This review highlights shared mechanistic pathways between preeclampsia and cardiovascular disease, identifying potential targets for future risk reduction trials.
Preeclampsia is a syndrome of hypertension in association with target organ dysfunction, including proteinuria, which manifests during pregnancy and the immediate postpartum period. The pathophysiology of preeclampsia originates from impaired trophoblastic invasion of the placental resulting in malperfusion and involves multiple mechanistic pathways that include anti-angiogenic factors, endothelial dysfunction, and immune dysregulation. Preeclampsia caries an increased risk of subclinical cardiovascular disease including left ventricular remodeling, diastolic dysfunction, coronary artery calcification, peripheral vascular abnormalities, and microvascular dysfunction and clinical cardiovascular disease including stroke, heart failure, myocardial infarction, and death from a cardiovascular cause. This review will highlight several common mechanistic pathways shared between preeclampsia and cardiovascular diseases that provide insight into potential targets for risk reduction and disease process mitigation that can be examined in future trials.
Countouris et al. (Thu,) studied this question.