cytotrophoblast cells from the placenta invade the
maternal spiral arteries during normal pregnancy.
This results in a striking increase in luminal diameter
and causes the vessels to lose their smooth muscle enabling
the expansion of vascular capacity necessary to support fetal
growth. Preeclampsia, growth restriction, recurrent abortion,
and preterm birth in many cases are caused by abnormal
implantation with failure of this process. Of these implantation
abnormalities, preeclampsia is well known to be associated
with later life cardiovascular disease.1,2 Furthermore,
several persistent metabolic and cardiovascular differences are
present in women with preeclamptic compared with normal
pregnancies. The data relating the other implantation disorders to
later life cardiovascular diseases are less compelling. It is
possible, however, in large population studies, to document
increased cardiovascular mortality in women with pregnancies
complicated by these disorders.1,3