title: Spiral artery remodeling and maternal cardiovascular risk: the spiral artery remodeling (SPAR) study.
abstract: Women with a history of placental bed disorders, including preeclampsia and intrauterine growth restriction have an increased long-term risk of cardiovascular disease (CVD). Further, similarities exist between atherosclerosis and abnormalities observed in placental bed spiral arteries in pregnancies affected by preeclampsia and intrauterine growth restriction, such as acute atherosis and defective remodeling. This suggests a common pathophysiological pathway underlying both disorders.
  
  
  
  The aim of this study was to investigate vascular and inflammatory lesions in the placental bed of women with preeclampsia and normal pregnancy using a systematic approach to characterize lesions of the placental bed, and relate spiral artery pathology to postpartum CVD risk assessment.
  
  
  
  Placental bed punch biopsies were performed following caesarean section and systematically studied to assess vascular pathology, arterial remodeling, and the presence of CD3, CD56, and CD68 cells. In addition, levels of modifiable CVD risk factors were assessed immediately postpartum.
  
  
  
  We found fewer spiral arteries with complete remodeling in women with preeclampsia than in the control group (21 vs. 68%; P = 0.008). Further, women with preeclampsia showed less presence of CD3 cells in both the decidua and the myometrium. Preliminary findings of CVD risk factor assessment postpartum suggest a correlation between acute atherosis and higher triglyceride and low-density lipoprotein cholesterol levels.
  
  
  
  Systematic study of vascular pathology in uterine spiral artery biopsy samples in relation to CVD risk factors provides valuable insight into the link between cardiovascular health and placental bed disorders.
authors.affiliation: aDivision Woman and Baby, Wilhelmina Children's Hospital Birth Center, Department of Obstetrics, University Medical Center Utrecht bDepartment of Pathology, University Medical Center Utrecht, Utrecht, The Netherlands cAcademic Unit of Human Development and Health, University of Southampton, Princess Anne Hospital, Coxford Road, Southampton, UK *Arie Franx and Bas B. van Rijn have contributed equally to the writing of this article.
authors.forename: Jan H W
authors.initials: JH
authors.lastname: Veerbeek
authors.forename: Laura
authors.initials: L
authors.lastname: Brouwers
authors.forename: Maria P H
authors.initials: MP
authors.lastname: Koster
authors.forename: Steven V
authors.initials: SV
authors.lastname: Koenen
authors.forename: Elvira O G
authors.initials: EO
authors.lastname: van Vliet
authors.forename: Peter G J
authors.initials: PG
authors.lastname: Nikkels
authors.forename: Arie
authors.initials: A
authors.lastname: Franx
authors.forename: Bas B
authors.initials: BB
authors.lastname: van Rijn
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000032:analysis; D015214:Antigens, Differentiation, Myelomonocytic / Q000032:analysis; D001158:Arteries / Q000473:pathology* / Q000503:physiopathology; D017252:CD3 Complex / Q000032:analysis; D019002:CD56 Antigen / Q000032:analysis; D002318:Cardiovascular Diseases / Q000503:physiopathology; D016022:Case-Control Studies; D008078:Cholesterol, LDL / Q000097:blood*; D003656:Decidua / Q000473:pathology; D005260:Female; D006801:Humans; D009215:Myometrium / Q000473:pathology; D010920:Placenta / Q000098:blood supply / Q000473:pathology*; D049590:Postpartum Period; D011225:Pre-Eclampsia / Q000473:pathology* / Q000503:physiopathology; D011247:Pregnancy; D012307:Risk Factors; D013601:T-Lymphocytes / Q000737:chemistry; D014280:Triglycerides / Q000097:blood*; D066253:Vascular Remodeling; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D017252:CD3 Complex; D019002:CD56 Antigen; D008078:Cholesterol, LDL; D014280:Triglycerides; C067980:CD68 antigen, human; D000097382:CD68 Molecule