May Ching Soh1, Fadia Dib2, Catherine Nelson-Piercy2, Magnus Westgren3, Lesley McCowan4, Dharmintra Pasupathy5. 1. Division of Women's Health, Women's Health Academic Centre, King's College London, King's Health Partners, London, UK Department of Obstetrics & Gynaecology, South Auckland Clinical School, University of Auckland & National Women's Health, Auckland, New Zealand. 2. Division of Women's Health, Women's Health Academic Centre, King's College London, King's Health Partners, London, UK. 3. Department of Clinical Science, Intervention and Technology Karolinska Institutet, Sweden. 4. Department of Obstetrics & Gynaecology, South Auckland Clinical School, University of Auckland & National Women's Health, Auckland, New Zealand. 5. Division of Women's Health, Women's Health Academic Centre, King's College London, King's Health Partners, London, UK dharmintra.pasupathy@kcl.ac.uk.
Abstract
OBJECTIVES: Women with SLE are at increased risk of cardiovascular events (CVEs), but a relationship with traditional cardiovascular and SLE-specific risk factors has not been established. In unselected populations, adverse pregnancy outcomes linked to maternal-placental syndrome (MPS) are associated with an increased risk of CVEs. However, the effect of MPS on CVEs is unknown in women with SLE. The aim of this study was to determine if MPS increased the risk and accelerated the development of CVEs in women with SLE. METHODS: Utilizing Swedish population registries, parous women with SLE were identified. Exposures were the following: MPS defined as hypertensive disorders of pregnancy; small-for-gestational-age; placental abruption and stillbirth; and preterm delivery <34 weeks. Outcomes were CVE encompassing cardiovascular morbidity and mortality. Risk of an event was modelled using Cox proportional hazards adjusted for year of delivery, age at CVE, severity of SLE and cardiovascular risk factors. Time-to-CVE was estimated using Kaplan-Meier methods. RESULTS: Over the 38-year study period, there were 3977 women with 7410 pregnancies, of whom 413 (10.2%) suffered a CVE. Hazard of CVE was higher in those with MPS, particularly when MPS (adjusted HR = 1.64; 95% CI: 1.31, 2.05) was combined with preterm delivery < 34 weeks' gestation (adjusted HR 1.99; 95% CI 1.39, 2.84). There was accelerated development of CVEs in women with MPS of 10.5% (vs 7.3% in uncomplicated pregnancies) over the 38-year interval (P < 0.05). CONCLUSION: Pregnancy complicated by MPS and preterm delivery exerts an independent effect to increase the risk and accelerate the development of CVEs in parous women with SLE.
OBJECTIVES:Women with SLE are at increased risk of cardiovascular events (CVEs), but a relationship with traditional cardiovascular and SLE-specific risk factors has not been established. In unselected populations, adverse pregnancy outcomes linked to maternal-placental syndrome (MPS) are associated with an increased risk of CVEs. However, the effect of MPS on CVEs is unknown in women with SLE. The aim of this study was to determine if MPS increased the risk and accelerated the development of CVEs in women with SLE. METHODS: Utilizing Swedish population registries, parous women with SLE were identified. Exposures were the following: MPS defined as hypertensive disorders of pregnancy; small-for-gestational-age; placental abruption and stillbirth; and preterm delivery <34 weeks. Outcomes were CVE encompassing cardiovascular morbidity and mortality. Risk of an event was modelled using Cox proportional hazards adjusted for year of delivery, age at CVE, severity of SLE and cardiovascular risk factors. Time-to-CVE was estimated using Kaplan-Meier methods. RESULTS: Over the 38-year study period, there were 3977 women with 7410 pregnancies, of whom 413 (10.2%) suffered a CVE. Hazard of CVE was higher in those with MPS, particularly when MPS (adjusted HR = 1.64; 95% CI: 1.31, 2.05) was combined with preterm delivery < 34 weeks' gestation (adjusted HR 1.99; 95% CI 1.39, 2.84). There was accelerated development of CVEs in women with MPS of 10.5% (vs 7.3% in uncomplicated pregnancies) over the 38-year interval (P < 0.05). CONCLUSION: Pregnancy complicated by MPS and preterm delivery exerts an independent effect to increase the risk and accelerate the development of CVEs in parous women with SLE.
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