Placental decidual arteriopathy and vascular endothelial growth factor A (VEGF-A) expression among women with and without HIV

Abstract

Background: Women with HIV (WHIV) are at higher risk of adverse birth outcomes. Proposed mechanisms for the increased risk include placental arteriopathy (vasculopathy) and maternal vascular malperfusion (MVM) due to antiretroviral therapy (ART) and medical comorbidities. However, these features and their underlying pathophysiologic mechanisms have not been well characterized in WHIV. Methods: We performed gross and histologic examination and immunohistochemistry staining for vascular endothelial growth factor A (VEGF-A), a key angiogenic factor, on placentas from women with one or more MVM risk factors including: weight <5th percentile, histologic infarct or distal villous hypoplasia, nevirapine-based ART, hypertension, and pre-eclampsia/eclampsia during pregnancy. We compared pathologic characteristics by maternal HIV serostatus. Results: A total of 27/41 (66%) placentas assessed for VEGF-A were from WHIV. Mean maternal age was 27 years. Among WHIV, median CD4 T-cell count was 440 cells/mm3 and HIV viral load was undetectable in 74%. Of VEGF-A stained placenta, both decidua and villous endothelium tissue layers were present in 36 (88%). VEGF-A was detected in 31/36 (86%) with decidua present, and 39/40 (98%) with villous endothelium present. There were no differences in VEGF-A presence in any tissue type by maternal HIV serostatus (P=0.28-1.0). MVM was more common in placentas selected for VEGF-A staining (51 versus 8%, P<0.001). Conclusions: VEGF-A immunostaining was highly prevalent, and staining pattern did not differ by maternal HIV serostatus among those with MVM risk factors, indicating the role of VEGF-A in placental vasculopathy may not differ by maternal HIV serostatus.