Multi-Fetal Pregnancy, Preeclampsia, and Long-Term Cardiovascular Disease. Issue 1 (July 2020)

• Record Type: Journal Article
• Authors: Bergman, Lina; Nordlöf-Callbo, Paliz; Wikström, Anna Karin; Snowden, Jonathan M.; Hesselman, Susanne; Edstedt Bonamy, Anna Karin; Sandström, Anna
• Is Part Of: Hypertension. Volume 76:Issue 1(2020)
• Publication Date: 2020-07
• Subjects: cardiovascular diseases -- phenotype -- preeclampsia -- pregnancy -- risk; Hypertension -- Periodicals; Hypertension -- Treatment -- Periodicals; 616.132005
• DOI: 10.1161/HYPERTENSIONAHA.120.14860
• Languages: English
• ISSNs: 0194-911X

Abstract

Abstract : This Swedish register-based cohort study determined the separate and joint contribution of preeclampsia and multi-fetal pregnancy on a woman's risk of cardiovascular disease (CVD) later in life. The study included 892 425 first deliveries between 1973 and 2010 of women born 1950 until 1971, identified in the Swedish Medical Birth Register. A composite outcome of CVD was retrieved through linkage with the National Patient and Cause of Death Registers. Cox proportional hazard regression was used to assess the risk of CVD in women who had preeclampsia in a singleton or multi-fetal pregnancy, adjusting for potential confounders, and presented as adjusted hazard ratios. Compared with women who had a singleton pregnancy without preeclampsia (the referent group), women with preeclampsia in a singleton pregnancy had an increased risk of CVD (adjusted hazard ratio 1.75 [95% CI, 1.64–1.86]). Women who had a multi-fetal pregnancy without or with preeclampsia did not have an increased risk of future CVD (adjusted hazard ratios 0.94 [95% CI, 0.79–1.10] and 1.25 [95% CI, 0.83–1.86], respectively). As opposed to preeclampsia in a first singleton pregnancy, preeclampsia in a first multi-fetal pregnancy was not associated with increased risk of future CVD. This may support the theory that preeclampsia in multi-fetal pregnancies more often occurs as a result of the larger pregnancy-related burden on the maternal cardiovascular system and excessive placenta-shed inflammatory factors, rather than the woman's underlying cardiovascular phenotype. Abstract : Supplemental Digital Content is available in the text.