Abstract
BackgroundSystemic inflammation, endothelial dysfunction and deficient vascularization of either uterus or myocardium are mechanistic hallmarks of early-onset preeclampsia and heart failure with preserved ejection fraction (HFpEF). HFpEF is especially prevalent in elderly women and preceded in middle age by preclinical left ventricular (LV) diastolic dysfunction.To detect if preeclampsia predisposes to HFpEF at later age, echocardiographic indices of LV function and of LV structure and biomarkers of systemic inflammation and of endothelial dysfunction were compared in middle-aged women with a history of early-onset preeclampsia or uncomplicated pregnancy.Methods and findingsMiddle-aged women with a history of early-onset preeclampsia (n = 131) or uncomplicated pregnancy (n = 56) were prospectively recruited 9 to 16 years after pregnancy.Women with a history of preeclampsia had higher body mass index (p = 0.006), blood pressure (p<0.001) and plasma levels of interleukin-6 (p = 0.005) and soluble intercellular adhesion molecule-1 (sICAM-1) (p = 0.014). They had thicker septal (p = 0.001) and posterior (p = 0.003) LV walls and worse diastolic LV function evident from reduced mean mitral annular lengthening velocity (E’mean; p = 0.007) and higher ratio of early diastolic mitral flow velocity (E) over E’mean (E/E’mean; p<0.001). Differences of sICAM-1, E’mean and E/E’mean remained significant after accounting for BMI and blood pressure.ConclusionsHistory of preeclampsia predisposes in middle age to worse LV diastolic function, which could increase the likelihood of later HFpEF development. This predisposition derives not only from persistent cardiovascular risk but may also be caused by persistent endothelial dysfunction hindering adequate vascularization in the uterus during pregnancy and in the myocardium in middle age.
Highlights
History of preeclampsia predisposes in middle age to worse left ventricular (LV) diastolic function, which could increase the likelihood of later heart failure with preserved ejection fraction (HFpEF) development
Early-onset preeclampsia is currently attributed to generalized maternal endothelial dysfunction mainly evident from arterial hypertension and proteinuria, which are respectively induced by disturbed vascular reactivity and glomerular leakage[1]
An emerging paradigm for HFpEF suggests HFpEF to be driven by a signalling cascade sharing many features with preeclampsia as it involves metabolic risk, systemic inflammation, endothelial dysfunction, oxidative stress and myocardial infiltration by macrophages[11,12,13]
Summary
Early-onset preeclampsia is currently attributed to generalized maternal endothelial dysfunction mainly evident from arterial hypertension and proteinuria, which are respectively induced by disturbed vascular reactivity and glomerular leakage[1]. Maternal endothelial dysfunction is presumed to result from placental release of antiangiogenic factors like sFlt-1, which counteract proangiogenic factors like PIGF in transforming small caliber uterine spiral vessels into large caliber capacitance vessels necessary to maintain normal placental function[2]. In accordance with this deranged equilibrium between antiangiogenic and proangiogenic factors, relative concentrations of sFlt-1 and PIGF were recently suggested to predict evolving preeclampsia[3]. To detect if preeclampsia predisposes to HFpEF at later age, echocardiographic indices of LV function and of LV structure and biomarkers of systemic inflammation and of endothelial dysfunction were compared in middle-aged women with a history of early-onset preeclampsia or uncomplicated pregnancy
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