Australian and New Zealand Journal of Obstetrics and Gynaecology 2009; 49: 364–370 DOI: 10.1111/j.1479-828X.2009.01018.x 364 © 2009 The Authors Journal compilation © 2009 The Royal Australian and New Zealand College of Obstetricians and Gynaecologists Blackwell Publishing Asia Original Article Do maternal- or pregnancy-associated disease states affect blood pressure in the early neonatal period? Alison L. KENT, 1,2 Bruce SHADBOLT, 2,3 Eric HU, 4 Sandra MESKELL, 5 Michael C. FALK 6 and Jane E. DAHLSTROM 4 Departments of 1 Neonatology, 4 Anatomical Pathology and 6 Nephrology, 3 Clinical Epidemiology Unit and 5 Centre for Neonatal Care, Canberra Hospital, and 2 Australian National University Medical School, Canberra, Australian Capital Territory, Australia Background: Placental vascular changes associated with maternal disease states may affect fetal vascular development. There is evidence suggesting that being born prematurely is associated with a higher blood pressure (BP) in later life. Aim: To determine whether maternal disease state affects BP in the early neonatal period. Methods: Cohort study of neonates admitted to neonatal intensive care unit with exposure to maternal hypertension and diabetes. Inclusion criteria were neonates greater than 27 weeks gestation not ventilated or requiring inotropes for more than 24 h, materna l hypertension (pregnancy induced or essential) or diabetes of any kind requiring treatment, and spontaneous delivery. Exclusion criteria included chromosomal or congenital anomaly and illicit maternal drug use. Oscillometric BP measurements taken until discharge on days 1, 2, 3, 4, 7, 14, 21 and 28. Placental histopathology was performed. Results: One hundred and ninety infants enrolled, 104 in the control and 86 in the study group. Sixty-five infants were born between 28–31 weeks and 125 infants between 32–41 weeks gestation. Those born between 28–31 weeks with a history of diabetes had a statistically higher systolic, mean and diastolic BP throughout the first 28 days of life (P = 0.001; P = 0.007; P = 0.02). Those born between 32–41 weeks gestation with placental pathology associated with altered uteroplacental perfusion had a higher systolic BP (P = 0.005). Conclusions: Maternal- or pregnancy-associated disease states appear to influence BP in the early neonatal period. Diabetes and altered placental perfusion were associated with higher BP readings. Clinical significance of these statistically elevated BPs in the early neonatal period is unknown. Key words: blood pressure, diabetes, hypertension, neonate, placenta. Introduction Hypertension is a major contributor to cardiovascular disease as it accelerates atherogenesis and leads to a two to three times increased risk of coronary heart disease. 1 In Australia, cardiovascular disease accounts for A$5.5 billion, or 10.9%, of the total direct health system costs. 2 Barker and Osmond first postulated that intrauterine and early nutrition may be associated with ischaemic heart disease in 1986. 3 That study has instigated much research into the association between low birthweight and hypertension and ischaemic heart disease in later life. However, a consistent relationship between low birthweight and systolic blood pressure (BP) has not been found, 4–13 and the association between low birthweight and ischaemic heart disease is also unclear. 14–16 The effect of prematurity on the development of hypertension or ischaemic heart disease in adulthood is unknown. A number of studies have shown that premature infants have a higher systolic or mean arterial BP in comparison to term controls. 17–20 Exposure to antenatal betamethasone has been found to affect insulin resistance in adults, but did not appear to have an affect on BP. 21 Maternal conditions such as diabetes and hypertension can be associated with distinctive placental pathology. 22 Pregnancy-induced hypertension (especially pre-eclampsia) can cause small placentas with multiple infarcts and decidual vessel vasculopathy (such as fibrinoid necrosis of the vessel wall, atherosis and lack of conversion of decidual vessels with persistence of smooth muscle in the media). The subsequent reduced uteroplacental perfusion can result in accelerated maturation of the villi (also known as distal villous hypoplasia) and occasionally chorangiosis (villous hypervascularity). Placentae of diabetic mothers may be large and also show altered villous maturation (delayed or accelerated), chorangiosis and decidual vasculopathy. 22 The long-term effect of these placental findings on fetal vascular development is unknown. Correspondence: Associate Professor Alison Kent, Department of Neonatology, Canberra Hospital, PO Box 11, Woden, ACT 2606, Australia. Email: alison.kent@act.gov.au Received 4 August 2008; accepted 31 March 2009.