664 M alnutrition contributes significantly to global mortality among children aged <5 years. 1,2 Undernutrition before and during pregnancy alters development, increasing offspring risk of obesity and cardiovascular disease. 3 Undernutrition in infancy while offspring remain developmentally plastic also increases the risk of cardiovascular disease in adulthood. 2,4,5 Little is currently known about the effect of childhood malnutrition on adult risk of cardiovascular disease. Pooled analyses on participants undernourished in early childhood from low- and middle-income countries showed that weight, height, and body mass index at age 2 years had strong negative relationships with adult systolic blood pressure, even adjust- ing for weight. 6 Dutch adults, exposed to famine as children or adolescents, had an excess coronary events, but lower stroke rates. 7 Rates of type 2 diabetes mellitus were 25% higher in those moderately exposed to the famine and 50% in those severely exposed. 8 Similar but larger risks were recorded for prenatal exposure to the acute malnutrition during preg- nancy in that famine; a 4-fold excess cardiovascular mortality occurred in female offspring exposed in utero to famine in early gestation. 9 Damage to cardiovascular structure or function arising from severe acute malnutrition (SAM) would have global public health significance. The damage could also differ between the 2 SAM syndromes: kwashiorkor and marasmus. We have used a retrospective cohort of adult survivors of SAM previously treated in the Tropical Metabolism Research Unit, Kingston, Jamaica, to explore the effects of malnutrition on adult cardio- vascular structure and function and shown that birth weight is 333 g lower in infants presenting with marasmus when Abstract—Malnutrition below 5 years remains a global health issue. Severe acute malnutrition (SAM) presents in childhood as oedematous (kwashiorkor) or nonoedematous (marasmic) forms, with unknown long-term cardiovascular consequences. We hypothesized that cardiovascular structure and function would be poorer in SAM survivors than unexposed controls. We studied 116 adult SAM survivors, 54 after marasmus, 62 kwashiorkor, and 45 age/sex/body mass index–matched community controls who had standardized anthropometry, blood pressure, echocardiography, and arterial tonometry performed. Left ventricular indices and outflow tract diameter, carotid parameters, and pulse wave velocity were measured, with systemic vascular resistance calculated. All were expressed as SD scores. Mean (SD) age was 28.8±7.8 years (55% men). Adjusting for age, sex, height, and weight, SAM survivors had mean (SE) reductions for left ventricular outflow tract diameter of 0.67 (0.16; P<0.001), stroke volume 0.44 (0.17; P=0.009), cardiac output 0.5 (0.16; P=0.001), and pulse wave velocity 0.32 (0.15; P=0.03) compared with controls but higher diastolic blood pressures (by 4.3; 1.2–7.3 mm Hg; P=0.007). Systemic vascular resistance was higher in marasmus and kwashiorkor survivors (30.2 [1.2] and 30.8 [1.1], respectively) than controls 25.3 (0.8), overall difference 5.5 (95% confidence interval, 2.8–8.4 mm Hg min/L; P<0.0001). No evidence of large vessel or cardiac remodeling was found, except closer relationships between these indices in former marasmic survivors. Other parameters did not differ between SAM survivor groups. We conclude that adult SAM survivors had smaller outflow tracts and cardiac output when compared with controls, yet markedly elevated peripheral resistance. Malnutrition survivors are thus likely to develop excess hypertension in later life, especially when exposed to obesity. (Hypertension. 2014;64:664-671.) • Online Data Supplement Key Words: blood supply ■ kwashiorkor ■ protein-energy malnutrition Received January 27, 2014; first decision February 10, 2014; revision accepted May 22, 2014. From the Tropical Medicine Research Institute (D.S.T., M.S.B.), Departments of Surgery, Radiology, Anaesthesia, and Intensive Care (I.A.T., A.T.B.), Medicine (Cardiology) (E.E.C., A.P.C.), and UWI Solutions for Developing Countries (T.E.F.), University of the West Indies, Mona, Kingston, Jamaica; Institute Biomedical Technology, Ghent University, Gent, Belgium (J.K., P.S.); MRC Lifecourse Epidemiology Unit (C.O.) and DOHAD Division (M.A.H.), University of Southampton, Southampton, United Kingdom; Centre for Human Evolution, Adaptation, and Disease, Liggins Institute, University of Auckland, Auckland, New Zealand (P.D.G.); and Division of Diabetes, Cardiovascular Medicine, and Nutrition, King’s College and King’s Health Partners, London, United Kingdom (J.K.C.). *These authors are joint last authors. The online-only Data Supplement is available with this article at http://hyper.ahajournals.org/lookup/suppl/doi:10.1161/HYPERTENSIONAHA. 114.03230/-/DC1. Correspondence to Terrence E. Forrester, UWI Solutions for Developing Countries, 25 West Rd, University of the West Indies, Mona, Kingston, Jamaica. E-mail terrence.forrester@uwimona.edu.jm Impaired Cardiovascular Structure and Function in Adult Survivors of Severe Acute Malnutrition Ingrid A. Tennant, Alan T. Barnett, Debbie S. Thompson, Jan Kips, Michael S. Boyne, Edward E. Chung, Andrene P. Chung, Clive Osmond, Mark A. Hanson, Peter D. Gluckman, Patrick Segers, J. Kennedy Cruickshank,* Terrence E. Forrester* © 2014 American Heart Association, Inc. Hypertension is available at http://hyper.ahajournals.org DOI: 10.1161/HYPERTENSIONAHA.114.03230 Acute Malnutrition and Hypertension by guest on May 1, 2016 http://hyper.ahajournals.org/ Downloaded from by guest on May 1, 2016 http://hyper.ahajournals.org/ Downloaded from by guest on May 1, 2016 http://hyper.ahajournals.org/ Downloaded from by guest on May 1, 2016 http://hyper.ahajournals.org/ Downloaded from by guest on May 1, 2016 http://hyper.ahajournals.org/ Downloaded from by guest on May 1, 2016 http://hyper.ahajournals.org/ Downloaded from by guest on May 1, 2016 http://hyper.ahajournals.org/ Downloaded from by guest on May 1, 2016 http://hyper.ahajournals.org/ Downloaded from