Human aging: Changes in structure and function

Lakatta, Edward G.; Mitchell, Jere H.; Pomerance, Ariela; Rowe, George G.

doi:10.1016/s0735-1097(87)80447-3

Cited by 243 publications

(139 citation statements)

References 18 publications

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“…As expected, left-ventricular work physiologically grows with age [50], although less than in both artificial cases, underlying the importance of the stiffening-remodelling compensation. In particular, removing arterial stiffening reduces the late systolic ventricular pressure but raises early values and enhances cardiac output, as shown in Fig 3f. Until about middle age, the resulting left-ventricular work is dominated by the concomitant increase of early systolic pressure and cardiac output, thus growing more than the physiological case.…”

Section: Resultssupporting

confidence: 72%

P5.5 Compensatory Effect Between Aortic Stiffening and Remodelling During Ageing

Guala¹,

Camporeale²,

Ridolfi³

2015

ARTRES

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The arterial tree exhibits a complex spatio-temporal wave pattern, whose healthy behaviour depends on a subtle balance between mechanical and geometrical properties. Several clinical studies demonstrated that such a balance progressively breaks down during ageing, when the aorta stiffens and remodels by increasing its diameter. These two degenerative processes however, have different impacts on the arterial wave pattern. They both tend to compensate for each other, thus reducing the detrimental effect they would have had if they had arisen individually. This remarkable compensatory mechanism is investigated by a validated multi-scale model, with the aim to elucidate how aortic stiffening and remodelling quantitatively impact the complex interplay between forward and reflected backward waves in the arterial network. We focus on the aorta and on the pressure at the ventricular-aortic interface, which epidemiological studies demonstrate to play a key role in cardiovascular diseases.

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Section: Resultssupporting

confidence: 72%

P5.5 Compensatory Effect Between Aortic Stiffening and Remodelling During Ageing

Guala¹,

Camporeale²,

Ridolfi³

2015

ARTRES

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“…16 In the load-bearing media of elastic arteries, the orderly arrangement of elastic fibers and laminae is gradually lost over time, and thinning, splitting, fraying, and fragmentation are observed. 17 The degeneration of elastic fibers is associated with an increase in collagenous material and in ground substance, often accompanied by calcium deposition in ground substance and in degenerate elastic fibers. Animal models of essential hypertension, such as spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHR-SP), can provide insight into the cellular and molecular determinants of arterial stiffness.…”

Section: Integrative Physiology Of Arterial Stiffness In Essential Hymentioning

confidence: 99%

Structural and Genetic Bases of Arterial Stiffness

2005

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Abstract-Arterial stiffness has independent predictive value for cardiovascular events. We review data concerning the heritability of arterial stiffness, and propose an integrated view of the structural and genetic determinants of arterial stiffness, based on a candidate gene approach and recent studies on gene expression profile. Arterial stiffness seems to have a genetic component, which is largely independent of the influence of blood pressure and other cardiovascular risk factors. In animal models of essential hypertension (SHR and SHR-SP), structural modifications of the arterial wall include an increase in the number of elastin/smooth muscle cell (SMC) connections, and smaller fenestrations of the internal elastic lamina, possibly leading to redistribution of the mechanical load toward elastic materials. These modifications may give rise to mechanisms that explain why changes in arterial wall material accompanying wall hypertrophy in these animals are not associated with an increase in arterial stiffness. In monogenic connective tissue diseases (Marfan, Williams, and Ehlers-Danlos syndromes) and the corresponding animal models, precise characterization of the arterial phenotype makes it possible to determine the influence of abnormal genetically determined wall components on arterial stiffness. Such studies have highlighted the role of extracellular matrix signaling in the vascular wall and have shown that elastin and collagen not only display elasticity or rigidity but also are involved in the control of SMC function. These data provide strong evidence that arterial stiffness is affected by the amount and density of stiff wall material and the spatial organization of that material.

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“…Excluding these individuals gives an estimate of 51 % for the prevalence of predominant ' diastolic CHF '. The high prevalence of ' diastolic CHF ' is understandable knowing that even normal ageing impairs diastolic function [30][31][32] and that both ischaemic heart disease and left ventricular hypertrophy are common in old age and can compromise left ventricular filling [4,5,33]. A limitation of our indirect diagnosis of ' diastolic CHF ' is that the reliability of our prevalence estimate depends on both the validity of our clinical definition of CHF and the accuracy of M-mode echocardiography in excluding systolic left ventricular dysfunction.…”

Section: Left Ventricular Function In Chfmentioning

confidence: 99%

Congestive heart failure in old age: prevalence, mechanisms and 4‐year prognosis in the Helsinki Ageing Study

Kupari

Lindroos

Iivanainen

et al. 1997

Journal of Internal Medicine

215

103

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Abstract. Kupari M, Lindroos M, Iivanainen AM, Heikkila$ J, Tilvis R. (Helsinki University Central Hospital, Helsinki, Finland). Congestive heart failure in old age : prevalence, mechanisms and 4-year prognosis in the Helsinki Ageing Study. J Int Med 1997 ; 241 : 387-94.Objective. To examine the prevalence, underlying diseases, abnormalities of left ventricular function and prognosis in congestive heart failure (CHF) of old age. Design. A population-based clinical and echocardiographic study with a 4-year mortality followup. Setting. University hospital. 1904, 1909 and 1914 (367 women). Main outcome measures. Presence of CHF by clinical and chest radiograph criteria ; left ventricular size and systolic function by echocardiography ; grade of aortic and mitral valve lesions by Doppler echocardiography ; 4-year total and cardiovascular mortality. Results. Forty-one of 501 participants (8.2 %) had CHF. Ischaemic heart disease (54 %), hypertension (54 %) and moderate-to-severe mitral or aortic valve Subjects. Five hundred and one individuals born in

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Human aging: Changes in structure and function

Cited by 243 publications

References 18 publications

P5.5 Compensatory Effect Between Aortic Stiffening and Remodelling During Ageing

P5.5 Compensatory Effect Between Aortic Stiffening and Remodelling During Ageing

Structural and Genetic Bases of Arterial Stiffness

Congestive heart failure in old age: prevalence, mechanisms and 4‐year prognosis in the Helsinki Ageing Study

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