Amalie Bjerke Rieber-Mohn1, Meryam Sugulle2, Gerd Wallukat3, Patji Alnæs-Katjavivi1, Gro Leite Størvold4, Nils Bolstad5, Christopher Wg Redman6, Ralf Dechend7, Anne Cathrine Staff1. 1. Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway; Division of Gynaecology and Obstetrics, Oslo University Hospital, Oslo, Norway. 2. Division of Gynaecology and Obstetrics, Oslo University Hospital, Oslo, Norway. Electronic address: uxsume@ous-hf.no. 3. Experimental and Clinical Research Center, a Joint Cooperation Between the Max-Delbrück Center for Molecular Medicine in the Helmholtz Association and the Charité Medical Faculty, Berlin, Germany. 4. Division of Gynaecology and Obstetrics, Oslo University Hospital, Oslo, Norway; Institute for Experimental Medical Research, Oslo University Hospital, Oslo, Norway. 5. Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway; Department of Medical Biochemistry, Oslo University Hospital, Oslo, Norway. 6. Nuffield Department of Obstetrics and Gynaecology, University of Oxford, Oxford United Kingdom. 7. Experimental and Clinical Research Center, a Joint Cooperation Between the Max-Delbrück Center for Molecular Medicine in the Helmholtz Association and the Charité Medical Faculty, Berlin, Germany; Department of Cardiology and Nephrology, HELIOS Klinikum Berlin, Germany.
Abstract
BACKGROUND: Uteroplacental acute atherosis is a pregnancy-specific lesion resembling early stages of atherosclerosis found frequently in preeclampsia. Preeclampsia is associated with an increased risk for future maternal atherosclerotic cardiovascular disease. The renin-angiotensin-system plays a role both in atherosclerosis and in preeclampsia. Circulating agonistic autoantibodies at the angiotensin-II type 1 receptor (AT1-AA) are increased in preeclampsia. We hypothesized an association between AT1-AA at delivery and postpartum with acute atherosis in pregnancy. MATERIAL AND METHODS: Maternal serum and decidua basalis tissue was collected at elective cesarean section (n = 41; 24 preeclampsia, 17 normotensive controls). Circulating AT1-AA were detected by a bioassay using spontaneously beating rat cardiomyocytes at delivery (n = 41) and 5-8 years postpartum in a subgroup (n = 10). Decidual acute atherosis was assessed by immunohistochemistry. RESULTS: Significantly less normotensive controls (18%; 3/17) than women with preeclampsia (58%; 14/24) were AT1-AA positive at delivery, p<0.01. Uteroplacental acute atherosis and circulating AT1-AA at delivery were not significantly correlated. Postpartum, 2 prior preeclamptic women had circulating AT1-AA, both without acute atherosis in pregnancy. CONCLUSIONS: Our results confirm that circulating AT1-AA are present significantly more often in preeclampsia than in normotensive pregnancy, however without association to acute atherosis. Whether circulating maternal AT1-AA or acute atherosis target young women at increased long-term cardiovascular risk warrants further investigations.
BACKGROUND:Uteroplacental acute atherosis is a pregnancy-specific lesion resembling early stages of atherosclerosis found frequently in preeclampsia. Preeclampsia is associated with an increased risk for future maternal atherosclerotic cardiovascular disease. The renin-angiotensin-system plays a role both in atherosclerosis and in preeclampsia. Circulating agonistic autoantibodies at the angiotensin-II type 1 receptor (AT1-AA) are increased in preeclampsia. We hypothesized an association between AT1-AA at delivery and postpartum with acute atherosis in pregnancy. MATERIAL AND METHODS: Maternal serum and decidua basalis tissue was collected at elective cesarean section (n = 41; 24 preeclampsia, 17 normotensive controls). Circulating AT1-AA were detected by a bioassay using spontaneously beating rat cardiomyocytes at delivery (n = 41) and 5-8 years postpartum in a subgroup (n = 10). Decidual acute atherosis was assessed by immunohistochemistry. RESULTS: Significantly less normotensive controls (18%; 3/17) than women with preeclampsia (58%; 14/24) were AT1-AA positive at delivery, p<0.01. Uteroplacental acute atherosis and circulating AT1-AA at delivery were not significantly correlated. Postpartum, 2 prior preeclamptic women had circulating AT1-AA, both without acute atherosis in pregnancy. CONCLUSIONS: Our results confirm that circulating AT1-AA are present significantly more often in preeclampsia than in normotensive pregnancy, however without association to acute atherosis. Whether circulating maternal AT1-AA or acute atherosis target young women at increased long-term cardiovascular risk warrants further investigations.
Authors: Ana I Rodriguez-Perez; Carmen M Labandeira; Maria A Pedrosa; Rita Valenzuela; Juan A Suarez-Quintanilla; María Cortes-Ayaso; Placido Mayán-Conesa; Jose L Labandeira-Garcia Journal: J Autoimmun Date: 2021-06-11 Impact factor: 7.094