About this trial

Pregnancy is considered a cardiovascular (CV) stress test, and complicated pregnancies are associated with an increased risk for cardiovascular disease (CVD) later in life. Moreover, it is known that often the pregnancy induced CV adaptation does not resolve completely after a short postpartum (PP) period and it is not clear whether these induced changes will resolve over a longer period of time (i.e. in the upcoming months/years after delivery).

Understanding the cardiac adaptation during pregnancy and the reversal process in the postpartum period, as well as the factors that influence this these processes, may provide us not only insight in this mechanism, but may help us in identifying factors that may be target points for modification.

Eligibility criteria

This trial accepts healthy volunteers

Qualifiers

Women aged ≥ 18 years

Controls: Women with an uncomplicated pregnancy at the moment of inclusion (i.e no foetal or maternal placental complications, such as pregnancy induced hypertension, preeclampsia or HELLP-syndrome, or small for gestational birth infancies)

Cases: Women diagnosed with a preeclamptic pregnancy at the moment of inclusion

Disqualifiers

Allergy or intolerance to glyceryl trinitrate, betablockers or iodinated contrast media.

Controls: Pre-existing chronic hypertension treated with antihypertensive medication or autoimmune disorder.

Trial population

The study population consists of pregnant women who either develop pre-eclampsia or have a normotensive pregnancy. For the shorter follow up period, participants are recruited from the (labour) ward and from the outpatient clinic in MUMC+. Participants are also recruited externally from other hospitals if they contact us with an interest in this study. For the longer follow up period, case participants took part in an earlier study and agreed to be contacted for future studies. These participants were recruited through a letter with information about the study. Control participants were recruited when they contacted us with interest in this study.

Trial design

Design model

Cohort

Time perspective

Prospective

Treatments tested in this trial

Not listed

Trial groups

226 Participants

are grouped into 6 trial groups

6

Trial groups

See each trial group below.

Group A: Short track controls

Group B: Short track early PE with IUGR

Group C: Short track early PE without IUGR

Group D: Short track late PE with IUGR

Group E: Short track late PE without IUGR

Group F: Long term follow up track cases

Trial outcomes

Primary outcomes

1

Relationship between placental acute atherosis and subclinical coronary atherosclerosis at 1 year postpartum

Acute atherosis will be defined as the presence of subendothelial lipid-filled foam cells on placental histopathological analysis. It will be measured as either present or absent. Subclinical coronary atherosclerosis will be measured using CT contrast angiography. This will be measured visually and split into the following categories: any atherosclerosis, wall irregularities, soft plaque and calcified plaque/stenosis. The incidence of acute atherosis will be compared with each of the subcategories of subclinical coronary atherosclerosis for the pre-eclamptic and normotensive groups at 1 year postpartum.

Time frame

1 year

2

Relationship between placental acute atherosis and subclinical coronary atherosclerosis at 15 years postpartum

Acute atherosis will be defined as the presence of subendothelial lipid-filled foam cells on placental histopathological analysis. It will be measured as either present or absent. Subclinical coronary atherosclerosis will be measured using CT contrast angiography. This will be measured visually and split into the following categories: any atherosclerosis, wall irregularities, soft plaque and calcified plaque/stenosis. The incidence of acute atherosis will be compared with each of the subcategories of subclinical coronary atherosclerosis for the pre-eclamptic and normotensive groups at 15 years postpartum.

Time frame

15 years

3

Relationship between decidual vasculopathy and subclinical coronary atherosclerosis at 1 year postpartum

Decidual vasculopathy will be defined as the presence of subendothelial lipid-filled foam cells, fibrinoid necrosis, mural hypertrophy, chronic perivasculitis, absence of spiral artery remodelling and/or persistence of intramural endovascular trophoblast in the third trimester on placental histopathological analysis. It will be measured as either present or absent. Subclinical coronary atherosclerosis will be measured using CT contrast angiography. This will be measured visually and split into the following categories: any atherosclerosis, wall irregularities, soft plaque and calcified plaque/stenosis. The incidence of decidual vasculopathy will be compared with each of the subcategories of subclinical coronary atherosclerosis for the pre-eclamptic and normotensive groups at 1 year postpartum.

Time frame

1 year

4

Relationship between placental decidual vasculopathy and subclinical coronary atherosclerosis at 15 years postpartum

Decidual vasculopathy will be defined as the presence of subendothelial lipid-filled foam cells, fibrinoid necrosis, mural hypertrophy, chronic perivasculitis, absence of spiral artery remodelling and/or persistence of intramural endovascular trophoblast in the third trimester on placental histopathological analysis. It will be measured as either present or absent. Subclinical coronary atherosclerosis will be measured using CT contrast angiography. This will be measured visually and split into the following categories: any atherosclerosis, wall irregularities, soft plaque and calcified plaque/stenosis. The incidence of decidual vasculopathy will be compared with each of the subcategories of subclinical coronary atherosclerosis for the pre-eclamptic and normotensive groups at 15 years postpartum.

Time frame

15 years

Secondary outcomes

1

Relationship between placental acute atherosis and clinical coronary atherosclerosis at 1 year postpartum

Acute atherosis will be defined as subendothelial lipid-filled foam cells on placental histopathological analysis. It will be measured as present or absent. Clinical coronary atherosclerosis will be measured using CT contrast angiography and the agatston score. Calcification score of their coronary arteries is based on the calcification seen on the CT scan. This is a continuous scoring system. The Agatston method uses the weighted sum of lesions with a density above 130 hounsfield units (HU), multiplying the area of calcium by a factor related to maximum plaque attenuation. The agatston score ranges from 0 and has no upper maximum. 0 = absent, 1-100 = low risk of coronary events, 101-400 = medium risk of coronary events, \>400 = high risk of coronary events. The incidence of acute atherosis will be compared with the average agatston score for the pre-eclamptic and normotensive groups at 1 year postpartum.

Time frame

1 year

2

Relationship between placental acute atherosis and clinical coronary atherosclerosis at 15 years postpartum

Acute atherosis will be defined as subendothelial lipid-filled foam cells on placental histopathological analysis. It will be measured as present or absent. Clinical coronary atherosclerosis will be measured using CT contrast angiography and the agatston score. Calcification score of their coronary arteries is based on the calcification seen on the CT scan. This is a continuous scoring system. The Agatston method uses the weighted sum of lesions with a density above 130 HU, multiplying the area of calcium by a factor related to maximum plaque attenuation. The agatston score ranges from 0 and has no upper maximum. 0 = absent, 1-100 = low risk of coronary events, 101-400 = medium risk of coronary events, \>400 = high risk of coronary events. The incidence of acute atherosis will be compared with the average agatston score for the pre-eclamptic and normotensive groups at 15 years postpartum.

Time frame

15 years

3

Relationship between placental decidual vasculopathy and clinical coronary atherosclerosis at 1 year postpartum

Decidual vasculopathy defined as subendothelial lipid-filled foam cells, fibrinoid necrosis, mural hypertrophy, chronic perivasculitis, absence of spiral artery remodelling and/or persistence of intramural endovascular trophoblast in the third trimester on placental histopathological analysis. (Present or absent) Clinical coronary atherosclerosis will be measured using CT contrast angiography and the agatston score. Calcification score of their coronary arteries is based on the calcification seen on the CT scan. This is a continuous scoring system. The Agatston method uses the weighted sum of lesions with a density above 130 HU, multiplying the area of calcium by a factor related to maximum plaque attenuation. Range 0 to no upper maximum. 0 = absent, 1-100 = low risk of coronary events, 101-400 = medium risk, \>400 = high risk. The incidence of decidual vasculopathy compared with average agatston score for the pre-eclamptic and normotensive groups at 1 year postpartum.

Time frame

1 year

4

Relationship between placental decidual vasculopathy and clinical coronary atherosclerosis at 15 years postpartum

Decidual vasculopathy defined as subendothelial lipid-filled foam cells, fibrinoid necrosis, mural hypertrophy, chronic perivasculitis, absence of spiral artery remodelling and/or persistence of intramural endovascular trophoblast in the third trimester on placental histopathological analysis. (Present or absent) Clinical coronary atherosclerosis will be measured using CT contrast angiography and the agatston score. Calcification score of their coronary arteries based on the calcification seen on the CT scan. This is a continuous scoring system. The Agatston method uses the weighted sum of lesions with a density above 130 HU, multiplying the area of calcium by a factor related to maximum plaque attenuation. Range 0 to no upper maximum. 0 = absent, 1-100 = low risk of coronary events, 101-400 = medium risk, \>400 = high risk. The incidence of decidual vasculopathy compared with average agatston score for the pre-eclamptic and normotensive groups at 15 years postpartum.

Time frame

15 years

PlacEntal Acute Atherosis RefLecting Subclinical Atherosclerosis

About this trial

Eligibility criteria

Qualifiers

Disqualifiers

Trial population

Trial design

Treatments tested in this trial

Trial groups

Trial outcomes

Primary outcomes

Secondary outcomes

Other outcomes

Sponsors and contacts