OBJECTIVE: To estimate the relative importance of positive maternal thrombophilia testing compared with additional pathological evidence of abnormal placentation with placental infarction. METHODS: We performed a retrospective cohort study over a 10-year period in 180 singleton high-risk pregnancies (delivery at 22-34 6/7 weeks of gestation) that had histologic evidence of placental infarction. The rate of positive maternal tests for antiphospholipid syndrome, factor V Leiden, and prothrombin gene mutation were compared with the rate of detection of one or more gross or histological features of abnormal placentation (impaired placental development or differentiation, maternal vascular underperfusion, fetal vascular underperfusion, chronic inflammation, or intervillous thrombosis). RESULTS: Only 14 of 108 (13.0%) of placentas with documented infarction were associated with a positive maternal thrombophilia result. In contrast, 67 of 108 (62.3%) placentas showed features of abnormal placental development or differentiation and 85 of 108 (78.7%) had evidence of noninfarct-related maternal vascular underperfusion (P<.001). Only four of 108 (3.7%) infarcted placentas had no other pathologic lesions. CONCLUSION: Our data indicate that gross and histologic features of abnormal placentation associate strongly with placental infarction in comparison with maternal thrombophilia tests. LEVEL OF EVIDENCE: II.
OBJECTIVE: To estimate the relative importance of positive maternal thrombophilia testing compared with additional pathological evidence of abnormal placentation with placental infarction. METHODS: We performed a retrospective cohort study over a 10-year period in 180 singleton high-risk pregnancies (delivery at 22-34 6/7 weeks of gestation) that had histologic evidence of placental infarction. The rate of positive maternal tests for antiphospholipid syndrome, factor V Leiden, and prothrombin gene mutation were compared with the rate of detection of one or more gross or histological features of abnormal placentation (impaired placental development or differentiation, maternal vascular underperfusion, fetal vascular underperfusion, chronic inflammation, or intervillous thrombosis). RESULTS: Only 14 of 108 (13.0%) of placentas with documented infarction were associated with a positive maternal thrombophilia result. In contrast, 67 of 108 (62.3%) placentas showed features of abnormal placental development or differentiation and 85 of 108 (78.7%) had evidence of noninfarct-related maternal vascular underperfusion (P<.001). Only four of 108 (3.7%) infarcted placentas had no other pathologic lesions. CONCLUSION: Our data indicate that gross and histologic features of abnormal placentation associate strongly with placental infarction in comparison with maternal thrombophilia tests. LEVEL OF EVIDENCE: II.