Andrew M South1,2,3,4, Norrina B Allen5. 1. Department of Pediatrics, Section of Nephrology, Brenner Children's, Wake Forest University School of Medicine, One Medical Center Boulevard, Winston-Salem, NC, 27157, USA. asouth@wakehealth.edu. 2. Division of Public Health Sciences, Department of Epidemiology and Prevention, Wake Forest University School of Medicine, Winston-Salem, NC, USA. asouth@wakehealth.edu. 3. Department of Surgery-Hypertension and Vascular Research, Wake Forest University School of Medicine, Winston-Salem, NC, USA. asouth@wakehealth.edu. 4. Cardiovascular Sciences Center, Wake Forest University School of Medicine, Winston-Salem, NC, USA. asouth@wakehealth.edu. 5. Department of Preventive Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
Abstract
PURPOSE OF REVIEW: Synthesize the clinical, epidemiological, and preclinical evidence for antenatal programming of hypertension and critically appraise paradigms and paradoxes to improve translation. RECENT FINDINGS: Clinical and epidemiological studies persistently demonstrate that antenatal factors contribute to programmed hypertension under the developmental origins of health and disease framework, including lower birth weight, preterm birth, and fetal growth restriction. Preclinical mechanisms include preeclampsia, maternal diabetes, maternal undernutrition, and antenatal corticosteroid exposure. However, clinical and epidemiological studies to date have largely failed to adequately identify, discuss, and mitigate many sources and types of bias in part due to heterogeneous study designs and incomplete adherence to scientific rigor. These limitations have led to incomplete and biased paradigms as well as persistent paradoxes that have significantly limited translation into clinical and population health interventions. Improved understanding of these paradigms and paradoxes will allow us to substantially move the field forward.
PURPOSE OF REVIEW: Synthesize the clinical, epidemiological, and preclinical evidence for antenatal programming of hypertension and critically appraise paradigms and paradoxes to improve translation. RECENT FINDINGS: Clinical and epidemiological studies persistently demonstrate that antenatal factors contribute to programmed hypertension under the developmental origins of health and disease framework, including lower birth weight, preterm birth, and fetal growth restriction. Preclinical mechanisms include preeclampsia, maternal diabetes, maternal undernutrition, and antenatal corticosteroid exposure. However, clinical and epidemiological studies to date have largely failed to adequately identify, discuss, and mitigate many sources and types of bias in part due to heterogeneous study designs and incomplete adherence to scientific rigor. These limitations have led to incomplete and biased paradigms as well as persistent paradoxes that have significantly limited translation into clinical and population health interventions. Improved understanding of these paradigms and paradoxes will allow us to substantially move the field forward.
Authors: David C Goff; Denis B Buxton; Gail D Pearson; Gina S Wei; Teri E Gosselin; Ebyan A Addou; Catherine M Stoney; Patrice Desvigne-Nickens; Pothur R Srinivas; Zorina S Galis; Charlotte Pratt; Kit Brian K Kit; Christine Maric-Bilkan; Holly L Nicastro; Renee P Wong; Vandana Sachdev; Jue Chen; Lawrence Fine Journal: Circ Res Date: 2019-02-15 Impact factor: 17.367