Maternal vascular malperfusion of the placental bed associated with hypertensive disorders in the Boston Birth Cohort

Abstract

Introduction The associations of maternal conditions, before or during pregnancy, with placental lesions have not been adequately studied in populations. Methods In the Boston Birth Cohort, we evaluated associations between three maternal medical conditions (hypertensive disorders [HDs], gestational/pre-gestational diabetes and obesity), and placental histological findings, using a standardized classification system proposed by the Amsterdam Placental Workshop Group. Placental pathology diagnoses and clinical data from 3,074 mothers with clinical indications who delivered singleton live births at the Boston Medical Center between October 1998 and November 2013 were evaluated. Associations between each maternal condition and maternal vascular malperfusion (MVM) of the placental bed and its standardized subgroups were examined using multivariate logistic and multinomial regressions. Results Women with HDs (chronic hypertension, eclampsia, preeclampsia, HELLP syndrome) had significantly increased odds of MVM lesions when compared to women with no HD (aOR 2.08 95% CI 1.74–2.50), after adjusting for demographics, substance use, diabetes and body mass index. No significant differences in frequencies or aORs were seen in women with and without diabetes, or across body mass index categories. Co-morbid condition patterns that included HDs were more likely to be associated with MVM than those without. Discussion Using a standardized classification system, we showed that MVM is strongly and specifically associated with maternal HDs, but not other maternal conditions. Additional studies are needed to confirm and validate our findings, and evaluate the role of maternal vascular lesions of the placental bed in relation to postnatal growth and development of the offspring and effect modifiers.

Maternal vascular malperfusion of the placental bed

“…The presence of features of MVM is higher in cases with severe preterm preeclampsia than it is with term preeclampsia, suggesting that later onset preeclampsia may have a different biologic mechanism that is yet to be understood . MVM can also be seen with other hypertensive disorders of pregnancy including chronic hypertension, eclampsia, and hemolysis, elevated liver enzymes, low platelets (HELLP) syndrome . In addition MVM lesions are associated with abnormal uterine artery Doppler flow and oligohydramnios, likely secondary to increased fetal vascular resistance, poor fetal/renal perfusion, and decreased urine output.…”

High normal blood pressure increase risks of developing adverse pregnancy outcomes

“…Additionally, risks of SGA birth increased by 2.0% (95% CI 1.5, 2.8) per each one mm Hg rise in DBP during pregnancy [8]. The possible biological rationale for this association is that high blood pressure, along with placental gene expression and function, affects critical components of maternal metabolism [18]. Study found that impaired maternal perfusion of the placenta (an extrinsic defect) and impaired placental development (an intrinsic defect) could cause SGA [19].…”

Pregnancy complications recur independently of maternal vascular malperfusion lesions

“…While accelerated villous maturation is often included as an MVM lesion [42], it is difficult to diagnose in term placentas [39], and so syncytial clumping was used instead. We used two different approaches to establish evidence of MVM: (A) corrected placenta weight below the 10th percentile and one of the MVM lesions described above [33,43] (which we term "MVM narrow "), or (B) one of the MVM lesions described, irrespective of placental weight [31,35] (which we term "MVM broad "). Although not all of the lesions currently used to define MVM were available in the NCPP data, there is substantial variability in the criteria used among recent studies ( Table 1), such that our study is as similar to some recent studies as the recent studies are to each other.…”

“…decidual vasculopathy [31,35,37,44,45], decidual vascular thrombosis [31]; decidual arteriopathy [30,42]; arterial thrombosis [42] decidua vessel thrombosis fibrinoid changes/necrosis in decidual vessels [31]; fibrinoid necrosis [42] decidua vessel fibrinoid acute atherosis [31,42], decidual vasculopathy atherosis [43];…”

“…These studies have not examined the placental pathology that may underlie these associations, but impaired placentation is thought to result in maternal vascular malperfusion (MVM) lesions [30], which are associated with pregnancy complications [31][32][33][34][35]. Indeed, there are associations between MVM lesions in one pregnancy and the incidence of adverse outcomes in a subsequent pregnancy [36,37].…”