Preeclampsia and Maternal Cardiovascular Disease: Consequence or Predisposition?

Abstract

Formerly preeclamptic women stand a higher chance of developing cardiovascular disease (CVD) later in life and may experience a shortened life span. This review updates the pathophysiology and definition of this complex disease and highlights the protective role of pregnancy by considering the relationship between pregnancy interval and likelihood of disease recurrence. The evidence for persistent maternal cardiovascular impairment following preeclampsia (PE) is considered, e.g. postpartum changes in CVD occurrence, blood pressure elevation and changes in the renin-angiotensin-aldosterone system). Since maternal endothelial dysfunction is a hallmark of PE, we summarize the evidence for reduced flow-mediated dilation in women with previous PE, and consider the utility and shortcomings of this clinical measure. In addition to viewing postpartum changes as a consequence of this disease, we consider the alternative view that PE might be the manifestation of a maternal phenotype that already has some predisposition to or is in the earlier stages of CVD; in this case, some of the postpartum residual deficits (or their antecedents) may have already been present prior to pregnancy. Finally, we consider the use of novel biomarkers for predicting or detecting PE prior to the appearance of clinical symptoms.

Hypertensive Disorders of Pregnancy and Future Maternal Cardiovascular Risk

“…Furthermore, preeclamptic women develop activating angiotensin II type 1 autoantibodies during pregnancy that persist after 18 months postpartum 33. Binding of these antibodies to the angiotensin 1 receptor has been shown to induce endothelial damage and may be a mechanistic link between preeclampsia and subsequent CVD risk 34. However, the relationship between preeclampsia and endothelial dysfunction is controversial, as other studies have failed to find an association between preeclampsia and functional markers of endothelial dysfunction, such as flow‐mediated dilation 35, 36.…”

Personalized Therapy Against Preeclampsia by Replenishing Placental Protein 13 (PP13) Targeted to Patients With Impaired PP13 Molecule or Function

“…Obese women who become pregnant at advanced maternal age have 21% risk for developing PE and later CVDs. The American Heart Association has published a white paper describing the life-long complications related to PE, and its association with a higher susceptibility to develop CVDs, and has issued specific guideline for the clinical surveillance of this group [45], [46].…”

Predicting the Risk to Develop Preeclampsia in the First Trimester Combining Promoter Variant -98A/C of LGALS13 (Placental Protein 13), Black Ethnicity, Previous Preeclampsia, Obesity, and Maternal Age

“…Single nucleotide polymorphisms (SNPs) have been identified as risk factors for PE leading to gestational hypertension [9], vasodilatation [10], angiogenesis regulation [11], interleukin-related inflammation [12], and human placental diseases [13, 14]. Affected pathways include: impaired placentation [15], immune-fetal rejection [16], anti-angiogenic state [17], and various cardiovascular disorders [18, 19]. …”