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20 - Programming the cardiovascular system

Published online by Cambridge University Press:  08 August 2009

By
Kent L. Thornburg
Edited by
Peter Gluckman  and
Mark Hanson
Kent L. Thornburg
Affiliation:
Oregon Health and Science University
Peter Gluckman
Affiliation:
University of Auckland
Mark Hanson
Affiliation:
University of Southampton
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Summary

Introduction

David Barker and colleagues first trained the spotlight on the idea that the prenatal environment shapes the lifelong health of the heart. They reported that the standardised mortality for ischaemic heart disease within a large population of English men and women was much higher in babies born at the 5- pound (2.3 kg) end of the birthweight scale compared to babies at the 9-pound (4.0 kg) end (Barker et al., 1989). Birthweight affected the death rate in men and women similarly across the weight range, with a significant sudden upturn in the heaviest babies studied. The latter group of heavier newborn babies may have included babies that were macrosomic and born to diabetic mothers. In a separate study, Rich-Edwards and coworkers (1997) found a similar relationship among >100,000 participants in the American Nurses study. In that study, the numbers of individuals who had symptoms for coronary disease and stroke increased with decreasing recalled birthweight.

The implications of the epidemiological findings of Barker's group are enormous. Cardiovascular disease is the most devastating disease on earth and, as a category, kills more men and women than any other disease. In the USA alone, the costs to society for cardiovascular disease currently exceed $350 billion annually. Furthermore, the rates of death due to cardiovascular events around the world are on the increase (American Heart Association 2004, World Health Organization, 2003, 2004a). Over half of all cardiovascular deaths worldwide are of women (World Health Organization 2004b, 2004c).

Type
Chapter
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Developmental Origins of Health and Disease , pp. 275 - 285
Publisher: Cambridge University Press
Print publication year: 2006

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References

Abrams, J. (2003). C-reactive protein, inflammation, and coronary risk: an update. Cardiol. Clin., 21, 327–31.CrossRefGoogle ScholarPubMed
American Heart Association (2004). International Cardiovascular Disease Statistics. www.americanheart.org/downloadable/heart/1077185395308FS06INT4(ebook).pdf Accessed 24 November 2004.
Anderson, D. F., Faber, J. J., Morton, M. J., Parks, C. M., Pinson, C. W. and Thornburg, K. L. (1985). Flow through the foramen ovale of the fetal and new-born lamb. J. Physiol., 365, 29–40.CrossRefGoogle ScholarPubMed
Andersson, K. and Stief, C. (2000). Penile erection and cardiac risk: pathophysiologic and pharmacologic mechanisms. Am. J. Cardiol., 86, 23–6F.CrossRefGoogle ScholarPubMed
Armitage, J. A., Khan, I. Y., Taylor, P. D., Nathanielsz, P. W., and Poston, L. (2004). Developmental programming of metabolic syndrome by maternal nutritional imbalance: how strong is the evidence from experimental models in mammals?J. Physiol., 561, 355–77.CrossRefGoogle ScholarPubMed
Arnett, D. K., las Fuentes, L., Broeckel, U. (2004). Genes for left ventricular hypertrophy. Curr. Hypertens. Rep., 6, 36–41.CrossRefGoogle ScholarPubMed
Bagby, S. P., LeBard, L. S., Luo, Z.et al. (2002). ANG II, AT(1) and AT(2) receptors in developing kidney of normal microswine. Am. J. Physiol. Renal. Physiol., 283, F755–64.CrossRefGoogle ScholarPubMed
Barbera, A., Giraud, G. D., Reller, M. D., Maylie, J., Morton, M. J. and Thornburg, K. L. (2000). Right ventricular systolic pressure load alters myocyte maturation in fetal sheep. Am. J. Physiol. Regul. Integr. Comp. Physiol., 279, R1157–64.CrossRefGoogle ScholarPubMed
Barker, D. J. P., Osmond, C., Golding, J., Kuh, D., Wadsworth, M. E. (1989). Growth in utero, blood pressure in childhood and adult life, and mortality from cardiovascular disease. BMJ, 298, 564–7.CrossRefGoogle ScholarPubMed
Bloomfield, F. H., Oliver, M. H., Hawkins, P.et al. (2004). Periconceptional undernutrition in sheep accelerates maturation of the fetal hypothalamic-pituitary-adrenal axis in late gestation. Endocrinology, 145, 4278–85.CrossRefGoogle ScholarPubMed
Brawley, L., Itoh, S., Torrens, C.et al. (2003). Dietary protein restriction in pregnancy induces hypertension and vascular defects in rat male offspring. Pediatr. Res., 54, 83–90.CrossRefGoogle ScholarPubMed
Broberg, C. S., Giraud, G. D., Schultz, J. M., Thornburg, K. L., Hohimer, A. R. and Davis, L. E. (2003). Fetal anemia leads to augmented contractile response to hypoxic stress in adulthood. Am. J. Physiol. Regul. Integr. Comp. Physiol., 285, R649–55.CrossRefGoogle ScholarPubMed
Bugiardini, R., Manfrini, O., Pizzi, C., Fontana, F. and Morgagni, G. (2004). Endothelial function predicts future development of coronary artery disease: a study of women with chest pain and normal coronary angiograms. Circulation, 109, 2518–23.CrossRefGoogle ScholarPubMed
Burrell, J. H., Boyn, A. M., Kumarasamy, V., Hsieh, A., Head, S. I. and Lumbers, E. R. (2003). Growth and maturation of cardiac myocytes in fetal sheep in the second half of gestation. Anat. Rec., 274A, 952–61.CrossRefGoogle Scholar
Chen, J. and Mehta, J. L. (2004). Role of oxidative stress in coronary heart disease. Indian Heart J., 56, 163–73.Google ScholarPubMed
Cooke, J. P. and Oka, R. K. (2001). Atherogenesis and the arginine hypothesis. Curr. Atheroscler. Rep., 3, 252–9.CrossRefGoogle ScholarPubMed
Davis, L., Roullet, J. B., Thornburg, K. L., Shokry, M., Hohimer, A. R. and Giraud, G. D. (2003). Augmentation of coronary conductance in adult sheep made anaemic during fetal life. J. Physiol., 547, 53–9.CrossRefGoogle ScholarPubMed
Davis, L. E. and Hohimer, A. R. (1991). Hemodynamics and organ blood flow in fetal sheep subjected to chronic anemia. Am. J. Physiol., 261, R1542–8.Google ScholarPubMed
Dawes, G. S. (1968). Foetal and Neonatal Physiology: a Comparative Study of the Changes at Birth. Chicago, IL:Year Book Medical Publishers.Google Scholar
Forsen, T. J., Eriksson, J. G., Osmond, C. and Barker, D. J. P. (2004a). The infant growth of boys who later develop coronary heart disease. Ann. Med., 36, 389–92.CrossRefGoogle Scholar
Forsen, T. J., Osmond, C., Eriksson, J. G. and Barker, D. J. P. (2004b). Growth of girls who later develop coronary heart disease. Heart, 90, 20–4.CrossRefGoogle Scholar
Godfrey, K. M. (2002). The role of the placenta in fetal programming: a review. Placenta, 23 (Suppl. A) S20–7.CrossRefGoogle ScholarPubMed
Groenendijk, B. C., Hierck, B. P., Gittenberger-de Groot, A. C. and Poelmann, R. E. (2004). Development-related changes in the expression of shear stress responsive genes KLF-2, ET-1, and NOS-3 in the developing cardiovascular system of chicken embryos. Dev. Dyn., 230, 57–68.CrossRefGoogle ScholarPubMed
Huang, W. L., Harper, C. G., Evans, S. F., Newnham, J. P. and Dunlop, S. A. (2001). Repeated prenatal corticosteroid administration delays myelination of the corpus callosum in fetal sheep. Int. J. Dev. Neurosci., 19, 415–25.CrossRefGoogle ScholarPubMed
Jobe, A. H. (2001). Glucocorticoids, inflammation and the perinatal lung. Semin. Neonatol., 6, 331–42.CrossRefGoogle ScholarPubMed
Kiserud, T., Ozaki, T., Nishina, H., Rodeck, C. and Hanson, M. A. (2000). Effect of NO, phenylephrine, and hypoxaemia on ductus venosus diameter in fetal sheep. Am. J. Physiol. Heart Circ. Physiol., 279, H1166–71.CrossRefGoogle ScholarPubMed
Kol, A. and Santini, M. (2004). Infectious agents and atherosclerosis: current perspectives and unsolved issues. Ital. Heart J., 5, 350–7.Google ScholarPubMed
Lamireau, D., Nuyt, A. M., Hou, X.et al. (2002). Altered vascular function in fetal programming of hypertension. Stroke, 33, 2992–8.CrossRefGoogle ScholarPubMed
Langley-Evans, S. C., Phillips, G. J., Benediktsson, R.et al. (1996). Protein intake in pregnancy, placental glucocorticoid metabolism and the programming of hypertension in the rat. Placenta, 17, 169–72.CrossRefGoogle ScholarPubMed
Leeson, C. P., Whincup, P. H., Cook, D. G.et al. (1997). Flow-mediated dilation in 9- to 11-year-old children: the influence of intrauterine and childhood factors. Circulation, 96, 2233–8.CrossRefGoogle ScholarPubMed
Li, G., Xiao, Y., Estrella, J. L., Ducsay, C. A., Gilbert, R. D. and Zhang, L. (2003). Effect of fetal hypoxia on heart susceptibility to ischaemia and reperfusion injury in the adult rat. J. Soc. Gynecol. Investig., 10, 265–74.CrossRefGoogle ScholarPubMed
Lingas, R. I. and Matthews, S. G. (2001). A short period of maternal nutrient restriction in late gestation modifies pituitary – adrenal function in adult guinea pig offspring. Neuroendocrinology, 73, 302–11.CrossRefGoogle Scholar
Martin, H., Gazelius, B. and Norman, M. (2000a). Impaired acetylcholine-induced vascular relaxation in low birthweight infants: implications for adult hypertension?Pediatr. Res., 47, 457–62.CrossRefGoogle Scholar
Martin, H., Hu, J., Gennser, G. and Norman, M. (2000b). Impaired endothelial function and increased carotid stiffness in 9-year-old children with low birthweight. Circulation, 102, 2739–44.CrossRefGoogle Scholar
McMullen, S., Gardner, D. S. and Langley-Evans, S. C. (2004). Prenatal programming of angiotensin II type 2 receptor expression in the rat. Br. J. Nutr., 91, 133–40.CrossRefGoogle ScholarPubMed
Newnham, J. P., Evans, S. F., Godfrey, M., Huang, W., Ikegami, M. and Jobe, A. (1999). Maternal, but not fetal, administration of corticosteroids restricts fetal growth. J. Matern. Fetal. Med., 8, 81–7.Google Scholar
Nishina, H., Green, L. R., McGarrigle, H. H., Noakes, D. E., Poston, L. and Hanson, M. A. (2003). Effect of nutritional restriction in early pregnancy on isolated femoral artery function in mid-gestation fetal sheep. J. Physiol., 553, 637–47.CrossRefGoogle ScholarPubMed
Ozaki, T., Nishina, H., Hawkins, P., Crowe, C., Poston, L. and Hanson, M. A. (2001). Isolated systemic resistance vessel function in hypertensive male rat offspring of mildly nutritionally restricted dams. J. Physiol., 513, 118p.Google Scholar
Pinson, C. W., Morton, M. J. and Thornburg, K. L. (1991). Mild pressure loading alters right ventricular function in fetal sheep. Circ. Res., 68, 947–57.CrossRefGoogle ScholarPubMed
Reller, M. D., Morton, M. J., Giraud, G. D., Reid, D. L. and Thornburg, K. L. (1989). The effect of acute hypoxaemia on ventricular function during beta-adrenergic and cholinergic blockade in the fetal sheep. J. Dev. Physiol., 11, 263–9.Google ScholarPubMed
Rich-Edwards, J. W., Stampfer, M. J., Manson, J. E.et al. (1997). Birthweight and risk of cardiovascular disease in a cohort of women followed up since 1976. BMJ, 315, 396–400.CrossRefGoogle Scholar
Schachinger, V., Britten, M. B. and Zeiher, A. M. (2000). Prognostic impact of coronary vasodilator dysfunction on adverse long-term outcome of coronary heart disease. Circulation, 101, 1899–906.CrossRefGoogle ScholarPubMed
Shaul, P. W. and Mineo, C. (2004). HDL action on the vascular wall: is the answer NO?J. Clin. Invest., 113, 509–13.CrossRefGoogle ScholarPubMed
Shiell, A. W., Campbell-Brown, M., Haselden, S., Robinson, S., Godfrey, K. M. and Barker, D. J. P. (2001). High-meat, low-carbohydrate diet in pregnancy: relation to adult blood pressure in the offspring. Hypertension, 38, 1282–8.CrossRefGoogle ScholarPubMed
Stocker, R. and Keaney, J. F. Jr. (2004). Role of oxidative modifications in atherosclerosis. Physiol. Rev., 84, 1381–478.CrossRefGoogle ScholarPubMed
Sundgren, N. C., Giraud, G. D., Stork, P. J., Maylie, J. G. and Thornburg, K. L. (2003a). Angiotensin II stimulates hyperplasia but not hypertrophy in immature ovine cardiomyocytes. J. Physiol., 548, 881–91.CrossRefGoogle Scholar
Sundgren, N. C., Giraud, G. D., Schultz, J. M., Lasarev, M. R., Stork, P. J. and Thornburg, K. L. (2003b). Extracellular signal-regulated kinase and phosphoinositol-3 kinase mediate IGF-1 induced proliferation of fetal sheep cardiomyocytes. Am. J. Physiol. Regul. Integr. Comp. Physiol., 285, R1481–9.CrossRefGoogle Scholar
Surat, D. R. and Adamson, S. L. (1996). Downstream determinants of pulsatility of the mean velocity waveform in the umbilical artery as predicted by a computer model. Ultrasound Med. Biol., 22, 707–17.CrossRefGoogle ScholarPubMed
Taylor, P. D., McConnell, J., Khan, I. Y.et al. (2005). Impaired glucose homeostasis and mitochondrial abnormalities in offspring of rats fed a fat-rich diet in pregnancy. Am. J. Physiol. Regul. Integr. Comp. Physiol., 288, R134–9.CrossRefGoogle ScholarPubMed
Thornburg, K. L. and Morton, M. J. (1986). Filling and arterial pressures as determinants of left ventricular stroke volume in fetal lambs. Am. J. Physiol., 251, H961–8.Google ScholarPubMed
Thornburg, K. L. and Reller, M. D. (1999). Coronary flow regulation in the fetal sheep. Am. J. Physiol., 277, R1249–60.Google ScholarPubMed
Vogel, R. A. and Corretti, M. C. (1998). Estrogens, progestins, and heart disease: can endothelial function divine the benefit?Circulation, 97, 1223–6.CrossRefGoogle ScholarPubMed
Watterberg, K. L. (2004). Adrenocortical function and dysfunction in the fetus and neonate. Semin. Neonatol., 9, 13–21.CrossRefGoogle ScholarPubMed
Wintour, E. M., Moritz, K. M., Johnson, K., Ricardo, S., Samuel, C. S. and Dodic, M. (2003). Reduced nephron number in adult sheep, hypertensive as a result of prenatal glucocorticoid treatment. J. Physiol., 549, 929–35.CrossRefGoogle ScholarPubMed
Woods, L. L. and Weeks, D. A. (2004). Naturally occurring intrauterine growth retardation and adult blood pressure in rats. Pediatr. Res., 56, 763–7.CrossRefGoogle ScholarPubMed
Woods, L. L., Weeks, D. A. and Rasch, R. (2004). Programming of adult blood pressure by maternal protein restriction: role of nephrogenesis. Kidney Int., 65, 1339–48.CrossRefGoogle ScholarPubMed
World Health Organization (2003). World Health Report, 2003. www.who.int/whr/2003/en. Accessed 24 November 2004.
World Health Organization (2004a). Cardiovascular Diseases. www.who.int/cardiovasculardiseases/en. Accessed 24 November 2004.
World Health Organization (2004b). WHO publishes definitive atlas on global heart disease and stroke epidemic. WHO Media Centre. www.who.int/mediacentre/releases/2004/pr68/en. Accessed 24 November 2004.
World Health Organization (2004c). Global cardiovascular infobase. WHO Collaborating Centre on Surveillance of Cardiovascular Diseases. www.cvdinfobase.ca. Accessed 24 November 2004.
Zhou, M. S., Schulman, I. H. and Raij, L. (2004). Nitric oxide, angiotensin II, and hypertension. Semin. Nephrol., 24, 366–78.CrossRefGoogle ScholarPubMed

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