Persistent Maternal Cardiac Dysfunction After Preeclampsia Identifies Patients at Risk for Recurrent Preeclampsia

Valensise, H.; Presti, D. Lo; Gagliardi, G.; Tiralongo, G.; Pisani, I.; Novelli, G. P.; Vasapollo, B.

doi:10.1161/hypertensionaha.115.06674

Cited by 54 publications

(54 citation statements)

References 41 publications

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“…44 In addition, these changes allow for early identification of women at highest risk of recurrent preeclampsia in their next pregnancy and, therefore may also provide an opportunity for intervention to mitigate future cardiovascular disease. 45 Once detected, subclinical changes in cardiac function may be amenable to cardioprotective therapies, such as β-blocker use. Previous work has demonstrated that in patients receiving cardiotoxic chemotherapy, β-blocker administration reversed worsening of longitudinal strain.…”

Section: Discussionmentioning

confidence: 99%

Circulating Antiangiogenic Factors and Myocardial Dysfunction in Hypertensive Disorders of Pregnancy

et al. 2016

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H ypertensive disorders of pregnancy (HDP) affect 5% to 10% of pregnant women, 1 are the most common medical complication of pregnancy in developed countries, 2 and are a leading cause of maternal and fetal death worldwide. 3 HDP include preeclampsia, gestational hypertension, chronic hypertension, and superimposed preeclampsia. Preeclampsia targets the vascular endothelium causing widespread maternal vascular endothelial dysfunction. Antiangiogenic proteins have been implicated as being pathogenic in the development of the observed vascular endothelial dysfunction. 4Overexpression of soluble fms-like tyrosine kinase-1 (sFlt1), an endogenous vascular endothelial growth factor inhibitor, is associated with preeclampsia-like phenotypes in a rodent model and symptoms diminish with the addition of vascular endothelial growth factor or placental growth factor. [5][6][7] Multiple human clinical studies have established that levels of the sFlt1 and soluble endoglin (sEng) increase in the circulation of pregnant women with preeclampsia. 4,6,[8][9][10] sFlt1 and sEng levels are elevated weeks before the clinical onset of preeclampsia, and the degree of elevation correlates with adverse maternal and fetal outcomes. 8,[11][12][13][14][15][16] Few adverse outcomes occur in the absence of angiogenic factor abnormalities. 17,18 Although previous studies have detected changes in myocardial function in HDP, 19,20 a direct association between preeclampsia biomarkers, including sFlt1 and sEng, has not been described. In other abnormal cardiovascular states such as congestive heart failure, increased circulating levels of antiangiogenic proteins have been associated with development of endothelial vascular dysfunction, myocardial dysfunction, and adverse cardiovascular outcomes. 21Women with HDP have abnormalities in both systolic and diastolic cardiac function that seem before clinical symptoms.19,22 Despite preservation of left ventricular ejection fraction (LVEF), 23 longitudinal muscle fiber shortening is decreased, suggesting the presence of subclinical left ventricular systolic dysfunction. 20 This finding suggests a Abstract-Hypertensive disorders of pregnancy (HDP) are associated with subclinical changes in cardiac function. Although the mechanism underlying this finding is unknown, elevated levels of soluble antiangiogenic proteins such as soluble fms-like tyrosine kinase-1 (sFlt1) and soluble endoglin (sEng) are associated with myocardial dysfunction and may play a role. We hypothesized that these antiangiogenic proteins may contribute to the development of cardiac dysfunction in HDP. We prospectively studied 207 pregnant women with HDP and nonhypertensive controls and evaluated whether changes in global longitudinal strain (GLS) observed on echocardiography is specific for HDP and whether these changes correlate with HDP biomarkers, sFlt1 and sEng. A total of 62 (30%) patients were diagnosed with preeclampsia (group A), 105 (51%) did not have an HDP (group B), and 40 (19%) were diagnosed with chronic or gestational hype...

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Section: Discussionmentioning

confidence: 99%

Circulating Antiangiogenic Factors and Myocardial Dysfunction in Hypertensive Disorders of Pregnancy

et al. 2016

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“…Interestingly, the list of predisposing factors for PE is almost the same as that for CKD, once more stressing the similarities between these diseases ( Table 2). Further elements, including genetic predisposition, are included in the list of risk factors for recurrent PE; once again, the similarities with CKD are evident [65][66][67][68][69][70][71][72][73][74][75][76][77][78][79]. However, in most of these lists there is an important overlap between predisposing maternal diseases, including CKD, and specific conditions that may impair placentation, including parity or genetic factors.…”

Section: Introductionmentioning

confidence: 99%

A best practice position statement on the role of the nephrologist in the prevention and follow-up of preeclampsia: the Italian study group on kidney and pregnancy

Piccoli

Cabiddu

Castellino³

et al. 2017

J Nephrol

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Preeclampsia (PE) is a protean syndrome causing a transitory kidney disease, characterised by hypertension and proteinuria, ultimately reversible after delivery. Its prevalence is variously estimated, from 3 to 5% to 10% if all the related disorders, including also pregnancy-induced hypertension (PIH) and HELLP syndrome (haemolysis, increase in liver enzyme, low platelets) are included. Both nephrologists and obstetricians are involved in the management of the disease, according to different protocols, and the clinical management, as well as the role for each specialty, differs worldwide. The increased awareness of the role of chronic kidney disease in pregnancy, complicating up to 3% of pregnancies, and the knowledge that PE is associated with an increased risk for development of CKD later in life have recently increased the interest and redesigned the role of the nephrologists in this context. However, while the heterogeneous definitions of PE, its recent reclassification, an emerging role for biochemical biomarkers, the growing body of epidemiological data and the new potential therapeutic interventions lead to counsel long-term follow-up, the lack of resources for chronic patients and the increasing costs of care limit the potential for preventive actions, and suggest tailoring specific interventional strategies. The aim of the present position statement of the Kidney and Pregnancy Study Group of the Italian Society of Nephrology is to review the literature and to try to identify theoretical and pragmatic bases for an agreed management of PE in the nephrological setting, with particular attention to the prevention of the syndrome (recurrent PE, presence of baseline CKD) and to the organization of the postpartum follow-up.

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“…This result aligns with findings of persistent cardiac hypertrophy up to a year postpartum in a subset of preeclamptic women. 7, 53 …”

Section: Discussionmentioning

confidence: 99%

Pregnancy-Associated Cardiac Hypertrophy in Corin-Deficient Mice: Observations in a Transgenic Model of Preeclampsia

Baird

Wang

et al. 2019

Canadian Journal of Cardiology

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Background: Preeclampsia increases the risk of heart disease. Defects in the protease corin, including the variant T555I/Q568P found in ~12% of blacks, have been associated with preeclampsia and cardiac hypertrophy. The objective of this study is to investigate the role of corin and the T555I/Q568P variant in preeclampsia-associated cardiac alterations using genetically modified mouse models. Methods: Virgin wild-type (WT) and corin knockout mice with or without a cardiac WT corin or T555I/Q568P variant transgene were mated at 3 or 6 months of age. Age- and genotype-matched virgin mice were used as controls. Cardiac morphology and function were assessed at gestational day 18.5 or 28 days postpartum by histological and echocardiographic analyses. Results: Pregnant corin knockout mice at gestational day 18.5 developed cardiac hypertrophy. Such a pregnancy-associated phenotype was not found in WT or corin knockout mice with a cardiac WT corin transgene. Pregnant corin knockout mice with a cardiac T555I/Q568P variant transgene developed cardiac hypertrophy similar to that in pregnant corin knockout mice. The cardiac hypertrophy persisted postpartum in corin knockout mice and was worse if the mice were mated at 6 instead of 3 months of age. There was no hypertrophy-associated decrease in cardiac function in pregnant corin knockout mice. Conclusions: In mice, corin deficiency causes cardiac hypertrophy during pregnancy. Replacement of cardiac WT corin, but not the T555I/Q568P variant found in blacks, rescues this phenotype, indicating a local anti-hypertrophic function of corin in the heart. Corin deficiency may represent an underlying mechanism in preeclampsia-associated cardiomyopathies.

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Persistent Maternal Cardiac Dysfunction After Preeclampsia Identifies Patients at Risk for Recurrent Preeclampsia

Cited by 54 publications

References 41 publications

Circulating Antiangiogenic Factors and Myocardial Dysfunction in Hypertensive Disorders of Pregnancy

Circulating Antiangiogenic Factors and Myocardial Dysfunction in Hypertensive Disorders of Pregnancy

A best practice position statement on the role of the nephrologist in the prevention and follow-up of preeclampsia: the Italian study group on kidney and pregnancy

Pregnancy-Associated Cardiac Hypertrophy in Corin-Deficient Mice: Observations in a Transgenic Model of Preeclampsia

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