Cardiovascular aging and heart failure

Oxenham, Helen; Sharpe, Norman

doi:10.1016/s1388-9842(03)00011-4

Cited by 115 publications

(71 citation statements)

References 69 publications

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“…5 In addition to these cardiac changes, arterial distensibility decreases from childhood to adulthood, 6 a stiffening of the arterial tree that increases afterload even in normotensive individuals. 7 …”

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confidence: 99%

Maturational and Adaptive Modulation of Left Ventricular Torsional Biomechanics

et al. 2006

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Background-Left ventricular (LV) torsional deformation, based in part on the helical myocardial fiber architecture, is an important component of LV systolic and diastolic performance. However, there is no comprehensive study describing its normal development during childhood and adult life. Methods and Results-Forty-five normal subjects (25 children and 20 adults; aged 9 days to 49 years; divided into 5 groups: infants, children, adolescents, and young and middle-age adults) underwent assessment of LV torsion and untwisting rate by Doppler tissue imaging. LV torsion increased with age, primarily owing to augmentation in basal clockwise rotation during childhood and apical counterclockwise rotation during adulthood. Although LV torsion and untwisting overall showed age-related increases, when normalized by LV length, they showed higher values in infancy and middle age. The proportion of untwisting during isovolumic relaxation was lowest in infancy, increased during childhood, and leveled off thereafter, whereas peak untwisting performance (peak untwisting velocity normalized by peak LV torsion) showed a decrease during adulthood. Conclusions-We have shown the maturational process of LV torsion in normal subjects. Net LV torsion increases gradually from infancy to adulthood, but the determinants of this were different in the 2 age groups. The smaller LV isovolumic untwisting recoil during infancy and its decline in adulthood may suggest mechanisms for alterations in diastolic function.

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confidence: 99%

Maturational and Adaptive Modulation of Left Ventricular Torsional Biomechanics

et al. 2006

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“…heart; mitochondria THERE IS INCREASING EVIDENCE for an age-dependent decline of cardiac performance (45). Several studies show this performance decline to be associated with oxidative stress (42,43,57,58), i.e., elevated levels of reactive oxygen species.…”

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confidence: 99%

Proteomic identification of 3-nitrotyrosine-containing rat cardiac proteins: effects of biological aging

Kański¹,

Behring²,

Pelling³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

207

160

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Proteomic techniques were used to identify cardiac proteins from whole heart homogenate and heart mitochondria of Fisher 344/Brown Norway F1 rats, which suffer protein nitration as a consequence of biological aging. Soluble proteins from young (5 mo old) and old (26 mo old) animals were separated by one-and two-dimensional gel electrophoresis. One-and two-dimensional Western blots with an anti-nitrotyrosine antibody show an age-related increase in the immunoresponse of a few specific proteins, which were identified by nanoelectrospray ionization-tandem mass spectrometry (NSI-MS/MS). Complementary proteins were immunoprecipitated with an immobilized anti-nitrotyrosine antibody followed by NSI-MS/MS analysis. A total of 48 proteins were putatively identified. Among the identified proteins were ␣-enolase, ␣-aldolase, desmin, aconitate hydratase, methylmalonate semialdehyde dehydrogenase, 3-ketoacyl-CoA thiolase, acetyl-CoA acetyltransferase, GAPDH, malate dehydrogenase, creatine kinase, electron-transfer flavoprotein, manganese-superoxide dismutase, F1-ATPase, and the voltage-dependent anion channel. Some contaminating blood proteins including transferrin and fibrinogen ␤-chain precursor showed increased levels of nitration as well. MS/MS analysis located nitration at Y105 of the electron-transfer flavoprotein. Among the identified proteins, there are important enzymes responsible for energy production and metabolism as well as proteins involved in the structural integrity of the cells. Our results are consistent with agedependent increased oxidative stress and with free radical-dependent damage of proteins. Possibly the oxidative modifications of the identified proteins contribute to the age-dependent degeneration and functional decline of heart proteins.heart; mitochondria THERE IS INCREASING EVIDENCE for an age-dependent decline of cardiac performance (45). Several studies show this performance decline to be associated with oxidative stress (42, 43, 57, 58), i.e., elevated levels of reactive oxygen species. For example, various biomarkers of oxidative stress such as oxo-2-deoxyguanosine, H 2 O 2 , 3-nitrotyrosine (3-NT), N-⑀-methyllysine, malondialaldehyde, and advanced glycation end products (14,22,47,48,55,62) increase with the age in cardiac tissue. Moreover, dietary restriction significantly reduces the age-dependent accumulation of these oxidative markers in heart, which indicates the importance of oxidative stress in cardiac aging (46).A causal role of reactive oxygen species in the age-dependent decline of cardiac dysfunction can, however, only be defined if biological targets of these species are identified and the physiological impact of biomolecular modification is characterized. A first step to establish molecular mechanisms of age-dependent cardiac dysfunction is the proteomic identification of oxidatively modified proteins. Various studies have indicated the formation of reactive nitrogen species in acute myocardiac disorders such as heart failure (1, 28, 31). These reactive nitrogen species are met...

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“…The functional capacity is associated with age and begins to decline after age 30, with a more exponential decrease in cardiorespiratory fitness and muscle strength after the age of 50 in apparently healthy individuals [20,21]. This represents a decline in peak VO 2 on average of 8% to 10% per decade [10][11][12]. Hence, age itself is an independent predictor for peak VO 2 .…”

Section: Discussionmentioning

confidence: 99%

“…Nevertheless, a progressive decline in cardiovascular system occurs with advancing age [10]. Age itself is an independent morbidity and mortality risk factor for a long list of diseases, hospitalization and length of hospitalization [11].…”

Section: Introductionmentioning

confidence: 99%

“…A few studies demonstrated that longitudinal rate of declining in peak VO 2 is on average 8% to 10% per decade in the general population and, at the age of 60, it is approximately two-thirds of that at 20 [10,14]. Recently it has been reported that peak VO 2 decreases with age in HF patients, however, these reports came from studies with patients classified as young, middle-aged and older, and the peak VO 2 was assessed using either a treadmill or cycle ergometer CPX [15,16].…”

Section: Introductionmentioning

confidence: 99%

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