Maternal Morbidity and Mortality: Are We Getting to the “Heart” of the Matter?

Figures

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  FIG. 1.. Signaling pathways, potential biomarkers, and therapeutic targets in PE. Placental ischemia-derived imbalance in proangiogenic (VEGF and PlGF) and antiangiogenic (sFlt-1 and sEng) factors, oxidative stress, and inflammation led to systemic vascular dysfunction reflected in hypertension and proteinuria in PE. Potential targeted interventions include blockade, removal, or competitive binding of sFlt-1 or supplementation of recombinant isoforms of proangiogenic factors. AT1-AA, AT1 receptor autoantibodies; PE, preeclampsia; PlGF, placental growth factor; sEng, soluble endoglin; sFlt-1, soluble fms-like tyrosine kinase-1; VEGF, vascular endothelial growth factor.

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  FIG. 2.. Pathophysiology of peripartum cardiomyopathy. In pathogenesis of peripartum cardiomyopathy, the role of cathepsin D-cleaved 16-kDa prolactin fragment, microRNA146a, and decreased VEGF signaling has been suggested. Suppression of prolactin production by bromocriptine had positive therapeutic effects in some preclinical and clinical studies. STAT3, signal transducer and activator of transcription 3.

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  FIG. 3.. Accumulation of cardiovascular risk factors from preconception through pregnancy and postpartum periods. Demographic, clinical, behavioral, social, and environmental risk factors for cardiovascular disease may contribute to adverse pregnancy outcomes. These may persist throughout pregnancy and postpartum periods. Additional cardiovascular risk may be acquired or uncovered during pregnancy, including maternal conditions (hypertensive disorders of pregnancy and gestational diabetes) and fetal conditions (small for gestational age). Preconception and pregnancy risks may persist during the postpartum period and/or emergence of additional cardiovascular risk factors may occur, including maternal conditions (hypertension, diabetes, and dyslipidemia).