted with Oscar. I was still 160/100 on the max dose of meds at my six week followup and was only able to wean off labetalol four-ish months postpartum, with bp that was borderline high for another year plus.
During my fourth pregnancy, my bp spiked immediately in the fifth week to ~130/85 from ~100/60, and I viewed that as likely an immune response to a foreign placenta. So I wasn't terribly surprised, just sad, when there was no heartbeat at week 16. And then in pregnancy number five, my bp was a steady ~100/60 through week 37…
Here's one of the publicly accessible recent papers on trophoblast invasion. It's ugly reading, very technical, but periodically there are sentences in normal English. http://www.reproduction-online.org/cont ... 3.full.pdf
"Traditionally, a view has been held that a high-resistance pattern in the first trimester represents normal physiology and that it is only when women have a persisting high- resistance pattern beyond the second trimester that it becomes significant or pathological. This tied in with initial theories of two stages of trophoblast invasion and remodelling (Pijnenborg et al. 1983), with an early shallow wave in the first trimester followed by a second wave of deep trophoblast invasion in the second trimester that is completed by 18–20 weeks and leads to the conversion of the uteroplacental circulation into a low-resistance bed. This view has been questioned (Lyall 2002), with suggestion that remodelling progresses as a dynamic and continuous process, which will vary between individuals due to interacting fetal and maternal factors."
I lean "dynamic and continuous" - it's just that you see a point where invasion has begun to deepen into the myometrium sometime after about 10-12 weeks, and it's handy to call that "second-stage invasion." If that doesn't happen normally, the oxygen flow that the fetus needs to establish in the second trimester never really materializes - which is what I assume happened in my fourth pregnancy. (Beautiful first-tri ultrasound, genetically normal fetus.) That's an immune-mediated response, but that's not the same thing as an autoimmune response - and it can vary tremendously depending on the environment, and the environment includes things like how well-controlled your hypertension is, the genes in the placenta, and how recently you've been pregnant/ how exploitable bits of the uterine environment are.
It's a really tricky thing to predict or negotiate - I think of it as a targeting problem (embed juuuust deeply enough) coupled to an arms race (conflict between maternal and paternal genes over depth of embedment.) I got lucky. But we do now have some epidemiological data that suggest you can bias the odds in your favor with a shorter interpregnancy interval. I want to be completely clear that this will not always work - again, I got lucky. But it's a useful thing to know when you are making your decisions about subsequent pregnancies.
I also liked this abstract, but don't read Dutch and need to find a translator: http://www.ncbi.nlm.nih.gov/pubmed/24330800
"Many doctors still tell some patients that a (subsequent) pregnancy is contraindicated. Aside from the fact that the desire to have a (or another) child is often extremely strong, which often results in ignoring the message, this type of advice may have serious negative consequences… Women may postpone a subsequent pregnancy out of fear of preeclampsia, while this in fact increases the recurrence risk."