Retinal vascular network architecture in low-birth-weight men

Chapman, Neil; Mohamudally, Anthoulla; Cerutti, Alessia; Stanton, Alice; Sayer, Avan Aihie; Cooper, Cyrus; Barker, David J.; Rauf, Abdul; Evans, Jennifer R; Wormald, Richard; Sever, Peter; Hughes, Alun D.; Thom, Simon

doi:10.1097/00004872-199715120-00012

Cited by 89 publications

(71 citation statements)

References 18 publications

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“…Martin et al 26 documented impaired skin microvascular endothelium-dependent vasodilatation in 3-day-old LBW infants, as well as in prepubertal children (mean age: 9Ϯ1.3 years) with a history of LBW. 7 Preterm birth was also associated with abnormal retinal vascularity in several studies, including narrower bifurcation angles, 27 narrower retinal arterioles, 28,29 and increased retinal arteriolar tortuosity. 30 Retinal arteriolar narrowing has been demonstrated in several population-based cohorts to predict the subsequent development of essential hypertension.…”

Section: Discussionmentioning

confidence: 96%

Low Birth Weight Infants Do Not Have Capillary Rarefaction at Birth

et al. 2011

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Abstract-Low birth weight predicts adult essential hypertension and is linked to increased cardiovascular mortality in adult life. A reduction in capillary density (ie, rarefaction) is a hallmark of essential hypertension, and evidence suggests that rarefaction precedes the onset of the rise in blood pressure, because it is found in normotensive individuals at high risk of developing hypertension, suggesting that rarefaction is likely to be a primary structural abnormality. We hypothesized that low birth weight infants would have significant capillary rarefaction at birth. We studied 44 low birth weight infants born to normotensive mothers (33 were born preterm, birth weight: 1823Ϯ446 g; and 11 were born at term, birth weight: 2339Ϯ177 g) and compared them with 71 infants born at term with normal weight (birth weight: 3333Ϯ519 g). We used orthogonal polarized spectroscopy to measure basal (ie, functional) and maximal (ie, structural) skin capillary densities. Low birth weight infants, whether born preterm or at term, had significantly higher functional capillary density (mean difference of 10.5 capillaries per millimeter squared; 95% CI: 6.6 -14.4 capillaries per millimeter squared; PϽ0.0001) and higher structural capillary density (mean difference of 11.1 capillaries per millimeter squared; 95% CI: 7.6 -14.5 capillaries per millimeter squared; PϽ0.0001) when compared with normal weight term infants. We conclude that low birth weight infants born to normotensive mothers do not have capillary rarefaction at birth. These results contradict what might have been predicted from the concept of the intrauterine origins of adult disease and suggest that microcirculatory abnormalities observed in individuals of low birth weight occur in postnatal life rather than during their intrauterine existence. (Hypertension. 2011;58:847-851.)Key Words: capillary rarefaction Ⅲ microcirculation Ⅲ hypertension Ⅲ low birth weight M icrocirculatory abnormalities and impaired tissue perfusion have been implicated in the pathogenesis of essential hypertension, obesity, diabetes mellitus, and insulin resistance. 1 In essential hypertension in particular, a reduction in the spatial density of arterioles and capillaries (ie, rarefaction) appears to play a central role. 2 We have shown previously that much of the capillary rarefaction in essential hypertension is attributed to the structural (ie, anatomic) absence of capillaries. 3 We have also shown significant capillary rarefaction in patients with borderline intermittent essential hypertension and in normotensive offspring of hypertensive parents, suggesting a familial predisposition in which capillary rarefaction represents a primary vascular abnormality that antedates the onset of sustained elevation of blood pressure (BP). 4,5 There is now a strong body of evidence showing that low birth weight (LBW), that is, birth weight of Ͻ2.5 kg regardless of gestation or causation, 6 is associated with structural and functional vascular abnormalities, 7 the development of essential hypertension, 8...

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Section: Discussionmentioning

confidence: 96%

Low Birth Weight Infants Do Not Have Capillary Rarefaction at Birth

et al. 2011

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“…Among men in Hertfordshire, those who had had low birth weight had narrow bifurcation angles in their retinal blood vessels (79). People with hypertension have similar changes in retinal vascular geometry.…”

Section: Possible Mechanismsmentioning

confidence: 95%

Fetal, Infant, and Childhood Growth Are Predictors of Coronary Heart Disease, Diabetes, and Hypertension in Adult Men and Women

Osmond¹,

Barker²

2000

Environmental Health Perspectives

145

130

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Many human fetuses have to adapt to a limited supply of nutrients. In doing so they permanently change their structure and metabolism. These programmed changes may be the origins of a number of diseases in later life, including coronary heart disease, hypertension and noninsulindependent diabetes. We review epidemiologic studies in which the incidence of these diseases has been related to the recorded, early growth of individuals, while considering factors in the adult lifestyle, such as obesity and socioeconomic status. We discuss possible mechanisms. For hypertension these mechanisms include placentation, maternal blood pressure, fetal undernutrition; childhood growth, activation of the renin-angiotensin system, renal structure, programming of the hypothalamic-pituitary-adrenal axis, vascular structure, and sympathetic nervous activity. For noninsulin-dependent diabetes we discuss mechanisms concerning both insulin resistance and insulin deficiency. We include a review of evidence for the programming of serum cholesterol and clotting factor concentrations. We address the timing of critical windows for coronary heart disease, reviewing studies that allow assessment of the relative importance of fetal, infant, and childhood growth. We argue for a research strategy that combines clinical, animal, and epidemiological studies.

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“…55 The biophysical basis of this influence is still poorly explored, although recent studies suggest a possible role for microvascular branching angles and related geometric parameters in hypertension-related cardiovascular disease. 56 …”

Section: Insulin Resistance Arterial Stiffness and Microvascular Fumentioning

confidence: 99%

Microvascular Dysfunction

Serné

Jongh

Eringa³

et al. 2007

Hypertension

208

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O besity and a central body fat distribution, hypertension, insulin resistance, glucose intolerance, dyslipidemia, and proinflammatory and prothrombotic factors are all part of the metabolic syndrome. The metabolic syndrome defines a clustering of metabolic risk factors which confers an increased risk for type 2 diabetes and cardiovascular disease. 1 In the past years a large amount of research has been aimed at elucidating the pathophysiology underlying this clustering of risk factors, because a better understanding may lead to new therapeutic approaches that specifically target underlying causes of the metabolic syndrome.Recently, it has become clear that microvascular dysfunction, by affecting both pressure and flow patterns, may have consequences not only for peripheral vascular resistance, but also for insulin-mediated changes in muscle perfusion and glucose metabolism, providing a novel pathophysiological framework for understanding the association between hypertension, obesity, and impaired insulin-mediated glucose disposal. [2][3][4] The present article examines recent data concerning the role of microvascular dysfunction as an explanation for the associations among hypertension, obesity, and impaired insulin-mediated glucose disposal.

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Retinal vascular network architecture in low-birth-weight men

Cited by 89 publications

References 18 publications

Low Birth Weight Infants Do Not Have Capillary Rarefaction at Birth

Low Birth Weight Infants Do Not Have Capillary Rarefaction at Birth

Fetal, Infant, and Childhood Growth Are Predictors of Coronary Heart Disease, Diabetes, and Hypertension in Adult Men and Women

Microvascular Dysfunction

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