Circulation, Vol 75, 956-963, Copyright © 1987 by American Heart Association
DJ Fitzgerald, SS Entman, K Mulloy and GA FitzGerald
Patients who develop pregnancy-induced hypertension exhibit a lesser
increment in prostacyclin biosynthesis than healthy pregnant subjects.
Whether this precedes the development of clinical disease and therefore may
be important in the pathogenesis of pregnancy-induced hypertension or is a
secondary event is unknown. We prospectively determined prostacyclin
biosynthesis in pregnant subjects at risk of developing pregnancy-induced
hypertension by use of noninvasive approach, measurement of the urinary
metabolite 2,3-dinor-6-keto-prostaglandin F1 alpha. Patients were recruited
at less than 20 weeks gestation. After delivery, patients were
retrospectively allocated by use of preset criteria, to one of four groups:
pregnancy-induced hypertension (n = 12), hypertension in labor (n = 22),
chronic hypertension (n = 9), and normotension (n = 24). There was a
significant increase in prostacyclin biosynthesis in all study groups
during gestation. However, patients who developed pregnancy-induced
hypertension exhibited a lesser increment and this difference persisted
throughout gestation. These results are consistent with a pathophysiologic
role for altered prostacyclin biosynthesis in women with pregnancy-induced
hypertension. In addition, decreased prostacyclin formation identifies a
population at risk of developing pregnancy-induced hypertension. Such
information would assist the design of clinical trials of drugs, such as
aspirin, that might prevent the development of this disease.
ARTICLES
Decreased prostacyclin biosynthesis preceding the clinical manifestation of pregnancy-induced hypertension
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