Collagen accumulation in heart ventricles as a function of growth and aging

Eghbali, Mahboubeh; Tf, Robinson; Seifter, Sam; Oo, Blumenfeld

doi:10.1093/cvr/23.8.723

Cited by 149 publications

(78 citation statements)

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“…Our results are also consistent with investigations showing that cardioprotective treatments are mediated by a restoration or up-regulation of antioxidant enzymes (42,45). It is recognized that an increase in collagen concentration is an integral part of the extracellular matrix remodeling that takes place in the LVs during the natural aging process (66) and as well as in response to a variety of pathologies resulting in hypertrophy of this chamber (67,68). In accordance with these studies, we showed evidence of an increase of collagen deposition with aging and its exacerbation in aged SHR.…”

Section: Discussionsupporting

confidence: 92%

Is Cardiac Hypertrophy in Spontaneously Hypertensive Rats the Cause or the Consequence of Oxidative Stress?

et al. 2008

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The aim of this work was to assess the possible correlation between oxidative damage and the development of cardiac hypertrophy in heart tissue from young (40-d-old) and older (4-, 11-and 19-month-old) spontaneously hypertensive rats (SHR) in comparison with age-matched Wistar (W) rats. To this end, levels of thiobarbituric acid reactive substances (TBARS), nitrotyrosine contents, NAD(P)H oxidase activity, superoxide production, and the activities of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) were determined. Compared to age-matched normotensive rats, SHR showed a significant increase in systolic blood pressure from 40 d of age and left ventricular hypertrophy (LVH) was significantly evident from 4 months of age. W rats (11-and 19-month-old) also showed an increase in LVH with aging. TBARS and nitrotyrosine levels were similar in young rats from both strains and were significantly increased with age in both strains, with the values in SHR being significantly higher than those in age-matched W rats. NAD(P)H activity was similar in young SHR and W rats, whereas it was higher in aged SHR compared with age-matched W rats. Compared to W rats, superoxide production was higher in aged SHR, and was abolished by NAD(P)H inhibition with apocynin. CAT activity was increased in the hearts of 4-month-old SHR compared to age-matched W rats and was decreased in the hearts of the oldest SHR compared to the oldest W rats. SOD and GPx activities decreased in both rat strains with aging. Moreover, an increase in collagen deposition with aging was evident in both rat strains. Taken together, these data showed that aged SHR exhibited higher cardiac hypertrophy and oxidative damage compared to W rats, indicating that the two undesirable effects are associated. That is, oxidative stress appears to be a cause and/or consequence of hypertrophy development in this animal model. (Hypertens Res 2008; 31: 1465-1476)

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Section: Discussionsupporting

confidence: 92%

Is Cardiac Hypertrophy in Spontaneously Hypertensive Rats the Cause or the Consequence of Oxidative Stress?

et al. 2008

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“…Earlier pathological studies in human and in rat have reported increased myocardial fibrosis in aged hearts (Tomanek et al 1972;Eghbali et al 1989;Besse et al 1993). Similarly our results showed that the total protein levels were maintained in the senescent group while the collagen levels were increased.…”

Section: Discussionsupporting

confidence: 88%

Age-related cardiac muscle sarcopenia: Combining experimental and mathematical modeling to identify mechanisms

Lin

Lopez

Jin³

et al. 2008

Experimental Gerontology

101

109

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Age-related skeletal muscle sarcopenia has been extensively studied and smooth muscle sarcopenia has been recently described, but age-related cardiac sarcopenia has not been previously examined. Therefore, we evaluated adult (7.5±0.5 months; n=27) and senescent (31.8±0.4 months; n=26) C57BL/6J mice for cardiac sarcopenia using physiological, histological, and biochemical assessments. Mice do not develop hypertension, even into senescence, which allowed us to decouple vascular effects and monitor cardiac-dependent variables. We then developed a mathematical model to describe the relationship between age-related changes in cardiac muscle structure and function. Our results showed that, compared to adult mice, senescent mice demonstrated increased left ventricular (LV) end diastolic dimension, decreased wall thickness, and decreased ejection fraction, indicating dilation and reduced contractile performance. Myocyte numbers decreased, and interstitial fibrosis was punctate but doubled in the senescent mice, indicating reparative fibrosis. Electrocardiogram analysis showed that PR interval and QRS interval increased and R amplitude decreased in the senescent mice, indicating prolonged conduction times consistent with increased fibrosis. Intracellular lipid accumulation was accompanied by a decrease in glycogen stores in the senescent mice. Mathematical simulation indicated that changes in LV dimension, collagen deposition, wall stress, and wall stiffness precede LV dysfunction. We conclude that age-related cardiac sarcopenia occurs in mice and that LV remodeling due to increased end diastolic pressure could be an underlying mechanism for age-related LV dysfunction.

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“…These areas of interstitial fibrosis, predominantly in the subendocardium of the left ventricle, increase with age and may be related to the loss of myocyte volume as "replacement fibrosis." 22,24 Connective tissue content and collagen cross-linking also decreased with endurance training. 25,26 Furthermore, exercise appears to have an antiapoptotic effect on myocytes that likely enhances chamber distensibility because myocytes are less stiff than collagen.…”

Section: Physiologic Differences Between Ventricular Compliance and Rmentioning

confidence: 97%

The Effects of Aging and Physical Activity on Doppler Measures of Diastolic Function

Prasad

Popović

Arbab‐Zadeh

et al. 2007

The American Journal of Cardiology

152

157

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Healthy aging results in changes in Doppler measures of diastolic function. It is unclear whether these alterations are a specific manifestation of the aging process or reflect a cardiac adaptation to a more sedentary lifestyle. It was hypothesized that healthy, but sedentary, aging would result in slowing of diastolic filling and myocardial relaxation, whereas lifelong endurance training would prevent such changes. Doppler data were measured in young subjects and sedentary and fit seniors across a broad range of loading conditions. Thirteen sedentary healthy (70 ± 4 years) and 12 fit Masters athlete (68 ± 3 years) seniors were recruited. Twelve young healthy (32 ± 9 years) subjects were used for comparison. Pulmonary capillary wedge pressure and Doppler variables were measured at the 6 loading conditions of baseline (twice), -15 and -30 mm Hg lower body negative pressure, and 2 levels of saline solution infusion. Doppler variables consisted of early and late mitral inflow velocity (E/A) ratio, isovolumetric relaxation time (IVRT), tissue Doppler velocities (TDI E mean ), and propagation velocity of mitral inflow. Aging resulted in a decrease in E/A ratio (p <0.001), TDI E mean (p <0.001), and propagation velocity of mitral inflow (p <0.001) and an increase in IVRT (p = 0.001). Lifelong endurance training did not completely prevent the changes in E/A ratio (p = 0.212), IVRT (p = 0.546), or propagation velocity of mitral inflow (p = 1.00). Fit seniors were able to achieve E/A ratios of 1.0 during baseline and saline solution infusion. TDI E mean was higher in fit versus sedentary seniors at baseline (p = 0.012) and during maximal lower body negative pressure (p = 0.036), but not during saline solution infusion (p = 0.493). In conclusion, age-associated abnormalities in Doppler measures of myocardial filling and relaxation are only partially minimized by lifelong endurance training and therefore may be more specific to the aging process than secondary to years of deconditioning.Normal aging, even in the absence of co-morbidities, results in marked changes in Doppler measures of ventricular filling and relaxation, including reversal of the early and late mitral inflow velocities (decreased E/A ratio) and prolongation of isovolumetric relaxation time (IVRT). 1 These variables, although reproducible, have several limitations in their ability to accurately reflect diastolic function, including significant preload dependence and lack of specificity for dynamic relaxation processes. 2 In addition, it is unclear whether alterations in these Doppler variables with senescence are a specific manifestation of the aging process or reflect a secondary cardiac adaptation to a more sedentary lifestyle. Recently, our laboratory showed that static left ventricular stiffness markedly increased during healthy sedentary aging, whereas lifelong endurance training preserved static left ventricular compliance. 4 These data showed that ≥1 component of diastole, namely static chamber compliance, was significantly influenced by fit...

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Collagen accumulation in heart ventricles as a function of growth and aging

Cited by 149 publications

References 0 publications

Is Cardiac Hypertrophy in Spontaneously Hypertensive Rats the Cause or the Consequence of Oxidative Stress?

Is Cardiac Hypertrophy in Spontaneously Hypertensive Rats the Cause or the Consequence of Oxidative Stress?

Age-related cardiac muscle sarcopenia: Combining experimental and mathematical modeling to identify mechanisms

The Effects of Aging and Physical Activity on Doppler Measures of Diastolic Function

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