Chronic hypertension and risk of placental abruption: is the association modified by ischemic placental disease?
OBJECTIVE
The purpose of this study was to evaluate whether the increased risk of placental abruption among women with chronic hypertension is modified by ischemic placental disease, specifically pregnancy-induced hypertension (PIH) and fetal growth restriction (FGR).


METHODS
We used the US linked natality and fetal death data files (1995-2002) and restricted the analysis to women who had a singleton birth at > or = 22 weeks of gestation and to fetuses who weighed > or = 500 g (n = 30,189,949). Fetal growth was defined both on a continuum (<1, 1-2, 3-4, 5-9, 10-19, ..., > or = 90) and as birthweight of < 10th percentile for gestational age (FGR) or birthweight of > 90th percentile (large for gestational age [LGA]). All analyses were adjusted for potential confounding factors through multivariable logistic regression.


RESULTS
Rates of abruption among women with and without chronic hypertension were 15.6 and 5.8 per 1000 pregnancies, respectively (relative risk [RR], 2.4; 95% CI, 2.3, 2.5). In comparison with normotensive women with appropriately grown babies (ie, 10th-90th percentile), the association between chronic hypertension and abruption was modified in the presence of FGR (RR, 3.8; 95% CI, 3.6, 4.1) and PIH (RR, 7.7; 95% CI, 6.6, 8.9). However, the highest risk was seen among women with chronic hypertension, PIH, and LGA (RR, 9.0; 95% CI, 7.2, 11.3). A dose-response relationship was observed between the risk of abruption and fetal growth (assessed on a continuum), with the risk being lowest among LGA babies.


CONCLUSIONS
The association between chronic hypertension and abruption is strong; ischemic placental disease (PIH and FGR) modified this relationship. These findings suggest an etiologic relationship between abruption and chronic placental disease. Chronic hypertension, if associated with LGA, is not associated with abruption; however, chronic hypertension with superimposed PIH accompanied by LGA is associated with significantly increased risk.
Ananth
Cande V
CV
Division of Epidemiology and Biostatistics, Department of Obstetrics, Gynecology, and Reproductive Sciences, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, NJ 08901-1977, USA. cande.ananth@umdnj.edu
Peltier
Morgan R
MR
Kinzler
Wendy L
WL
Smulian
John C
JC
Vintzileos
Anthony M
AM
D000037:Abruptio Placentae / Q000209:etiology*; D000328:Adult; D002908:Chronic Disease; D005260:Female; D005317:Fetal Growth Retardation / Q000209:etiology*; D005865:Gestational Age; D006801:Humans; D006973:Hypertension / Q000150:complications*; D046110:Hypertension, Pregnancy-Induced / Q000209:etiology*; D007511:Ischemia / Q000209:etiology*; D010920:Placenta / Q000098:blood supply*; D011247:Pregnancy; D012307:Risk Factors