3/14/2023 0 Comments Linear association scatter plotThe purpose of this study was to sample left-ventricular PCr/ b ATP ratios derived from the healthy, male subjects serving as control groups in previous publications of our study group. End-diastolic and end–systolic volumes as well as longitudinal left ventricular function decrease with age, whereas myocardial mass and mass-to-volume index increase. Moreover, it is known that ageing is associated with reduction in early-to-atrial peak ratio probably caused by accumulation of collagen within the myocardium resulting in increased myocardial stiffness. Both mitochondrial and lysosomal damages are supposed to result in functional heart failure and death of cardiac myocytes. Furthermore, myocardial lysosomes also suffer from different alterations with increasing age leading to an impaired autopha- gocytosis of defective mitochondria due to an overload of heavy lipofuscine and decreased efficiency of lysosomal enzymes. First, decreased mitochondrial oxidative phosphorylation has been supposed to contribute to impaired cellular metabolism during ageing. At the present time, it is well known that mitochondrial function becomes impaired and declines with age. A recent study, however, supported our findings and reported also on a decrease in left-ventricular PCr/ATP ratios with age in 49 healthy subjects. The latter study group calculated absolute concentrations for PCr and c -ATP, demonstrating moderate decreases in both with age, but not in the ratio. detected reduced PCr and ATP concentrations in elderly but not reduced PCr/ATP ratios, whereby the number of subjects enrolled in each of both studies was relatively small. At this time, data on impact of ageing on myocardial PCr/ ATP ratios were controversial. We also detected a significant effect of age on cardiac high-energy metabolism, showing a decrease in left ventricular PCr/ATP ratio with age. Our study group has shown that cardiac high-energy metabolism correlates positively with exercise capacity and negatively with cardiovascular risk factors. Furthermore, several previous studies have shown that the cardiac PCr/ATP ratios are clearly reduced in patients suffering from hereditary disorders with mitochondrial involvement. Previous 31P MRS studies have shown that cardiac PCr/ATP ratios are significantly but unspecifically reduced in ischemic and structural heart diseases as well as in diabetes and other metabolic disorders. Mitochondrial insufficiency can be caused by defects in key mitochondrial enzymes, increased mitochondrial proton leak, impaired supply of reducing equivalents or insufficient mitochondrial PO2. Consequently, the PCr/ATP ratio reflects the creatine rephosphorylation rate and, therefore, the mitochondrial function in the myocardium. This metabolic homeostasis, also known as ‘‘stability paradox’’, is enabled by a complex cellular regulation of mitochondrial respiration, which has extensively reviewed by Saks et al. The myocardial HEP metabolism is characterized by a remarkable metabolic stability maintaining almost constant levels of PCr and ATP during increases of workload. The ratios between phosphocreatine (PCr) and adenosine-triphosphate (ATP) obtained by 31P MRS are mainly used as an important physiological index for cardiac energy metabolism. magnetic resonance spectroscopy (31P MRS) is a unique tool to investigate human myocardial high-energy phosphate (HEP) metabolism in vivo.
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