Cardiac tissue remodeling in healthy aging: the road to pathology

Tracy, Evan; Rowe, Gabrielle; LeBlanc, Amanda J.

doi:10.1152/ajpcell.00021.2020

Cited by 30 publications

(26 citation statements)

References 186 publications

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“…To test this hypothesis, future studies should consider ovariectomizing rats at an older age. Finally, although impaired myocardial deformation has been observed with age in both male and female participants in human studies, 52,53 the age-induced observations in the current study may not be extrapolated to male rats due to the absence of male groups.…”

Section: Discussionmentioning

confidence: 61%

“…52,53 This age-associated impairment has been posited to be a consequence of increased myocardial stiffening that ultimately diminishes the contribution of myocardial elasticity to adequate fiber contraction and motion during systole. 30,52 The current study has some limitations. First, the circulating estrogen concentrations were not determined.…”

Section: Discussionmentioning

confidence: 99%

“…Our findings are congruent with previous studies in which healthy elderly adults have shown impaired myocardial deformation compared with young and middle-aged adults. 52,53 This age-associated impairment has been posited to be a consequence of increased myocardial stiffening that ultimately diminishes the contribution of myocardial elasticity to adequate fiber contraction and motion during systole. 30,52 The current study has some limitations.…”

Section: Discussionmentioning

confidence: 99%

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The effects of estrogen deficiency and aging on myocardial deformation and motion in normotensive female rats

2021

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Objective: Estrogen deficiency is associated with left ventricular (LV) dysfunction in postmenopausal women and ovariectomized rats. Whether the relationship between estrogen deficiency and LV dysfunction is independent of cardiovascular disease (CVD) risk factors remains uncertain. This study assessed the effects of short-term and long-term estrogen deficiency on cardiac structure and function using conventional and speckle tracking echocardiography, independent of traditional CVD risk factors.Methods: Female Sprague-Dawley rats were divided into short-term (6 wks) ovariectomized (n ¼ 9), short-term sham-operated (n ¼ 10), long-term (6 mo) ovariectomized (n ¼ 8), and long-term sham-operated (n ¼ 9) groups. Cardiac geometry, systolic and diastolic function, and myocardial deformation and motion were measured using echocardiography.Results: Ovariectomy had no effect on conventional echocardiography measures of cardiac structure or function. Compared with short-term, long-term groups had reduced LV internal diameter (false discovery rate [FDR] adjusted P ¼ 0.05) and impaired relaxation (e'; FDR adjusted P ¼ 0.0005) independent of body mass and blood pressure (BP). Global longitudinal strain was impaired in ovariectomized compared with sham-operated rats (FDR adjusted P ¼ 0.05), but not after adjusting for body mass and BP (FDR adjusted P ¼ 0.16). Global longitudinal strain (FDR adjusted P ¼ 0.05), strain rate (FDR adjusted P ¼ 0.002), and velocity (FDR adjusted P ¼ 0.04) were impaired in long-term compared with short-term groups. Global longitudinal strain rate remained impaired after adjustments for body mass and BP (FDR adjusted P ¼ 0.02).Conclusions: Estrogen deficiency does not independently cause cardiac remodeling, LV dysfunction, or impaired myocardial deformation. Traditional CVD risk factors accompanying estrogen deficiency may account for cardiac remodeling and dysfunction observed in postmenopausal women.

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Section: Discussionmentioning

confidence: 61%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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The effects of estrogen deficiency and aging on myocardial deformation and motion in normotensive female rats

2021

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“…Diğer teoriye göre, damar yapısını koruyan nitrik oksit (NO) sentezinin azalması ve endotel hücrelerde apopitoz sinyallerinin çoğalmasıdır. NO azalması dolaşımdaki ROS miktarının çoğalmasından kaynaklanır (48).…”

Section: Vasküler Değişimlerunclassified

Does Cardiac Physiology also Take Age in Geriatric Population?

KARADÜZ

Yurdalan

2021

Geriatrik Bilimler Dergisi

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Aging is a process characterized by a decreasing anabolic metabolism and regeneration capacity of the body, leading to irreversible changes in structure and functions. As the older population increases globally, recent studies have focused on a better understanding of the aging changes in the cardiac structure causing mortality and morbidity. It was proven that physiological changes with aging are the leading risk factor for cardiovascular diseases. This review aims to examine cellular mechanisms and investigate changes in the cardiac structure and physiology with the aging process in light of current information. Many theories explain cellular and molecular changes that play a significant role in aging. Decreased autophagy, increased mitochondrial oxidative stress, telomere length changes, mitochondrial dysfunction, changes in mTOR signals, errors in RNA coding, increase in cardiac fibrosis, altered Insulin Like-Growth Factor is fundamental accepted cellular theories currently. As a result of these processes at the cellular level, the effects of aging are seen as structural-functional differentiations in the myocardium, cardiovascular and nervous systems. Changes in the vascular system begin in endothelial cells, and the loss of vascular elasticity over time paves the way for basic functional changes. In addition, hypertrophy of the myocardium and blockages resulting from autonomic nervous system dysfunction are the most notable changes. Cardiovascular diseases such as cardiac hypertrophy, arrhythmia, and heart failure are the major problems as a result of these changes. Studies have also proven that the incidence of the diseases increases in parallel with age. It is thought that a better understanding of the consequences of the cardiac aging process will contribute to both promoting the healthy aging process and presenting more effective methods in the treatment of cardiovascular diseases for older individuals.

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“…5,22 Pre-LVAD implantation prediction of cardiac recovery HF is a progressive disorder that is characterized by compensatory mechanisms designed to reduce wall stress, sustain LV function, and maintain cardiac output 23 ; however, these systems become overwhelmed leading to symptomatic HF. 24 Clinical factors associated with myocardial recovery include several features suggesting patients are earlier in this disease progression: a short HF duration (<5 years), 9,25,26 non-ischemic cardiomyopathy (NICM), 27 younger age <50, 16,25,28 normal or mildly impaired renal function (<1.2 mg/dl), and not-large left ventricular end diastolic diameter (LVEDD) (<6.5 cm). 9,10,27 Of patients fitting these characteristics, nearly half will experience improvement of LV function sufficient to permit LVAD explant, with long-term freedom from the need for transplant or LVAD reinsertion.…”

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confidence: 99%